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Walking: Still the Starting Line for Fitness

Published: September 06, 2018

Source:https://www.cancercompass.com/cancer-news/article/62674.htm

(HealthDay News) -- Being physically active is one of the most important steps people of all ages can take to improve their health.

Yet despite everything we know about the benefits of exercise, only half of U.S. adults and only about a quarter of high school students get the amount recommended in national guidelines.

If you haven't gotten onboard with the program, it's easy to start -- and walking is a perfect path to fitness. That's because it doesn't require any special skills or expensive equipment -- just a good pair of shoes.

Walking not only gets you aerobically fit, it can help with problems such as insomnia, diabetes and even a depressed mood. Walking also has a lower risk of injury than high-impact activities like running. And you can walk year-round, indoors or out.

Start at your own speed and walk in short increments, say for five minutes three times a day. Then gradually increase both length and intensity over time as you develop stamina.

Depending on where you live, however, you may not be able to just walk out of your front door and go. More than 30 percent of people 16 or older live in neighborhoods without sidewalks. The U.S. Surgeon General has called on communities to make walking more accessible to residents. Until then, ironically, you may have to drive to take a walk at a park or on a school track, for instance.

Keep in mind that you can walk at your convenience if you have a home treadmill. These machines aren't just for running, plus they can also keep track of miles logged and calories burned, and many can be set to increase the difficulty of your workouts.


Over 1.4 Billion of World's Adults Face Disease Because of Inactivity, WHO Says

Published: September 05, 2018

Source:https://www.cancercompass.com/cancer-news/article/62667.htm

(HealthDay News) -- Couch potatoes, take note: Sedentary living has put more than one quarter of the world's adults at risk for serious disease, a new study says.

More than 1.4 billion adults face a higher risk for heart disease, diabetes, dementia and certain types of cancer because they get too little physical activity, World Health Organization (WHO) researchers concluded.

The researchers analyzed findings from hundreds of surveys that included 1.9 million adults, 18 and older, in 168 countries.

In 2016, nearly one-third of women and one-quarter of men worldwide did not get the recommended levels of physical activity to stay healthy, the researchers found. Weekly guidelines call for at least 150 minutes of moderate-intensity physical activity or 75 minutes of vigorous-intensity physical activity.

The study was published Sept. 4 in The Lancet Global Health.

"Unlike other major global health risks, levels of insufficient physical activity are not falling worldwide, on average, and over a quarter of all adults are not reaching the recommended levels of physical activity for good health," lead author Regina Guthold said in a journal news release.

Women were less active than men in all regions of the world except in East and Southeast Asia.

Of particular concern were increases in already low levels of physical activity for men and women. Insufficient physical activity rose 5 percent in high-income countries, and increased just 0.2 percent in low-income countries.

The transition toward more sedentary occupations and motorized transportation in richer countries could help explain the higher levels of inactivity, researchers said.

It's important that governments provide infrastructure that promotes more walking and bicycling to work and active sports and recreation, they noted.

Eliminating inequalities in physical activity levels between men and women will be critical to achieving global activity targets, study co-author Fiona Bull said. And this will require efforts "to promote and improve women's access to opportunities that are safe, affordable and culturally acceptable," she noted.

Melody Ding, a researcher from the University of Sydney in Australia, authored an accompanying journal editorial. In it, she said in certain parts of the world women face more environmental, social and cultural barriers to participate in physical activity.

Those restrictions likely contribute to overall low activity levels. In restrictive Saudi Arabia and Iraq, for instance, more than half of all adults were insufficiently active, the study found.

Comparatively, around 40 percent of U.S. adults and 36 percent of British adults got too little activity.

Also, "although high-income countries have a higher prevalence of insufficient physical activity, it is important to note that low- and middle-income countries still bear the larger share of the global disease burden of physical inactivity," Ding wrote.


Working Workouts Into Your Life

Published: September 04, 2018

Source:https://www.cancercompass.com/cancer-news/article/62649.htm

(HealthDay News) -- Weekly fitness guidelines can seem like a laundry list of to-do's that you just can't get done -- 30 minutes of cardio at least five days, resistance training two or three days, and at least two flexibility sessions … each and every week.

Yet each type of exercise does the body good, so it's important to find ways to meet these goals.

First, recognize that an exercise program will mean changes to your daily routine, and you'll likely need to cut out other, less important activities. Aim for a gradual transition and look for non-essential pastimes to replace, like watching TV and web surfing.

Next, draw up a realistic schedule that works with your lifestyle and, for a better chance of sticking to it, write it down. Realize that, if you have a family that expects you home at 6 p.m. for dinner, hitting the gym after work won't work for you. Instead block out 30 minutes after the kids go to bed or get up 30 minutes early and get in a workout while the house is still quiet. And you might double up on workouts on those days you do get to the gym by taking both cardio and flexibility classes.

Make exercise convenient. Maybe the gym near your home makes more sense than the one near your office. If you spend a lot of time just hanging out when your kids are at soccer or lacrosse practice, look for a nearby nature trail or track and spend your waiting time moving instead.

If you'll be working out at home, create a designated exercise space and outfit it with essentials, like a mat, free weights and DVDs you can pop into a laptop.

And don't forget to plan weekend family outings that involve walking or other exercise -- no one said you can't have fun and togetherness while getting fit.


What Every Woman Needs to Know About Ovarian Cancer

Published: September 02, 2018

Source:https://www.cancercompass.com/cancer-news/article/62641.htm

(HealthDay News) -- Women need to know the symptoms of ovarian cancer and see a doctor if they have them, an ob-gyn expert says.

Ovarian cancer is the fifth-leading cause of death in American women, claiming more lives than any other cancer of the female reproductive system, according to the American Cancer Society.

About 22,240 women in the United States will be diagnosed with the disease in 2018, and over 14,000 will die from it, according to the U.S. National Cancer Institute.

September is Ovarian Cancer Awareness Month.

"Any woman who experiences unexplained bloating, an upset stomach, an urgency to urinate or abdominal pain for a few weeks, should go see a doctor, and if her doctor does not take these symptoms seriously, she should see another doctor," said Dr. Stephanie Blank. She is director of gynecologic oncology for the Mount Sinai Health System in New York City.

Other symptoms include pelvic pain, fatigue, unexplained weight change, and abnormal bleeding or any bleeding after menopause.

"Too often, women are sent to the wrong doctor, or [are] told they're just aging or gaining weight when experiencing these kinds of symptoms, and by then they have lost valuable time," Blank said in a Mount Sinai news release.

Women who are diagnosed with ovarian cancer before it has spread have a five-year survival of 93 percent, researchers have found. But detection of ovarian cancer is difficult and often delayed.

Women with BRCA1 and BRCA2 gene mutations are at increased risk for ovarian cancer, and the risk for all women increases with age. Half of all ovarian cancers are diagnosed in women who are 63 and older.

 

Long-term use of birth control pills reduces the risk of ovarian cancer by about 50 percent, according to the news release. Removing fallopian tubes and ovaries is the best means of ovarian cancer prevention, but is not appropriate for all women.


Common household products contain flame retardant chemicals that cause thyroid cancer

Published: August 26, 2018

Source:https://www.naturalnews.com/2018-08-26-common-household-products-contain-flame-retardant-chemicals.html

(Natural News) If you value your thyroid gland, you should cut back on your use of all kinds of household products. An article in Natural Health 365 stated that these products contain flame retardant chemicals that can increase your risk of developing papillary thyroid cancer.

The thyroid gland handles the production of thyroid hormones that regulate the metabolism of the body. Like all parts of the body, its tissues can develop carcinoma when exposed to various toxic substances. Thyroid cancer, in particular, has the fastest rising rates among all types of cancer. The most common form of this disease is papillary thyroid cancer.

Experts theorize that environmental factors are partly responsible for the increasing frequency of thyroid cancers. Flame retardant chemicals are one of their primary suspects. Companies have been adding increasing amounts of these chemicals to the consumer products they manufacture. Their intended reason is to reduce the flammability of the items in question, which are often fire hazards. However, in their attempt to improve the safety of their household products, the companies inadvertently endangered the health of consumers by using chemicals that affect the thyroid.

Is there a connection between increasing thyroid cases and flame retardants?

Researchers from Duke University took samples of house dust from the homes of 140 participants. The latter were all required to have occupied their home for 11 years so that the researchers could study their long-term consequence in much better shape. The participants were also evenly split between thyroid cancer patients and healthy people.

The researchers evaluated the level of flame retardant in the house dust samples. Then they compared that with the rates of thyroid cancer at the time.

They also matched up the participants according to the latter’s age, body mass index, ethnicity, and sex. They also included education level, household income, and level of education.

In their paper, the Duke researchers discovered that the risk of papillary thyroid cancerincreased alongside the exposure level to flame retardants. The same held true regarding the severity of the disease.

Based on their findings, the research team believed there is a link between increasing levels of flame retardants and the recent rise in thyroid cancer incidences.

Earlier studies warned that certain flame retardants interfere with the endocrine system. The thyroid gland is part of this vital system.

Toxic flame retardants can disrupt the thyroid gland’s normal functions

The flame retardants are similar to thyroid hormones. When these endocrine disruptors are absorbed by accident, they affect the function and balance of the organ.

Polybrominated diphenyl ethers (PBDE) comprise a class of such fire retardants that impair the endocrine system. Two, in particular, are very closely linked with thyroid cancer: tris(2-chloroethyl) phosphate (TCEP) is used in chairs, couches, nursing pillows, and strollers, while decabromodiphenyl ether (BDE209) is found in carpet backings, furniture cushions, mattresses, and upholstery textiles.

High levels of BDE-209 levels in household dust was linked with much higher chances of thyroid cancer.

The Duke researchers checked this connection by sampling blood from the participants and examining the sample for key biomarkers of PBDE and BDE209 flame retardants. They found that participants who lived in houses with high amounts of TCEP were more than 400 percent more likely to have thyroid cancer.

Meanwhile, participants with the highest concentration of BDE209 are 14 times more vulnerable to thyroid cancer. Even if they did not have the BRAF V600E gene mutation, they still experience a much higher chance of developing papillary thyroid cancer. Women are also much more prone to getting this kind of aggressive cancer.


Study Explores New Way to Stop Cancer's Spread

Published: August 22, 2018

Source:https://www.cancercompass.com/cancer-news/article/62535.htm

(HealthDay News) -- Scientists say they're researching a way to destroy cancer cells that travel to other parts of the body.

Many cancers become especially dangerous only when they spread (metastasize) from the initial location to other tissues such as the lungs, brain or bone, the University of Colorado Cancer Center researchers explained.

The investigators found that when a crucial part of cellular recycling is turned off in metastatic cancer cells, they can't survive the stresses of traveling through the body.

"Highly metastatic cells leave their happy home and have all these stresses on them. One way that the cell is able to deal with stresses is through disposing of cellular wastes or damaged cell components and recycling them," study co-author Michael Morgan said in a university news release.

"When we turn off the activity of cellular structures called lysosomes, which a cell uses to do this recycling, the metastatic cells become unable to survive these stresses," Morgan explained.

Morgan was an assistant research professor at CU Cancer Center during the study. He is now assistant professor of biology at Northeastern State University in Oklahoma.


HPV Test May Replace Pap for Some Women, New Guidelines Say

Published: August 21, 2018

Source:https://www.cancercompass.com/cancer-news/article/62524.htm

(HealthDay News) -- The Pap smear has long been the gold standard for cervical cancer screening, but an expert panel now says the HPV (human papillomavirus) test is also an option for women over 30.

These women now have three choices under new recommendations issued by the U.S. Preventive Services Task Force (USPSTF):

  • A Pap test screening every three years.
  • An HPV test alone every five years -- HPV is a virus known to cause cervical cancer.
  • Both tests every five years.

The task force also recommended a Pap test alone every three years for women between the ages of 21 and 29.

"It's very important for all women to get screened for cervical cancer. Screening can reduce deaths from cervical cancer," said Dr. Douglas Owens, vice chair of the USPSTF.

"There are three good options for screening for cervical cancer in women 30 to 65. Our recommendation is that women have a conversation with their clinician about which option is best for them," Owens added.

A Pap test looks for changes in cells from the cervix that indicate cancer or precancerous changes, according to the U.S. Office on Women's Health. The HPV test looks for evidence of the virus in cells, but not for cancerous changes, according to the American Cancer Society (ACS).

Almost all cases of cervical cancer are caused by high-risk HPV infections, according to background information in the recommendations. Both tests use samples collected from a woman's cervix. A woman won't be able to tell a difference in the tests, the ACS said.

The task force didn't recommend HPV testing or co-testing for younger women.

Debbie Saslow, senior director of HPV-related and women's cancers for the ACS, explained why it's not a good idea to test for HPV in women under 30. "Almost everybody gets HPV, but more than 99 percent of the time, HPV goes away on its own. If you test for HPV in younger women [before the infection has a chance to clear on its own], it would be unnecessarily alarming," she said.

Dr. George Sawaya, author of an editorial accompanying the new recommendations, agreed.

"HPV testing sooner [than age 30] will lead to more 'false alarms,'" he said. "In other words, some women will have invasive diagnostic procedures and be found to have no cervical problem." Sawaya is a professor of obstetrics and gynecology at the University of California, San Francisco.

The task force also made recommendations about who doesn't need cervical cancer screening. This included women under 21, women who've had a hysterectomy that included removal of the cervix, women aged 65 and older who have had adequate screening in the past and aren't at a high risk of HPV.

Saslow said the most important message women need to take away from the new recommendations is simple: get screened.

"Most cervical cancer is in women who don't ever get screened or who get screened rarely. Whatever test is available to you, get screened. If you have a choice, and you're over 30, ask for an HPV test," she suggested.

Sawaya concurred. "Regardless of the method used for screening, the most important thing for women is to have easy access to affordable screening," he said.

Saslow also pointed out that young people should be sure to get the HPV vaccine if they didn't get it in their pre-teen years. Men and women can get the HPV vaccine up until age 26, though younger is better, she added.


Insight into development of lung cancer

Published: August 18, 2018

Source:https://www.sciencedaily.com/releases/2018/08/180818115627.htm

Lung cancer is the leading cause of preventable cancer death. A disease of complex origin, lung cancer is usually considered to result from effects of smoking and from multiple genetic variants. One of these genetic components, a chromosome named 15q25.1, has been previously identified as a leading influencer of susceptibility to lung cancer, smoking behavior, and nicotine addiction. However, no previous study has investigated the mechanisms of this lead agent, or documented the susceptibility pathways that allow this chromosome to modify development of disease.

A research team led by Xuemie Ji, MD, PhD, Research Associate in Department of Biomedical Data Science at Dartmouth's Geisel School of Medicine, helped solve this central problem. The team identified two main pathways involving the mechanism by which the chromosome 15q25.1 locus influences lung cancer risk. The first pathway is an interaction pathway in the nervous system that is implicated in nicotine dependence. The other pathway can control key components in many biological processes, such as transport of nutrients and ions, and the human immune system.

The results have been newly published in Nature Communications. "Our findings in pathways uncover insights into the mechanism of lung cancer etiology and development, which will potentially shorten the interval between increasing biological knowledge and translation to patient care," says Ji. "Blocking genes downstream or in parallel pathways might provide a strategy to treat such cancer."

The study used two independent cohorts of 42,901 individuals with a genome-wide set of genetic variants, as well as an expression dataset with lung tissue from 409 lung cancer patients to validate findings. Two different methods were used to analyze data, and confirm that the findings are reliable and can be repeated with different methods. "To our knowledge, this is the first study to explore the pathogenic pathways related to the mechanisms of chromosome 15q25.1 and the first to use a novel analysis approach to analyze data and to validate the findings," says Ji. "The ability to block the damaging genetic variants downstream or in parallel pathways might improve lung cancer prognosis and survival, and therefore provide alternative strategies to treat such cancer."

The team is working to identify more mechanisms contributing to the increased risk of lung cancer. They aim to provide more explanation for the large unexplainable division of lung cancer occurrences.


Survive colon cancer by eating more Omega-3s, says new study

Published: August 17, 2018

Source:https://www.naturalnews.com/2018-08-17-survive-colon-cancer-by-eating-more-omega-3s-says-new-study.html

(Natural News) An observational study has concluded that increasing your intake of omega-3s found in oily fish can reduce your risk of dying from colon cancer by 70 percent. These findings, published in the medical journal Gut, suggest that colon cancer and other related conditions can be managed with proper diet, among other things.

Dr. Jules Garbus, a colorectal surgeon at Winthrop University Hospital in Mineola, N.Y. said in an article on Health.com, “We have long suspected the health benefits of omega-3 fatty acid supplementation. This study begins to show a correlation between ‘healthy living’ and reducing death from colorectal cancer.”

The study was led by Dr. Andrew Chan, of Massachusetts General Hospital in Boston. Dr. Chan and his team tracked data from 1,659 people diagnosed with colon cancer over a period of 10 years. The researchers found that out of 561 patients who died over the course of their study, 169 deaths were due to associated conditions caused by colon cancer, 153 deaths were from heart disease, and 113 deaths were from other types of cancer. The other cases were attributed to other factors. However, what was more noteworthy was the observation that patients who consumed at least 0.3 grams of omega-3 fatty acids from oily fish daily after their cancer diagnosis had a 41 percent reduction of dying from the disease, compared with those who consumed less than 0.1 gram per day. Dr. Chan found that the reduction of risk was associated with omega-3s coming from both food and fish oil supplements, although only a few of the patients they tracked used supplements.

Furthermore, the study noted that increasing omega-3 fatty acid intake by at least 0.15 grams a day after a colon cancer diagnosis reduced the risk of dying from the disease by 70 percent. A reduction of daily intake was also linked to a 10 percent higher risk of death from the disease. Those who increased their intake of omega-3s also had a 13 percent lowered risk of dying from other causes compared to a 21 percent increased risk who decreased their intake.

Despite these praise-worthy results, other cancer experts remain unconvinced. Dr. Arun Swaminath, who directs the inflammatory bowel disease program at Lenox Hill Hospital in New York City has cautioned that more research is necessary to validate these results. This study, he said, took data on intake of omega-3s from “food frequency questionnaires,” which “have significant weaknesses to the point that some have questioned whether they should be abandoned altogether.” Moreover, Dr. Swaminath recalled previous studies that claimed fish oil to be good for heart health until subsequent, more rigorous research “punctured the idea that fish oil was good medicine….it’s not clear if [Chan’s study] falls into the same trap as previous studies that found similar associations, but didn’t stand up to rigorous scrutiny.”

That being said, Dr. Swaminath added that should “this association… turn out to be true, then it will be great for patients, and I see little downside [other than out-of-pocket costs] to adopting this strategy.”

Omega-3 fatty acids provide many health benefits

Even excluding for caution and thinly-veiled disbelief, there are several benefits to increasing your intake of omega-3s. An article on AuthorityNutrition.com lists some health benefits to take note of:

The blues brothers no more — Omega-3s have been studied to alleviate the symptoms of depression and anxiety. Depressed patients who regularly consumed omega-3 supplements were found to be less depressed after a few weeks.

“Eye” can see you — Omega-3s have also been studied to improve eye health. Those who consumed ample amounts of omega-3s every day had a significantly reduced risk of macular degeneration, studies have concluded.

Baby, one more time — Researchers have noted that omega-3s are crucial to the brain and development of infants.

These are just a few benefits omega-3s have been proven to give. Whatever their relationship is with colon cancer, it wouldn’t hurt to add oily fish in your diet today.


Childhood exposure to secondhand smoke may increase risk of adult lung disease death

Published: August 16, 2018

Source: https://www.sciencedaily.com/releases/2018/08/180816081452.htm

A new study suggests that long-term exposure to secondhand smoke during childhood increases the risk of chronic obstructive pulmonary disease (COPD) death in adulthood. The study also suggests secondhand smoke exposure as an adult increases the risk of death not only from COPD but also several other conditions.

Secondhand smoke is known to have adverse effects on the lung and vascular systems in both children and adults. But it is unknown whether childhood exposure to secondhand smoke is associated with mortality in adulthood. To explore the issue, American Cancer Society epidemiologists led by W. Ryan Diver, MSPH, examined associations of childhood and adult secondhand smoke exposure with death from all causes, ischemic heart disease, stroke, and chronic obstructive pulmonary disease among 70,900 never-smoking men and women from the Cancer Prevention Study II Nutrition Cohort. Study participants, primarily ages 50 to 74 at the beginning of the study, answered questions about their secondhand smoke exposure during childhood and as adults and were followed for 22 years.

Those who reported having lived with a daily smoker throughout their childhood had 31% higher mortality from chronic obstructive pulmonary disease compared to those who did not live with a smoker. In a calculation done for this release, Diver says the increase in COPD mortality corresponds to about 7 additional deaths per year per 100,000 never-smoking study participants. Although the study counted only deaths, the increase in fatal COPD implies that living with a smoker during childhood could also increase risk of non-fatal COPD.

In addition, secondhand smoke exposure (10 or more hours/week) as an adult was associated with a 9% higher risk of all-cause mortality, a 27% higher risk of death from ischemic heart disease, a 23% higher risk of death from stroke, and a 42% higher risk of death from COPD.

"This is the first study to identify an association between childhood exposure to secondhand smoke and death from chronic obstructive pulmonary disease in middle age and beyond," said Diver. "The results also suggest that adult secondhand smoke exposure increases the risk of chronic obstructive pulmonary disease death. Overall, our findings provide further evidence for reducing secondhand smoke exposure throughout life."


Rare cancer could be caught early using simple blood tests

Published: August 14, 2018

Source:https://www.sciencedaily.com/releases/2018/08/180814101412.htm

A pioneering study into myeloma, a rare cancer, could lead to GPs using simple blood tests to improve early diagnosis.

The study investigated the best combination of blood tests that could be used to diagnose myeloma in GP practices.

The research was a collaboration between the University of Oxford, the University of Exeter and Chiddenbrook Surgery, Crediton, funded by the National Institute for Health Research (NIHR) and is published in the British Journal of General Practice.

Researchers investigated how useful a number of different measures were for indicating the presence of the disease, and suggested what combinations of these tests were sufficient to rule out the disease, and to diagnose it, saving the patient from the worry of specialist referral.

Blood tests of 2703 cases taken up to five years prior to diagnosis were analysed and compared with those of 12,157 patients without the cancer, matching cases with control patients of similar age amongst other relevant parameters.

They demonstrated that a simple combination of two blood parameters could be enough to diagnose patients. Such blood tests are routinely conducted in GP surgeries.

Constantinos Koshiaris, lead author of the study, from Oxford University, said: "The combination of levels of haemoglobin, the oxygen carrier in the blood, and one of two inflammatory markers (erythrocyte sedimentation rate or plasma viscosity) are a sufficient test rule out myeloma. If abnormalities are detected in this test, it should lead to urgent urine protein tests which can help speed up diagnosis."

Each year approximately 5,700 people are diagnosed with myeloma in the UK alone. It can lead to symptoms such as bone pain, fatigue and kidney failure. It has the longest diagnosis process of all common cancers, and a large number of patients are diagnosed after emergency care, over a third of which having had at least three primary care consultations.

Professor Willie Hamilton, of the University of Exeter Medical School, is principal investigator on the study. He said "Ordinarily a GP will see a patient with myeloma every five years -- and early diagnosis matters. More timely treatment could significantly improve survival rates for this disease. We report a simple way a GP can check patients presenting symptoms such as back, rib and chest pain, or recurrent chest infections, and determine whether they have myeloma or not."

The authors also suggest the possibility of integrating a system in the electronic health record to alert clinicians to relevant symptoms or changes in blood parameters related to myeloma.


Obesity and breast cancer: Scientists explain how being overweight makes breast cancer cells more aggressive

Published: August 13, 2018

Source:https://www.naturalnews.com/2018-08-13-scientists-explain-how-being-overweight-makes-breast-cancer-cells-more-aggressive.html

(Natural News) Researchers from Helmholtz Zentrum München, Technische Universität München (TUM), and Heidelberg University Hospital carried out a study on how extra weight makes breast cancer cells more aggressive. Using human tissue from breast cancer metastases, the researchers found that the enzyme known as ACC1 (acetyl-CoA-carboxylase 1) — a key component of fatty acid synthesis — is inhibited by high levels of cytokines. They found that obesity causes the release of cytokines into the bloodstream that affect the metabolism of breast cancer cells, which in turn make them more aggressive.

“ACC1 is a key component of fatty acid synthesis,” said Mauricio Berrel Diaz of Helmholtz Zentrum München and one of the leaders of the study. “However, its function is impaired by the cytokines leptin and TGF-?.”

Extremely overweight subjects have been found to have increased levels of cytokines in the blood. The researchers discovered that when ACC1 is inhibited, it results to the accumulation of the fatty acid precursor acetyl-CoA, which is passed on to particular gene “switches” that in turn stimulate the metastatic capacity of cancer cells through switching on a certain gene program.

In an experimental model, the researchers blocked the yet unknown signaling pathway with an antibody that is directed against the leptin receptor. This resulted to a significantly lowered metastatic spread of breast cancer cells.

The researchers aim to prove the data on the recently discovered mechanism in future studies. Moreover, they are taking into consideration the related intervention points that could potentially be used for treating breast cancer.

“Blocking the signaling pathways and switching off the metastasis-related genes could be a therapeutic target,” explained Stephan Herzig of TUM and co-leader of the study. “As part of the so-called neoadjuvant therapy, the risk of metastases or the recurrence of tumors could be reduced prior to the surgical removal of the tumor.”

The findings of the study was published in the journal Cell Metabolism.

How body weight influences the risk of breast cancer

Being overweight or obese can result to health consequences. According to the Centers for Disease Control and Prevention (CDC), more than one-third or 36.5 percent of adults in the U.S. are obese. This makes them more vulnerable to serious health conditions, such as diabetes, cardiovascular disease, and some types of cancer. Women who became overweight or obese after menopause are more prone to having breast cancer.

According to an article by the American Cancer Society, before menopause, the ovaries produce most of the estrogen in the body, while fat tissue only produces a small amount. But after menopause, the ovaries stop producing estrogen, so most of a woman’s estrogen comes from fat tissue. Therefore, having more fat tissue after menopause can increase estrogen levels and raise the risk of developing breast cancer. Furthermore, women who are overweight or obese are more likely to have higher blood sugar levels, which have been associated to some types of cancer such as breast cancer.

Although this link is complicated, studies indicate that the increased risk seems to be on women who gained weight during their adulthood and not on those who have been overweight since childhood. In addition, having excess fat around the waist may increase the risk more compared to having excess fat in the hips and thighs.

In another entry by the American Cancer Society, it was written that breast cancer is the most common type of cancer in American women, except for skin cancers. A woman in the U.S. have one out of eight chance of developing breast cancer sometime in her life. Moreover, around 252,710 new cases of invasive breast cancer will be diagnosed in women and approximately 40,610 women will die from this cancer.


Do your moles put you at risk of melanoma? Find out through ABCDE

Published: August 12, 2018

Source:https://www.naturalnews.com/2018-08-12-do-your-moles-put-you-at-risk-of-melanoma.html

(Natural News) Moles are a common sight on a person’s body. These dark-colored clusters of pigmented cells usually appear during childhood, but can fade or disappear with age. While most are harmless, some moles may become deadly over time. Moles can be a risk factor for melanoma, a type of skin cancer. Melanoma may sound scary but it’s actually one of the most treatable cancers and, if caught early, can be taken out in its entirety by simply removing the mole. Dermatologists have listed five warning signs to watch out for; so if you want to know if your mole is cancerous, just remember ABCDE:

  • Asymmetry — Draw a line through the middle of a benign mole, and the two halves will match. If you do the same to another mole and the two sides aren’t equal, then it’s an asymmetrical mole. An irregularly-shaped mole is one that puts you at a higher risk of melanoma.
  • Borders — A regular mole has smooth and even borders. On the other hand, an early melanoma tends to have ragged and uneven edges, with some cases displaying notched or scalloped edges.
  • Color Change — Exposure to sunlight can make moles darker, but the sun won’t make a single mole a multi-colored one. A variety of distinct colors in one mole is a warning signal that your mole could be cancerous. The colors to keep an eye on are different shades of black, tan, or brown. According to SkinCancer.org, a melanoma could even become white, red, or blue.
  • Diameter — If you notice one mole that’s slowly grown larger over time, you need to have it checked. While most moles will be no larger than a pencil eraser (at one-fourth of an inch or six mm), the malignant ones usually become much bigger in diameter.
  • Elevation or Evolution — Depending on which dermatologist you speak to, “E” could be either “Elevation” or “Evolution”. Dermatologists that use “Elevation” will advise you to watch out for moles with a raised surface, while dermatologists that prefer “evolution” will warn against moles that have displayed any changes in color, shape, or even bleeding.

Despite how easy it is to spot a cancerous mole, some people wouldn’t even bother. Dr. David Fischer, Director of the Melanoma Program at Massachusetts General Hospital, told the DailyMail.co.uk that these same people might even be too scared to check. “It’s one of those fear and denial-type things. People would rather not know than find out something scary or devastating,” Fisher said before adding: “But the thing is, six out of seven melanoma cases are cured just by catching it early and removing it. In other words, early detection could be life-saving. That statistic should help motivate people to be really proactive, to realize that there’s a benefit to this.”

Aside from moles, there are other factors that put you at risk of melanoma. If you’re predisposed to developing moles or birthmarks, have a family history of melanoma, frequently use tanning beds, or are under direct sunlight a lot, then you might just have a higher chance than most people.

Don’t fret, however. As was mentioned earlier, melanoma is treatable if the warning signs are spotted at an early stage. In the words of Fraser: “Not every cancer has that type of opportunity to catch it so early. This type of cancer does.”


Tomatoes are your best bet to prevent stomach cancer

Published: August 09, 2018

Source:https://www.naturalnews.com/2018-08-09-tomatoes-are-your-best-bet-to-prevent-stomach-cancer.html

(Natural News) Eating tomatoes may not only be good for your skin, but it may also help you prevent stomach cancer. According to a study published in the Journal of Cellular Physiology, tomato extracts can inhibit the growth of stomach cancer cells, which may be potentially useful in supporting conventional treatments.

Stomach cancer is one of the most common types of cancer worldwide. It is more likely to occur in smokers, particularly men, and people over the age of 55. It also commonly affects people who are overweight or obese and those that have poor eating habits, such as consuming smoked and salted food, and a diet low in fiber.

The disease has also been linked to Helicobacter pylori infection, as well as genetic causes.

The researchers at the Sbarro Institute for Molecular Medicine at Temple University in Philadelphia opined that the anti-tumor properties of tomatoes were not related to “specific components” such as lycopene, but that the tomatoes “should be considered in their entirety,” said Daniela Barone, a researcher at the Oncology Research Center of Mercogliano (CROM), and one of the study authors.

After analyzing whole tomato lipophilic extracts, the scientists found that two Southern Italy cultivars, San Marzano and Corbarino, were able to inhibit the development, growth, and proliferation of cancer cells. The tomato extracts also induced apoptosis or cell death in malignant cells.

The findings also showed that treatment with the whole tomato extracts affected key processes within the cells which hindered their migration ability. This prevented the cells from moving around and spreading throughout the body.

 “Our results prompt further assessment of the potential use of specific nutrients not only in the cancer prevention setting but also as a supportive strategy along with conventional therapies,” said Professor Antonio Giordano, Director of the Sbarro Institute for Molecular Medicine, Temple University and Professor of Pathology and Oncology at the University of Siena in Italy.

The researchers believe that the study findings could give way to further research using different tomato varieties, analyzing them for different health benefits, and potentially applying the information in treatment and prevention methods for stomach cancer.

In the same vein, a study published in the Journal of Cellular Physiology revealed that regular consumption of tomatoes could reduce the development of skin cancer tumors.

Researchers found that mice that were fed a diet of tomato powder daily for 35 weeks had a 50 percent decrease in skin cancer tumors after exposure to UV (ultraviolet) light, compared to those which did not receive the tomato treatment.

Tomatoes are a staple in the Mediterranean diet

The future of stomach cancer treatments using tomatoes looks promising enough, but eating tomatoes, in general, promote better health and overall quality of life, thanks to their phytochemical content, which includes antioxidants, carotenoids, dietary fiber, and various vitamins and minerals. Tomatoes are also known to decrease the risk of cardiovascular diseases such as heart attack and stroke.

Tomatoes have been used as an ingredient in numerous kinds of foods, including pasta dishes, ketchup, and pizzas.

One particular type of diet highlights tomatoes as one of its staple ingredients. The Mediterranean diet has become regarded as highly beneficial to overall health and weight management. It has also been associated with a reduced risk of cancer and many other chronic conditions.


New Treatment for Non-Hodgkin Lymphoma Approved

Published: August 08, 2018

Source:https://www.cancercompass.com/cancer-news/article/62380.htm

(HealthDay News) -- Poteligeo (mogamulizumab) injection has been approved by the U.S. Food and Drug Administration to treat adults with two types of non-Hodgkin lymphoma.

The drug was approved to treat relapsed or refractory mycosis fungoides (MF) and Sézary syndrome (SS) after the patient has had at least one prior therapy delivered through the bloodstream.

"Mycosis fungoides and Sézary syndrome are rare, hard-to-treat types of non-Hodgkin lymphoma and this approval fills an unmet medical need for these patients," Dr. Richard Pazdur, director of the FDA's Oncology Center of Excellence, said in an agency news release.

Non-Hodgkin lymphoma is a cancer that starts in immune-boosting white blood cells called lymphocytes. When these cells become cancerous, the skin develops itchy rashes and lesions that may spread beyond the original site.

Poteligeo's approval was based on clinical studies involving 372 people with relapsed MF or SS, who were given either Poteligeo or a chemotherapy drug called vorinostat. Progression-free survival averaged 7.6 months for those who took Poteligeo, versus 3.1 months among those who took vorinostat, the agency said Wednesday.

Poteligeo's most common side effects included rash, injection-site reactions, fatigue, diarrhea, bone/muscle pain and respiratory tract infections. More serious side effects could include toxic skin reactions, autoimmune reactions and infections, the FDA said.

The drug is produced by the Japanese drugmaker Kyowa Kirin Inc.


Heart Monitoring a Must for Breast Cancer Patients on Herceptin

Published: August 07, 2018

Source:https://www.cancercompass.com/cancer-news/article/62352.htm

(HealthDay News) -- The widely used chemotherapy drug trastuzumab (Herceptin) can be life-saving for women with HER2-positive breast cancer, a particularly aggressive form of the disease.

But new research now adds to mounting evidence that the treatment can take a toll on the heart, increasing the risk for heart failure.

The complication is uncommon, and in many cases, the benefits of the chemotherapy still outweigh the risks. But the study authors stressed that regular heart monitoring of these high-risk patients, including younger women, should be a priority during treatment.

"This is an important finding, as to the best of our knowledge this is the first study to calculate the rates of cardiotoxicity in younger women using insurance claim data," said the study's lead author, Mariana Henry. She's a graduate student at the Yale School of Public Health.

The study used diagnoses and insurance billing codes for nearly 16,500 women with non-metastatic invasive breast cancer who were a median age of 56 years old, and were treated with chemotherapy within six months of diagnosis. Of these patients, 4,325 of the participants received Herceptin, or trastuzumab-based chemotherapy.

The researchers found that 4.2 percent of the study patients developed heart failure. But rates of the condition were higher among those treated with Herceptin: 8.3 percent of these patients developed heart failure compared with 2.7 percent of those who did not receive this type of chemotherapy.

And the risk of heart failure increased with age.

Taking other chemotherapy drugs, known as anthracyclines, could also increase the likelihood of heart problems, the investigators found.

"While we were unable to directly look at obesity, comorbidities such as diabetes, which tend to be associated with obesity, were associated with a higher risk of heart failure," Henry noted.

The researchers concluded that breast cancer patients treated with Herceptin require regular heart monitoring. Heart disease is the second leading cause of death among breast cancer survivors mainly due to the toxic effects of some cancer treatments, the study authors pointed out.

According to Dr. William Hundley, a cardiology professor at Wake Forest Baptist Medical Center, in Winston-Salem, N.C., "There is a surveillance program with echocardiograms during receipt of trastuzumab for this very purpose."

This usually involves undergoing an echocardiogram, a procedure that uses ultrasound waves to assess heart function, every three months during treatment, explained Hundley, who was not involved in the new study. He added that treatment discussions between breast cancer patients and their oncologist should cover both the risks and benefits of any appropriate therapies.

In their study, Henry and her colleagues also analyzed the rate of heart-monitoring adherence among the chemotherapy patients.

Only 46 percent of those treated with Herceptin or trastuzumab-based chemotherapy had their heart function assessed before starting chemotherapy and received the recommended heart monitoring during treatment, the findings showed.

It's unclear why rates of heart monitoring were low among these patients. The study authors suggested that some doctors may view it as unnecessary, particularly for younger women with fewer underlying health issues or other heart-related risks.

The researchers pointed out that younger women with long life expectancies may receive more aggressive treatment, which could increase their need for more careful heart monitoring.

If heart changes are detected, patients can talk to their doctor and make informed decisions about their treatment. In some cases, heart medications can help improve heart health during treatment, according to the American Heart Association.

Hundley added that scientists are also actively investigating if lifestyle adjustments -- such as diet and exercise -- could also help reduce the risk for heart problems among high-risk chemotherapy patients.


Chemotherapy found to stop new brain cells from growing, worsening depression in brain cancer patients

Published: August 06, 2018

Source:https://www.naturalnews.com/2018-08-06-chemotherapy-found-to-stop-new-brain-cells-from-growing-worsening-depression.html

(Natural News) Chemotherapy is depressing enough, but a drug used in the procedure may heighten it and make it worse, according to a study by researchers from King’s College London.

Depression is considered one of the least recognizable symptoms of cancer since the condition is commonly attributed to the shock of the patient upon hearing the news. The results of a new study, however, bring new light to the condition being an actual symptom of the disease rather than psychological distress stemming from receiving a cancer diagnosis.

Research has demonstrated that depression is prevalent in sufferers of brain cancer. According to studies, an estimated 30 percent of patients with brain cancer deal with it. However, this symptom is under-diagnosed; only less than 10 percent report experiencing symptoms of depression and 20 percent of patients are classified to have clinical depression.

Chemotherapy is a treatment that brings side effects of its own – most famous of which is hair loss.

Using data from animal studies, researchers were able to determine the chemotherapy may also affect neurogenesis or the growth of new brain cells. In this study, researchers questioned whether the effects of chemotherapy on neurogenesis significantly disrupted biological brain mechanism and if these changes increased a patient’s vulnerability to depression.

For this study, researchers gave healthy mice a chemotherapy drug known as temozolomide (TMZ), which is commonly used in treating brain cancer for humans. After the mice were administered with TMZ, researchers saw a decline in the production of new neurons in the hippocampus – the part of the brain that is related to emotion and memory. Results also indicated a direct link between neurogenesis and stress, with neurogenesis declining in direct response to the increased production of stress hormones.

This meant that people undergoing chemotherapy not only have lesser brain cells but have a greater level of stress when exposed to it.

Researchers also observed substantial changes in the behavior of mice who had undergone chemotherapy, most notable of which is the lack of pleasure seeking or behavioral despair. The changes mimic behavior observed in people who experience depression, such as a lack of motivation and resignation.

The results may be based on mice and may not accurately represent what is actually happening to patients who have depression, but researchers believe that these findings could help improve patient care.

“Our results suggest that chemotherapy may stunt the growth of new brain cells, which has biological and behavioral consequences that may leave people less able to cope with the stress of having cancer,” Martin Egeland, a co-author of the study, explained. “Understanding the specific effects of chemotherapy on mood could lead to improved treatments and increase the quality of life for those affected by cancer.”

While there is no way to test these findings in humans, further studies that would be undertaken for the study include the effect of intervention methods, such as cognitive training, for patients and how it can protect them from depression.

“We will have to determine when is the best time to intervene and how much time we have. Treating the cancer is the priority of course,” according to senior author Sandrine Thuret. “However, if we can improve the quality of life of the patient, it can also be a step forward and may reduce their vulnerability to mental health problems.”

The National Cancer Institute lists depression as a symptom of cancer. While there are many risk factors for developing depression, the agency notes that going to counseling programs can be a way to deal with depression. Developing relaxation skills and stress-reduction exercises are also other ways to combat it.


Fried foods, especially overcooked potatoes, dramatically increase cancer risk

Published: August 03, 2018

Source:https://www.naturalnews.com/2018-08-03-fried-foods-overcooked-potatoes-dramatically-increase-cancer-risk.html

(Natural News) Fried potatoes and other foods cooked at high temperatures significantly increase cancer risk, according to research. Because of this, the Food Standards Agency (FSA), a government body in the U.K., issued a public warning over the risks of these foods.

When foods are cooked at high temperatures or over 120 degrees Celsius, a chemical compound called acrylamide forms. This chemical compound can trigger cancer cell growth. Fried foods, especially fried potatoes, contain the highest amounts of acrylamide.

Apparently, acrylamide can also be found in other foods, such as packed crackers, cookies, dry cereals, toasted nuts, peanut butter, canned black olives, prune juice, and roasted cocoa beans. The chemical compound is also found in bread crusts and many foods that are roasted, such as nuts.

Acrylamide arises in certain carbohydrates, proteins, and starchy foods that are exposed to high or prolonged heat during processing or cooking. it is formed when simple sugars, such as glucose, exposed to intense heat react with the amino acid asparagine.

In addition, studies in mice have revealed that exposure to high levels of acrylamide can lead to neurological damage.

Ways to reduce acrylamide consumption

In line with the FSA’s warning, the government body also suggested simple ways to reduce people’s consumption of acrylamide.

One of the ways to avoid acrylamide formation in foods is to aim for a golden yellow color or lighten when frying, roasting, baking, or toasting starchy foods. People should also follow the cooking instructions on packaging properly to ensure that foods are not cooked for too long or at extreme temperatures.

The FSA also advised that raw potatoes should not be kept in the fridge. Putting potatoes in the fridge can increase overall levels of acrylamide. Rather, raw potatoes should be stored in a dark, cool place with temperatures over 6C. In addition, potatoes should not be stored for a long period because more acrylamide can form.

Other ways to reduce acrylamide consumption include eating chunky chips on occasion instead of fries. Moreover, cutting potatoes into larger wedges decreases their surface area, thus reducing the level of acrylamide that can form. To reduce one’s overall risk of cancer, adhere to a varied, balanced diet.

Increased early death risk, another reason to ditch french fries

Cancer is not the only risk of eating fried potatoes. It can also increase the risk of early death. A study published in the journal American Journal of Clinical Nutrition found that people who eat fried potatoes two or more times each week could increase their risk of premature death by two times.

Researchers in Italy analyzed the data of 4,440 adults who participated in the Osteoarthritis Initiative (OAI) cohort study. The participants were between the ages of 45 and 79 at the beginning of the study, and they were followed up for an average of eight years. They were tasked to accomplish a food frequency questionnaire as part of the OAI study. Researchers of the current study used these data to measure the participants’ total weekly potato intake and weekly consumption of fried and unfried potatoes.

During the follow-up period, a total of 236 participants died. Although overall potato consumption did not affect their death risk, consumption of two to three portions of fried potatoes like french fries, potato chips, or hash browns every week doubled the risk of early death. Eating more than three portions further increased the risk. There was no link found between the consumption of unfried potatoes and early death risk.


Irrefutable evidence proves that honey and bee pollen improve menopausal symptoms in breast cancer patients

Published: August 02, 2018

Source:https://www.naturalnews.com/2018-08-02-honey-and-bee-pollen-improve-menopausal-symptoms-in-breast-cancer-patients.html

(Natural News) As the most common cancer among women around the world, breast cancer is one of the biggest health issues of our time. It’s also quite controversial, as you might expect, from a problem that has the potential to generate so many profits. In addition to living with a constant worry of developing this potentially deadly disease, women have to deal with overdiagnosis, dishonest surgeons who prey on their fear, and questionable charities that don’t put their funds toward finding a cure as claimed. A diagnosis can be extremely traumatic as women face questions about their mortality, and for those who are undergoing treatment, there’s a whole slew of side effects that can make their make life pretty miserable.

Some breast cancer patients undergo chemical hormone suppression as part of their treatment. Drugs like Tamoxifen and Arimidex often add to the trauma of breast cancer by causing hair loss, libido crashes, hot flashes, and fatigue, to name just a few side effects. It gets so bad that some women quit their treatment, while others are given psychotropic drugs like Prozac or Lyrica that pile on even more side effects.

It might seem like it’s just an endless series of bad news when it comes to breast cancer, but a new study has found that there could be some help in the form of honey and bee pollen. Researchers set out to see if bee pollen could reduce menopause-like symptoms in those taking hormone-suppressive drugs for breast cancer. They got the idea after a trial showed that bee pollen extracts enhanced menopausal women’s quality of life and reduced their hot flashes.

Researchers surprised by honey finding

Not only did they find that the bee pollen was indeed effective, but they discovered something else completely unexpected at the same time. In the study, they used honey as the placebo, but to their surprise, they discovered that it was every bit as effective as the bee pollen when it came to reducing symptoms!

In the randomized crossover trial, the researchers assessed the menopausal complaints of 46 breast cancer patients who were receiving anti-hormonal treatment. An incredible 70.9 percent noted improvements when taking bee pollen, while an equally remarkable 68.3 percent noted improvements in her symptoms when taking honey. In fact, the difference between the two groups was so small that it was not considered significant, making them essentially equally good choices.

These results were confirmed in a follow-up. The researchers mention that honey actually raises estrogen levels, which goes against the idea behind suppressing hormones in the first place – even if it did lead to improvements in symptoms in the study. Nevertheless, they believe that women who are looking to discontinue treatment because they aren’t finding symptom relief from alternatives like acupuncture could be offered bee pollen. They also called for future tests to look into the use of honey and bee pollen in relieving menopausal symptoms in healthy women.

Of course, it’s important to keep in mind that finding relief from the symptoms caused by hormone-suppressive drugs does not actually protect the body from their dangers. Sometimes a bad reaction is your body’s way of telling you that whatever you’re taking should be avoided. For example, extended tamoxifen use has been linked to endometrial and liver cancer.

Nevertheless, many women feel compelled to continue the treatment their doctors have prescribed, and anything that can make this a more pleasant experience naturally and without side effects is worth consideration.


For Women Worldwide, Lung Cancers Rise as Breast Cancers Decline

Published: August 01, 2018

Source:https://www.cancercompass.com/cancer-news/article/62310.htm

(HealthDay News) -- As women around the world wage war against cancer, good news on the breast cancer front is tempered by predictions that lung cancer deaths could rise more than 40 percent.

Researchers in Spain reported that between 2015 and 2030, lung cancer deaths among women worldwide will likely increase 43 percent.

During that same period, however, breast cancer deaths are projected to fall 9 percent.

"While we have made great strides in reducing breast cancer mortality globally, lung cancer mortality rates among women are on the rise worldwide," said study author Jose Martinez-Sanchez. He's director of public health, epidemiology and biostatistics at the International University of Catalonia (UIC Barcelona).

For the study, researchers analyzed World Health Organization data gathered from 52 countries between 2008 and 2014. The study authors concluded that the worldwide lung cancer death rate among women will increase from just over 11 percent in 2015 to 16 percent in 2030.

The highest rates in 2030 are projected in Europe and Oceania, and the lowest rates in North America and Asia. Only Oceania is predicted to see a dip in the rate of women's lung cancer deaths -- and that's just from 17.8 percent in 2015 to 17.6 percent in 2030.

The study was published Aug. 1 in the journal Cancer Research.

"If we do not implement measures to reduce smoking behaviors in this population, lung cancer mortality will continue to increase throughout the world," Martinez-Sanchez warned in a journal news release.

Meanwhile, he said, "we are seeing an increase in breast cancer mortality in Asia because this culture is adapting a westernized lifestyle, which often leads to obesity and increased alcohol intake, both of which can lead to breast cancer."

Breast cancer is associated with many lifestyle factors, Martinez-Sanchez explained.

"On the other hand, we are witnessing a decrease in breast cancer mortality in Europe," he added. There may be greater awareness of breast cancer among Europeans, he suggested, leading to active participation in screening programs and treatment improvements.


Turning off protein could boost immunotherapy effectiveness on cancer tumors

Published: July 31, 2018

Source:https://www.sciencedaily.com/releases/2018/07/180731104248.htm

Researchers at the Bloomberg~Kimmel Institute for Cancer Immunotherapy in the Johns Hopkins Kimmel Cancer Center discovered inhibiting a previously known protein could reduce tumor burdens and enhance the effectiveness of immunotherapy treatments.

In order to investigate the role of the Yes-associated protein, or YAP, in T-cells in the cancer setting, scientists used mice genetically engineered to lack YAP in several T-cell populations, including regulatory T-cells, known as Tregs. This was the first time the relationship between YAP and Tregs has been explored.

The study was published in Cancer Discovery on June 15, 2018.

Tregs are important for health, because they prevent autoimmune diseases but can be a major obstacle in the mounting of immune responses to tumors and immunotherapy. YAP can be found in a subset of those regulatory T-cells.

Scientists tested the antitumor effects of YAP inhibitors alone and in combination with immunotherapies. Their encouraging results showed YAP plays a role in the suppression of antitumor immunity by Tregs and demonstrated by turning off YAP's abilities, tumor killing with less restrained immune cells is possible.

Fan Pan, M.D., Ph.D., senior author of the study and associate professor of cancer immunology, said blocking YAP or the signaling pathways under its control boosted the effects of both a tumor vaccine and a checkpoint inhibitor (anti-PD1 antibody) to produce even stronger antitumor activity. He said the approach of therapeutically targeting YAP was effective over a broad scope of cancer types in mice.

Since Tregs are notorious for dampening the effectiveness of tumor-directed immunity in cancer patients, this study's finding may pave the way for a new and promising strategy to unleash the patient immune response from the stifling grip of suppressor cell control.

While Pan and study authors are optimistic that further work could lead to effective YAP-targeting immunotherapies for cancer, they pointed out therapies aimed at enhancing YAP activity may have potential use for the treatment of autoimmune diseases.


Shield Yourself From the Summer Sun

Published: July 28, 2018

Source:https://www.cancercompass.com/cancer-news/article/62277.htm

(HealthDay News) -- When you're out having fun in the sun this summer, remember to take steps to prevent sunburn.

Along with being painful, sunburns can cause lasting damage that can lead to a number of skin problems, including skin cancer, warned Dr. Suzanne Olbricht, chief of dermatology at Beth Israel Deaconess Medical Center in Boston.

"The sun's UV rays damage the DNA in the cells of your skin," she explained in a medical center news release. "These harmful DNA changes can be quite profound and you will sometimes see the damage in the form of peeling skin."

All skin types can burn, Olbricht added.

"The darker one's skin, the more melanin is present and therefore the greater the UV protection," she said. "But no matter the color, your skin can burn. Everyone should take precautions when heading out into the sun."

Use a broad spectrum sunscreen with a strong sun protection factor (SPF).

"SPF measures how well the sunscreen protects your skin compared to if you were not wearing it," Olbricht said. "For example, if it normally takes 20 minutes for your skin to turn red, a product with SPF 15 will typically prevent sunburn 15 times longer."

Use lots of sunscreen and reapply regularly. One ounce, or a shot glass full, of sunscreen will cover your entire body, including your face, ears and scalp.

"A rule of thumb for reapplying is every two hours," Olbricht said. "But if you're swimming or sweating a lot, you will want to reapply more often."

Try to stay out of the sun when its rays are strongest, between 10 a.m. and 2 p.m. Wear sunglasses with UV protection, a wide-brimmed hat, and clothing with UPF protection (ultraviolet protection factor).

"A lot of children's summer clothing and swim attire can be found with UPF 50+, which helps block 98 percent of UVA/UVB rays," Olbricht said.


3-Pronged Approach to Cancer Prevention

Published: July 26, 2018

Source:https://www.cancercompass.com/cancer-news/article/62262.htm

(HealthDay News) -- Need another reason to improve your diet and start exercising? Doing so could help ward off cancer, a new study finds.

"Keep in mind that every lifestyle factor counts and it is never too late to adopt a healthy lifestyle," said study co-author Bernard Srour, of the French National Institute of Health and Medical Research.

Eating healthful foods, engaging in physical activity and avoiding alcohol is tied to lower overall cancer risk, as well as lower breast and prostate cancer risks, Srour's team found.

Researchers analyzed data from more than 41,000 adults in France, age 40 and older, who had never been diagnosed with cancer. Between May 2009 and January 2017, nearly 1,500 cases of cancer were diagnosed in the group.

But those who fared best cancer-wise adhered more closely to dietary guidelines developed by the World Cancer Research Fund (WCRF) and the American Institute for Cancer Research (AICR), the researchers said.

A 1-point increase on the guidelines' score of healthy eating was associated with a 12 percent decrease in overall cancer risk, a 14 percent decrease in breast cancer risk, and a 12 percent decrease in prostate cancer risk.

The study was published July 26 in the journal Cancer Research.

The study authors concluded that the "synergistic contribution" of a healthy diet was more significant than any single dietary recommendation in reducing cancer risk.

For example, antioxidants from fruits and vegetables may counteract some of the cancer risks posed by red meat and processed meat. Similarly, by lowering blood pressure, exercise could partly offset the effects of high-salt foods.

"This emphasizes the role of an overall healthy lifestyle -- nutrition and physical activity and alcohol avoidance -- in cancer prevention," Srour said in a journal news release.

The researchers said the WCRF/AICR recommendation to avoid alcohol most likely contributed to that diet's role in reducing cancer risk.

"In its last report, the WCRF stated that there is now strong, convincing evidence that alcohol consumption increases the risks of oropharyngeal, esophagus, liver, colorectal and postmenopausal breast cancers," said study co-author Mathilde Touvier, also of the French Institute of Health and Medical Research and the University of Paris.

It appears alcohol is linked with stomach and premenopausal breast cancers as well, Touvier added.


One of the most powerful superfoods, honey protects you from cancer and keeps your immune system strong

Published: July 25, 2018

Source:https://www.naturalnews.com/2018-07-25-one-of-the-most-powerful-superfoods-honey-protects-you-from-cancer-and-keeps-your-immune-system-strong.html

(Natural News) Honey has been used in medicine for well over 5,000 years. Now, researchers from United Arab Emirates University have found that honey from certain regions – particularly those that have arid climates – can be used to treat major chronic diseases, including cancer. The results of their study, published in BMC Complementary and Alternative Medicine, investigated the antioxidant and anti-inflammatory properties of arid region honey and compared it with popular varieties from non-arid regions using in vitro testing.

“Most of the antioxidant benefits of honey are associated with the presence of polyphenols,” researchers noted in their study. “The content of these polyphenols is different depending on the source and floral origin of honey. The climate where honey is made also significantly influences the polyphenol content and profile.”

For this study, researchers compared six varieties of honey: Four of these were grown in the Middle East, which is known to have dry, desert-like conditions, and two were from non-arid regions like Germany and New Zealand. To note, the following varieties were selected.

  • Those that are predominantly from wild jujube (Ziziphus spina-csisti) grown in the United Arab Emirates (UAE)
  • Monofloral (from one nectar) and heterofloral (from different nectars) varieties of the umbrella thorn tree (Acacia tortilis) from the UAE and Yemen
  • Monofloral manuka (Leptospermum scoparium) honey from New Zealand, and heterofloral manuka from Germany

All honey varieties underwent multiple tests in the study. In particular, researchers measured each variety’s ability to protect specific red blood cells, called erythrocytes, from destruction after being exposed to peroxide, as determined by MDA (malondialdehyde) levels after the test. Its immunomodulatory effect was also tested using a prostate cancer cell line, including PBMC (peripheral blood mononuclear cells). The team looked at IL-6 (interleukin 6) and NO (nitric oxide) levels in the cells after they had been incubated with honey overnight.

The results showed that honey grown in arid regions had protected the erythrocyte membrane after exposure to oxidation. “Arid region honey showed a greater antioxidant effect than non-arid honey as shown by the prevention of oxidative damages to erythrocytes,” the researchers wrote. This was confirmed by a reduced level of MDA in arid region honey samples.

In addition, the polyphenols found in arid region honey successfully lowered the expression of pro-inflammatory IL-6 markers in PBMC samples. This demonstrates the immunomodulatory effect of arid region honey in specific cancer cells.

“All of this is in favor of a promising use of arid region honey as a therapeutic product for major chronic diseases, especially cancer,” the team concluded. In particular, the group stressed that the erythrocyte membrane protective function of honey could significantly reduce inflammation, a significant risk factor for multiple chronic diseases.

The sweet benefits of honey

The benefits of honey don’t just stop with it being a potent antioxidant. Here are other benefits of adding honey to your diet.

  • It can help lower blood pressure. The antioxidants present in honey have been lined to modest reductions in blood pressure in animal and human studies.
  • It improves “good” cholesterol levels. Honey significantly raises high-density lipoprotein (or “good” cholesterol) levels in the body, while keeping bad cholesterol levels at bay. This reduces the risk of cardiovascular disease and stroke.
  • It can lower triglycerides. Increased triglyceride levels are linked to heart disease and Type 2 diabetes. Honey can reduce the risk, especially if used to replace table sugar.
  • It promotes wound healing. If used topically, honey can help treat burns, wounds, and other skin conditions.

Blood test can predict optimal treatment for advanced prostate cancer, study finds

Published: July 24, 2018

Source:https://www.sciencedaily.com/releases/2018/07/180724174332.htm

An international collaborative study between Lawson Health Research Institute, Memorial Sloan Kettering Cancer Center, the Royal Marsden and Epic Sciences is one of the first to demonstrate that a blood test can predict how patients with advanced prostate cancer will respond to specific treatments, leading to improved survival.

The study used a liquid biopsy test developed by molecular diagnostics company Epic Sciences that examines circulating tumour cells (CTCs) in blood samples from patients with advanced prostate cancer who are deciding whether to switch from hormone-targeting therapy to chemotherapy. CTCs are cancer cells that leave a tumour, enter the blood stream and invade other parts of the body, causing the spread of cancer.

The test identifies whether or not a patient's CTCs contain a protein called AR-V7 in the cell's nucleus. The research team set out to determine whether the presence of this protein predicted which treatment would best prolong a patient's life. They found that patients who tested positive for the protein responded best to taxane-based chemotherapy while those who tested negative for the protein responded best to hormone-targeting therapy with drugs called androgen-receptor signaling (ARS) inhibitors. These are the two most widely used drug classes to treat advanced prostate cancer.

"The study focused on a critical decision point when patients and their oncologists are choosing what therapy to pursue next," says Dr. Alison Allan, a scientist at Lawson and Chair, Department of Anatomy & Cell Biology at Western University's Schulich School of Medicine & Dentistry. "We are addressing a critical unmet need by validating that a blood test or liquid biopsy can be used to select a therapy most likely to extend a patient's life."

Research participants included 142 patients with advanced prostate cancer from the London Regional Cancer Program at London Health Sciences Centre (LHSC) in London, Ontario; Memorial Sloan Kettering Cancer Center in New York; and the Royal Marsden in London, England. The patients had already undergone at least one round of hormone-targeting therapy without success and were working with their oncologist to decide whether to switch to a different hormone-targeting therapy or to chemotherapy as their next line of treatment.

Hormone-targeting therapies like ARS inhibitors work by slowing or stopping the growth of cancers that use hormones to grow. Prostate cancer growth relies on hormones called androgens, which include testosterone. Androgen deprivation therapy like ARS inhibitors blocks the production of male hormones to treat the recurrence or spread of prostate cancer.

"ARS inhibitors are the preferred first line of treatment because they target the hormones that provide the fuel for prostate cancer cells to grow," explains Dr. Allan. "However, at some point, cancer cells can figure out a way to survive without this fuel and become resistant to ARS inhibitors, in many cases through production of the AR-V7 protein. That's why chemotherapy is sometimes used a second line therapy."

While this study looked at predicting the best treatment for patients who had already undergone at least one round of hormone-targeting therapy, a future goal of the team is to assess the use of this test or similar CTC blood tests in determining optimal therapy at earlier decision points in advanced prostate cancer care. The team also plans to collaborate further with Epic Sciences to evaluate different versions of the CTC blood test for other types of cancer, such as lung cancer.

Through Epic Sciences' partnership with Genomic Health, the CTC blood test is now commercially available in the United States as the Oncotype DX AR-V7 Nucleus Detect.


The powerful antioxidant and anti-cancer effects of arid region honey

Published: July 22, 2018

Source:https://www.naturalnews.com/2018-07-22-the-powerful-antioxidant-anti-cancer-effects-of-arid-region-honey.html

(Natural News) The arid region honey can be used as a therapeutic product for chronic diseases, including cancer, according to researchers from United Arab Emirates University. The study, published in BMC Complementary and Alternative Medicine, compared varieties of honey from desert climates against those from non-arid regions to establish which variety contained more antioxidant and anti-inflammatory activities.

  • Researchers tested in vitro both monofloral and heterofloral types of honey from arid and non-arid regions.
  • The following were conducted to determine certain physicochemical properties of honey: hemolysis assay (to determine erythrocyte membrane protection effect), PC-3 prostate cancer cells and PBMC (to measure interleukin 6 and nitric oxide levels), and 24-hour incubations (to test PC-3 cell viability).
  • Honey varieties from arid regions showed better erythrocyte membrane protection effect – with H4 samples reaching 1.3 (± 0.042) micromol Trolox Equivalents per gram of dry matter (mMTE/g), as well as H2 samples measuring 1.122 ± 0.018mMTE/g.
  • MDA (malondialdehyde) levels were reduced in arid region honey, as well as cell population in PC-3 after a 24-hour incubation with honey.
  • Interleukin 6 (IL-6) was also reduced by honey varieties, and nitric oxide levels moderately increased in both cultures.

The findings suggest that arid region honey possesses potent antioxidant activity, as well as potential anti-inflammatory properties.


5 Good reasons to include more magnesium-rich foods in your diet

Published: July 21, 2018

Source:https://www.naturalnews.com/2018-07-21-5-good-reasons-to-include-more-magnesium-rich-foods-in-your-diet.html

(Natural News) You may not realize it, but magnesium is one of the nutrients your body needs the most. According to the Human Genome Project, there are 3,751 proteins with binding sites for this mineral, which only adds to why you need to eat food items that have an abundance of it.

Increasing your magnesium intake can provide you with a wide range of health benefits.

Lower your risk of dying from cardiovascular disease

Numerous studies have linked low magnesium levels in the body to an increased risk of developing cardiovascular disease and dying from it. It was also found that increasing your magnesium intake can be therapeutic for conditions like hypertension, arrhythmia, atherosclerosis, and dysfunctional endothelium.

One such study, published in Atherosclerosis, found that low magnesium levels double your likelihood of dying from heart disease. You will also be seven times more likely to die from all causes.

Manage diabetes and its symptoms

Type 2 diabetics, particularly those suffering from neuropathy and coronary heart disease, usually lack magnesium. This is because having higher glucose levels in your blood also increases the amount of magnesium in your urine, meaning you lose more of the nutrient every time you pee compared to people without diabetes. A study from Harvard Universityfound that supplementing with 320 mg of magnesium for 16 weeks can improve both fasting blood sugar levels and good cholesterol (HDL).

Mitigate the risk of developing colon cancer

Several studies have found links between higher magnesium intake and a lower risk of developing colon cancer. A Chinese review revealed that the highest magnesium intake reduced colorectal cancer risk by 11 percent compared to the lowest intake. Another meta-analysis, this time from London, found that every time you increase your intake of magnesium by 100 mg, you decrease your colorectal cancer risk by 13 percent.

Make your bones stronger

Magnesium stimulates calcitonin, a hormone that helps draw calcium from the blood and soft tissues so it can be used in the bones instead. Aside from strengthening your bones, this also lowers your risk for conditions related to having too much calcium, such as heart attack, arthritis, kidney stones, and osteoporosis. Magnesium’s effects are such that even when you decrease your daily calcium intake from the 1,200 mg recommended by the U.S. government to just 500 mg, you will still be able to increase your bone density.

Reduce symptoms of metabolic syndrome

Metabolically obese, normal-weight (MONW) individuals have a normal body mass index (BMI) of 25, but suffer from insulin resistance and hypertension, increasing their risk for both diabetes and cardiovascular disease. A Mexican study found that supplementing with magnesium helped ease both systolic and diastolic pressure, as well as improve triglyceride and blood glucose levels.

Increase your magnesium intake with the right diet

Magnesium levels tend to go down with age, so it is essential that you supply your body with this nutrient through proper diet. Here are some healthy, magnesium-rich food items:

  • Legumes – Lentils, beans, and peas are packed with nutrients, including magnesium. They also contain lots of plant protein, which makes them great for people who want a good source of this nutrient which, unlike red meat, does not increase their risk for heart disease.
  • Seeds – Pumpkin, chia, and flax seeds, among others, contain magnesium. They are also rich in fiber, which makes them extremely good for your heart.
  • Nuts – Cashews, almonds, and Brazil nuts are rich in magnesium. Aside from having fiber, they also possess anti-inflammatory properties that make them excellent if you want a heart-friendly snack.
  • Fatty fish – Salmon, halibut, mackerel, and certain fatty fish are not just packed with protein, they also contain magnesium and omega-3 fatty acids. These nutrients make them great for maintaining healthy blood vessels and cardiovascular function.
  • Leafy greens – Spinach, kale, collard greens, and other leafy vegetables are among the best sources of magnesium. A single cup of spinach is enough to supply 39 percent of the recommended daily intake (RDI) for the nutrient. They also provide antioxidants that help protect your body from oxidative stress and maintain normal cellular function.

Study Confirms Added Cancer Risk for Diabetics, Especially Women

Published: July 20, 2018

Source:https://www.cancercompass.com/cancer-news/article/62171.htm

(HealthDay News) -- The increased risk of cancer in people with diabetes is higher for women than men, a new study finds.

Previous research identified the link between diabetes and cancer risk, but this study looked at whether that risk differs between men and women.

The takeaway: Among people with diabetes, women have a 6 percent higher risk of cancer than men, the researchers said.

And based on the researchers' analysis of data from 47 studies, diabetics of both sexes are at greater risk of cancer than people without diabetes.

For women with type 1 or type 2 diabetes, the cancer risk is 27 percent higher compared to other women. And men with diabetes have a 19 percent higher cancer risk than men who don't have the blood sugar disease, the findings showed.

The researchers also examined specific types of cancer in people with diabetes and found that, compared to men, women have a 15 percent higher risk of leukemia, a 14 percent higher risk of stomach cancer, a 13 percent higher risk of oral cancer, and an 11 percent higher risk of kidney cancer.

But women have a 12 percent lower risk than men for liver cancer, according to the report.

"Further studies are needed to clarify the mechanisms underlying the sex differences in the diabetes-cancer association," the study authors concluded.

The report, from Toshiaki Ohkuma of the University of New South Wales in Australia and colleagues at the University of Oxford in England, was published July 19 in the journal Diabetologia.

Cancer is the second leading cause of death worldwide, accounting for 8.7 million deaths in 2015. About one in four women and one in three men will develop cancer during their lifetime, the study authors noted in a journal news release.

In addition, in 2015, there were 415 million adults worldwide with diabetes and 5 million diabetes-related deaths.


Could an Early Supper Lower Breast, Prostate Cancer Risk?

Published: July 18, 2018

Source:https://www.cancercompass.com/cancer-news/article/62131.htm

(HealthDay News) -- Having a late dinner and heading straight to bed may boost your risk of breast or prostate cancer, a new study suggests.

Spanish researchers analyzed data from 621 prostate cancer patients and 1,205 breast cancer patients, as well as 872 men and 1,321 women without these cancers.

People who ate their evening meal before 9 p.m. or waited at least two hours after supper before going to sleep had a 20 percent lower cancer risk than those who ate supper after 10 p.m. or those who ate and went to bed soon after, according to the study.

The research only found an association and does not prove late-night eating causes these cancers.

"Our study concludes that adherence to eating patterns [during the day] is associated with a lower risk of cancer," said lead author Manolis Kogevinas, a researcher at the Barcelona Institute for Global Health (ISGlobal).

The findings "highlight the importance of assessing circadian rhythms in studies on diet and cancer," Kogevinas said in an institute news release.

If the findings are confirmed, "they will have implications for cancer prevention recommendations, which currently do not take meal timing into account," Kogevinas said.

He added that the impact could be especially important in places like southern Europe, where people have supper late.

More research is needed to understand the findings, but co-author Dora Romaguera said that "everything seems to indicate that the timing of sleep affects our capacity to metabolize food." Romaguera is a researcher at ISGlobal.

Though extensive research has probed links between types of food and cancer risk, little attention has been paid to how cancer risk might be affected by mealtimes and what people do before and after eating, the study authors said.


New target protein for colon cancer identified

Published: July 17, 2018

Source: https://www.sciencedaily.com/releases/2018/07/180717182320.htm

Researchers at Boston University School of Medicine (BUSM) have identified a new potential target protein (c-Cbl) they believe can help further the understanding of colon cancer and ultimately survival of patients with the disease.

They found colon cancer patients with high levels of c-Cbl lived longer than those with low c-Cbl. Even though scientists have studied this protein in other cancers, it has not been explored in colon cancer until now.

The researchers examined the level of c-Cbl in tumors that were removed from people with colon cancer. Based on the level of this protein, c-Cbl, patients were split into two groups, high c-Cbl and low c-Cbl.

The researchers then wanted to find out what happens to cells when this protein was turned off. They did this by using two types of colon cancer cells split into three groups each. One group consisted of un-manipulated colon cancer cells, one group had increased expression of normal c-Cbl and the other group had increased expression of the "off" version of c-Cbl. This off version of c-Cbl lacked an essential function of c-Cbl called ubiquitin ligase activity. Cells that were given the "off" version of c-Cbl grew more tumors than those that were given the "on" version.

For tumors to grow and metastasize they need blood vessels. The next step was to look at how c-Cbl affected blood vessel growth by using three experimental models, (one group was normal, one group was given the c-Cbl protein and the third group was given the "off" version of the protein). The model that was given the "off" version of c-Cbl grew more blood vessels. "This helps us to understand the role of the ubiquitin ligase activity of c-Cbl in preventing tumors from growing and reducing tumor's ability to grow blood vessels," explained corresponding author Vipul Chitalia, MD, PhD, associate professor of medicine at BUSM.

According to the researchers, this study suggests that c-Cbl might improve the survival of patients with colon cancer. "This information will help cancer researchers understand colon cancer better and possibly design new treatments to better cure colon cancer and help patients live longer."


Health Tip: Take Care of Yourself During Radiation Therapy

Published: July 16, 2018

Sourcehttps://www.cancercompass.com/cancer-news/article/62113.htm

(HealthDay News) -- Radiation therapy to help fight cancer may be physically and emotionally draining.

It's important to get plenty of sleep, eat a healthy and balanced diet and to stay as healthy as possible during your treatments.

The American Cancer Society recommends:

  • Get enough sleep. This may include naps during the day, as fatigue can be a major side effect of radiation that can last up to six weeks after treatments end.
  • Eat a healthy and balanced diet. Discuss your diet with your medical team, particularly if you are having side effects that make it difficult to eat.
  • Clean the skin affected by radiation with a mild soap. Do not use any other products to clean the skin without your doctor's approval.
  • Tell your medical team about all medicines and supplements you take.

Natural solution for damage done by chemo: Omega 3s found to treat wounds from inflamed mucous membranes in cancer patients

Published: July 13, 2018

Source:https://www.naturalnews.com/2018-07-13-omega-3s-found-to-treat-wounds-from-inflamed-mucous-membranes-in-cancer-patients.html

(Natural News) Omega-3 fatty acids can be used to treat and prevent oral mucositis in patients undergoing mucotoxic cancer chemotherapy. The double-blind, randomized study, published in the journal Wounds, detailed the effectiveness and route of administration of omega-3 fatty acids in patients receiving chemotherapy in Iranian hospitals.

Mucositis is characterized by soreness or swelling in the mouth which can result in painful ulcers in the area. The condition is a common side effect of chemotherapy drugs used in cancer treatment. In particular, mucositis is prevalent in patients undergoing high-dose chemotherapy, and 80 percent of individuals with head and neck cancers. Aside from the formation of ulcers, people with mucositis experience severe pain, an increased risk of local and systemic infections, dysfunction, and bleeding from the mouth, oral cavity and pharynx – all of which could affect a person’s quality of life. In some cases, the condition can lead to complications such as septicemia. It can also be an economic burden, as it prolongs hospital stays to heal and manage the pain and other conditions.

The main focus of traditional cancer treatment is to inhibit the condition, with little emphasis given to situations that come out of it. Mucositis, in particular, has no specific treatment; current practices aim to reduce infections until the area is healed.

Earlier studies have shown that omega-3 fatty acids can be used effectively in wound treatment. In particular, animal tests have indicated that omega-3 fatty acids improve the healing time for skin burn in both healthy and diabetic samples, and had a positive effect on oral wound recovery in rats. Moreover, clinical trials have revealed that omega-3 fatty acids can be used to aid the healing of stomach and duodenal ulcers in patients. Authors believe that this is because fatty acids increase the production of “pro-inflammatory cytokines” in the wounded area, allowing it to be used safely in wound healing.

The authors noted that there is no definitive examination of the effect of omega-3 fatty acids in mucositis; thus the need for the study. To evaluate their theory, they conducted a randomized trial using patients that had grade 1 oral mucositis. The group was divided into those that would receive the omega-3 fatty acid and those that would receive a placebo. At the time of the trials, the patients were under the initial chemotherapy stage and had not received any radiation therapy. Patients had been examined prior the trial, and they underwent follow-up examinations on a weekly basis.

Results indicated that patients who were given omega-3 fatty acids experienced less pain than those in the placebo group. In addition, people who were given omega-3 fatty acids had significantly lower severity of mucositis compared to those in the placebo group.

Those in the omega-3 group recovered quicker as well. On average, the mucositis lasted for 5.5 days in the omega-3 group, while the control group needed at most 16 days before they recovered from the condition. That meant that those in the omega-3 group were able to eat better than those in the placebo group. Irritation sores from mucositis were also noted to be significantly different in both groups as well.

The authors of the study concluded: “According to the findings in this study, omega-3 fatty acids in oral form have a significant effect on wound healing induced by oral mucositis.”


Immune-Based Therapy May Help When Melanoma Spreads to Brain

Published: July 12, 2018

Source:https://www.cancercompass.com/cancer-news/article/62075.htm

(HealthDay News) -- A type of therapy that harnesses the immune system is giving new hope to people battling a once hopeless cancer -- melanoma that's spread to the brain.

New research involving more than 2,700 U.S. patients is confirming what specialists in the field have long known -- that "checkpoint blockade" treatment can beat back these devastating tumors.

"Physicians who treat patients with melanoma brain metastases have seen first-hand the dramatic improvements in survival that immunotherapy can achieve," said one such specialist, Dr. Jason Ellis.

"This study provides data to support our individual clinical observations," said Ellis, a neurosurgeon at Lenox Hill Hospital in New York City. He wasn't involved in the new study.

Checkpoint blockade agents are not chemotherapy -- instead of acting directly on tumor cells, they manipulate the patient's immune system so that it targets and destroys the melanoma cells.

This type of "immunotherapy" was approved by the U.S. Food and Drug Administration in 2011.

The new research was led by Dr. J. Bryan Iorgulescu, a postdoctoral fellow in pathology at Brigham and Women's Hospital/Harvard Medical School in Boston. His team explained that about one in every 54 Americans will develop a melanoma skin cancer in their lifetime.

Luckily, most cases are detected early and easily cured via surgery. But sometimes the tumor has had time to spread, even to the brain. In fact, advanced melanomas are now the third-leading cause of metastatic brain cancer, the research team noted.

In its analysis, Iorgulescu's group tracked outcomes from 2,753 patients with melanoma that had spread to the brain. The patients were treated at cancer centers nationwide between 2010 and 2015.

The study found that first-line treatment with checkpoint blockade immunotherapy was associated with a rise in median overall survival from 5.2 months to 12.4 months.

Treatment was also tied to an increase in the four-year overall survival rate: Just over 28 percent of patients who got the immunotherapy survived at least four years, compared to about 11 percent who didn't get the therapy, the findings showed.

The researchers noted that survival benefits were even greater for those patients whose melanoma had not already spread beyond the brain, to organs such as the liver or lungs.

"Our findings build on the revolutionary success of checkpoint blockade immunotherapy clinical trials for advanced melanoma, and demonstrate that their substantial survival benefits also extend to melanoma patients with brain metastases," Iorgulescu said in a Brigham and Women's news release.

Dr. Michael Schulder helps direct neurosurgery at Long Island Jewish Medical Center in New Hyde Park, N.Y. He wasn't involved in the new analysis, but agreed it confirms what many cancer specialists have long known, "namely, that the use of checkpoint inhibitors has revolutionized the treatment and outlook for patients with metastatic melanoma."

The Boston researchers did offer one caveat, however: Not every patient has equal access to this expensive treatment. Insurance status was a real barrier to immunotherapy for some patients with these advanced tumors, and uninsured patients were much less likely to get the treatment compared to people with private insurance or those on Medicare.


Top 10 ways to avoid ever getting cancer in the first place

Published: July 11, 2018

Source:https://www.naturalnews.com/2018-07-11-top-10-ways-to-avoid-ever-getting-cancer-in-the-first-place.html

(Natural News) Millions of humans binge on junk food every meal and think doctors will be able to “fix” their health problems later with medicine and surgery. So what exactly is “junk food,” because most people think what they’re eating is not really “that bad.” Plus, most diets people choose are the ones that cater to their weaknesses, and that food regimen simply includes more junk science substitutes – replacing one chemical-laden food choice with another, and another, and another. It’s a costly cycle with the ultimate price being your life.

Cancer doesn’t show up over night, in fact, it’s a cumulative effect from overloading your body with toxins day after day, year after year. Consuming toxic foods daily and hoping cancer won’t eventually kick in is like walking on the edge of a cliff with a blindfold on… hoping everything will be just fine. It’s not that difficult to join the cancer prevention mission, and you don’t have to give up all the food you love, just take off the “blindfold” and stay on the safe paths, away from the cliff’s edge.

Cancer is not inherited and it’s not contagious, so get smart and prevent it

The type of cancer that 1 in 3 Americans get is not contagious and you’re not born with it. Still every medical doctor in America wants to talk about whether it “runs in the family” and wants to “find a cure” using chemical medicine, which will never happen. Ever try to put out a fire with gasoline and a blow dryer?

Cancer is caused by the consumption of chemicals, so NO chemical or combination of chemicals will ever be the solution. That’s why allopathic medicine is one of the worst ways to treat cancer, and also one of the main causes. Let’s take an inside look at what starts the “fire” and the fuel that spreads it.

Deny cancer its sources of fuel, and there won’t be a “forest fire” to try to put out later — avoid these top 10 cancer fuels

#1. Never eat sodium nitrates (processed meats)

#2. Avoid or filter tap water

#3. Stop eating GMOs

#4. Quit using artificial sweeteners

#5. Don’t buy or eat conventional meat (hormones, antibiotics, parasites, pathogens)

#6. End all processed (homogenized) dairy product consumption

#7. See if a naturopathic physician can get you off any and all chemical pharmaceuticals

#8. Never ever get another flu shot (as vaccines almost always contain cancer-causing ingredients such as stealth viruses like SV40)

#9. Eliminate all foods from your intake that are imported from China (they’re often loaded with heavy metal toxins)

#10. Always ignore the mass “mainstream” media because they lie about everything that’s good for you and they promote everything that’s bad for you

There are always healthy options to everything Big Food and Big Pharma have made toxic, you just have to know where to look

Sodium nitrates are used to kill wild boars. Little tablets are used as bait and because the pigs don’t sweat like humans, the toxins can’t escape. Imagine how toxic sodium nitrates and nitrites are too all animals, they just take longer to kill certain species. Avoid hot dogs, bacon, deli meats and sausage at all costs. Check out liquid aminos, organic tamari, and organic garlic for spicing up your meals.

Tap water contains a powerful and deadly insecticide called sodium fluoride. It also contains other people’s medications, heavy metal toxins, and chlorine. You can buy an inexpensive water filtration system for your home and save thousands of dollars in the long run – it’s called Big Berkey and it’s the best on the market for the money.

Consuming genetically modified organisms means you’re eating chemical forms of bug killer and weed killer. Are you a bug or a weed? There is no way to prevent cancer if you eat chemicals all day, every day.

Artificial sweeteners trick your body into ingesting them, thus altering your cells. Don’t mutate your cells on purpose, because they will fight you later. Knowledge is power so use it.

There is a monstrous difference between conventional meat and organic. Organic won’t contain hormones or antibiotics, and the animals will not have been fed GMO corn, soy and alfalfa. You are what you eat, so don’t eat cancer. Plus, CAFO meat is usually ridden with pathogens and parasites from the unkempt quarters where they suffer, including cows, chickens, turkeys and pigs.

Conventional dairy products come from CAFO cows also, and then they’re processed through pasteurization and homogenization in order to remove some of the toxins and most of the nutrition, while adding new toxins.

Prescription medications, taken “as directed,” have killed more Americans than every war in history put together. Many pharmaceutical meds are opiate-based now, meaning you’re taking a diluted form of heroin.

Vaccines contain neurotoxins that humans should never even touch or eat, much less inject into muscle tissue. Beware of mercury (loaded in flu shots), formaldehyde, and infected African Green monkey kidney cells. Read the vaccine insert before even considering “immunizations.”

Even certified organic foods that are imported from China are loaded with heavy metal toxins from massive industry pollution. The USDA does not regulate this atrocity.

Go to Food.news for real news on healthy food versus toxic food. Only YOU can prevent cancer “fires.”


Infertility, Not Fertility Drugs, Linked to Raised Risk of Ovarian Cancer

Published: July 06, 2018

Source:https://www.cancercompass.com/cancer-news/article/62020.htm

(HealthDay News) -- Fertility drugs do not increase a woman's risk of ovarian cancer, a new study suggests.

It did find that infertility itself is associated with an increased risk of ovarian cancer.

The researchers examined data from more than 58,000 women in Denmark who had infertility treatments (ART, or assisted reproduction technology) between 1994 and 2015. The investigators then compared them with more than 549,000 women who did not undergo ART.

"We found that the higher risk of ovarian cancer among women having assisted reproduction treatment was only present among those with diagnosed female infertility," said study author Anja Pinborg. She is a professor in the fertility department at Rigshospitalet, Copenhagen University Hospital, in Denmark.

"And in a general population we saw that ovarian stimulation does not seem to increase the risk of ovarian cancer," she added.

The findings were presented July 3 at a meeting of the European Society of Human Reproduction and Embryology, in Barcelona. The study addresses long-held concerns that the fertility drugs could be a risk factor for ovarian cancer.

In a meeting news release, Pinborg said the results are "reassuring," and added that she "would advise infertile women contemplating ART treatment to go ahead. Ovarian stimulation itself is not introducing any excess risk of ovarian cancer."


Obesity affects prostate cancer test results

Published: July 05, 2018

Source:https://www.sciencedaily.com/releases/2018/07/180705114009.htm

University of Adelaide research shows that the results of the most widely used test for prostate cancer may be affected by obesity.

With increasing prevalence of obesity in high-income countries, this study published by the Society for Endocrinology, has important implications for detecting and monitoring the most common form of cancer in men.

Using data from 970 South Australian men from the Florey Adelaide Male Ageing Study, PhD student and medical oncologist Dr Adel Aref from the University's Adelaide Medical School and the Freemasons Foundation Centre for Men's Health, studied the effects of obesity on PSA levels detected in blood and the influence of the hormones, testosterone and estrogen.

Elevated levels of prostate specific antigen (PSA) in the blood can be an indicator of prostate cancer and lead to further diagnostic investigations," says Dr Aref.

PSA is increased by the male sex steroid hormone, testosterone. "We have shown for the first time that the concentration of PSA in the blood is lower in men with severe obesity (with a body mass index or BMI of 30 or higher) than in lean men, and that this can be attributed to lower concentrations of circulating testosterone."

"The results of this study have important implications for how we should interpret PSA levels in men who are obese," says project supervisor Professor Gary Wittert, Director of the Freemasons Foundation Centre for Men's Health and the Adelaide Medical School at the University of Adelaide and SAHMRI.

"Obesity is a major risk factor in the development of cancer, as well as other diseases. More than 65% of men in Australia are overweight or obese and this level is predicted to increase.

"Further studies are now required to investigate effective strategies for applying this knowledge in clinical practice" says Professor Wittert.


New tools used to identify childhood cancer genes

Published: July 03, 2018

Source:https://www.sciencedaily.com/releases/2018/07/180703190748.htm

Using a new computational strategy, researchers at UT Southwestern Medical Center have identified 29 genetic changes that can contribute to rhabdomyosarcoma, an aggressive childhood cancer. The group used Bayesian analysis, a method for statistical inference, in conjunction with screening using CRISPR/Cas9, the much-heralded gene-editing tool, to confirm the statistical predictions.

Their work helps to explain "the engine" driving formation of rhabdomyosarcoma and suggests potential treatments. Furthermore, their research method can be used to identify genetic drivers of other cancers.

Nearly all genes occur in cells as pairs. This research focused on genes for which there was only one copy or for which there were three or more copies.

"We came up with the idea that the altered expression of key cancer genes may be driven by genomic copy-number amplifications or losses. We then developed a new computational algorithm called iExCN to predict cancer genes based on genomewide copy-number and gene expression data," said Dr. Stephen Skapek, Chief of the Division of Pediatric Hematology-Oncology and with the Harold C. Simmons Comprehensive Cancer Center.

The work also used several new experimental tools, including CRISPR/Cas9 screening technology, to verify the function of these predicted cancer genes in rhabdomyosarcoma.

"The iExCN algorithm was developed based on Bayesian statistics, which is fundamentally different from commonly used statistics methodologies, and usually provides more accurate estimation of statistical associations, though it involves more complicated computation and longer processing time," said Dr. Lin Xu, Instructor in the Departments of Clinical Sciences and Pediatrics and with the Quantitative Biomedical Research Center.

Rhabdomyosarcoma, a cancer of developing skeletal muscle, is the most common soft tissue cancer in children. Using the algorithm to analyze genomic data from 290 rhabdomyosarcoma tumors, the researchers identified 29 associated genes, many of which had not previously been linked to rhabdomyosarcoma.

Dr. Yanbin Zheng, Assistant Professor of Pediatrics, used customized CRISPR/Cas9-based screens to verify these statistically predicted genetic causes of rhabdomyosarcoma. "Among the validated rhabdomyosarcoma genes, EZH2, CDK6, and RIPK2 are particularly worthy of further investigation because there are already drugs that target these genes that are either FDA-approved or in clinical trials," Dr. Zheng said.

Dr. Skapek, who holds the Distinguished Chair in Pediatric Oncology Research, said the group need to further verify the cancer-causing role of the iExCN-identified genes, but that the research is exciting. "We are exploring new strategies for targeted therapies that zero in on these genes," he said. "More important, our study represents a general approach that can be applied to identify oncogenic drivers and tumor-suppressor genes in other cancer types for which we have previously failed to uncover targetable vulnerabilities."


Sitting Tied to Raised Risk of Death From 14 Diseases

Published: July 02, 2018

Source:https://www.cancercompass.com/cancer-news/article/61989.htm

(HealthDay News) -- Get up off of the couch: Sitting too much may kill you even if you exercise regularly.

If you sit for six hours a day or more, your risk of dying early jumps 19 percent, compared with people who sit fewer than three hours, an American Cancer Society study suggests.

And, the study authors added, sitting may kill you in 14 ways, including: cancer; heart disease; stroke; diabetes; kidney disease; suicide; chronic obstructive pulmonary disease (COPD); lung disease; liver disease; peptic ulcer and other digestive disease; Parkinson's disease; Alzheimer's disease; nervous disorders; and musculoskeletal disorders.

"The simple message is that we should be moving more," said lead researcher Alpa Patel. She's strategic director of the cancer society's prevention study-3.

"The less sitting you do, the better it is for you," she said. "Breaking up an hour of sitting with 2 minutes of standing or light activity can improve cholesterol, blood sugar and blood pressure."

The study couldn't prove cause and effect, but it's clear that Americans are spending more time in their seats -- watching TV, working and playing on computers and smartphones. With age people sit more, and people with chronic disease spend even more sedentary time, the researchers noted.

An Australian study estimated that 90 percent of non-working time was sedentary, and that more than half of it was spent watching TV or sitting at computers.

It's not clear why prolonged sitting is unhealthy, Patel said. It's possible that people who spend a lot of time on the couch also have other unhealthy behaviors, such as excess snacking, she suggested.

In addition, prolonged sitting has been linked to higher levels of triglycerides, blood sugar, blood pressure and insulin. Sitting has also been tied to inflammation caused by obesity.

These consequences might explain why sitting was linked with death from heart, liver and kidney disease, as well as cancer, diabetes and COPD, Patel said.

It's less clear why death from suicide, Parkinson's and Alzheimer's, as well as nervous and musculoskeletal disorders, seems associated with sitting. For these, she said, it's possible that the conditions themselves result in more sedentary time.

The increased mortality risk differed by disease, ranging from 10 percent for cancer to 60 percent for musculoskeletal disease, Patel said.

For the study, Patel's team collected data on nearly 128,000 men and women who were part of an American Cancer Society prevention study. At the start of the study, all were free of major chronic diseases. During 21 years of follow-up, nearly 49,000 people died.

Dr. David Katz, director of the Yale-Griffin Prevention Research Center in Derby, Conn., said, "We have known for some time now that sitting for extended periods daily is injurious to health."

He noted that this study links excessive sitting to an increased risk of dying early from an array of causes -- everything from heart disease to suicide.

"Does this mean that sitting excessively increases suicide risk? That seems implausible," Katz said. "Perhaps depressed people lack the motivation to get up and go out. But then again, we know that routine activity is important to mental health, so some contribution of sedentariness to the severity of depression is not out of the question."

Even though more study is needed to figure out why sitting appears to boost the risk of early death, what to do about it is no mystery, he said.

"The remedy is at hand -- stand up, stretch, walk around; repeat often," said Katz, who's also a past president of the American College of Lifestyle Medicine.


Up to half of childhood cancer survivors will develop hormone disorders

Published: June 29, 2018

Source:https://www.sciencedaily.com/releases/2018/06/180629150142.htm

The Endocrine Society today issued a Clinical Practice Guideline advising healthcare providers on how to diagnose and treat the endocrine disorders that affect a significant portion of childhood cancer survivors in the United States today.

The guideline, titled "Hypothalamic-Pituitary and Growth Disorders in Survivors of Childhood Cancer: An Endocrine Society Clinical Practice Guideline," was published online and will appear in the July 2018 print issue of The Journal of Clinical Endocrinology & Metabolism (JCEM), a publication of the Endocrine Society. Recent data shows that almost 50 percent of these survivors will develop an endocrine disorder over their lifetime. The guideline provides recommendations on how to diagnose and manage certain endocrine and growth disorders commonly found in childhood cancer survivors.

Childhood cancer is relatively rare, and due to improvements in treatment and patient care, the current five-year survival rates exceed 80 percent. It's estimated that by 2020, there will be half a million childhood cancer survivors in the United States. These survivors face a greater risk of developing serious medical complications, even decades after cancer treatment ends. Endocrine disorders are especially prevalent among this population, often as a result of their previous treatments, particularly exposure to radiation therapy.

"Childhood cancer survivors have a high risk of developing endocrine disorders," said Charles A. Sklar, M.D., of the Memorial Sloan Kettering Cancer Center in New York, N.Y. Sklar chaired the writing committee that developed the guideline. "Our new guideline addresses the growing risk of endocrine disorders among childhood cancer survivors and suggests best practices for managing pituitary and growth disorders commonly found in this population. The guideline stresses the importance of life-long screening of these survivors for earlier detection and optimal patient care."

Recommendations from the guideline include long-term screening of childhood cancer survivors who underwent radiation therapy to the brain. This population should be screened for growth disorders, pituitary hormone deficiencies, and early puberty. If a condition is diagnosed, in most instances, clinicians should treat these survivors with the same approaches as other patients who develop endocrine conditions.

Other members of the Endocrine Society writing committee that developed this guideline include: Zoltan Antal of the New York Presbyterian Hospital, Weill Cornell Medical College and the Memorial Sloan Kettering Cancer Center in New York, N.Y.; Wassim Chemaitilly of St. Jude Children's Research Hospital in Memphis, Tenn.; Laurie E. Cohen of Boston Children's Hospital in Boston, Mass.; Cecilia Follin of Skane University Hospital in Lund, Sweden; Lillian R. Meacham of Emory University School of Medicine in Atlanta Ga.; and M. Hassad Murad of Mayo Clinic in Rochester, Minn.

The Society established the Clinical Practice Guideline Program to provide endocrinologists and other clinicians with evidence-based recommendations in the diagnosis, treatment, and management of endocrine-related conditions. Each guideline is created by a writing committee of topic-related experts in the field. Writing committees rely on evidence-based reviews of the literature in the development of guideline recommendations. The Endocrine Society does not solicit or accept corporate support for its guidelines. All Clinical Practice Guidelines are supported entirely by Society funds.

The Clinical Practice Guideline was co-sponsored by the European Society of Endocrinology and the Pediatric Endocrine Society. The Pituitary Society endorsed the guideline.


Study Confirms Denser Breasts Are More Prone to Cancer

Published: June 26, 2018

Source:https://www.cancercompass.com/cancer-news/article/61942.htm

(HealthDay News) -- Using automated breast density measurements, Norwegian researchers were able to more precisely confirm that women with dense breasts have a higher risk of breast cancer.

The study included more than 100,000 women and more than 300,000 screening exams.

"We found that screening examinations of women having dense breasts showed higher rates of recall and biopsy, and higher odds of screen-detected and interval breast cancers than women with non-dense breasts," said the study's senior author, Solveig Hofvind. She is a researcher and head of BreastScreen Norway for the Cancer Registry of Norway.

Dense breasts pose a challenge when it comes to cancer screening, because dense tissue shows up white on a mammogram. That's also how breast tumors look on a mammogram. Dense breast tissue can actually hide or mask cancers, according to Hofvind.

The findings were published June 26 in Radiology.

Dr. Liane Philpotts wrote an accompanying editorial. She is chief of breast imaging at the Yale School of Medicine.

"Dense breasts are not something that a patient feels. You can only tell if someone has dense breast tissue on a mammogram," Philpotts said.

Radiologists identify breast density using a standardized scoring technique from the American College of Radiology (ACR). The scoring system runs from A to D. A woman with an A or B doesn't have dense breasts, but someone with a C or D does, she explained.

About half of American women who are screened for breast cancer have dense breast tissue. As women age, their breasts often become less dense, Philpotts said.

Instead of using the ACR technique, which relies on a radiologist's subjective judgment, the new study used automated software -- known as automated volumetric analysis -- to classify breast density.

The Norwegian women in the study were between 50 and 69 years old. The automated software found dense breasts in 28 percent of their screening tests.

The rates of cancer were 6.7 per 1,000 exams for women with dense breasts and 5.5 for women with non-dense breasts, according to the findings.

"This study really shows that women with dense breasts did have more cancers. It wasn't a huge amount. It was a small increase, but it was an increase," Philpotts said.

In addition, women with dense breasts had more interval cancers. These are cancers found between screenings -- for example, when a woman feels a lump in her breast.

The study found that women with dense breasts were called back for more testing due to suspicious findings and were more likely to have a biopsy to check tissue for cancer than women without dense breasts.

Women with dense breasts also tended to have larger tumors when cancer was detected -- average of 17 millimeters (mm) vs. 15 mm for women without dense breasts.

The study also confirmed that it's harder to accurately identify breast cancers in dense breast tissue. Cancers were accurately detected in women with dense breasts 71 percent of the time compared to 82 percent for women without dense breasts.

"Automated volumetric breast density measurements may be considered a future standard for breast cancer screening, ensuring an objective density classification," Hofvind said.

Philpotts pointed out that the findings don't necessarily translate to a U.S. population, because the women screened in the study were older, and they were screened every other year instead of annually.

She said more research is needed to gauge the risks and benefits of the automated software. Hofvind agreed.

Women with dense breasts generally don't need to be screened more often, according to Philpotts. But they will need some sort of supplemental imaging such as ultrasound or MRI that's better at seeing the difference between dense tissue and cancerous tissue.


You are NOT born to be fat: Correct eating habits, not genetics, dictate how much you weigh

Published: June 23, 2018

Source:https://www.naturalnews.com/2018-06-23-you-are-not-born-fat-correct-eating-habits-not-genetics.html

(Natural News) Obesity is a complex medical condition in which excess body fat has already accumulated and may cause adverse effects on one’s health. It is usually defined by the body mass index and evaluated in terms of fat distribution and total cardiovascular risk factors. According to data gathered from the National Health and Nutrition Examination Survey, at least two in three adults were considered to be overweight or are suffering from obesity. Recently, between 2005 and 2014, there has been a significant increase in the prevalence of this condition among both men and women.

In the U.S. alone, 39.8 percent of their population is affected by obesity. It is estimated that the annual medical cost of a person who has obesity was $1,429 higher than those of normal weight.

Various risk factors come into play that directly lead to obesity – lifestyle and diet being the two most common. However, recent scientific studies have suggested that genetics may also play a significant role in determining why a person weigh so much.

It is known that genes can cause obesity in some disorders like Bardet-Biedl syndrome and Prader-Willi syndrome. However, the mechanism through which we understand the connection between genes and obesity has not been established clearly. While genes may cause obesity, there are still other environmental factors leading to this assumption.

Some of the main factors that need to be considered are eating habits, dietary consumption, and lifestyle. With this, a study was conducted and published in The American Journal of Clinical Nutrition wherein researchers explored whether eating behaviors can mediate or modify genetic susceptibility to obesity.

The study is designed to determine genetic risk factors by calculating the BMI of 3515 and 2145 adults in the FENLAND and EDEN population-based cohort studies. Meanwhile, a validated questionnaire was also given out to pinpoint the eating behavior of these adults. Eating behaviors were classified into different sectors – uncontrolled eating, emotional eating and cognitive restraint.

Cognitive restraint was defined as a conscious effort to limit and monitor one’s food intake to achieve their desired weight. With the use of Sobel test, researchers tested and assessed the mediating effect of each eating behavior associated with BMI-GRS and measured BMI. The researchers tried to determine whether eating behaviors lead to a significant increase or decrease of the respondent’s risk of genetic obesity.

The results of the study indicated that the association between BMI and BMI-GRS are intermediated by both uncontrolled eating and emotional eating behaviors of both sexes. Meanwhile, cognitive restraint is not associated with this mediator, except among EDEN women population.

This means that genetic susceptibility to obesity has a direct link in one’s eating behavior and habit. Reigning in on the top tier of risk factors are uncontrolled eating and emotional eating behavior.

This proves that even though a particular person is genetically designed to be obese, healthy eating habits still plays a major role in determining how much a person weighs. This rang true among EDEN women in this study who practices cognitive dietary restraint.

In achieving one’s desired weight and maintain be able to maintain good health, it is imperative to start with the basics of eating healthy. Daily exercise combined with proper diet can help combat obesity and other health conditions.

This study proved the assumption that people were not born to be fat and that with a little amount of hard work, genetics can no longer define a person – or weight, for that matter.


Novel therapy makes oxidative stress deadly to cancer

Published: June 21, 2018

Source:https://www.sciencedaily.com/releases/2018/06/180621000344.htm

Oxidative stress can help tumors thrive, but one way novel cancer treatments work is by pushing levels to the point where it instead helps them die, scientists report.

Adoptive T cell therapy appears to reprogram the metabolism of tumor cells, increasing their level of reactive oxygen species, or ROS, and their destruction, says Dr. Gang Zhou, immunologist at the Georgia Cancer Center and Department of Medicine at the Medical College of Georgia at Augusta University.

Scientists treated mice that had large, localized colorectal tumors with adoptive T cell therapy after preconditioning them with a chemotherapy drug known to help with the expansion and persistence of these infused T cells. The T cells are a patient's own cells, but engineered to better fight cancer.

The therapy appeared to deliver a deadly double-whammy to the cancer cells, says Zhou, corresponding author of the study in the journal Cell Metabolism.

The scientists found the treatment interfered with production of glutathione, a natural antioxidant found in all cells, as it heightened production and accumulation of ROS inside tumor cells.

Results included increased production by T cells of proinflammatory cytokines -- including tumor necrosis factor alpha -- which regulate many functions cancer needs to control like cell proliferation, differentiation and death.

"We started by asking questions about how immunotherapy can change the metabolism of tumor cells. Our studies show tumor necrosis factor alpha can act directly on tumor cells and induce ROS inside them," Zhou says.

The bottom line of the metabolic changes include, for example, complete tumor regression in nearly all the tested mice.

The scientists found similar effects -- higher ROS levels correlated with high tumor cell death -- when the therapy was used in models of breast cancer and lymphoma.

Tumor necrosis factor alpha appears key to these desired results following adoptive T cell therapy, because when the scientists eliminated it from the equation, tumor cell death decreased dramatically.

Scavenging ROS had a similar effect. When they gave the antioxidant N-acetylcysteine -- a precursor to glutathione -- it also hampered the curative effect of adoptive T cell therapy, they report.

They also found that tumor necrosis factor alpha synergizes with chemotherapy to increase oxidative stress and cancer cell death. And, that giving pro-oxidants -- drugs known to raise ROS levels -- can somewhat replicate the tumor-killing benefit of adoptive T cell therapy. It's known that these drugs may increase oxidative stress in cancer cells and push them toward death, or apoptosis, Zhou says.

"Their baseline is already high and if you further disrupt their ability to deal with these free radicals, they will go toward apoptosis," Zhou says.

In fact, in an apparent failed attempt to fight off the higher ROS, the scientists found increased expression of several antioxidant genes in treated tumor cells.

The significant, cancer-lethal ROS increases they found were limited to the tumor cells, not other nearby cell types.

The scientists note that the direct killing of tumors by ROS they saw does not negate the possibility that tumor necrosis factor alpha also is working through its previously known method of killing off blood supplies to tumors.

Antioxidant therapy in patients with active cancer has drawn mixed results, but most studies indicate that it worsens cancer, particularly in smokers, according to the National Cancer Institute. Preclinical studies in mice indicate the therapy promotes tumor growth and metastasis. Studies exploring the benefit of antioxidant therapy in preventing cancer have largely shown no benefit or harm, the NCI says.

Tumors are known to impact T cells. In fact scientists have shown that the two can compete for nutrition and energy in the tumor microenvironment, remote sites tumors establish to successfully spread, the scientists write. It's T cells that usually get short shrift in the struggle.

Comparatively little focus has been on what T cells do to tumors, Zhou and his colleagues report. But better understanding of that impact should help improve immunotherapies, like adoptive T cell therapy, that seek to enable T cells to better target tumors.

Adoptive T cell therapy is still under development for treatment of colorectal cancer. This therapeutic approach was already known to essentially poke holes in cancer cells to kill them.

ROS are chemicals like peroxide and superoxide that are byproducts of necessary body functions like the use of oxygen and energy production by cell powerhouses called mitochondria. One reason cancer cells have naturally higher ROS levels is they have a high energy demand, Zhou says, constantly working to grow and spread.

Some level of ROS also benefits our healthy cells, including cell proliferation and differentiation. But, too much is also deadly to normal cells, even damaging to DNA.

The research was supported by the National Institutes of Health and an American Cancer Society Research Scholar grant.


How pancreatic tumors lead to weight loss

Published: June 20, 2018

Source:https://www.sciencedaily.com/releases/2018/06/180620150153.htm

Patients with pancreatic cancer usually experience significant weight loss, which can begin very early in the disease. A new study from MIT and Dana-Farber Cancer Institute offers insight into how this happens, and suggests that the weight loss may not necessarily affect patients' survival.

In a study of mice, the researchers found that weight loss occurs due to a reduction in key pancreatic enzymes that normally help digest food. When the researchers treated these mice with replacement enzymes, they were surprised to find that while the mice did regain weight, they did not survive any longer than untreated mice.

Pancreatic cancer patients are sometimes given replacement enzymes to help them gain weight, but the new findings suggest that more study is needed to determine whether that actually benefits patients, says Matt Vander Heiden, an associate professor of biology at MIT and a member of the Koch Institute for Integrative Cancer Research.

"We have to be very careful not to draw medical advice from a mouse study and apply it to humans," Vander Heiden says. "The study does raise the question of whether enzyme replacement is good or bad for patients, which needs to be studied in a clinical trial."

Vander Heiden and Brian Wolpin, an associate professor of medicine at Harvard Medical School and Dana-Farber Cancer Institute, are the senior authors of the study, which appears in the June 20 issue of Nature. The paper's lead authors are Laura Danai, a former MIT postdoc, and Ana Babic, an instructor in medicine at Dana-Farber.

Starvation mode

In a 2014 study, Vander Heiden and his colleagues found that muscle starts breaking down very early in pancreatic cancer patients, usually long before any other signs of the disease appear.

Still unknown was how this tissue wasting process occurs. One hypothesis was that pancreatic tumors overproduce some kind of signaling factor, such as a hormone, that circulates in the bloodstream and promotes breakdown of muscle and fat.

However, in their new study, the MIT and Dana-Farber researchers found that this was not the case. Instead, they discovered that even very tiny, early-stage pancreatic tumors can impair the production of key digestive enzymes. Mice with these early-stage tumors lost weight even though they ate the same amount of food as normal mice. These mice were unable to digest all of their food, so they went into a starvation mode where the body begins to break down other tissues, especially fat.

The researchers found that when they implanted pancreatic tumor cells elsewhere in the body, this weight loss did not occur. That suggests the tumor cells are not secreting a weight-loss factor that circulates in the bloodstream; instead, they only stimulate tissue wasting when they are in the pancreas.

The researchers then explored whether reversing this weight loss would improve survival. Treating the mice with pancreatic enzymes did reverse the weight loss. However, these mice actually survived for a shorter period of time than mice that had pancreatic tumors but did not receive the enzymes. That finding, while surprising, is consistent with studies in mice that have shown that calorie restriction can have a protective effect against cancer and other diseases.

"It turns out that this mechanism of tissue wasting is actually protective, at least for the mice, in the same way that limiting calories can be protective for mice," Vander Heiden says.

Human connection

The intriguing findings from the mouse study prompted the research team to see if they could find any connection between weight loss and survival in human patients. In an analysis of medical records and blood samples from 782 patients, they found no link between degree of tissue wasting at the time of diagnosis and length of survival. That finding is important because it could reassure patients that weight loss does not necessarily mean that the patient will do worse, Vander Heiden says.

"Sometimes you can't do anything about this weight loss, and this finding may mean that just because the patient is eating less and is losing weight, that doesn't necessarily mean that they're shortening their life," he says.

The researchers say that more study is needed to determine if the same mechanism they discovered in mice is also occurring in human cancer patients. Because the mechanism they found is very specific to pancreatic tumors, it may differ from the underlying causes behind tissue wasting seen in other types of cancer and diseases such as HIV.

"From a mechanistic standpoint, this study reveals a very different way to think about what could be causing at least some weight loss in pancreatic cancer, suggesting that not all weight loss is the same across different cancers," Vander Heiden says. "And it raises questions that we really need to study more, because some mechanisms may be protective and some mechanisms may be bad for you."


Hypnosis may help reduce fear of cancer treatment in children

Published: June 19, 2018

Source:https://www.sciencedaily.com/releases/2018/06/180619122514.htm

Hypnosis could help to reduce the fear of medical procedures in children and young people with cancer.

New research led by the University of Exeter found promising evidence that hypnosis can reduce the fear and worry associated with injections and other needle procedures, such as extracting bone marrow.

Previous research has shown that these procedures often provoke more anxiety in children and young people than the cancer itself. Up to half of children with cancer experience clinically significant emotional distress. This can cause additional anguish for the child and for their families and have a long-lasting impact on mental health.

The Exeter team worked with Devon Integrated Children's Service to analyse all the available evidence on ways to reduce this anxiety without using drugs. The study is published in Psycho-Oncolgy and was supported by the National Institute for Health Research (NIHR) Collaboration for Leadership in Applied Health Research and Care South West Peninsula (PenCLAHRC).

Tamsin Ford, Professor of Child and Adolescent Psychiatry at the University of Exeter Medical School, said: "Getting a cancer diagnosis as a child is clearly extremely distressing for both the young person and their family. We must do all we can do to improve their mental health during this highly emotional time. Hypnosis is inexpensive to deliver, and our research found promise that it could help to reduce the fear and anxiety of multiple needle procedures. We now need high quality trials to demonstrate whether hypnosis should be adopted in clinics ."

The team also looked at evidence around listening to music, virtual reality and cognitive behavioural therapy, however the research was contradictory.

The paper, Effectiveness of non-pharmacological interventions to reduce procedural anxiety in children and adolescents undergoing treatment for cancer: a systematic review and meta-analysis, is published in Psycho-Oncolgy. Authors were Michael Nunns, Dominic Mayhew, Tamsin Ford, Morwenna Rogers, Christine Curle, Stuart Logan, and Darren Moore.


Laser-sonic scanner aims to replace mammograms for finding breast cancer

Published: June 18, 2018

Source:https://www.sciencedaily.com/releases/2018/06/180618102645.htm

For women over 40, mammography is a necessary yet annoying procedure to endure every year or two. The technique, while valuable for reducing breast cancer deaths, is less than ideal because it exposes patients to X-ray radiation and requires their breasts to be painfully squished between plates. The plates flatten the breast so the X-rays can more easily pass through it and produce a clear image.

Early detection has been shown to increase breast cancer survival rates, but many women avoid having their mammograms taken as often as they should because of the discomfort involved. A 2013 study found that as many as half of women who were avoiding their mammograms cited pain as the reason why.

Mammography also has trouble with breasts, such as those in young women, that are "radiographically dense," or somewhat opaque to X-rays. And mammography tends to overdiagnose, causing around half of women to receive a false-positive diagnosis at some point in their lives.

Caltech researchers say they have developed something better: a laser-sonic scanner that can find tumors in as little as 15 seconds by shining pulses of light into the breast. The scanning system, known as photoacoustic computed tomography, or PACT, was developed in the lab of Lihong Wang, Caltech's Bren Professor of Medical Engineering and Electrical Engineering.

PACT works by shining a near-infrared laser pulse into the breast tissue. The laser light diffuses through the breast and is absorbed by oxygen-carrying hemoglobin molecules in the patient's red blood cells, causing the molecules to vibrate ultrasonically. Those vibrations travel through the tissue and are picked up by an array of 512 tiny ultrasonic sensors around the skin of the breast. The data from those sensors are used to assemble an image of the breast's internal structures in a process that is similar to ultrasound imaging, though much more precise. PACT can provide a clear view of structures as small as a quarter of a millimeter at a depth of 4 centimeters. Mammograms cannot provide soft-tissue contrast with the level of detail in PACT images, Wang says.

Because the laser light at the currently used wavelength is so strongly absorbed by hemoglobin, PACT can construct images that primarily show the blood vessels present in the tissue being scanned. That's useful for finding cancer because many tumors grow their own blood vessels, surrounding themselves with dense networks of vascular tissue. Those vessels provide the tumors with large amounts of blood and allow the tumors to grow quickly.

During a PACT scan, the patient lies face down on a table that has a recess containing ultrasonic sensors and the laser. One breast at a time is placed in the recess, and the laser shines into it from underneath. Since the scan is quick, taking only 15 seconds, the patient can easily hold their breath while being scanned, and a clearer image can be developed.

"This is the only single-breath-hold technology that gives us high-contrast, high-resolution, 3-D images of the entire breast," Wang says.

The speed with which a PACT scan can be performed gives it advantages over other imaging techniques. For example, magnetic resonance imaging (MRI) scans can take 45 minutes. MRI scans are also expensive and sometimes requires contrast agents to be injected into the patient's blood.

"Gadolinium, for example, is a common contrast agent for MRI which is not totally innocuous," Wang says. "Gadolinium may cause nausea and vomiting, and can remain in the brain for years, with unknown long-term effects. In comparison, PACT is entirely safe; the blood serves as an intrinsic contrast agent, and the laser exposure is well within the safety limits."

In a recent pilot study, the researchers scanned the breasts of eight women using PACT, and correctly identified eight of the nine breast tumors that were present.

The PACT technology has already been licensed by a company, of which Wang is a founder and shareholder, that plans to commercialize it and conduct large-scale clinical studies, Wang says.

"Our goal is to build a dream machine for breast screening, diagnosis, monitoring, and prognosis without any harm to the patient," he says. "We want it to be fast, painless, safe, and inexpensive."

Wang says future research may focus on using PACT for imaging other parts of the body. It could give medical personnel the ability to assess the health of the vascular tissue in the extremities of a patient with diabetes, for example. Diabetes damages blood vessels and, if not properly diagnosed and treated, can cause tissue death, particularly in the feet. PACT is also able to differentiate between oxygenated and non-oxygenated blood; Wang says that could further improve the device's ability to find tumors, since cancer tissue, with its high oxygen demands, deoxygenates blood more rapidly than healthy tissue.


Vitamin D May Guard Against Colon Cancer

Published: June 15, 2018

Source:https://www.cancercompass.com/cancer-news/article/61860.htm

(HealthDay News) -- The sun you get when you mow the lawn or run errands could protect you against colon cancer, new research shows.

How? Sunlight prompts the production of vitamin D, and people with sufficient levels of the vitamin had a 22 percent lower risk of colon cancer, said lead researcher Marjorie McCullough. She's senior scientific director of epidemiology research for the American Cancer Society.

That risk also appears to decrease further as vitamin D levels rise, though the study did not prove that sunlight causes colon cancer risk to drop.

The chances of developing colon cancer decline about 19 percent in women and 7 percent in men for every incremental increase in blood vitamin D levels, the researchers found.

"It appeared across most of the range we were looking at, the relationship was linear," McCullough said.

Colon cancer is the third most common cancer and the third leading cause of cancer-related deaths in both men and women in the United States, with about 140,250 new cases and 50,630 deaths expected during 2018, the researchers said in background notes.

About 1 in every 24 women and 1 in every 22 men will develop colon cancer during their lifetime, they said.

"It has long been postulated that vitamin D deficiency can cause other problems besides osteoporosis and immune system dysfunction," said Dr. Len Horovitz, an internist with Lenox Hill Hospital in New York City who was not involved with the study.

"The suspicion that vitamin D deficiency might be responsible for the development of cancer is corroborated in this study, where vitamin D deficiency and colorectal cancer are linked," Horovitz said.

Don't start baking yourself to avoid colon cancer, however.

Only about 7 percent of the U.S. population have levels of vitamin D deficiency low enough to increase their risk of colon cancer, McCullough said.

"If you live in a sunny area year-round, or if you're living in an area where the spring and summer months are warmer, your levels will be higher just incidentally," McCullough said. "We do not recommend people seek sun exposure to raise their vitamin D levels, because UV radiation is a strong risk factor for skin cancer."

Vitamin D has long been associated with bone health, but the nutrient hasn't been recommended to protect against colon cancer or other health problems due to scant research, McCullough said.

When the U.S. National Academy of Medicine put out its vitamin D guidelines in 2011, it concluded that the medical evidence of vitamin D benefits for cancer were not sufficient enough to make a recommendation, she said.

To clear this up, McCullough and her colleagues combined data from 17 different studies involving 5,706 people with colon cancer and 7,107 healthy participants from the United States, Europe and Asia.

The researchers even reanalyzed blood samples from about a third of the participants, so they could perform a more direct apples-to-apples comparison across all of the 17 studies.

They concluded that vitamin D does indeed appear to provide protection against colon cancer, particularly for women.

Most people get enough vitamin D just by living their lives, McCullough said.

The sunlight you get from a casual walk down the street, running errands, and even walking from the car or train to your office building is sufficient to stimulate proper vitamin D production in your body, she said.

People also get vitamin D from fortified foods like milk, cereal and orange juice, and from fatty fish like salmon, tuna, trout and swordfish, McCullough said.

Because of this, people shouldn't rely on supplements to get their vitamin D, McCullough said. Heavy doses of vitamin D can be toxic.

"High-dose individual supplements are not recommended," she said.

It's not known exactly why vitamin D could protect against cancer, but researchers suspect the vitamin plays a role in controlling cell growth and promoting programmed cell death, McCullough said.

"Cancer occurs when there's uncontrolled growth and spread of abnormal cells," she said. "Experimental studies have shown that vitamin D can help to limit proliferation of abnormal cells."


Tomato extracts KILL stomach cancer cells, new study shows

Published: June 13, 2018

Source: https://www.naturalnews.com/2018-06-13-tomato-extracts-kill-stomach-cancer-cells-new-study-shows.html

(Natural News) When you think of cancer-fighting foods, what usually comes to mind? Perhaps you think of turmeric, ginger, or green tea, but what about tomatoes? You’re probably aware they’re good for you, but did you know they can actually reduce your risk of stomach cancer?

That was the finding of a study carried out by Temple University and the Mercogliano Oncology Research Center in Italy. The researchers analyzed the lipophilic extracts of whole tomatoes to determine their impact on the neoplastic features of cell lines in gastric cancer. They discovered that extracts taken from two tomato varieties in particular, San Marzano and Corbarino, could stop malignant stomach cancer cells from cloning and growing. The whole tomato extracts stopped the cells from migrating away from the primary tumor, causing them to die.

If you’re into cooking, you’re probably already familiar with San Marzano tomatoes, which are the preferred variety for pizza sauce. These plum tomatoes grow near Mount Vesuvius, where the rich volcanic soil gives them their distinctive sweet flesh and low acidity. Their meaty texture, thick skin, and relatively low amount of seeds combine to make them quite different from ordinary tomatoes. Corbarino tomatoes grow in the same area and boast similar characteristics.

The researchers say that the anti-tumor effects of these tomatoes do not come from specific components like lycopene alone; instead, their results indicate that the entire tomato needs to be consumed to reap the benefits. It’s a significant finding when you consider that stomach cancer is the world’s most common type of cancer. Their findings were published in the Journal of Cellular Physiology.

Tomatoes full of cancer-fighting lycopene

Despite being a staple in the Mediterranean diet, this is one of just a handful of studies to look at the effects of the entire tomato. However, different components of tomatoes have been studied extensively over the years for their cancer-fighting abilities. Lycopene, for example, has been explored in-depth for its ability to destroy free radicals. The antioxidant is what gives the tomatoes their red color. While small amounts can be found in watermelon, grapefruit, and guava, four-fifths of the lycopene in the average American’s diet comes from tomatoes and tomato products such as tomato juice, spaghetti sauce, and ketchup.

Studies have shown that lycopene can prevent cancers of the lung, prostate, stomach, colon, pancreas, esophagus, cervix, and breast. In addition, it can help reduce a person’s risk of cardiovascular disease thanks to its cholesterol and blood pressure lowering effects.

Further research is needed to explore whether other types of tomatoes could have a similar effect. It’s possible that some varieties have a greater effect than others, and it would be useful to find out which ones are the most powerful cancer fighters.

Start eating more organic tomatoes today

In the meantime, you can’t go wrong by incorporating more tomatoes into your diet. Choose organic varieties and try to buy local whenever possible. Cooking them increases the bioavailability of lycopene, as does consuming them with a fat like olive oil or cheese.

If you’re not a fan of cooked tomato dishes, experiment with different ways of consuming them raw – for example, sliced and drizzled with balsamic vinegar, chopped up in a green or pasta salad, or with other vegetables as part of a fresh homemade salsa. Don’t miss out on this powerful gift from nature!


Balanced Diet May Be Key to Cancer Survival

Published: June 12, 2018

Source:https://www.cancercompass.com/cancer-news/article/61823.htm

(HealthDay News) -- Eating a nutritionally balanced high-quality diet may lower a cancer patient's risk of dying by as much as 65 percent, new research suggests.

The finding that total diet, rather than specific nutritional components, can affect a cancer patient's prognosis "was particularly surprising to us," said the study's lead author, Ashish Deshmukh.

Total diet, he explained, was one that appeared to be "balanced" and "nutrient-rich" with a wide variety of vegetables, fruits, whole grains, proteins and dairy.

Deshmukh is an assistant professor with the University of Florida's College of Public Health and Health Professions.

To explore the impact of nutrition on cancer, the researchers sifted through data collected between 1988 and 1994 by the Third National Health and Nutrition Examination Survey (NHANES III). Almost 34,000 people were included in the survey, which asked all participants to offer up a 24-hour diet diary.

The team then used the U.S. Department of Agriculture's (USDA) "Dietary Guidelines for Americans" as a yardstick for ranking the nutritional quality of the diets used by 1,200 people who had been diagnosed with cancer.

The USDA guidelines specify serving recommendations for fruits, vegetables, whole grains, proteins, dairy, saturated fat, cholesterol and sodium.

In turn, all 1,200 patients were then tracked for an average of 17 years, with researchers verifying all subsequent deaths -- up to 2011 -- through the U.S. National Center for Health Statistics Linked Mortality Files.

By that point, half the cancer patients had died.

But the research team found that those who had consumed the most nutritious diets overall had a 65 percent lower risk for dying -- either from cancer or any other cause -- than those who had consumed the worse diets.

Deshmukh noted that the investigation did not assess the exact length of the survival benefit, nor did the researchers explore how exercise or other types of healthy behavior may impact cancer outcomes. Only an association was seen between diet and death risk, not a cause-and-effect link.

But the researchers noted that the overall strength of the protective benefit of eating well held up even after digging deeper to look at the specific risk of dying from certain types of cancer, including skin cancer and breast cancer.

"It is most critical that cancer survivors and their health care providers start talking about [a] balanced diet," said Deshmukh. "It is also crucial that cancer survivors work with their dietitians to identify a balanced diet regimen, and then follow that regimen.

"There are no harms [from] healthful eating," he added.

Marjorie Lynn McCullough is a senior scientific director of epidemiology research with the American Cancer Society. She noted that the "study had some limitations, such as not controlling for smoking, and evaluating older nutrition guidelines which have since been modified." She was not involved with the study.

But, she added, the findings are "generally consistent with growing evidence supporting recommendations to eat a healthy diet for cancer survivors."

Like the guidelines for cancer prevention, McCullough said, that means lowering the intake of sugar and empty calories by consuming "a mostly plant-based diet, including a variety of vegetables, whole fruits and whole grains, in addition to exercise and achieving and maintaining a healthy body weight.

"However, nutrition needs can vary during treatment, recovery and over the long term," she cautioned, "so cancer survivors should work with their health care practitioner to tailor advice on nutrition and physical activity to their situation."


Genetic markers for prostate cancer

Published: June 11, 2018

Source:https://www.sciencedaily.com/releases/2018/06/180611133830.htm

An international team of researchers including USC scientists has found scores of new genetic markers in DNA code that increase prostate cancer risk -- powerful knowledge likely to prove useful to detect and prevent the disease.

Focusing on DNA of more than 140,000 men worldwide, researchers were able to identify 63 new genetic markers associated with prostate cancer risk. That greatly increases the number of genetic risk regions, bringing the total to more than 170 and moving scientists closer to using genetic information for clinical treatment.

The results will help bridge the gap between cancer research diagnosis and treatment, equipping physicians with tools to screen at-risk patients. The study, based at USC with collaborators worldwide, including the London-based Institute of Cancer Research, was published today in Nature Genetics.

"This is not a cure, but the information can help to identify men at high risk of developing prostate cancer who may benefit from enhanced screening and future targeted prevention," said Christopher A. Haiman, professor of preventive medicine at the Keck School of Medicine of USC and a principal investigator for the project.

Prostate cancer is the second-most common cancer in American men, with one in nine men being diagnosed in their lifetime, and the third-leading cause of cancer death for men.

To identify genetic markers associated with prostate cancer risk, the researchers used "OncoArray," a new DNA analysis, to compare more than half a million single-letter changes in the DNA code of nearly 80,000 men with prostate cancer and more than 61,000 men without the disease. The researchers identified 63 new variants in DNA, which when inherited increased a man's risk of prostate cancer. Each individually had only a small effect on risk, but the combined effect of inheriting multiple variants could be dramatic.

The findings show that 1 percent of men at highest risk were 5.7 times more likely than the general population to develop prostate cancer -- an increase in absolute risk from about one in 11 to one in two. The researchers were able to identify that high-risk population because it inherited many of the harmful genetic variants.

And the top 10 percent in the population risk distribution were 2.7 times more likely to develop the disease than the general population -- corresponding to a risk of almost one in four.

With the addition of dozens more genetic markers to previously known markers, almost 30 percent of a man's inherited risk of prostate cancer has been accounted for -- which may now be enough to start using the information in practical testing strategies, according to the study.

"We now have the ability to identify men at greater risk of prostate cancer," Haiman said. "We now need to figure out how to use this genetic information to prevent the disease."

These genetic markers may also one day help guide treatment for prostate cancer. Many of the new genetic variants were found in the region of genes involved in communication among cells of the immune system and other cells in the body. This implies that genetic errors in immune pathways may be affecting prostate cancer risk, which could have important implications for potential future treatment of prostate cancer with immunotherapies.

The study comes with caveats. For example, it focuses on white males only. Haiman said parallel studies are underway to study other ethnic groups. For reasons unknown, African-American men face a 74 percent greater risk of prostate cancer than in non-Hispanic white men, according to the American Society of Clinical Oncology.

The global scope of the project enabled researchers to collect massive amounts of DNA and compare genetic variants, which was key to achieving critical mass to make new discoveries. About 200 researchers worldwide participated, including experts from the United States, United Kingdom, Sweden, Canada, Germany, China, Finland, Belgium, Spain, Poland, Malaysia and Croatia, among others.

Five scientists from the Keck School of Medicine participated in the study, including Haiman, Sue Ann Ingles, Mariana C. Stern, David V. Conti and the late Brian E. Henderson, who proposed the study more than three years ago. Henderson was a former dean of the Keck School, first director of the Zilkha Neurogenetic Institute and director of the USC Norris Comprehensive Cancer.

Aside from non-melanoma skin cancer, prostate cancer is the most common cancer among men in the United States. It is also one of the leading causes of cancer death among men of all races. The U.S. Centers for Disease Control estimates 172,258 men in the United States were diagnosed with prostate cancer and 28,343 men died from prostate cancer in 2014, the most recent year such data is available.

The study was supported by a National Institutes of Health grant (U19CA148537). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.


Not just for coffee: Cinnamon found to have potent anti-cancer effects in latest research

Published: June 10, 2018

Source:https://www.naturalnews.com/2018-06-10-not-just-for-coffee-cinnamon-potent-anti-cancer-effects-research.html

(Natural News) A study published in BMC Complementary and Alternative Medicine has established that Cinnamomum cassia, or more commonly known as Chinese cinnamon, has been found to have anti-cancer effects.

The study was a collaborative effort from researchers at the National Institute of Forest Science, Andong National University, and Kyonggi University in South Korea. In particular, they took an extract from the twigs of the Chinese cinnamon, which they studied its ability to prevent cell growth and induce cell death (apoptosis) in human colorectal cancer cells. To understand the antiproliferative effect, that is, the ability to inhibit growth, of the extract – as well as the change of protein or mRNA levels – of the extract, researchers used an MTT assay to check cell activity, including a Western blot, and RT-RCR, respectively.

Based on the findings, researchers discovered that extracts derived from the twigs of the Chinese cinnamon were able to reduce the chances of human colorectal cancer cells to infiltrate other cells successfully. In particular, this was successful because the extract decreased cyclin D1 protein levels, which had a role in cell proliferation. They also found that the extract stimulated apoptosis by activating ROS-dependent NF-κB and ATF3.

The researchers then concluded that Chinese cinnamon could be used as an agent in treating colorectal cancer. “This study may support the anti-cancer property of TC-HW [C. cassia extracts] from and our data will provide the complementary and alternative use of TC-HW for cancer treatment,” they wrote.

Cinnamon and its other health benefits

In the U.S., the most common type of cinnamon sold is the cassia variety. On the other hand, Ceylon cinnamon (C. zeylanicum) is another variety of cinnamon that is more difficult to find, making it more expensive. Cinnamon is made by cutting the stems of the Cinnamomum tree, in which the inner bark is then extracted while the woody parts are removed. Upon drying, it forms strips that curl into rolls called cinnamon sticks, which can be grounded to form the cinnamon powder. The oily part of cinnamon gives its distinct smell and flavor. This part is also abundant in a compound called cinnamaldehyde. This compound is responsible for most of the beneficial effects of cinnamon. More than just a spice, cinnamon has been known for its medicinal properties for thousands of years. Listed below are some of the health benefits of cinnamon:

  • It is rich in antioxidants – Cinnamon is rich with powerful antioxidants, such as polyphenols, which protect the body from oxidative stress.
  • It fights inflammation – Inflammation is good for the body, but it becomes a problem when it is chronic and is directed against the body’s own tissues. Some studies suggest that the antioxidants of cinnamon have anti-inflammatory effects that may help reduce the risk of disease.
  • It may lower the risk of heart problems – According to studies, cinnamon can improve cholesterol, triglycerides, and blood pressure — all of which are key risk factors for heart disease.
  • It improves insulin sensitivity and lowers blood sugar levels – Cinnamon can significantly reduce insulin resistance. It can also lower blood sugar by reducing the amount of glucose that enters the bloodstream after a meal. Cinnamon also has a compound that can act on cells by imitating insulin, improving glucose uptake by cells.
  • It may be beneficial on neurodegenerative diseases – Cinnamon has been shown to improve Alzheimer’s disease and Parkinson’s disease in various animal studies.

Breaking through a tumor's defenses

Published: June 7, 2018

Source:https://www.sciencedaily.com/releases/2018/06/180607112732.htm

In research published today, Babraham Institute researchers have shown that some tumours use not one but two levels of protection against the immune system. Knocking out one level boosted the protective effects of the second and vice versa. The research demonstrates that a two-pronged approach targeting both cell types simultaneously may offer a promising route for the development of new cancer immunotherapies.

The development and growth of a cancerous tumour often occurs despite a fully functioning immune system, capable of recognising and killing cancer cells. Tumours hijack certain cells in our immune system to create a growth-permissive environment and give protection from the anti-tumour elements. In particular, tumours recruit immune cell allies, cells called tumour-associated macrophages (TAMs) and regulatory T cells (Treg), to evade immune attack.

Specifically inhibiting the recruitment of TAMs by blocking the actions of a protein called colony-stimulating factor 1 (CSF1) reduces tumour growth in mouse models. Although clinical trials of inhibitors targeting TAMs are underway, results in patients haven't been as effective as hoped. A lack of understanding of how TAMs promote tumour progression potentially limits the therapeutic value of these inhibitors.

Likewise, inhibiting the action of Treg cells in mice by inactivating a key enzyme called PI3K delta gives protection against a range of tumours. A PI3K delta inhibitor is approved for treatment of chronic lymphocytic leukaemia (CLL) and follicular non-Hodgkin lymphoma (NHL), but the potential for PI3K delta inhibitors for the treatment of solid cancers in humans is yet to be demonstrated.

The research published today used a mouse model of colorectal cancer to explore the synergy between TAMs and Treg cells, showing that each cell type was able to compensate for the effects of the loss of the other to maintain the tumour's protection from the immune system. However, jointly inhibiting TAMs and Treg cells substantially inhibited tumour growth.

Dr David Gyori, first author on the paper, said: "Strikingly, preventing tumour immunosuppression by both TAMs and Treg cells caused almost complete tumour rejection by the immune system and half of the mice became completely tumour-free. Taken together, our findings provide a convincing rationale for assessing the clinical value of combinatorial therapies targeting the CSF1 receptor and PI3K delta."

Professor Klaus Okkenhaug, one of the authors on the study by Gyori et al. and a parallel study by Lim et al. said: "Harnessing the power of the immune system to kill cancer cells is becoming a successful therapeutic strategy. These studies demonstrate the importance of fully understanding the interplay between the many elements of the immune system to ensure that combinatorial therapies are both synergistic and effective."


Colonoscopies, Endoscopies Carry Greater Infection Risk Than Thought: Study

Published: June 6, 2018

Source:https://www.cancercompass.com/cancer-news/article/61772.htm

(HealthDay News) -- Getting a colonoscopy or an endoscopy may be riskier than you thought.

Researchers report that the rate of infections following these procedures at outpatient ambulatory surgery centers could be 100 times higher than previously believed, a new study finds.

Bacterial infections such as E. coli and Klebsiella can strike 1 in 1,000 patients after a screening colonoscopy, nearly 2 in 1,000 after a non-screening colonoscopy, and more than 3 in 1,000 after an endoscopy, the study authors said.

Previously, it had been believed that the rate of infection after endoscopy was 1 in 1 million, the researchers noted.

"Though patients are routinely told that common endoscopic procedures are safe, we found that post-endoscopic infections are more common than we thought, and that they vary widely from one … facility to another," said lead researcher Susan Hutfless, an assistant professor of medicine at Johns Hopkins University in Baltimore.

More than 15 million colonoscopies and 7 million upper-GI endoscopies are performed with an endoscope each year in the United States. An endoscope is a reusable optical instrument that let's an endoscopist view a patient's gastrointestinal tract. The scopes can be used to check for diseases such as colon cancer, or to perform a number of procedures, such as polyp removal, without the need for invasive surgery, the study authors said.

Using an insurance claim database, Hutfless and her colleagues gathered data from six states -- California, Florida, Georgia, Nebraska, New York and Vermont. They tracked emergency room visits for infections and hospital admissions for seven and 30 days after a colonoscopy or endoscopy at an outpatient specialty center.

Hutfless' team also found that people who had been hospitalized before one of the procedures had even a greater risk of infection.

In fact, nearly 45 in 1,000 patients hospitalized within 30 days before a screening colonoscopy went to the hospital within a month suffering from an infection. For those hospitalized before an endoscopy, the rate of infections was more than 59 per 1,000.

Although outpatient centers that perform these procedures were established more than 40 years ago, they have gained popularity over the last 20 years because they are more convenient and less expensive than hospitals.

In 2017, according to the Ambulatory Surgery Center Association, 64 percent of these clinics were owned by doctors and 28 percent were affiliated with hospitals or health care systems. Because these centers often don't maintain electronic medical records, they are not likely to be aware that patients are being infected during their procedures.

"If they don't know their patients are developing these serious infections, they're not motivated to improve their infection control," Hutfless said in a Hopkins news release.

While the majority of these outpatient centers follow strict infection-control guidelines, the researchers found that rates of infections at some centers were more than 100 times higher than expected.

Endoscopy and colonoscopy have revolutionized treatment and prevention of gastric diseases, but patients should be aware of the risk of infection associated with these procedures, the researchers concluded.


Here’s why you should avoid a high-carb diet if you have cancer

Published: June 5, 2018

Sourcehttps://www.naturalnews.com/2018-06-05-heres-why-you-should-avoid-a-high-carb-diet-if-you-have-cancer.html

(Natural News) Most people think that having cancer is like winning a twisted lottery: Your chances of being selected are pretty slim, but once you are picked, your life changes forever. There’s just one problem – cancer isn’t something you get, it’s a disease primarily caused by unhealthy diets and poor lifestyle choices.

In particular, people who are yet to undergo cancer treatment still consume a diet full of carbohydrates and various forms of sugar increase their risk of cancer recurrence, and in severe cases, mortality, according to an article in the International Journal of Cancer. In the study, lead author Anna Arthur of the University of Illinois at Urbana–Champaign added that conversely, eating fats and starchy foods in moderation could reduce these risks.

Researchers looked at what cancer patients were eating before and after their treatment and their corresponding health outcomes. The study, which ran for over two years, involved 400 patients from the University of Michigan Head and Neck Specialized Program of Research Excellence (Head and Neck SPORE) who were recently diagnosed and treated for head and neck squamous cell carcinoma (HNSCC).

HNSCC is the collective term for cancers that develop from the squamous cells that line mucosal surfaces inside the head and neck. The usual areas where HNSCC develop include the oral cavity, throat, larynx (or voice box), the paranasal sinuses and sinus cavity, and the salivary glands.

Using the Harvard Food Frequency Questionnaire, the researchers were able to identify which food items, beverages, and supplements patients had taken a year before they were diagnosed with cancer. The team discovered that those who ate the most amounts of total carbohydrates and sugars – especially sucrose, fructose, lactose, and maltose – a year prior to their treatment were most likely to die from any cause during their follow-up period, according to Arthur. In the same vein, these people consumed, on average, at least 4.4 servings of simple carbohydrates, which included refined grains, desserts, and sugar-sweetened beverages – a far cry from the 1.3 servings of those who ate the lowest amounts. Also, the most commonly diagnosed HNSCC types include the tonsils and the base of the tongue including its surrounding tissues, with nearly 70 percent of diagnoses made at the later stages of the disease.

In the follow-up period, more than 17 percent of patients had a recurring case, with 42 patients dying from it. Researchers also noted that 70 participants died from other causes.

Of the results, Arthur explained that the cancer type and stage also played a role in concert with carbohydrate consumption. Those who consumed the highest amounts of carbohydrates and sugars had oral cavity cancer. Likewise, the two factors were also linked to an uptick in mortality risk in people with stages 1-3 cancer, but not stage 4.

“Although in this study we found that higher total carbohydrate and total sugar were associated with higher mortality in head and neck cancer patients, because of the study design we can’t say that there’s a definitive cause-effect relationship,” she added. “The next step would be to conduct a randomized clinical trial to test whether carbohydrate restriction has a protective effect on survival rates.”

There’s still a silver lining to this study: Eating a moderate amount of various forms of fat and starch after treatment may improve a patient’s survival rate and increase his chances of remission, researchers pointed out.

“Our results, along with the findings of other studies, suggest that diet composition can affect cancer outcomes,” co-author Amy Goss of the University of Alabama at Birmingham (UAB) explained. “We’d like to determine if this is true using a prospective, intervention study design and identify the underlying mechanisms. For example, how does cutting back on sugar and other dietary sources of glucose affect cancer growth?”

For patients with HNSCC, this is great news: Among all cancers, the five-year survival rates of patients with this type of cancer are low since these are detected in later stages.

“This observational study is noteworthy because it focuses on a serious cancer that is difficult to treat, and little is known about how nutrition can best help a patient battling it,” added Dr. Laura Rogers, a co-author of the study and a professor of nutrition sciences at UAB. “This study reiterates the importance of additional intervention studies that test optimal diet recommendations for cancer survivors.”


Many breast cancer patients can skip chemo, big study finds

Published: June 4, 2018

Source:http://www.foxnews.com/health/2018/06/03/many-breast-cancer-patients-can-skip-chemo-big-study-finds.html

Most women with the most common form of early-stage breast cancer can safely skip chemotherapy without hurting their chances of beating the disease, doctors are reporting from a landmark study that used genetic testing to gauge each patient's risk.

The study is the largest ever done of breast cancer treatment, and the results are expected to spare up to 70,000 patients a year in the United States and many more elsewhere the ordeal and expense of these drugs.

"The impact is tremendous," said the study leader, Dr. Joseph Sparano of Montefiore Medical Center in New York. Most women in this situation don't need treatment beyond surgery and hormone therapy, he said.

The study was funded by the National Cancer Institute, some foundations and proceeds from the U.S. breast cancer postage stamp. Results were discussed Sunday at an American Society of Clinical Oncology conference in Chicago and published by the New England Journal of Medicine. Some study leaders consult for breast cancer drugmakers or for the company that makes the gene test.

MOVING AWAY FROM CHEMO

Cancer care has been evolving away from chemotherapy — older drugs with harsh side effects — in favor of gene-targeting therapies, hormone blockers and immune system treatments. When chemo is used now, it's sometimes for shorter periods or lower doses than it once was.

For example, another study at the conference found that Merck's immunotherapy drug Keytruda worked better than chemo as initial treatment for most people with the most common type of lung cancer, and with far fewer side effects.

The breast cancer study focused on cases where chemo's value increasingly is in doubt: women with early-stage disease that has not spread to lymph nodes, is hormone-positive (meaning its growth is fueled by estrogen or progesterone) and is not the type that the drug Herceptin targets.

The usual treatment is surgery followed by years of a hormone-blocking drug. But many women also are urged to have chemo to help kill any stray cancer cells. Doctors know that most don't need it, but evidence is thin on who can forgo it.

The study gave 10,273 patients a test called Oncotype DX, which uses a biopsy sample to measure the activity of genes involved in cell growth and response to hormone therapy, to estimate the risk that a cancer will recur.

WHAT THE STUDY FOUND

About 17 percent of women had high-risk scores and were advised to have chemo. The 16 percent with low-risk scores now know they can skip chemo, based on earlier results from this study.

The new results are on the 67 percent of women at intermediate risk. All had surgery and hormone therapy, and half also got chemo.

After nine years, 94 percent of both groups were still alive, and about 84 percent were alive without signs of cancer, so adding chemo made no difference.

Certain women 50 or younger did benefit from chemo; slightly fewer cases of cancer spreading far beyond the breast occurred among some of them given chemo, depending on their risk scores on the gene test.

WILL PEOPLE TRUST THE RESULTS?

All women like those in the study should get gene testing to guide their care, said Dr. Richard Schilsky, chief medical officer of the oncology society. Oncotype DX costs around $4,000, which Medicare and many insurers cover. Similar tests including one called MammaPrint also are widely used.

Testing solved a big problem of figuring out who needs chemo, said Dr. Harold Burstein of the Dana-Farber Cancer Institute in Boston. Many women think "if I don't get chemotherapy I'm going to die, and if I get chemo I'm going to be cured," but the results show there's a sliding scale of benefit and sometimes none, he said.

Dr. Lisa Carey, a breast specialist at the University of North Carolina's Lineberger Comprehensive Cancer Center, said she would be very comfortable advising patients to skip chemo if they were like those in the study who did not benefit from it.

Dr. Jennifer Litton at MD Anderson Cancer Center in Houston, agreed, but said: "Risk to one person is not the same thing as risk to another. There are some people who say, 'I don't care what you say, I'm never going to do chemo,'" and won't even have the gene test, she said. Others want chemo for even the smallest chance of benefit.

Adine Usher, 78, who lives in Hartsdale, New York, joined the study 10 years ago at Montefiore and was randomly assigned to the group given chemo.

"I was a little relieved. I sort of viewed chemo as extra insurance," she said. The treatments "weren't pleasant," she concedes. Her hair fell out, she developed an infection and was hospitalized for a low white blood count, "but it was over fairly quickly and I'm really glad I had it."

If doctors had recommended she skip chemo based on the gene test, "I would have accepted that," she said. "I'm a firm believer in medical research."


How might baking soda boost cancer therapy?

Published: June 1, 2018

Source:https://www.sciencedaily.com/releases/2018/06/180601134720.htm

A Ludwig Cancer Research study has uncovered an entirely novel mechanism by which cells enter a state of dormancy as tissues starved of oxygen become increasingly acidic. The study, led by Chi Van Dang, scientific director of the Ludwig Institute for Cancer Research, has potentially significant implications for cancer therapy: Large swaths of solid tumors are often deprived of oxygen, and cells in such patches are thought to be a major source of drug resistance and disease relapses.

Published today in the journal Cell, the study details how in response to acidity cells turn off a critical molecular switch known as mTORC1 that, in ordinary conditions, gauges the availability of nutrients before giving cells the green light to grow and divide. That event, Dang and his colleagues show, shuts down the cell's production of proteins, disrupting their metabolic activity and circadian clocks, and pushing them into a quiescent state. They also demonstrate that this acid-mediated effect might be relatively easy to reverse -- a finding that could help improve a variety of cancer therapies.

"In tumors grafted into mice, we see mTOR activity in spotty places where there's oxygen," says Dang who is also a professor in the Molecular and Cellular Oncogenesis Program at The Wistar Institute. "But if you add baking soda to the drinking water given to those mice, the entire tumor lights up with mTOR activity. The prediction would be that by reawakening these cells, you could make the tumor far more sensitive to therapy."

Baking soda had previously been reported to enhance cancer immunotherapy by one of the co-authors of the new study, Robert Gillies of the H. Lee Moffitt Cancer Center, though the mechanism underlying the effect was unclear.

Dang's team, including co-corresponding author Zandra Walton, an MD-PhD student at the University of Pennsylvania Perelman School of Medicine, discovered that mechanism through an intricate series of experiments done at the University of Pennsylvania and Dang's Ludwig lab at the Wistar Institute. It centers on the behavior of lysosomes -- a sack-like cellular organelle that digests proteins and that mTOR moves to when it is ready for action.

The researchers show that in acidic conditions protein motors propel lysosomes carrying mTOR away from the area around the nucleus, where they're ordinarily located. This separates mTOR from a protein required for its activation, RHEB, which continues to hang around at that location. Lacking one of its key activation signals, mTOR remains dormant, suspending the synthesis of proteins -- including the components of the cell's molecular clock -- along with most metabolic activity.

"Cells don't want to make proteins or other biomolecules when they're under stress," says Dang. "They want to slow things down and only awaken when things return to normal."

The researchers show that baking soda can reverse this effect. When given to mice in their drinking water, it surprisingly sufficed to neutralize the acidity of hypoxic patches in tumors. This sent lysosomes zipping back to the nuclear periphery in cells -- where RHEB was waiting -- and restored the activity of mTOR.

All this is relevant to cancer because researchers have long known that quiescent cells cannot typically be killed by chemotherapy. Notably, Dang and his team also found that T cell activation, which is essential to most immunotherapies, is similarly compromised under acidic conditions.

"We started out with a question about oxygen starvation and the circadian clock, and we ended up discovering a new mechanism by which acidic conditions in tissues shut off a lot of things -- including the cell's molecular clock," muses Dang.

The finding that something as simple as baking soda could possibly help reverse this effect and render quiescent cancer cells susceptible to cancer therapies excites Dang.

"The concept is so easy," he says. "It's not some $100,000 per year drug. It's literally just baking soda." Dang and his team are now looking into how acidity might affect immunotherapy and further exploring the acid-induced quiescence of cancer cells.


Many Breast Cancer Survivors Not Getting Needed Mammograms

Published: May 31, 2018

Source:https://www.cancercompass.com/cancer-news/article/61713.htm

(HealthDay News) -- After surviving a diagnosis of breast cancer, women still need regular screening. But many of them, especially black women, aren't getting the mammograms they need, a new study finds.

It's essential to screen for a return of cancer so it can be treated before symptoms appear, the researchers explained.

"The use of regular mammograms to detect a return of breast cancer before any symptoms appear is associated with better overall survival," said lead researcher Dr. Kathryn Ruddy, director of cancer survivorship at the Mayo Clinic Cancer Center in Rochester, Minn.

"Therefore, clinicians need to make sure that their patients are fully aware of the role these annual mammograms play in screening for new breast cancers as well as for local recurrences," she added. "Creating and implementing survivorship care plans with clear follow-up instructions may help ensure that more survivors adhere to recommended screening schedules."

For the study, Ruddy and her colleagues followed more than 27,000 women for several years after breast cancer surgery. Women who had both breasts removed were excluded, because mammograms are no longer needed for them.

Of the nearly 4,900 women remaining in the study after five years, the researchers tracked how well they kept up with their annual breast cancer screening.

One year after surgery, 13 percent of the women had not had a mammogram. Five years later, the number of women who hadn't had a mammogram in the past year rose to 19 percent, the researchers found.

Over five years, only 50 percent of the women had at least one mammogram each year, Ruddy's team found.

The researchers also found that black women were less likely than white women to get yearly mammograms. Lack of screening may contribute to higher death rates among black women, because recurrence of breast cancer is a major cause for poor outcomes in black women, the researchers said.

The findings were published May 24 in the Journal of the National Comprehensive Cancer Network.

"This lack of imaging follow-up represents a missed opportunity for identifying recurrent or new breast cancers among a high-risk patient subgroup," said Dr. Benjamin Anderson in a journal news release. He is a professor of surgery and global health medicine at the University of Washington and vice chair of the network's Guidelines Panel for Breast Cancer.

"Of equal importance, this finding illustrates that our health care system can fail to track sizable groups of cancer patients after completion of treatment," Anderson said.


New Guidelines Lower Colon Cancer Screening Age to 45

Published: May 30, 2018

Source:https://www.cancercompass.com/cancer-news/article/61693.htm

(HealthDay News) -- Most people should now begin colorectal cancer screening at age 45, say new guidelines that were spurred by the rising rate of the disease among younger Americans.

For years, the American Cancer Society (ACS) and other medical groups have advised people at average risk of colon and rectal cancer to begin screening at age 50. Earlier screening has been reserved for people at increased risk.

But the ACS is now changing that advice -- a shift largely driven by the fact that colorectal cancers are increasingly being diagnosed in younger Americans.

Media personality Katie Couric, a longtime advocate in the fight against colon cancer, applauded the move.

"I have seen first-hand the dangers of early onset colon cancer. My late husband, Jay Monahan, was just 41 when he was diagnosed more than 20 years ago," she said in a statement.

"Doctors have noticed an alarming trend -- an increase in people like Jay, under age 50, being diagnosed with the disease," Couric added. "I'm thrilled that the American Cancer Society has responded and revised its guidelines, lowering the recommended age to start screening to 45."

Just last year, an ACS study found that since the mid-1990s, colon cancer rates among Americans aged 20 to 54 have been steadily inching up -- by between 0.5 percent and 2 percent each year. Rectal cancer has risen more rapidly, by 2 percent to 3 percent per year.

Someone born in 1990 now has twice the risk of colon cancer, and four times the risk of rectal cancer, as someone born in 1950, the new report noted.

"It's going up at a pretty alarming rate. And we don't know why," said Dr. Andrew Wolf, who led the ACS guidelines development group.

"Everyone wants to say that it's the obesity epidemic, poor diet and lack of exercise," Wolf said. "But those things do not fully explain the rise."

And, since most people do not start colorectal cancer screening until age 50, changes in screening rates would not account for the increase among younger Americans, he added.

However, it's not certain that screening at age 45 will save more lives, according to Wolf. Clinical trials are the "gold standard" for proving that -- and most trials of screening have not included people younger than 50.

But the ACS commissioned a "modeling" study in developing the new guidelines. It used existing data to estimate the effects of screening at age 45. The conclusion was that earlier screening had a better "benefit-risk ratio" than screening at age 50.

Americans aged 45 to 49 do have a lower rate of colorectal cancer than those aged 50 to 54 -- at about 31 cases per 100,000 people, versus 58 per 100,000.

But, the ACS said, the higher rate among people in their early 50s is partly because they have more early cancers detected through screening. So, the true risk of the disease among people in their late 40s may actually be similar.

The risks of screening, meanwhile, are low, Wolf said. Those hazards are mainly confined to colonoscopies -- which can, rarely, puncture the colon wall or cause significant bleeding.

But those low odds would be even lower in younger people, Wolf explained. Plus, he added, colonoscopy is only one of the options for screening. Others include a yearly stool test looking for hidden blood, or a DNA-based stool test done every three years.

The ACS is not recommending any particular approach.

"The choice should be based on what tests are available, and the patient's personal preferences," Wolf said. "People should be informed of all their choices."

Guidelines from other groups still recommend age 50 as the screening starting point for most people. They do, however, advise earlier screening for certain people at heightened risk -- such as those with a strong family history of the disease.

The American College of Gastroenterology already recommends that black people begin at age 45, due to their relatively higher risk.

The group is in the process of updating its screening guidelines, a spokesperson said.

Earlier this year, Memorial Sloan Kettering Cancer Center, in New York City, launched a program for colon cancer patients younger than 50. One goal is to research the reasons for the rising incidence, said Dr. Andrea Cercek, an oncologist at Sloan Kettering.

She said rates are not only increasing among people in their 40s, but also among those in their 20s and 30s (though the incidence at those ages remains low). So, screening at age 45 does not address the whole issue, Cercek noted.

To her, there is a key message for people of all ages: "If you do develop persistent gastrointestinal symptoms -- lasting longer than a few days -- don't dismiss them," Cercek said.

Some red flags include a persistent change in bowel habits; abdominal pain or cramping; stool that is dark or has visible blood; and unintended weight loss.

In a young person, Cercek noted, gastrointestinal symptoms likely stem from an infection or other non-cancerous condition.

"But the point is to have it checked out," she said.

If it is colorectal cancer, early detection makes a huge difference. "It's very curable when we catch it early," Cercek said.


How to Do a Self-Check for Skin Cancer

Published: May 26, 2018

Source:https://www.cancercompass.com/cancer-news/article/61677.htm

(HealthDay News) -- Learning how to do a skin self-exam could save your life.

"Skin cancer is one of the few cancers you can see with the naked eye," said Dr. Ali Hendi, an assistant clinical professor of dermatology at Georgetown University Medical Center in Washington, D.C.

"Yet sadly, many people don't know how to be their own hero when it comes to skin cancer, including what to look for on their skin or when to see a board-certified dermatologist," he added in an American Academy of Dermatology news release.

Skin cancer is the most common cancer in the United States. One in five Americans develops skin cancer, and one person dies every hour from melanoma, the deadliest form of the disease.

To check your skin, use a full-length mirror to examine your entire body, front and back. Then, raise your arms and look at your right and left sides, Hendi said.

Bend your elbows and carefully check your forearms, underarms and palms. Look at the backs of your legs and feet, between your toes, and the soles of your feet. With nail polish removed, check your fingernails and toenails, as well.

Use a hand mirror to check the back of your neck and scalp, and part your hair for a closer look. Finally, check your back and buttocks with a hand mirror. Ask a partner to help check your back and other hard-to-see areas.

"While performing a skin self-exam, keep in mind that skin cancer can develop anywhere on the skin, not just in areas that are exposed to the sun," Hendi said.

"If you notice any new spots on your skin, scalp or nails, spots that look different from other spots on your body, or spots that are changing, itching or bleeding, make an appointment to see a board-certified dermatologist," he advised.

Hendi also explained the ABCDEs of checking for melanoma.

A is for Asymmetry: One half of a spot is unlike the other half.

B is for Border: The spot has an irregular, scalloped or poorly defined edge.

C is for Color: Colors vary from one area of the spot to another, from shades of tan, brown or black, for instance, or areas of white, red or blue.

D is for Diameter: When diagnosed, melanomas are usually larger than 6 millimeters (about the size of a pencil eraser), but can be smaller.

E is for Evolving: The spot looks different or is changing in size, shape or color.

See a medical professional if you have any of these signs or notice an existing mole start to change in any way.

"When detected early, skin cancer, including melanoma, is highly treatable, making it imperative to check your skin regularly," Hendi said. "It only takes a few minutes to check your skin, and it could save your life."


Heavier Women May Face Higher Cancer Risks, Study Finds

Published: May 24, 2018

Source:https://www.cancercompass.com/cancer-news/article/61661.htm

(HealthDay News) -- Excessive weight gain is never a good idea for health. Now, new research supports the notion that putting on pounds raises cancer risks for middle-aged women.

The study, which tracked more than 137,000 Norwegian women for 18 years, found that the odds of developing certain cancers rose as waistlines expanded.

The take-home message: "maintaining stable weight in middle adulthood … as well as avoiding excess body weight are both of importance for prevention of several obesity-related cancers in women," the researchers said.

For the study, Marisa da Silva and colleagues at the Arctic University of Norway in Tromso collected data on women who took part in the Norwegian Women and Cancer study from 1991 to 2011.

The researchers looked specifically for the risk of obesity-related cancers, including certain myelomas and cancers of the breast, colon, endometrium (lining of the uterus), ovaries, pancreas, kidneys, gallbladder, stomach, liver, esophagus, brain and thyroid.

Over 18 years of follow-up, nearly 10,000 women developed obesity-related cancers, da Silva's team found.

Although the study couldn't prove cause and effect, obesity was tied to a rise in the risk of postmenopausal breast cancer by 20 percent and kidney cancer by 95 percent.

The largest increase was seen in endometrial cancer, with obese women more than twice as likely to develop it, compared with women of normal weight.

The researches also focused on 82,000 women whose weight changed over the follow-up period. More than 5,300 of these women developed obesity-related cancers over the study period.

Among women who gained 22 pounds or more, the risk for breast cancer rose 36 percent and 40 percent for endometrial cancer. But the largest risk was for pancreatic cancer, which saw a 91 percent increased risk for women who gained this level of weight in middle age.

Two U.S. obesity experts said they weren't surprised by the connections.

"It is widely known that obesity increases your risk of medical conditions such as hypertension, sleep apnea and diabetes," said Dr. Heather McMullen, who directs bariatric surgery at Northwell Health's Syosset Hospital in Syosset, N.Y.

"This article highlights that obesity, as well as significant weight gain in women, increases risk of certain cancers," she said.

The exact reasons for the link remain unclear, added Dr. Mitchell Roslin, chief of obesity surgery at Lenox Hill Hospital in New York City.

He noted that increases in an older woman's weight can trigger a rise in estrogen and other hormones that, in turn, have been linked to higher odds for endometrial and breast cancer. The elevated blood sugar levels that accompany obesity might also have ties to cancer risk, Roslin said.

Whatever the link, "we need to begin to understand that what we eat can be a powerful medicine or alternatively a promoter of disease," Roslin said. "While the impact of obesity on diabetes and heart disease gets attention, the impact of obesity on cancer is not discussed as frequently."

The results of the study were scheduled to be presented Wednesday at the European Congress on Obesity, in Vienna, Austria. Research presented at medical meetings is typically considered preliminary until published in a peer-reviewed journal.


Lycopene, the pigment that gives tomatoes their color, is one of the most powerful anti-cancer agents yet discovered

Published: May 22, 2018

Source:https://www.naturalnews.com/2018-05-22-lycopene-tomatoes-powerful-anti-cancer-agent.html

(Natural News) Whether or not tomatoes are your favorite part of a salad (or pizza), there are certainly good reasons to include as many of them in your diet as possible. One of the greatest reasons is the fact that the lycopene that gives tomatoes their beautiful color is one of the most potent anti-cancer agents yet discovered by scientists.

Though researchers have been aware of lycopene’s powerful anti-cancer capabilities for over 30 years, more recently, a significant amount of research has gone into unlocking just how this compound can best be used as part of the cancer fighting arsenal.

LifeExtension Magazine notes that cancer is the second leading cause of death in the United States, affecting over 21 million Americans at any given time. The fact that lycopene can effectively prevent and treat cancer is therefore vitally important.

What is lycopene and how does it work?

Lycopene is found not only in tomatoes, but also in pink grapefruit, papaya and watermelon. It is a carotenoid – a type of pigment that gives some red fruits their beautiful hue. Lycopene is a powerful antioxidant that neutralizes free radicals in the body, preventing DNA damage and helping cells to function optimally. (

As reported by FitDay, in addition to its cancer fighting credentials, lycopene has also been proven to reduce heart disease risk by 50 percent, reduce the risk of arteriosclerosis (a build-up of plaque in the arteries), protect the skin from UV radiation damage caused by excessive sun exposure, and fight the signs of aging.

What the science says about lycopene and cancer

NaturalHealth365 recently reported on various studies confirming lycopene’s ability to fight prostate, ovarian and skin cancer:

A new review of studies published in Journal of Biological Regulators and Homeostatic Agents credits lycopene with interfering with the proliferation of cancer cells and slowing the progression of the disease. The team reported that lycopene also helps prevent malignant tumors from metastasizing, or spreading to other sites in the body.

Another study, published in the Journal of Cellular Physiology, found that tomato extracts interfere with the ability of cancer cells to clone themselves.

Extensive studies have also been undertaken to examine the potential of lycopene to fight ovarian cancer – considered to be the most lethal of all gynecological cancers.

A study published in the American Journal of Cancer Research found that when mice which had been implanted with human ovarian cancer cells were given lycopene, their tumors were dramatically reduced in number. In addition, when some of the mice were given conventional chemotherapy drugs like paclitaxel and carboplatin, the effects of the drugs were enhanced by the lycopene, meaning that fewer toxic drugs needed to be administered.

With regard to prostate cancer, way back in the mid-1980s, researchers at the prestigious Harvard University Medical School discovered that the lycopene in tomatoes can protect men from developing this fairly common cancer.

Skin cancer doesn’t stand a chance against lycopene, either. A recent study published in the Journal of Cellular Biology found that when skin cells were exposed to lycopene before being subjected to high levels of UV radiation, the likelihood of developing skin cancer was reduced and apoptosis – cancer cell “suicide” – was encouraged.

All things considered, there are many reasons to eat as many tomatoes as possible. And growing your own fresh, delicious varieties at home will be a rewarding experience in more ways than one.


Berries and Grapes May Keep You Breathin' Easy

Published: May 21, 2018

Source:https://www.cancercompass.com/cancer-news/article/61612.htm

(HealthDay News) -- Adding more grapes and berries to your diet is a tasty way to give your lung health a boost, new research suggests.

Folks who ate the most foods with a particular type of flavonoid, called anthocyanins, maintained the best lung function as they aged, researchers said. Anthocyanins are found in dark-pigmented fruits and vegetables such as red grapes, blueberries and purple potatoes.

"A diet rich in fruits and vegetables can help protect the lungs against damage, preserving their functionality and reducing the risk of developing respiratory diseases later in life," said the study's lead author, Vanessa Garcia-Larsen.

She explained that by the time people are 30 years old, they've generally reached their peak lung capacity.

"After this time, lung function started to slowly decline for everyone. The speed of decline will vary from one person to another, depending on several factors, such as smoking, physical activity, exposure to certain pollutants and the presence of other medical conditions," Garcia-Larsen explained. She's an assistant professor of human nutrition at Johns Hopkins Bloomberg School of Public Health in Baltimore.

Processed foods, such as cured meats, have been shown in previous studies to be linked with a steeper decline in lung function, according to Garcia-Larsen.

But the new study found that those who ate a large amount of dark-colored fruits and vegetables had a slower per year decline in lung function compared to those who ate fewer of these anthocyanin-filled foods.

"This slower decline was evident even after taking into account other important factors, such as smoking and age," she said.

However, the study was only designed to find an association; it cannot prove cause and effect.

Samantha Heller, a registered dietician at NYU Langone Health System in New York City, said the findings make sense.

"Anthocyanins have been shown to have really positive health effects. They're full of antioxidants, and if you eat a whole piece of fruit, you're getting a whole lot of other healthy compounds, too," she said.

"Plus, there's less room on the plate for the less healthy foods. And, it's not just one type of food that's key for good health," Heller noted. "Everything that's plant-based works together to help fight disease and protect against cell damage."

The study included 463 adults from Norway and England. Their average age was 44.

The participants all completed dietary questionnaires and a lung function test at the start of the study. Ten years later, their lung function was tested again.

The researchers saw a relationship between anthocyanin consumption and lung health -- the more people ate, the better their lung health.

According to Garcia-Larsen, "Foods rich in anthocyanin flavonoids might protect the lungs through their antioxidant and anti-inflammatory properties, which have been extensively demonstrated in experimental studies."

She added that a few hours after eating foods such as berries, there's evidence of the flavonoids in lung tissue. This "suggests that [anthocyanin-foods] might have a functional role protecting the lungs against the pollutants and other environmental insults," such as smoking, Garcia-Larsen noted.

These dark-pigmented fruits and vegetables seemed to be most helpful for people who never smoked and those who had quit smoking. Smokers should stop, Garcia-Larsen said, because it's the best thing they can do for their lungs.

The toxins in smoke may impair the ability of antioxidants or anti-inflammatory effects to counteract smoking damage. But when smokers quit, she said, they did get a benefit from anthocyanin in fruits and veggies.

Garcia-Larsen is scheduled to present the findings Monday at an American Thoracic Society meeting in San Diego. Findings presented at meetings are typically viewed as preliminary until they've been published in a peer-reviewed journal.


Men May Gain More From Cancer Immunotherapy

Published: May 17, 2018

Source: https://www.cancercompass.com/cancer-news/article/61569.htm

(HealthDay News) -- Male cancer patients seem to fare significantly better following immunotherapy treatment than female patients, new research indicates.

"Both sex and gender can potentially affect the strength of the body's immune response," explained study author Dr. Fabio Conforti, from the European Institute of Oncology in Milan, Italy.

For example, Conforti noted that women generally show stronger immune responses than men in reaction to medical treatment. That, he said, seems to explain why infections occur less frequently -- and are often less serious -- among women than men, and why women also typically respond better to vaccines than men.

"On the other hand, women account for roughly 80 percent of all patients with systemic autoimmune diseases worldwide," Conforti said. "Therefore, it's possible that differences in the immune system of women and men could be relevant to the natural course of chronic inflammatory conditions such as cancer, and potentially how they respond to drugs."

The new finding is based on a review of 20 studies that assessed survival rates among cancer patients. All were treated with immunotherapy drugs, a type of advanced cancer therapy developed over the last decade that has now become the standard treatment for several types of cancer, including melanoma and non-small-cell lung cancer.

Taken together, the studies had enrolled more than 11,000 patients. Researchers found that all the patients fared better on immunotherapy treatment than they would have on another treatment (or no treatment at all). But following treatment, male cancer patients saw their survival extended by twice as much as female patients.

Patients in the studies were struggling with advanced cancers, including melanoma, kidney cancer, urothelial cancer, head and neck cancer, and lung cancer.

The investigators noted an important caveat in their finding: In roughly half of the studies women only accounted for less than a third of participants, making it hard to conclusively identify gender differences in outcomes.

Conforti and his colleagues reported their findings in the May 17 issue of The Lancet Oncology.

In an accompanying editorial, Omar Abdel-Rahman, of Ain Shams University in Cairo, Egypt, and the University of Calgary in Canada, wrote that "caution needs to be exercised before jumping directly to radical conclusions and before changing the current standard of care."

He noted that the analysis includes a diverse group of solid tumors that might act differently in men and women.

"Moreover, there are also lifestyle or behavioral characteristics that differ between men and women that might also have confounding effects," Abdel-Rahman added.


Colon Polyp Type May Be Key to Cancer Risk

Published: May 15, 2018

Source:https://www.cancercompass.com/cancer-news/article/61546.htm

(HealthDay News) -- The type of colon polyp that's spotted during a colonoscopy may help predict the likelihood of colon cancer, new research shows.

These polyps -- also called adenomas -- can be labeled advanced or non-advanced, explained researchers at the University of Pittsburgh School of Medicine.

Their study of almost 16,000 patients who underwent colonoscopy found that the long-term risk for colon cancer was 2.5 times greater for those with advanced polyps, compared to people without such growths.

On the other hand, non-advanced polyps did not increase the likelihood of developing the disease. These patients had the same risk as those who didn't have polyps, the investigators found.

"That's a provocative finding," said study lead researcher Dr. Robert Schoen. "It would suggest that if you have a polyp that is non-advanced, which is the case in about one-third of people undergoing screening, you don't need to come back as frequently for colonoscopy because your risk of cancer is the same as if you didn't have any polyps."

Schoen is a professor of medicine and epidemiology at the university. The study was funded by the U.S. National Institutes of Health.

Colonoscopies can spot early cancers and in many cases can even prevent the disease as doctors remove potentially harmful polyps.

"One can actually prevent people from getting cancer, which is far better than just detecting it early," Schoen said. "But polyps are commonly found, and patients can find themselves returning for frequent follow-up colonoscopy procedures."

To find out if the type of colon polyp influences a patient's prognosis, Schoen's group tracked 15-year outcomes for 15,900 people who underwent a colonoscopy as part of a major U.S. cancer screening trial.

When the study began, colonoscopies revealed that 18 percent of patients had an advanced polyp, 32 percent had a non-advanced polyp, and 50 percent did not have any pre-cancerous polyps.

The study, published May 15 in the Journal of the American Medical Association, found that those with advanced polyps had a higher risk for colon cancer for the duration of the study.

"After an advanced polyp has been removed, the whole colon remains at risk for cancer, and periodic colonoscopy is needed," Schoen said.

But people with non-advanced polyps had the same long-term risk for cancer as those without polyps.

Schoen noted that, in the United States, people with one or two non-advanced polyps are typically advised to return for a repeat screening in five to 10 years.

The new study questions whether that might be necessary.

"Bringing everyone back at five years is incurring a lot of testing that may not be preventing much cancer because only a small fraction of polyps will ever turn into cancer," Schoen said. "Millions of people are receiving follow-up colonoscopy exams for non-advanced polyps. We need to find out what is necessary. Potentially, this is an area where we could reduce testing and costs."

Dr. David Weinberg is chair of the department of medicine at Fox Chase Cancer Center in Philadelphia. Looking over the new findings, he stressed that most people will never develop advanced colon polyps.

Weinberg agreed that the new findings question the wisdom of routine 5-year follow-up colonoscopies for people with low-grade polyps versus advanced growths.

"Colonoscopy is a relatively finite resource, even in the United States," he said. "Given the higher risk over time in patients with advanced adenomatous polyps, particular efforts should be devoted to making sure that these patients are regularly followed to identify colon polyps and remove them."


What Causes Cancer? Misconceptions Abound.

Published: May 14, 2018

Source:https://www.cancercompass.com/cancer-news/article/61527.htm

(HealthDay News) -- Many people are clueless about what can actually cause cancer, a new study finds.

Not stress, microwave ovens or food additives, British experts say.

But a survey of more than 1,300 people in England found many folks believe otherwise.

"It's worrying to see so many people endorse risk factors for which there is no convincing evidence," said study author Samuel Smith, of the University of Leeds.

More than a third wrongly believed that electromagnetic frequencies and eating genetically modified food were cancer risk factors.

Others believed microwave ovens (19 percent) or drinking from plastic bottles (15 percent) caused cancer, despite a lack of scientific evidence.

The researchers also found that more than 4 out of 10 thought stress or food additives caused cancer.

When it came to known causes of cancer, 88 percent of respondents correctly said smoking, 80 percent cited secondhand smoke, and 60 percent said sunburn.

People who had mistaken beliefs about the causes of cancer were not more likely to have risky lifestyle habits. But those who knew more about proven causes of cancer were less likely to smoke, according to the study.

"Compared to past research it appears the number of people believing in unproven causes of cancer has increased since the start of the century," Smith said in a Cancer Research UK news release.

It could be related to changes "to how we access news and information through the internet and social media," he speculated.

"It's vital to improve public education about the causes of cancer if we want to help people make informed decisions about their lives and ensure they aren't worrying unnecessarily," Smith added.


Cancer Docs: We Need More Research on Medical Marijuana

Published: May 10, 2018

Source:https://www.cancercompass.com/cancer-news/article/61513.htm

(HealthDay News) -- Most cancer doctors say they don't know enough about medical marijuana to provide an informed opinion to patients.

Nevertheless, many go ahead and give its use their blessing, a national survey reveals.

Seven out of 10 oncologists surveyed in the United States said they aren't informed enough about the risks and benefits of medical marijuana to recommend its use to patients, according to findings published May 10 in the Journal of Clinical Oncology.

But eight out of 10 cancer doctors said they've discussed medical marijuana with patients in the past year, and 46 percent have gone so far as to recommend its use in cancer treatment.

This is a "concerning discrepancy," said Dr. Ilana Braun, chief of Dana-Farber Cancer Institute's division of adult psychosocial oncology, in Boston.

"We can think of few other instances in which physicians would offer clinical advice about a topic on which they do not feel knowledgeable," Braun said.

Currently, there are 30 states with medical marijuana laws on the books, and almost all name cancer as a qualifying condition for its use, Braun said.

However, pot remains an illegal substance under federal law, restricting research opportunities into its effectiveness as a medical treatment. "The scientific evidence base supporting use of medical marijuana in oncology remains thin," Braun said.

To assess how cancer doctors are grappling with this issue, Braun and her colleagues surveyed a nationally representative random sample of 400 oncologists.

The responses revealed that:

Only 30 percent of cancer doctors felt sufficiently informed to make recommendations regarding medical marijuana.

About 46 percent recommended its use, regardless.

Of those who recommended its use, 56 percent admitted that they did not consider themselves well-informed enough to have done so.

Braun said more research needs to be done regarding the medical effectiveness of marijuana, as well as potential harmful effects.

For example, patients with immune systems wrecked by chemotherapy could be at increased risk of a fungal infection from pot use, she noted.

The best review of medical marijuana's usefulness, released in 2017 by the National Academy of Sciences, found very mixed evidence when it comes to cancer treatment, Braun said.

The report found conclusive evidence that oral medications containing THC, the intoxicating chemical in pot, can reduce the impact of chemotherapy-induced nausea and vomiting.

But the report found no evidence one way or the other regarding medical marijuana's ability to treat the lack of appetite and wasting caused by cancer.

There's substantial evidence that pot is an effective treatment for chronic pain in adults, but it's not known if marijuana can help fight cancer pain in particular.

Braun's survey found that 67 percent of cancer doctors felt that medical pot could be a useful adjunct to standard pain management, and 65 percent said it could help patients with their lack of appetite.

Dr. Andrew Epstein, an oncologist with Memorial Sloan Kettering Cancer Center in New York City, said doctors may not have a full grasp of the issue, but that should not necessarily cause great concern.

"If oncologists are recommending something which is blatantly unsafe, then that would be one thing. I think marijuana has a lack of evidence behind some things for benefit and may have some downsides, but I do not think marijuana, per se, is a highly risky therapy," Epstein said. "I am less concerned than the authors about this."

In fact, Epstein argues that the debilitating effects of cancer and cancer treatment -- pain, appetite loss, nausea, depression -- "are potentially more debilitating than any potential medication interactions this plant would have with cancer treatments."

Cancer doctors appropriately consider medical marijuana as an adjunct therapy to be used alongside other established treatments, Epstein said.

"Oncologists are welcoming something that might have benefit outweighing harm in their toolbox, along with all the other things they already have," he said.

At the same time, Epstein agrees with Braun that more research and better medical education is needed, so doctors can provide patients the most well-informed advice they can.

Better medical education surrounding marijuana "would help with the knowledge base of these things, so oncologists could become even more knowledgeable participants in helping guide patients and families," Epstein said.


A new connection between glucose and lipid regulation in cancer metabolism

Published: May 08, 2018

Source:https://www.sciencedaily.com/releases/2018/05/180508102206.htm

Researchers at Albert Einstein College of Medicine and Shanghai Jiao Tong University School of Medicine in China have identified an enzyme that helps cancer cells make the building materials they need to quickly proliferate. Inhibiting this enzyme could be a strategy to slow down cancer growth, leading to more effective treatments. The study was published in the April 27 issue of the Journal of Biological Chemistry.

Whereas healthy human cells get most of the fatty acids and cholesterol they need to build their cell membranes from the bloodstream, cancer cells cannot wait for their building materials to be delivered by this route. Instead, cancer cells frequently ramp up the activity of the enzymes involved in synthesizing lipids right in the cell.

One of these families of enzymes is the sterol regulatory element binding proteins, or SREBPs. SREBPs travel into cell nuclei and turn on genes involved in lipid production, usually in response to specific signals. In some cancer cell lines, including certain liver, colon and breast cancers, a particular SREBP called SREBP1a is overactive.

Fajun Yang, an associate professor of developmental and molecular biology at Albert Einstein, studies exactly how cancer cells supply themselves with lipids. The newly published research on SREBP1a began when Xiaoping Zhao, the lead author on the new study, was a postdoctoral fellow in Yang's lab, and continued as a collaboration when Zhao started his own lab at Shanghai Jiao Tong University.

In the new study, the team found that SREBP1a was able to be overactive in cancer cells thanks to another enzyme, pyruvate kinase M2 (PKM2). PKM2 was coincidentally also known to be involved in supplying hungry cancer cells with surplus energy through a different mechanism: by chemically modifying a small molecule called pyruvate during glucose metabolism. In the new study, the researchers showed that PKM2 was also able to modify SREBP1a.

"Nobody had previously said that this guy, PKM2, regulates lipid metabolism," Yang said. "So actually we saw that this is a new connection between a glucose metabolism regulator and a lipid metabolism regulator. In cancer cells, both become abnormally activated."

When PKM2 and SREBP1a interact, the SREBP1a becomes more stable, the study showed. This allows SREBP1a to turn on genes involved in lipid synthesis. Using a small protein that could block the interaction, the authors were able to stop the excess lipid production and slow down cancer cell growth.

"The cancer cell kind of feels like, 'Oh, I'm fasting to death!'" Yang said. "The tumor cells become especially sensitive; even though they can suck up lots of glucose, they cannot make the building blocks of the cell membrane. If combined with another drug, then this is a potential therapeutic approach."

The approach is promising because it targets proteins that are not highly expressed in healthy cells. If cancer cell growth could be slowed down by blocking this pathway, patients might require lower doses of the toxic drugs that actually kill the cancer cells, and thus experience fewer side effects.

The study was funded by the National Natural Science Foundation of China and the National Institutes of Health.


Study confirms curable state between single and widespread cancers

Published: May 07, 2018

Source:https://www.sciencedaily.com/releases/2018/05/180507084829.htm

In 1995, two University of Chicago-based cancer specialists suggested there was an intermediate state -- somewhere between curable localized cancers and lethal widespread disease -- for patients with metastatic cancer.

Those physicians, Samuel Hellman and Ralph Weichselbaum, both still at the University of Chicago, labeled that clinically significant intermediate state "oligometastasis," Greek for "a few that spread." They focused on tumors that had migrated from an initial cancer in the colon or rectum to one or a few distant sites.

They also made the controversial suggestion that many of these patients, depending on the extent of disease burden, could be cured with surgery or targeted radiation therapy.

Twenty-three years later, Weichselbaum, Hellman, the Pritzker Distinguished Service Professor Emeritus and former dean of the biological sciences at the University of Chicago, and colleagues, working with patients in treatment for colorectal cancer, have confirmed their oligometastasis hypothesis and for the first time have identified molecular patterns that can be used to predict which patients are most likely to benefit from surgery, leading to long-term survival.

"This is a paradigm shift in the treatment of metastatic disease," said Weichselbaum, MD, the Daniel K. Ludwig Distinguished Service Professor, chair of radiation and cellular oncology at UChicago and director of the Ludwig Center for Metastasis Research.

"Our results point to a molecular basis for oligometastasis that can pretty reliably predict clinical outcomes. In a series of colorectal cancer patients with limited spread of disease to the liver, we were often able to achieve prolonged survival. We think this approach could be applied to many types of cancer."

In the May 4, 2018, issue of the journal Nature Communications, the researchers describe results from 134 patients (median age 61) with cancer of the colon (72 percent) or rectum (28 percent) that had spread to the liver. These patients were treated with perioperative chemotherapy (5-flourouracil based) followed by surgical removal of all detectable signs of cancer that had spread to the liver.

"We performed DNA sequencing, RNA sequencing for gene expression, microRNAs and microsatellite instability for each patient," Weichselbaum said. The data sort patients into three distinct groups -- subtypes 1, 2 and 3 -- with about a third in each group. "This is a separation, primarily based on molecular analysis," Weichselbaum said.

Group 2 had the highest 10-year survival rates, followed by Group 1 and Group 3 with just 20 percent.

When the team took a closer look at the tumor microenvironment around cancers that had spread to the liver, however, they found that subtype-2 tumors seemed to trigger an immune response that helped rein in new tumor growth.

So they selected those subtype 2 tumors and reclassified them, based on their molecular determinants combined with clinical data.

This predicted a robust difference in survival for the low-risk group. They had a 94 percent chance of 10-year overall survival. In this revised classification system, Groups 1 and 3 had 10-year overall survivals of 45 percent and 19 percent, respectively.

Our results "open the door to look at broader sets of metastasis," Weichselbaum said. "Oligo is just a subset, a lower bound of metastasis. We want to know what happens when a patient has a little more than oligo. We arbitrarily started thinking of treating one to five metastases. Now we want to see if maybe, combined with other therapies, we could treat 10 or 20."

The findings provide a "framework for integrated classification and treatment of metastasis," the authors wrote. This study, the first to combine clinical and molecular data to treat limited metastatic disease, was able to amplify predicted differences. The results should improve treatment of patients with potentially curable colorectal liver metastases.


Debunking cancer myths: Few cancers come from an inherited gene, according to the scientists

Published: May 04, 2018

Source:https://www.naturalnews.com/2018-05-04-debunking-cancer-myths-few-cancers-come-from-an-inherited-gene-according-the-scientists.html

(Natural News)  Is cancer genetic? While many people believe that cancer simply runs in their family, science tells us that very few cancers are actually caused by genes inherited from our parents. In fact, estimates suggest that only about 5-to-10 percent of all cancers stem from an inherited gene. Even the National Cancer Institute admits the fact that hereditary cancers are, in reality, quite rare.

In spite of this, many people wrongly believe that they are doomed to get cancer just because a family member had it. But as the American Cancer Society notes, cancers that appear to run in families are not inherently caused by faulty genes. Families often share similar lifestyle habits — whether it be in regards to diet, exercise, tobacco use or alcohol consumption, these are all things that can influence your cancer risk independent of your genetics. It’s well-established that kids often pick up on their parents’ habits.

By definition, cancer is a genetic disease — but not in the way we typically think of “genes.” This too can be confusing; we often think of genes as being what we inherit from our parents and pass down to our children. But your genes are so much more than that: They are the blueprint which lays the foundation for every cell in your body.

Cancer is caused by changes to genes which disrupt the way your cells function, particularly regarding cell growth and division. In this way, cancer is a “genetic” disease — if effects genes. But for the vast majority of cases, these are not cellular changes passed down through families. As the American Cancer Society explains, most cancers are caused by acquired mutations.

These kinds of mutations are changes that are acquired throughout the course of a lifetime — often thanks to exposure to carcinogenic substances. Whether it be the food you’re eating, the cigarettes you’re smoking or the pesticides you’re spraying on your lawn — these are the kinds of things that silently cause cancer over time.

Natural News has reported on cancer-causing foods and chemicals for years, and even the lowly cancer industry admits that these are things that cause cancer. Yet few people are truly aware of this fact, and many erroneously believe that if cancer runs in their family, they’re out of luck.

The truth is that nearly half of all cancers can be directly linked to lifestyle factors — with some research suggesting that figure is even higher. Some researchers believe that upwards of 90 percent of cancers are caused by some sort of controllable factor.

A recent study found that 24 lifestyle factors contributed to 41 percent of cancer cases. As the study authors noted:

“We estimated summary population attributable risk estimates for 24 risk factors (smoking [both passive and active], overweight and obesity, inadequate physical activity, diet [inadequate fruit and vegetable consumption, inadequate fiber intake, excess red and processed meat consumption, salt consumption, inadequate calcium and vitamin D intake], alcohol, hormones [oral contraceptives and hormone therapy], infections [Epstein-Barr virus, hepatitis B and C viruses, human papillomavirus, Helicobacter pylori], air pollution, natural and artificial ultraviolet radiation, radon and water disinfection by-products) by combining population attributable risk estimates for each of the 24 factors that had been previously estimated.”

These are not genetic cancers — they are cancers caused by the litany of toxins we expose our bodies to, in one way or another, on a daily basis. Indeed, there is no shortage of cancer-causing chemicals in modern life; from added sugars and artificial dyes to pesticides and herbicides, these hazards are virtually everywhere. And to make matters worse, modern medicine often relies on more cancer-causing chemicals to treat disease.


More evidence emerges that cell phones trigger abnormal cell growth and cancer

Published: May 03, 2018

Source:https://www.naturalnews.com/2018-05-03-more-evidence-cellphones-trigger-abnormal-cell-growth-and-cancer.html

(Natural News) Cell phones have been classified as a possible carcinogen since 2011. Since then, numerous studies have confirmed that the electromagnetic field (EMF) radiation emitted by cell phones can indeed cause anomalous cell growth and cancer, according to a Waking Times article.

In March 2018, the Ramazzini Institutepublished the results of a long-term animal study where rats were exposed to the radio frequency (RF) radiation generated by cell phones throughout their lives. The Italian researchers reported that heavy exposure to cell phone radiation was linked with increased appearances of Schwann cell tumors in the brain and heart.

The Ramazzini researchers urged that cell phones should be re-classified as “probable” carcinogens instead of merely “possible” ones.

Their findings found support in a separate investigation of the increasing instances of a highly dangerous type of brain tumor in the U.K. The cases of glioblastoma multiforme more than doubled from 1995 to 2015.

The authors of the U.K. study believe that widespread environmental or lifestyle factors – such as the increasing use of cell phones – brought about this startling rise of brain tumors.

Cell phone EMF radiation causes DNA and cellular damage

Constant exposure to radiation is known to have serious effects on health. Since cell phones constantly talk to cell towers via microwave energy and we usually have them near us, we are almost always exposed to the microwave radiation they emit.

Animal experiments performed by the U.S. Navy’s Office of Naval Research exposed the brains of animals to microwave radiation similar to the ones emitted by cell phones. The results showed that such radiation could break down cell membranes and the blood-brain barrier that keeps out toxins in the blood.

Given cell phones are usually held close to the head, it’s implied their radiation could drop the natural defenses of the brain, allowing toxins to contaminate brain cells.

A related study by Dr. Martin Pall showed that similar microwave radiation opens channels in the outer membrane of your cells. When opened, these voltage-gated calcium channels (VGCCs) flood the cell with unneeded calcium ions.

The end result is the formation of oxidant stressors that are suspected to cause many chronic diseases. Peroxynitrite stressors, for example, are linked to atherosclerosis, amyothrophic lateral sclerosis, inflammatory bowel disease, myocardial ischemia, and septic lung disease. They could also damage DNA.

Finally, a McGill University professor reported that EMFs can affect the water that comprises 70 percent of the human body. He believes magnetic fields can disrupt the water channels used by enzymes to produce ATP for the body. This starves the body of much-needed energy, causing a cascade of problems such as higher chances of developing chronic disease.

American report downplays links between cell phone radiation and tumors

The results of the Ramazzini report was identical to the lifetime exposure study carried out by the U.S. National Toxicology Program (NTP). The American researchers found that exposing mice and rats to microwave radiation for nine hours a day caused various tumors to manifest in the brain, heart, liver, pancreas, and prostate.

In particular, the heart tumors of rats are similar to acoustic neuroma, a benign tumor that develops in the nerve connecting the ear and the brain of humans. Acoustic neuromashave been traced to heavy use of cell phones. EMF radiation also damages DNA.

However, the NTP researchers only considered the radiation to be a “weak” carcinogen. They also expressed insufficient confidence in the results of their own findings, especially since they believed that non-ionizing RF radiation should not be able to harm DNA.


Add 7 disability-free years to your life by simply practicing healthy lifestyle habits

Published: May 02, 2018

Source:https://www.naturalnews.com/2018-05-02-add-7-disease-free-years-to-your-life-by-simply-practicing-healthy-lifestyle-habits.html

(Natural News) It looks like its time to get up from the couch, turn off the TV, and put on your running shoes.

Aside from making you fit and strong, a study has confirmed that living a healthy lifestyle can also help add seven disability-free years to your life.

The results of the research, which was published in Health Affairs, determined that several healthy lifestyle factors can boost your longevity by as much as seven years. Most of those years can even be spent free of any disability.

The study findings noted that to some extent, alcohol consumption, being obese/overweight, and quitting smoking are connected with more disability-free years of life. The researchers examined data gleaned from the Health and Retirement Study. The study the scientists referenced looked into the health outcomes of over 14,000 individuals aged 50 to 89 from 1998 to 2012.

Using the data, the researchers determined that individuals who lived healthy lifestyles were able to increase their longevity by at least seven years with a delay in disability onset of about six years.

Men who didn’t smoke, drank in moderation, and weren’t obese had an average life expectancy of 11 years, unlike people in the same age group who took part in high-risk behaviors. Meanwhile, the women lived 12 more healthy years compared to peers who drank heavily, were overweight, and smoked. 

 The researchers categorized disability as limitations in one of these five daily activities:

  1. Bathing
  2. Eating
  3. Getting dressed
  4. Getting in/out of bed
  5. Walking

Dr. Mikko Myrskylä, co-author and executive director of the Max Planck Institute for Demographic Research in Rostock, Germany, noted that one benefit of living more years disability-free is the need for fewer health care services. With a healthy, productive population, both individuals and communities can enjoy a greater quality of life.

Although the three risk factors were linked to early onset of disability, obesity had a greater link to it. The researchers did state that their study didn’t take genetic factors that could influence risk behaviors into account.

Dr. Myrskylä emphasized the need for a more effective policy that can minimize risky health behaviors, such as the promotion of the dangers of tobacco and encouraging moderate drinking, which were both public health successes. But obesity has proven to be more challenging since experts have yet to finalize the most effective way of addressing this risk factor.

Dr. Myrskylä shared that individuals older than 50 who drink excessively, are smokers, or are obese shouldn’t feel dismayed by these findings since it’s not too late to make lifestyle changes that can improve their health conditions.

He concluded, “For example, we observed that former smokers had almost as long healthy lifespan as never-smokers.” Individuals who take action right away and make healthier life choices can still enjoy “massive health gains.”

Tips to live a healthy lifestyle

Aside from drinking moderately, quitting smoking, and staying in shape, here are other tips to help you live a healthy lifestyle:

  • Consume more fruits and vegetables – Try to eat more than three servings of fruits and vegetables a day to improve your health. Eating fruits and vegetables regularly, which are rich in fiber and vitamins, may help lower your risk of heart disease by 76 percent.
  • Exercise regularly – This may seem like common sense, but not enough people exercise regularly despite its many health benefits. If you’re up for it, regular high-intensity exercise, like running, can add about four years to your life. Any kind of regular exercise is food for the heart, mind, and metabolism. If you want something slower paced, taking a 30-minute brisk walk daily can also help lower your risk of heart problems.
  • Get busy in the bedroom – Having sex regularly, or at least two to three times weekly, may add at least three years to your life. Sex can burn as many calories as running for 30 minutes, and having sex regularly can even help boost your immunity, lower your blood pressure, and strengthen your heart.
  • Spend time with family and friends – Not spending enough time with your loved ones can increase your risk of heart disease. Loneliness might even cause inflammation, and even if you’re healthy, this can be just as dangerous as having high cholesterol or smoking regularly.
  • Switch off the TV – Spending too much idle time just watching TV can be bad for your health. If you can’t say goodbye to your favorite shows, make an effort to limit your binge-watching to less than two hours daily.

New insights into the origins of mutations in cancer

Published: May 01, 2018

Source:https://www.sciencedaily.com/releases/2018/05/180501085135.htm

Researchers at the European Bioinformatics Institute (EMBL-EBI), the University of Dundee and the Wellcome Sanger Institute have used human and worm data to explore the mutational causes of cancer. Their study, published today in Genome Research, also shows that results from controlled experiments on a model organism -- the nematode worm C. elegans -- are relevant to humans, helping researchers refine what they know about cancer.

Enigmatic DNA mutation and repair

Cancer is caused by DNA mutations which can be triggered by a range of factors, including UV radiation, certain chemicals and smoking, but also errors occurring naturally during cell division. A cell recognises most of these mutations and corrects them through multiple repair mechanisms. However, DNA repair is not perfect, so it can leave certain mutations unrepaired or repair them incorrectly leading to changes in DNA. Understanding the footprints of these mutational processes is an important first step in identifying the causes of cancer and potential avenues for new treatments.

"The DNA mutations we see in cancer cells were caused by a yin and yang of DNA damage and repair," explains Moritz Gerstung, Research Group Leader at EMBL-EBI. "When we study a patient's cancer genome, we're looking at the final outcome of multiple mutational processes that often go on for decades before the disease manifests itself. The reconstruction of these processes and their contributions to cancer development is a bit like the forensic analysis of a plane crash site, trying to piece together what's happened. Unfortunately, there's no black box to help us.

Controlled experiments in model organisms can be used to mimic some of the processes thought to operate on cancer genomes and to establish their exact origins."

What worms can tell us

Previous research has shown that one of the first DNA repair pathways associated with an increased risk of cancer is DNA mismatch repair (MMR). The current study uses C. elegans as a model system for studying MMR in more detail.

"Dr Bettina Meier in my team initiated this project by assessing the kinds of mutations that arise when C. elegans is defective for one specific DNA repair pathway," says Professor Anton Gartner, Principal Investigator in the Centre for Gene Regulation and Expression at Dundee. "As it only takes three days to propagate these worms from one generation to the next, the process of studying how DNA is passed on is greatly expedited. DNA mismatch repair is propagated for many generations and this allowed us to deduce a distinct mutational pattern. The big question was if the same type of mutagenesis also occurred in human cancer cells."

To address this question, EMBL-EBI PhD student Nadia Volkova compared the C. elegans results with genetic data from 500 human cancer genomes.

"We found a resemblance between the most common signature associated with mutations in MMR genes in humans and the patterns found in nematode worms," explains Volkova. "This suggests that the same mutational process operates in nematodes and humans. Our approach allows us to find the exact profile of MMR deficiency and to understand more about what happens when DNA repair goes wrong."

These findings could lead to a better understanding of the causes of cancer and potentially help to identify the most appropriate treatment.


Identifying the mechanism in obesity's link to colon cancer

Published: April 30, 2018

Source:https://www.sciencedaily.com/releases/2018/04/180430160421.htm

In a recent new finding, doctoral candidates Wiecang Wang and Jianan Zhang, with their advisor Guodong Zhang in the department of food science at the University of Massachusetts Amherst, report that they have identified a new molecular mechanism to explain the link between obesity and increased risk of colon inflammation, which is a major risk factor in colorectal cancer.

The research team, which includes scientists at the University of California Davis, suggest for the first time that inhibiting an enzyme known as soluble epoxide hydrolase, sHE, may abolish this risk of obesity-induced colonic inflammation, say Zhang and colleagues. They note that a few sEH inhibitors, known to be a factor in other inflammatory diseases but not colon cancer before, are now in human clinical trials.

Senior author Zhang says, "In our mouse studies, obesity-induced colon inflammation can be eliminated by inhibiting sEH. So we discovered a new therapeutic target for a very important disease."

Because sEH inhibitors are already being explored as a treatment for other diseases such as pain and hypertension, he notes, medical researchers using it would not need to reinvent a whole new approach. "We hope it will be a promising treatment in humans, but mice and humans are very different," Zhang cautions. Details appear in an early online issue of Proceedings of the National Academy of Sciences.

As the authors point out, more than one-third, or 34.9 percent, of adults in the United States are obese, and obese individuals have a 30-60 percent higher risk of developing colorectal cancer, the third most common and the second leading cause of cancer-related death in the nation. Colon inflammation is an early warning sign of this cancer, and the new research shows why and how obesity increases risk.

In this study, the investigators used a liquid chromatography tandem mass spectrometry (LC-MS/MS)-based metabolomics approach to analyze the profiles of signaling lipids in the colon of groups of lean and obese mice. This allowed them to identify new bioactive lipids which are deregulated in the colon tissues of obese mice.

"Metabolomics is a very powerful tool to find new biomarkers and pathways of human diseases," says first author Wang. "We found that the concentrations of sEH-produced metabolic products are higher in colons of obese mice. This leads to our discovery that sEH is over-expressed in the colons of obese mice and it is involved in obesity-induced colonic inflammation."

To validate their findings, the research team used three different approaches to investigate the roles of sEH in obesity-induced colonic inflammation. These included using two different sEH inhibitors in experiments as well as a knockout mouse genetically modified not to produce sEH. Results were similar in all cases, reports co-first author Jianan Zhang, no relation to her professor. "Blocking the enzyme prevents the mouse from developing colonic inflammation. Even in the mice on a high-fat diet, by inhibiting sEH you can completely block colon inflammation," she says.

To explore further, the researchers conducted another study in both lean and obese mice who had experimentally-induced colon inflammation. They used molecular analyses to follow a pathway called Wnt because about 90 percent of sporadic colorectal cancers have activating mutations within the Wnt pathway, the professor notes. They found that obesity increases activation of Wnt signaling in the colon, but it too can be eliminated by the two different inhibitors and the knockout.


Size matters when fighting cancer

Published: April 27, 2018

Source:https://www.sciencedaily.com/releases/2018/04/180427155745.htm

Doctors could be a step closer to finding the most effective way to treat cancer with a double whammy of a virus combined with boosting the natural immune system, according to a pioneering study by researchers at The University of Texas Health Science Center at Houston (UTHealth) and The Ohio State University.

"The findings of this research are very exciting because it helps unravel the complex yin and yang relationship between the natural cancer-fighting power intrinsic to our immune system and externally added cancer-killing cells that are given as a therapy. It's very significant because it shows, contrary to recent scientific claims, that virotherapy can be combined with cell therapy for a positive effect," said the study's corresponding author Balveen Kaur, Ph.D., professor and vice chair of research in the Vivian L. Smith Department of Neurosurgery at McGovern Medical School at UTHealth.

Previous scientific wisdom has discredited combining virotherapy and externally added NK cell therapy to the body's natural killer (NK) cells, but there could be clear cancer-fighting benefits -- providing enough external NK cells are deployed to destroy the tumor and stop its spread, as revealed in the paper published this week in Proceedings of the National Academy of Sciences.

To reach this conclusion, physicians devised a mathematical formula unlocking the complex interactive relationship between externally introduced viruses and NK cells in addition to the immune system's existing NK cells to calculate cancer cell-killing potency. The mathematical modeling was able to predict how a virus-treated tumor would respond to NK cell therapy, depending on the number of NK cells introduced to the tumor. It showed that when the number of externally introduced NK cells is increased, the ability to fight cancer is strengthened. While the patient's own NK cells, present in smaller numbers, concentrate on clearing the virus and therefore have an adverse effect on virotherapy by limiting the virus's cancer-busting power, this impact can be reversed to destroy more of the tumor by introducing greater numbers of external NK cells. The theory behind these equations was subsequently confirmed in practice by experiments on mice with brain tumors, paving the way for further work.

NK cells are an essential part of the innate immune system and they play a critical role in protecting the body from cancer. The primary function of NK cells is to fight infections, which means they attack the introduced virus, thus thwarting its therapeutic capacity. However, if sufficient numbers of extra NK cells are added, they can kill more tumor cells directly and compensate for this negative influence.

"Natural NK cells sense and kill infected cancer cells, thus clearing viruses. But by adding exogenous NK cells in sufficient quantities, they can also destroy the residual tumor. Our tests showed when you get this ratio right, there's a significant improvement in cancer-fighting efficacy," said Kaur, who is a member of The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences. "So it's a big step forward, which should create more opportunities for further research and development of clinical trials for the treatment of cancer in humans and animals."


Neonicotinoids may alter estrogen production in humans

Published: April 26, 2018

Source:https://www.sciencedaily.com/releases/2018/04/180426125939.htm

Neonicotinoids are currently the most widely used pesticides in the world and frequently make headlines because of their harmful effects on honeybees and other insect pollinators. Now, a study published in the journal Environmental Health Perspectives, indicates they may also have an impact on human health by disrupting our hormonal systems. This study by INRS professor Thomas Sanderson indicates that more work must be done on the potential endocrine-disrupting effects of neonicotinoids.

The Quebec government has recently decided to more strictly regulate the use of certain pesticides, including neonicotinoids, which are widely used by Quebec farmers to control crop pests. Neonicotinoids act on insects' nervous systems, killing them by paralysis. Very little research has been done on their effects on human health, but INRS Professor Sanderson and Ph.D. student Élyse Caron-Beaudoin have taken on the challenge.

Both researchers have long been interested in the mechanisms of endocrine disrupting chemicals and they wanted to determine whether neonicotinoids belong to this class of compounds. "Endocrine disrupters are natural or synthetic molecules that can alter hormone function," says Caron-Beaudoin, the study's main author. "They affect the synthesis, action, or elimination of natural hormones, which can lead to a wide variety of health effects."

The research duo has developed methods to test the effect of neonicotinoids on the production of estrogens, essential hormones with several biological functions. By targeting aromatase, a key enzyme in the synthesis of estrogens, they were able to test the impact of three neonicotinoids on breast cancer cells in culture after exposure to concentrations similar to those found in the environment in agricultural areas.

The results of the study show an increase in aromatase expression and a unique change in the pattern in which aromatase was expressed, which is similar to that observed in the development of certain breast cancers. "However, as these results were obtained in a cellular model of breast cancer, we cannot necessarily conclude that exposure to pesticides at concentrations similar to those in the human environment would cause or promote cancer," cautions Professor Sanderson. This study is the first evidence that neonicotinoids have an effect on aromatase gene expression and may potentially alter estrogen production. Hormonal disturbance by these pesticides will need to be confirmed in future studies, but the results obtained by the INRS team indicate that it caution should be exercised in the management and use of neonicotinoid insecticides.


New breath and urine tests detect early breast cancer more accurately

Published: April 25, 2018

Source:https://www.sciencedaily.com/releases/2018/04/180425120253.htm

A new method for early and accurate breast cancer screening has been developed by researchers at Ben-Gurion University of the Negev and Soroka University Medical Center, using commercially available technology.

The researchers were able to isolate relevant data to more accurately identify breast cancer biomarkers using two different electronic nose gas sensors for breath, along with gas-chromatography mass spectrometry (GC-MS) to quantify substances found in urine.

In their study published in Computers in Biology and Medicine, researchers detected breast cancer with more than 95 percent average accuracy using an inexpensive commercial electronic nose (e-nose) that identifies unique breath patterns in women with breast cancer. In addition, their revamped statistical analyses of urine samples submitted both by healthy patients and those diagnosed with breast cancer yielded 85 percent average accuracy.

"Breast cancer survival is strongly tied to the sensitivity of tumor detection; accurate methods for detecting smaller, earlier tumors remains a priority," says Prof. Yehuda Zeiri, a member of Ben-Gurion University's Department of Biomedical Engineering. "Our new approach utilizing urine and exhaled breath samples, analyzed with inexpensive, commercially available processes, is non-invasive, accessible and may be easily implemented in a variety of settings."

The study reports breast cancer is the most commonly diagnosed malignancy among females and the leading cause of death around the world. In 2016, breast cancer accounted for 29 percent of all new cancers identified in the United States and was responsible for 14 percent of all cancer-related deaths.

Mammography screenings, which are proven to significantly reduce breast cancer mortality, are not always able to detect small tumors in dense breast tissue. In fact, typical mammography sensitivity, which is 75 to 85 percent accurate, decreases to 30 to 50 percent in dense tissue.

Current diagnostic imaging detection for smaller tumors has significant drawbacks: dual-energy digital mammography, while effective, increases radiation exposure, and magnetic resonance imaging (MRI) is expensive. Biopsies and serum biomarker identification processes are invasive, equipment-intensive and require significant expertise.

"We've now shown that inexpensive, commercial electronic noses are sufficient for classifying cancer patients at early stages," says Prof. Zeiri. "With further study, it may also be possible to analyze exhaled breath and urine samples to identify other cancer types, as well."


Scientists unearth vital link between fat, immunity and heat regulation

Published: April 24, 2018

Source:https://www.sciencedaily.com/releases/2018/04/180424112901.htm

Scientists have just made a surprising discovery involving fat and special immune cells that live within it -- it turns out that 'gd T cells' are the key cogs in the biological wheel that regulates our body heat and protects us against cold shock. The discovery thus reveals a peculiar and previously unknown aspect of the immune system -- as well as driving our response to infection, it also plays a role in regulating our metabolism. In addition, this discovery has put the spotlight on a potential new target for therapies designed to help individuals either lose or gain weight.

There are two quite distinct types of fat -- white and brown. The main job of white fat is to store the energy from the food we eat for when we need it. Of course, the more energy we take in without using, the fatter we get. The job of brown fat, contrastingly, is to burn the fat to produce heat in the body. This is particularly important when babies are born as it regulates their temperatures until they develop more white fat, but it's also important in protecting us from hypothermia.

Both white and brown fat tissues also have their own immune systems, and scientists are only just beginning to understand how these work. The latest research, led by Associate Professor in Immunology at Trinity College Dublin, Lydia Lynch, adds greatly to this understanding. The findings have just been published in journal Nature Immunology.

Gamma delta T cells (gd T cells) are usually found at barrier sites in the body to guard the body from infection, but in the current study the scientists found a special population of them in fat. Unlike other immune cells that traffic in and out of fat, these gd T cells live there all the time, suggesting they play an important role where they are housed.

To find out what they do, the scientists removed them from fat tissue in mice and were surprised to learn that the mice became much colder, even at room temperature. When the mice were moved into cold environments, they were unable to regulate their body temperature and died.

Professor Lynch said: "Surprisingly, we found that the immune cells in fat respond to cold temperatures -- they play an integral part in regulating thermogenesis by 'turning on' the burning of white fat, or by stimulating the conversion of white fat into brown fat, which generates the heat required to keep us warm in the cold. This heat generation happens when the lipids in the white fat are burned up, and, when this occurs, weight loss is the chief side effect."

"We have essentially identified a special immune cell population that is not only responsible for turning white fat brown, but also for protecting us against the cold. Indeed the main function of these fat-dwelling gd T cells is not to defend against pathogens or cancer, as initially seemed likely, but instead to protect the body from typically non-immune related dangers such as cold."

This discovery opens the door to a new potential target for therapeutic research -- in patients living with obesity, or in those who are experiencing wasting, for example. For people with obesity, activating the biological pathway and kick-starting the body into burning white fat may induce weight loss, while for those experiencing wasting (often associated with cancer and AIDS), switching off the pathway may induce desirable weight gain.


Positioning During Cancer Radiation May Be Key to Heart Risks

Published: April 23, 2018

Source:https://www.cancercompass.com/cancer-news/article/61357.htm

(HealthDay News) -- If you have lung or throat cancer, exactly how you are positioned during your radiation treatments may alter your chances of beating the disease.

New research suggests that even tiny shifts can mean the radiation may harm organs around tumors in the chest, most notably the heart.

"We already know that using imaging can help us to target cancers much more precisely and make radiotherapy treatment more effective," said researcher Corinne Johnson, a Ph.D. student at the Manchester Cancer Research Center in England.

"This study examines how small differences in how a patient is lying can affect survival, even when an imaging protocol is used," Johnson explained. "It tells us that even very small remaining errors can have a major impact on patients' survival chances, particularly when tumors are close to a vital organ like the heart."

When cancer specialists prepare to perform radiation therapy, they scan the patient's body to determine the exact position and size of the tumor, the researchers explained. Before every treatment that follows, more images are used to ensure that the patient and the tumor are in the same position.

For the study, the researchers recruited 780 patients undergoing radiation therapy for non-small cell lung cancer. For each treatment, patients were positioned on the machines and an image was taken to ensure they were lying within 5 millimeters (mm) of their original position.

The researchers used the images to assess how precisely the radiation was delivered, and to determine if it shifted closer or farther away from the heart.

The patients whose radiation shifted slightly towards their heart were 30 percent more likely to die than those who experienced a similar shift away from their heart, the investigators found.

When the analysis was repeated with 177 throat cancer patients, the researchers noted an even larger difference -- about 50 percent -- even after they took other factors, such as the patients' ages, into account.

The findings were scheduled for presentation Sunday at the European Society for Radiotherapy and Oncology (ESTRO) annual meeting, in Barcelona, Spain. Research presented at meetings should be viewed as preliminary until published in a peer-reviewed journal.

"By imaging patients more frequently and by reducing the threshold on the accuracy of their position, we can help lower the dose of radiation that reaches the heart and avoid unnecessary damage," Johnson said in a news release from the meeting.


Treatment of cancer could become possible with adenovirus

Published: April 20, 2018

Source:https://www.sciencedaily.com/releases/2018/04/180420122859.htm

Adenovirus is a common virus that causes infectious diseases of the respiratory tract, eyes and gastrointestinal tract in humans and animals. Researchers at Umeå University study molecular mechanisms of infection in order to understand how adenovirus causes disease.

The researchers in Umeå, together with research groups from Germany, the UK and Hungary, have now discovered a new type of mechanism used by a rare adenovirus type to attack cells.

Human Adenovirus type 52 (HAdV-52) is one of the few adenoviruses that has two different types of fiber proteins on its surface, which are 'used' by the virus for the attachment to target cells. In collaboration with researchers in the Glycosciences Laboratory at Imperial College in London, who are world leading in the research field of glycobiology, the scientists have shown that the shorter fiber binds to an unusual type of carbohydrate-based receptor, polysialic acid (a long chain of repeated sialic acids). Annasara Lenman working with Niklas Arnberg has subsequently corroborated that HAdV-52 binds to polysialic acid on target cells, and that this leads to infection. In collaboration with experts in structural biology at the University of Tübingen, the interaction between the short fiber and polysialic acid has been mapped at the atomic level.

"We knew earlier that the short fiber binds to sialic acid, but not how the underlying carbohydrate chain was constructed," explains Annasara Lenman postdoc at the Department of Clinical Microbiology and The Laboratory for Molecular Infection Medicine Sweden (MIMS) at Umeå University, Sweden.

As polysialic acid is overexpressed on cancer cells in the brain and lungs, our findings could open new possibilities to use HAdV-52 for treatment for the corresponding types of cancer.

For a long time, adenovirus and other viruses have been considered suitable weapons for the treatment of different types of cancer. Viruses can kill cancer cells themselves, but in recent years it has also been understood that a virus infection in a tumor can activate the immune system against the cancer cells. You can also "arm" viruses with different genes that can for example counteract the development of resistance against different drugs. A major challenge has been to target viruses specifically against the cancer cells.

"Most adenoviruses tested so far have only one type of cell-binding fiber. HAdV-52 has two different fibers, one of which has a natural predilection for cancerous cells that express polysialic acid. This opens up a more effective harnessing of viruses against the right kind of cells," Annasara Lenman explains.

The results can also be of importance in other research areas:

"Perhaps the most important function of polysialic acid is its contribution to the brain's development. However, one has not known much about how polysialic acid interacts with its environment. Our research makes it pertinent to investigate whether polysialic acid plays a part in brain development by interacting with specific cellular molecules." says Annasara Lenman.


Could a Tattoo Someday Spot Your Cancer?

Published: April 19, 2018

Source: https://www.cancercompass.com/cancer-news/article/61325.htm

(HealthDay News) -- Tattoos serve many purposes, perhaps expressing artistry, loyalty or love. Now, scientists working with mice say they've engineered a medical "tattoo" that can screen for early signs of major disease.

The biomedical tattoo is made up of cells embedded with sensors that measure levels of blood calcium.

It's initially invisible when implanted under the skin. But the sensors become apparent if blood calcium levels rise. This indicates a condition called hypercalcemia, which is a marker for several cancers and other major diseases.

"Forty percent of all cancers -- including colon cancer, lung cancer, breast cancer and prostate cancer -- disrupt calcium balance (homeostasis)," said study lead author Martin Fussenegger.

"The biomedical tattoo is designed to catch mild hypercalcemia," which produces no symptoms, he said.

Appearance of the tattoo may signal that some of those cancers may start to develop, said Fussenegger, of ETH Zurich's department of biosystems science and engineering in Basel, Switzerland.

When elevated blood calcium persists, the implant releases melanin, producing a telltale dark patch on the skin, he said. (Melanin is a dark pigment responsible for tanning.)

But whether this is just a fun gimmick or a reliable diagnostic tool remains to be seen.

Dr. Janice Dutcher is a medical oncologist with the Cancer Research Foundation in New York City.

She described the innovation as a "neat gimmick."

"I guess in the context of looking for new and inventive ways to screen for disease, it's a reasonable idea," she said. "It's always nice to try and conceive of a new, simple and accurate way to screen for disease."

But Dutcher cautioned that screening for high calcium levels is not always an effective way to detect cancer early. Some cancers -- kidney cancer, for example -- only prompt high calcium after the disease has progressed, she said.

Dr. Norman Edelman, senior medical advisor for the American Lung Association, seconded that point.

In his experience, "the bulk" of tumor-related hypercalcemia occurs at a late stage, when cancer has spread. "It is also a late finding in kidney failure," he added.

"So this is really fun science. But I would not spend a lot to license the patent," Edelman said.

To test their design, the researchers implanted the engineered cells under the skin of mice with either cancerous tumors that cause hypercalcemia or tumors that do not alter calcium blood levels.

The tattoos only surfaced on the skin of mice with elevated blood calcium levels, according to the report.

In theory, said Fussenegger, a tattoo diagnosis would happen at such an early stage of disease "that over 95 percent of the above-mentioned cancer types will be cured."

He and his colleagues were "impressed by the precision and sensitivity of the tattoo," he said. A skin patch arose only when high calcium levels persisted, he explained, adding this would reduce the likelihood of false diagnoses.

Still, "animal experiments do not always translate to people," Fussenegger acknowledged. Human trials are set to begin within five years, he said.

The goal is a human tattoo "universal system" that could detect multiple health issues at once. If all goes according to plan, Fussenegger predicted it could be available within 10 to 15 years.

Besides cancer, Fussenegger said the approach could be linked to other slow-developing diseases. These might include neurodegenerative disorders like Parkinson's and Alzheimer's, he said.


Cancer is a lifestyle disease: 4 in 10 cancers can be entirely avoided

Published: April 18, 2018

Source:https://www.naturalnews.com/2018-04-18-cancer-is-a-lifestyle-disease-4-in-10-cancers-can-be-entirely-avoided.html

(Natural News) Those who think they shouldn’t worry about cancer because they have no family history of the dreaded disease are grossly misinformed. Scientists have found time and again that genes are not the reason people get cancer. A new study shows that lifestyle is a frequent culprit. The research suggests that 2,500 cases of cancer could be prevented weekly if Britons changed their lifestyle by exercising more and losing weight. Cancer Research UK reports that almost 40 percent of cancer cases in the UK is preventable.

Smoking, the number one cause of cancer, is now giving way to obesity as the top culprit. This is why experts warn that excess weight can someday be the biggest reason why people get the disease. In fact, Cancer Research UK chief executive Sir Harpal Kumar remarked that in the next decades, obesity can be the new smoking if people don’t watch out.

Research published in the British Journal of Cancer revealed that excess weight leads to 13 kind of cancer, including bowel, breast, womb and kidney. It also shows that over 20 cases of cancer could be prevented if people maintained a healthy weight.

The good news is excess weight is a choice. Wellness expert Dani Walker, author of the book Education Beats Medication, suggests these natural ways of beating obesity:

  • Drink eight ounces of lemon water upon waking up in the morning — It jump-starts your metabolism and helps rid your body of toxins that accumulate with fat intake. Organic lemon will also help balance balance your alkaline or pH levels. Avoid zero calorie food and artificial sweeteners. Don’t be fooled by the phrase “zero calories” and stay away from artificial sweeteners that could make you ask for more. Opt for natural sweeteners like honey, molasses, raw whole sugar, or organic fruit juice.
  • Take organic apple and grapefruit as often as you can — Organic fruits and greens have live enzymes and nutrients that help cleanse the body of toxins and provide nutrition. They also suppress appetite and burn fat.
  • Go big on breakfast — A whopping 80 percent of overweight people eat a small breakfast or skip it altogether.
  • Hydrate — Take six to eight glasses of filtered water daily. Filtered water flushes fat and toxins away. This, in turn, helps you lose excess weight.
  • Walk for an hour nonstop daily — Walking is slow rhythmic movement that reboots your weight set point and develops a thin, lean body. It’s something people young and old can do. You’ll see and feel the dramatic difference in 30 days.

Cancer is no longer the death sentence is used to be. Still, prevention is better than cure. Why get sick, when a change in lifestyle will keep you healthy and strong?

Wellness is a choice, which, like most good things, need time and patience to achieve. You can choose to quit smoking and lose weight today, and look forward to spending more time with your loved ones in the future. Or, you can turn a deaf ear to all the warning signs about unhealthy living, and suffer from disease.


Some Blood Pressure Meds Tied to Pancreatic Cancer Risk in Women

Published: April 17, 2018

Source:https://www.cancercompass.com/cancer-news/article/61306.htm

(HealthDay News) -- Certain drugs prescribed to treat high blood pressure may boost a woman's risk for developing pancreatic cancer after menopause, new research suggests.

In a large study of postmenopausal women, those who had ever taken a short-acting calcium channel blocker (CCB) saw their pancreatic cancer risk shoot up by 66 percent.

And women who had used a short-acting CCB for three years or more faced more than double the risk for pancreatic cancer, compared with those who had taken other types of blood pressure drugs.

This class of drugs includes short-acting nifedipine (brand names Procardia, Adalat CC); nicardipine (Cardene IV); and diltiazem (Cardizem).

The short-acting CCBs were the only blood pressure drugs linked to higher pancreatic cancer risk, according to study lead author Zhensheng Wang.

However, people taking this class of drugs shouldn't panic, because their absolute risk of developing pancreatic cancer still remains very low. According to the U.S. National Cancer Institute, just 1.6 percent of Americans will develop the cancer during their lifetime. That means that -- even after accounting for a bump up in risk from taking a CCB -- an individual's odds for the disease remains minimal.

Still, the new finding was unexpected, said Wang, a postdoctoral associate at Baylor College of Medicine in Houston.

Prior investigations had hinted that CCBs might even protect against pancreatic cancer by boosting levels of a protein (sRAGE) known to keep inflammation in check, said Wang.

Reduced inflammation is typically associated with a lower risk for a range of cancers.

So what might explain the current results?

Wang noted that short-acting CCBs are "the least effective" blood pressure drug available. That could mean many of the women in the study had not achieved good blood pressure control to begin with, which could have boosted their risk for diabetes. And diabetes is a known risk factor for pancreatic cancer.

Wang also said blood samples taken from more than half the pancreatic cancer patients revealed that those who had ever taken a short-acting CCB also had notably lower levels of the sRAGE protein, compared with women who had taken other types of blood pressure drugs. That would mean less inflammation control and, therefore, potentially higher cancer risk.

Finally, he hypothesized that women who are prescribed short-acting CCBs might differ in some way from patients prescribed other types of blood pressure control.

CCBs tamp down blood pressure by preventing calcium from entering cells in the heart and blood vessel walls, thereby decreasing cardiac stress and workload.

In 1996, the U.S. Food and Drug Administration took steps to discourage doctors from prescribing short-acting nifedipine. It warned that some researchers had linked the drug to an increased risk for heart attack and stroke.

The current study followed more than 145,000 participants in the Women's Health Initiative study. They were between 50 and 79 years old at the start of the study, and medication use -- but not dosage -- was monitored between 1993 and 1998.

By 2014, more than 800 had developed pancreatic cancer, with risk up only among those who had been prescribed a short-acting CCB, Wang's team found.

For those who'd used the drugs three years or more, risk of pancreatic cancer was 107 percent higher than for those who took other blood pressure drugs.

Longer-acting CCB drugs were not associated with any risk elevation. Neither were beta blockers, diuretic drugs or ACE inhibitors.

Wang and his colleagues plan to present their findings this week at a meeting of the American Association for Cancer Research in Chicago.

He said the findings need to be reconfirmed. Also, research presented at meetings is usually considered preliminary until peer-reviewed for publication in a medical journal.

One cancer specialist agreed that more investigation is warranted.

"There is no doubt more research needs to be done on this," said Dr. Victoria Rutson, chief medical officer for the Pancreatic Cancer Action Network in Manhattan Beach, Calif.

But for now, Rutson advised patients to "consult with their doctors before removing or adding any medications."

"Removing hypertension medications can be extremely dangerous, especially if someone has a history of high blood pressure," she warned.

Rutson also said if pancreatic cancer runs in your family, you might want to consult a doctor.

"If you have a familial history of pancreatic cancer, it is important to visit with a gastroenterologist, especially if you begin to exhibit any symptoms that are new or out of the ordinary," Rutson added.

Pancreatic cancer is the fourth leading cause of cancer deaths in the United States. Wang said it typically strikes older adults with chronic medical conditions, such as high blood pressure.


Combination therapy doubles survival in metastatic lung cancer

Published: April 16, 2018

Source:https://www.sciencedaily.com/releases/2018/04/180416101413.htm

The immunotherapy drug pembrolizumab, when combined with chemotherapy, doubles survival in patients with non-squamous non-small cell lung cancer (NSNSCLC) lacking genetic changes in the EGFR or ALK genes, when compared to chemotherapy alone, according to an international, Phase III clinical trial.

Principal investigator Leena Gandhi, MD, PhD, director of the thoracic medical oncology program at Perlmutter Cancer Center at NYU Langone Health and associate professor of Medicine in the division of Medical Oncology at NYU School of Medicine, presented these findings April 16 at the American Association for Cancer Research (AACR) Annual Meeting 2018 in Chicago. The data from this study were simultaneously published online April 16 in the New England Journal of Medicine.

A total of 616 patients with untreated, metastatic NSNSCLC without EGFR or ALK alterations, from 118 international sites, were randomly allocated for the trial -- 405 patients were treated with both pembrolizumab and platinum + pemetrexed, and 202 received platinum + pemetrexed with a saline placebo.

Response rates, overall survival and progression-free survival rates were superior in the pembrolizumab and chemotherapy combination-treatment group.

Of those treated with pembrolizumab and platinum + pemetrexed, the risk of death was reduced by 51%, compared to those treated with platinum + pemetrexed alone. Among patients treated with the combination therapy, the chance of progression or death was reduced by 48%. In other words, chance of overall and progression free survival doubled.

"The data show that treatment with pembrolizumab and chemotherapy together is more effective than chemotherapy alone," says Gandhi. "Using this combination therapy to treat patients with such an aggressive disease could be an important advance in keeping patients alive and well for longer."

The risk of severe side effects was similar in both groups (67.2% in the combination group and 65.8% in the standard treatment group), although there was an increased risk of acute kidney injury with the combination treatment (5.2% vs. 0.5%). The most common side effects experienced by both groups were nausea, anemia and fatigue.

Non-small cell lung cancer is the leading cause of all cancer death, in part because in the majority of cases, the cancer has already spread at the time of diagnosis. Pembrolizumab in combination with chemotherapy is FDA-approved to treat these patients, based on a previous phase II trial on which Dr. Gandhi was one of the lead investigators.

"Although some non-small cell lung cancer patients have increased benefit of targeted therapy or immunotherapy instead of chemotherapy, for some groups of patients with NSNSCLC, chemotherapy has been the standard treatment for more than 30 years," Gandhi notes. "But for patients with NSNSLC without EGFR or ALK alterations, this study may suggest a new standard of care."


Japanese study confirms vitamin D reduces cancer risk

Published: April 15, 2018

Source:https://www.naturalnews.com/2018-04-15-japanese-study-confirms-vitamin-d-reduces-cancer-risk.html

(Natural News) Vitamin D is an essential nutrient that is good for the health, and scientists continue to explore its other health benefits. In fact, a new study found that vitamin D reduces the risk of cancers. The large Japanese cohort study, published in the BMJ, aimed to determine whether vitamin D was associated with the risk of total cancer and certain cancers.

The researchers conducted the study using data of 33,736 participants from the Japan Public Health Center-based Prospective (JPHC) Study. The participants were aged between 40 and 69 years. At the beginning of the study, they provided detailed information on their medical history, diet, and lifestyle. Their blood samples were also taken to measure vitamin D levels.

Then, the researchers divided the participants into four groups, depending on their levels of vitamin D. After that, they observed the participants for an average of 16 years, in which they recorded more than 3,300 new cases of cancer. The study also included 4,044 randomly selected sub-cohort participants.

After cancer risk factors, such as age, weight, physical activity levels, smoking, alcohol consumption, and diet, were considered, the researchers found that participants with a higher level of vitamin D had a 20 to 25 percent lower risk for all cancers. For liver cancer, they showed a 30 to 55 percent lower risk of cancer, and the association was more evident in men than in women. In addition, they found that vitamin D levels lower the risk for pre-menopausal breast cancer, but not for prostate and lung cancer.

Furthermore, they observed a ceiling effect for total cancer risk, which suggested that no further benefit would be provided beyond a certain vitamin D blood concentration. However, they failed to determine the optimal vitamin D concentration that reduced the risk of cancer.

“We observed that a higher circulating concentration of vitamin D was associated with a lower risk of subsequent cancer in a large Japanese population. Our findings support the hypothesis that vitamin D may confer protection against the risk of cancer,” said Sanjeev Budhathoki, first author of the study.

Ways to get your daily vitamin D needs

Vitamin D is especially good for the bones. Studies also suggested that it can help prevent colds and fight depression. Thus, it is important to get enough vitamin D. 

Here are some ways to get your daily vitamin D needs:

  • Get exposed to sunlight – Vitamin D is synthesized when the skin is exposed to sunlight. Getting around 20 to 25 minutes of sunlight exposure is helpful, but too much of it can increase the risk of cancer.
  • Eat foods rich in vitamin D – If you are unable to get exposed to sunlight, especially during winter, get vitamin D from fatty fish, such as salmon, trout, mackerel, tuna, and eel. Fatty fish is not only a good source of the vitamin but also of the heart-healthy omega-3 fatty acids. Other foods that are good sources of vitamin D include beef liver, cod liver oil, egg yolks, fortified milk, and fortified cereals.
  • Take vitamin D supplements – Vitamin D can also be obtained from supplements. However, you must only take a proper daily dosage of these supplements. This is because too much vitamin D can be harmful. The safe upper limit of vitamin D per day for people aged nine and over is 4,000 IU, which includes all sources – sun, food, and supplements.

Want to Help Beat Colon Cancer? Live Healthy

Published: April 12, 2018

Source:https://www.cancercompass.com/cancer-news/article/61254.htm

(HealthDay News) -- More than 1.3 million Americans are diagnosed with colon cancer, but new research suggests that adopting a healthy lifestyle goes a long way toward boosting survival.

The study followed nearly 1,000 patients with advanced colon cancer for an average of seven years.

It found that people who ate right and exercised had a 42 percent lower risk of dying during the study period, compared to those who had less healthy lifestyles.

The take-home message: "Having a health body weight, being physically active, and eating a diet rich in vegetables, fruits and whole grains after a diagnosis of stage 3 colon cancer was associated with a longer survival," the researchers reported April 12 in the journal JAMA Oncology.

The new research was led by Erin Van Blarigan, from the University of California, San Francisco. She and her colleagues noted that in 2001, the American Cancer Society published guidelines advocating a healthy lifestyle during and after colon cancer treatment.

But does healthy living really make a difference with survival?

To find out, Van Blarigan's team tracked outcomes for 992 colon cancer patients who enrolled in a chemotherapy trial from 1999 through 2001. The participants' health -- and levels of nutrition and exercise -- were then followed until 2016-2017.

People who most closely adhered to the lifestyle recommendations on diet and exercise fared much better in terms of survival, the data showed. And when the researchers took into account healthy alcohol intake, patients did even better -- a 51 percent reduction in death risk during the study period.

Writing in an accompanying editorial, a team of cancer specialists led by Dr. Michael Fisch of AIM Specialty Health in Chicago said the findings confirm the power of healthy living for cancer patients.

Their advice to doctors? If there was any uncertainty before about whether or not to urge colon cancer patients to eat right and exercise, the new findings "should put those concerns to rest."

The experts stressed, however, that a cancer diagnosis can be overwhelming for patients, and improving lifestyles in such a context is often easier said than done.

Still, the new findings "strengthen the call to take aim at extending and improving lives for cancer survivors through changing behaviors related to nutrition and physical activity."

Dr. Jeffrey Farma is associate professor of surgical oncology at Fox Chase Cancer Center in Philadelphia. He said that far from being a secondary consideration, a "focus on improving lifestyle through nutrition and activity are moving to the forefront of a lot of cancer-related research for all stages of treatment."

And while the new study is encouraging, "there is still much work to be done to further validate these intriguing findings," said Farma, who wasn't involved with the research.

Specifically, what's needed is "for us to look at ways to integrate and support health and lifestyle changes into our practices in treating all cancer patients," he said.


Belly Fat Tied to Lower Kidney Cancer Survival Odds in Women

Published: April 09, 2018

Source:https://www.cancercompass.com/cancer-news/article/61225.htm

(HealthDay News) -- Belly fat reduces a woman's chances for surviving kidney cancer, but not a man's, a new study suggests.

The study included 77 women and 145 men with kidney cancer. Half of the women with high amounts of belly fat died within 3.5 years of diagnosis. Meanwhile, more than half of women with low amounts of belly fat were still alive after 10 years.

Researchers at Washington University School of Medicine in St. Louis found no link between belly fat and men's kidney cancer survival.

The findings suggest kidney cancer develops and progresses differently in men and women, the study authors said.

"We're just beginning to study sex as an important variable in cancer," study senior author Dr. Joseph Ippolito said in a university news release. Ippolito is an instructor in radiology.

"Men and women have very different metabolisms. A tumor growing in a man's body is in a different environment than one growing inside a woman, so it's not surprising that the cancers behave differently between the sexes," he explained.

Excess weight is a major risk factor for kidney cancer, but does not necessarily affect a patient's chance of survival. This study suggests, however, that the distribution of body fat affects women's survival odds. But it does not prove a cause-and-effect relationship.

"We know there are differences in healthy male versus healthy female metabolism," Ippolito said. "Not only in regard to how the fat is carried, but how their cells use glucose, fatty acids and other nutrients. So the fact that visceral [belly] fat matters for women but not men suggests that something else is going on besides just excess weight."

This line of research could lead to better ways to treat women with kidney cancer, Ippolito added.


New immunotherapy for lung cancer shows promise of success

Published: April 05, 2018

Source:https://www.sciencedaily.com/releases/2018/04/180405183626.htm

In a groundbreaking development, results from a recent clinical trial to treat lung cancer show that a novel immunotherapy combination is surprisingly effective at controlling the disease's progression. The study, published April 4 in the journal The Lancet Oncology, focused on non-small cell lung cancer, which is the most common form of lung cancer.

Immunologist John Wrangle, M.D., of the Hollings Cancer Center at the Medical University of South Carolina said it's a promising therapy that can be delivered in an outpatient setting. "People don't talk about 'curing' patients with metastatic lung cancer. We now get to flirt with the idea for certain patients using immunotherapy. And at the very least we have a significant proportion of patients enjoying prolonged survival even if we can't call them 'cured'," he said.

He, along with his colleague Mark Rubinstein, Ph.D. also of the Hollings Cancer Center, designed a clinical trial that started in 2016.

Patients with metastatic non-small cell lung cancer will always progress after chemotherapy, so most patients go on to be treated with immunotherapy, a type of therapy that uses the body's immune system to fight cancer. One class of immunotherapeutic drugs is known as "checkpoint" inhibitors, as they target checkpoints in immune system regulation to allow the body's natural defenses, such as white blood cells, to more effectively target the cancer.

Rubinstein said checkpoint therapies work by cutting the brake cables on the white bloods cells that are inherently able to kill tumor cells. "Tumor cells often produce suppressive factors which essentially turn the brakes on tumor-killing white blood cells. What's unique about the therapy that we're testing is that in addition to cutting the brake cables on white blood cells, we're providing fuel to them so that they can more effectively kill cancer cells."

Wrangle and Rubinstein's therapy is a combination of a checkpoint drug, nivolumab, with a new and powerful immune stimulation drug, ALT-803. "What's unique about our trial is that it's two completely different types of drugs that have never been combined in humans before, and the trial demonstrated that these drugs can be safely administered, and also, there's evidence that it may help patients where checkpoint therapy is not good enough alone," said Rubinstein.

Patients who have stopped responding to checkpoint therapy may be helped significantly by adding ALT-803. Pre-clinical studies have shown that ALT-803 activates the immune system to mobilize lymphocytes against tumor cells and could potentially serve as an important component in combination treatments. Of the 21 patients treated, nine previously either had stable disease or responded to single-agent immunotherapy before becoming resistant to this treatment. Of these nine patients, 100 percent either had stable disease or had a partial response to the treatment used in this study.

"We can reassert control, at least in terms of stable disease, in essentially everybody we've treated so far," Wrangle said.

This novel combination is a huge step forward in cancer treatment. "Whereas for decades the modalities of therapy were surgery, radiation, and chemotherapy, the last decade has brought targeted therapy, and more recently, immunotherapy. It fundamentally alters the balance of power between your body and your cancer," Wrangle said.

A lung cancer specialist, Wrangle said 75 percent of lung cancer patients unfortunately are diagnosed at an incurable stage. "If 10 years ago you were talking about defining a five-year survival rate for metastatic non-small cell lung cancer patients, someone would laugh in your face. It would be a joke. It's just a very different time now," he said of the progress being made in the treatment of lung cancer.

He credits Rubinstein's work, instrumental in the development of ALT-803, in helping to make this advance. Research into ALT-803 started years ago while Rubinstein was doing his postdoctoral training at the Scripps Research Institute. It was there that he co-discovered the powerful immune system stimulator used in this trial. The stimulator, known as IL-15 complexes, is actually a combination of an immune system growth factor and its soluble receptor. IL-15 is a growth factor for certain kinds of white blood cells including natural killer cells and T cells.

Wrangle explained that natural killer cells are the chief arm of the innate immune response. "They are an important part of anti-cancer response that haven't been really talked about for a long time."

Wrangle said his collaboration with Rubinstein is a powerful example of what team science can accomplish.

"His ownership of the intellectual foundation of this therapy is manifest," Wrangle said of Rubinstein's contribution. "He is brilliant and just works furiously to help understand how we can develop this therapy."

Successful trials for the treatment of cancer are incredibly rare, he said. "There are very few people in human history who get the privilege of developing a new therapy for any human disease, much less cancer. Mark and I are now in this weird micro-club of folks who have developed the promise of a new therapy for cancer. That's such an amazing privilege to be able to do that," he said.

In contrast to other immunotherapies that require admission to a hospital, this new therapeutic combination can be administered in an outpatient setting. "The plan was to do it all as an outpatient therapy because inpatient therapy is just infeasible. My patients feel like they have the flu, but they go about their day, and it's totally manageable. That's the kind of revolutionary part with regard to this class of agent," Wrangle said.

Wrangle and Rubinstein are surprised and elated at the success demonstrated in their latest study. Wrangle said the landscape of oncology is "eyeball-deep in failed trials," so he and Rubinstein are hopeful this will provide more treatment options for patients. "The number of trials that work is miniscule, so was I surprised? I was ecstatic that it was working," he said.

Rubinstein agreed, adding that the success of the trial is a testament to the commitment, hard work and incredible insight that Wrangle has for making a difference for his patients. "He has an amazing vision for how to bridge the gap between basic and clinical research."

Wrangle said there's still plenty of work to do before the new combination of drugs can be used outside of a clinical trial. "We have a lot to figure out about how to use this therapy, and we need to treat a few hundred patients in order to get a better sense of how to refine the synergy of these two classes of drugs. That's just going to take time," he said.

Both of the researchers, who are in their early forties, said they were motivated by the need to give lung cancer patients better options. Wrangle plans to frame the study's publication. "I think this manuscript will be the thing that we have on the wall that we look back at 20 years from now, when we're still working together and discovering new therapies."


A potential new therapeutic target for Ewing sarcoma

Published: April 05, 2018

Sourcehttps://www.sciencedaily.com/releases/2018/04/180405101722.htm

The sarcoma research group of the Bellvitge Biomedical Research Institute (IDIBELL), led by Dr. Òscar Martínez-Tirado, has identified a potential new therapeutic target for Ewing sarcoma, the second most frequent bone cancer in children and adolescents, and a tumor known by its aggressiveness and tendency to metastasize. The research, published in International Journal of Cancer, has been funded almost entirely by the Alba Pérez Foundation, a non-profit organization dedicated to this disease.

For years, the main line of research of the Ewing sarcoma group focused on the caveolin 1 protein (CAV1), which has been associated to treatment resistance and metastasis, among other issues. However, the location of this protein in the cell makes its use as a therapeutic target virtually impossible. "That is why we were looking for a CAV1 cofactor with an equally relevant role but a more accessible location," explains Dr. Martínez-Tirado, "and the EphA2 membrane receptor, already described in previous studies, meets these requirements."

In their latest work, researchers not only demonstrate the connection between the EphA2 receptor and caveolin 1, but also establish a correlation between the phosphorylation of EphA2 and the aggressiveness of tumors in Ewing sarcoma. "In several in vitro and in vivo tests, we observed that this membrane receptor plays a key role in the migration of tumor cells."

Regarding in vivo studies, the research team used two different models. The artificial model of metastasis, more experimental, allows researchers to assess the ability of cells to adhere to the pulmonary epithelium in adverse conditions. On the other hand, the new orthotopic model developed by the same group a few months ago induces a spontaneous metastasis, much more similar to what can be observed in a clinical setting.

"In the lab, we have shown that the lack of EphA2 receptor significantly decreases the incidence and number of metastases," says Dr. Martínez-Tirado, "and thanks to our collaboration with Hospital Virgen del Rocío, we also saw that 90% of Ewing sarcoma patients express this receptor (mimicking caveolin 1), a fundamental fact when it comes to selecting EphA2 as a therapeutic target. At the same time, working with patient samples also allowed us to correlate EphA2 ligand-independent activity, associated with its phosphorylation, with lower survival. "

Thanks to the stable financial support of the Alba Pérez Foundation, IDIBELL researchers will keep on working on the development of treatments based on blocking the activity of this receptor. "Through drug nanoengineering techniques, we aim to develop a molecule with a double effect, capable of blocking EphA2 in tumor cells and delivering other targeted drugs at the same time," concludes the IDIBELL researcher.


Making headway in infant leukemia research

Published: April 04, 2018

Sourcehttps://www.sciencedaily.com/releases/2018/04/180404114751.htm

Around 600 children under the age of 15 are diagnosed with leukemia each year in Germany. The effects are especially dramatic if this severe illness develops at birth or shortly afterwards. Research carried out at the Division of Genetics at Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) with support from the Institute for Human Genetics has now discovered another molecular cause for a particularly aggressive type of leukemia in infants. The results have been published in the journal Blood.

While tumours tend to affect the health of older people, leukemia (blood cancer) frequently affects children. A special type of leukemia, which is particularly difficult to treat and often occurs in very young patients, is the subject of research carried out by Prof. Robert Slany and his team at the Division of Genetics at FAU.

With this type of cancer, the genes in the white blood cells affected change slightly, causing two chromosomes to cross. This produces an abnormal protein that disrupts cell growth control. 'The longer we study these classes of proteins, the clearer it becomes how adept these molecules are at interfering with cellular growth to such an extent that makes normal control virtually impossible,' says Prof. Slany.

The latest research results show that these proteins not only disrupt the production mechanism of the cells by accelerating the transcription mechanism of certain genes, but also change the structure of the gene itself, which intensifies the abnormal implementation of the genetic information even further. 'It's like driving a car on black ice -- braking is impossible,' explains Prof. Slany. The challenge for the future now lies in finding a suitable type of 'grit' for this black ice that slows down the proliferation of leukemia cells to normal levels without damaging the other healthy cells in the body. The research findings have now been published in the journal Blood with the following title: 'The interaction of ENL with PAF1 mitigates polycomb silencing and facilitates murine leukemogenesis'.


How to fight side effects of hormone therapy for prostate cancer

Published: April 03, 2018

Source:https://www.sciencedaily.com/releases/2018/04/180403140352.htm

Men on hormone therapy for prostate cancer may benefit significantly from hitting the gym with fellow patients and choosing more veggies and fewer cheeseburgers, a new study suggests.

Androgen deprivation therapy is a powerful tool against prostate cancer, and more and more men are opting for the treatment as a growing array of hormone-based therapies become available.

But it comes with a cost. Suppressing male hormones, including testosterone, that fuel cancer growth also means that patients lose strength and muscle mass and gain fat. And that puts the men at risk for other health problems, including heart disease and diabetes.

But diet and moderate exercise proved to be valuable tools in fending off those side effects in the new research from The Ohio State University. The study appears in the journal Annals of Behavioral Medicine.

"We found that a comprehensive exercise and diet program in a group setting can make a difference for prostate cancer patients, and the difference was greater than I expected in a short period of time," said lead author Brian Focht, a professor of human sciences at Ohio State.

"As they gain fat and lose muscle during hormone therapy, these men are at significant risk for chronic health problems including metabolic disorder, a precursor to diabetes and heart disease."

While this isn't the first study to show that exercise is good for prostate cancer patients and survivors, it is the first to employ this type of group approach and one of the first to also focus on diet, said Focht, also an investigator at Ohio State's Comprehensive Cancer Center.

"We think the group approach is important, because it creates social support for a group of men who have experienced shared challenges, and that can increase the chances of long-term behavior change," Focht said. "We wondered if prostate cancer patients would view this approach as feasible and acceptable, and we heard a resounding 'yes.' They fully embraced it."

The study included 32 prostate cancer patients treated at Ohio State's Arthur G. James Cancer Hospital. Half the men participated in a 12-week personalized program that included group exercise and nutrition counseling. The other half received some basic education related to their cancer diagnosis, and the opportunity for exercise education at the end of the study. Before the study, all of the men were sedentary, exercising less than an hour a week in the previous six months.

The research team evaluated the men at the start of the study, two months after the program and three months after the program and found significant differences between the men who had the intervention and those who did not.

The exercise and diet group saw gains in mobility and muscle strength and decreases in fat mass three months after the intervention, while those three measures moved in the opposite, undesirable, direction for the other group of men.

Men in the intervention group, on average, lost about 4.4 pounds, 4 pounds of which was fat. Their body fat percentage dropped by more than 2 percent. Meanwhile, the control group gained a third of a pound and almost 2 pounds of fat mass, on average. Their body fat percentage increased by 1.8 percent.

Similarly, mobility (measured with walking and stair-climbing tests) increased for the exercise group and decreased for the control group. Muscular strength (measured by pounds lifted on leg extension and chest press exercises) improved by about 20 pounds in the exercise group. After three months, the control group saw little difference in how much weight they could lift.

Exercise regimens were tailored to each man's ability and increased in intensity during the three-month experiment and included two one-hour supervised sessions per week. Workouts included weight-bearing exercise such as leg extensions and bicep curls, and aerobic exercise on a treadmill, stationary bike or elliptical trainer.

The research team also encouraged the men to exercise on their own, per national guidelines that recommend at least 150 minutes of physical activity a week and 10,000 steps per day. The men in the study did not experience any serious medical problems or injuries as a result of the exercise program.

Nutrition counseling was led by a registered dietitian, who gave advice during small group sessions after workouts and on brief phone calls. Men were encouraged to adopt a plant-based diet and follow other nutritional guidelines supported by the federal government and by medical groups including the American Cancer Society.

"This is not a one-size-fits-all approach. Each man needs to work within his own limits, and each has different needs nutritionally," said Focht, who wants to replicate the research with about 200 prostate cancer patients to see if the findings in this small pilot study hold true.

"There's an increasingly recognized focus on the holistic treatment of cancer patients. We not only want to add years to life, but we want to add life to their years," Focht said.


Eating nuts increases survival in colon cancer patients

Published: April 02, 2018

Source:https://www.naturalnews.com/2018-04-02-eating-nuts-increases-survival-in-colon-cancer-patients.html

(Natural News) The regular consumption of nuts significantly increases the prognosis of people with stage III colon cancer, according to a study published in the Journal of Clinical Oncology.

The study was led by researchers at Yale Cancer Center who looked at the the effect of nuts consumption on colon cancer recurrence and survival. In conducting the study, the research team examined 826 individuals with stage III colon cancer. The participants reported their dietary intake on food frequency questionnaires. At the same time, they were enrolled onto a randomized adjuvant chemotherapy trial. The research team followed-up on the participants after an average of six and a half years after they were treated with surgery and chemotherapy.

The results of the study showed that cancer patients who ate two or more servings of nuts every week exhibited 42 percent improvement in disease-free survival as well as a 57 percent improvement in overall survival, in comparison to those who did not eat nuts.

As the researchers further analyzed the results, they found that disease-free survival increased by 46 percent among the subgroup of nut consumers who ate tree nuts, such as almonds, walnuts, hazelnuts, cashews, and pecans, instead of peanuts.

“These findings are in keeping with several other observational studies that indicate that a slew of healthy behaviors, including increased physical activity, keeping a healthy weight, and lower intake of sugar and sweetened beverages, improve colon cancer outcomes,” said Temidayo Fadelu, the lead author of the study.

Fadelu also said that their findings emphasized the importance of dietary and lifestyle factors in surviving colon cancer. In addition, their study highlighted the links between biological mechanisms that worsen disease, not only in colon cancer, but also in certain chronic diseases, such as type-2 diabetes. This finding is in line with previous studies that reported nuts can help reduce insulin resistance, which is a condition wherein the body finds it hard to process the insulin hormone. Insulin resistance results in unhealthy levels of sugar in the blood as well as a predecessor to type-2 diabetes and related diseases. Furthermore, previous studies among colon cancer patients found that their condition worsens when they follow a lifestyle that increase insulin resistance, such as being obese, lacking of exercise, and eating a diet rich in carbohydrates.

“These studies support the hypothesis that behaviors that make you less insulin resistant, including eating nuts, seem to improve outcomes in colon cancer,” said Charles S. Fuchs, senior author of the study.

Fuchs also noted that nuts might satisfy hunger with less consumption of carbohydrates or other foods linked to negative results. He also said that patients may not be eating nuts because of concerns regarding its high fat content, which could lead to obesity and worse outcomes. However, contrary to this, regular eaters of nuts in the study were found to be leaner.

More reasons why you should eat nuts

Nuts are technically considered a fruit, although they are not sweet and are rich in fat. The most commonly consumed nuts are almonds, Brazil nuts, cashews, hazelnuts, macadamia nuts, pecans, pecans, pine nuts, pistachios, and walnuts. Nuts are highly nutritious, which is one of the reasons why you should eat nuts. Nuts are also low in carbs and a great source of nutrients like magnesium, manganese, and selenium. Another reason why you should eat nuts is because they are packed with antioxidants, which help fight free radicals that harm the body. Nuts may also help in losing weight, managing cholesterol and triglyceride levels, reducing inflammation, and lowering the risk of heart attack and stroke.


Researchers discover how viruses manipulate the immune system to cause cancer

Published: March 30, 2018

Source:https://www.naturalnews.com/2018-03-30-researchers-discover-how-viruses-manipulate-the-immune-system-to-cause-cancer.html

(Natural News) Viruses drive the rapid reproduction of infected cells, and this hastens the creation of more viruses. Excessive cellular proliferation is a telltale sign of cancer.

According to a review by researchers from the University of Colorado Cancer Center (CU Cancer Center), viruses can manipulate the human immune system to ensure their survival and even promote cancer.

Fortunately, this discovery can be used to boost the effectiveness of immune-based therapies to fight cancer.

Dr. Sharon Kuss-Duerkop, a research instructor working in the lab of CU Cancer Centerinvestigator Dr. Dohun Pyeon, said that causing cancer may be a side effect of viruses manipulating the immune system.

Viruses “edit” human DNA via the insertion of their own genetic code into the DNA so that new viruses are created when the DNA is replicated. But the scientific review detailed that viruses can’t actually “turn off” the immune system when it manipulates genes.

Viruses actually “mute” the immune system through epigenetic regulation. Instead of changing the actual code of genes, viruses modify how genes are expressed.

Viruses modify gene expression through DNA methylation. During this process, parts of the human genome become unreadable. When this happens, sections of the genome called DNA promoter regions are methylated.

These promoter regions act as on-off switches for next-door genes, and when a promoter region is methylated, this switch is turned off. The gene it controls isn’t read and expressed.

Dr. Kuss-Duerkop explained, “You get lack of access by things that would be driving transcription.”

This means that methylating DNA promoter regions allow viruses to turn off genes. However, the virus alone can’t do this. They enlist human proteins which then methylate DNA to turn off the other crucial sections of human DNA.

Dr. Kuss-Duerkop added that viruses encode certain proteins that are able to regulate DNA methyltransferases. In essence, viruses make human proteins over-methylate human DNA.

Viruses target genes that the immune system uses to fight the virus itself, such as interferon-b, “a highly anti-viral gene expressed in virtually all cell types; or genes that T cells need to recognize virus-infected cells.”

This results in a weaker immune system fighting off the virus, and – if it’s a cancer-causing virus – a “microenvironment” by the tumor where the immune system is suppressed. This occurs in various cancers, and tumors may even hide themselves from the immune system. Tumors can even suppress the immune system more globally by the places they grow.

To prevent these cancer-causing viruses from spreading and halting their ability to manipulate the immune system, medical experts are looking into a way that will allow the immune system to fight off cancer. They hope to do this by boosting the immune system’s resistance to these same cancers.

Researchers are already making progress. For instance, PD-1 inhibitors can negate the “cloak” that cancers use to fool the immune system. Meanwhile, CAR-T cell therapies rely on specially engineered T-cells to target cancer-specific proteins and eliminate the cancer cells that they are attached to.

However, immune-based therapies against cancer aren’t that easy to create. There’s also the fact that not all patients will respond to these therapies.

To boost the effectiveness of immune therapies, or even identify which patients can benefit the most from immune therapies, experts must learn how viruses and cancers have evolved to circumvent the immune system.

It’s possible that if virus-related cancers have methylated DNA promoter regions of immune-related genes, demethylating these genes can help boost the effectiveness of immune-based therapies against cancer.

Kuss-Duerkop noted that caution is advised to avoid turning down methylation globally, which may cause the over-activation of all genes in the cell. Instead, demethylating certain gene promoter regions selectively can help restore an immune system inactivated by cancer-causing viruses.

Viruses are causing these tumors to form, and they also control the immune system to allow tumors to keep growing. Dr. Kuss-Duerkop concluded that these same mechanisms can help prevent tumors via immune-based therapies. They may even prevent cancer from developing in the first place.

Foods that fight cancer and boost the immune system

To strengthen your immune system so it can fight cancer, try to eat more of the foods below:

  • Curcumin (turmeric) – Curcumin is the main ingredient of turmeric. It has cancer-fighting and cancer-prevention properties.
  • Flax – Flax has lignans, which are compounds that prevent cancerous changes in cells.
  • Garlic – Garlic has allium compounds which boost immune cell activity, help break down cancer-causing substances, and prevent carcinogens from entering cells.
  • Hot Peppers – Hot peppers like cayenne (chili peppers) are rich in capsaicin, a chemical that fights cancer and helps neutralize certain cancer-causing nitrosamines.

Childhood Obesity May Be Driving More Cancers in Young Adults

Published: March 29, 2018

Source:https://www.cancercompass.com/cancer-news/article/61143.htm

(HealthDay News) -- Obesity rates in children have been rising for years, and the consequences of that extra weight may be showing up in cancer cases.

A new review found that certain cancers associated with people over 50 now affect people at younger ages more frequently. And obesity may be to blame.

Of the 20 most common cancers in the United States, the study found that nine are occurring in young adults. Approximately one in four new thyroid cancers were diagnosed in people aged 20 to 44, and about one in 10 new breast cancer cases occurred in that same age group, the researchers reported.

"Scientists have known for some time that obesity increases cancer risk, and when obese people get cancer, they're more likely to have a worse prognosis. And now it appears that obesity accelerates the development of cancer," said study author Dr. Nathan Berger. He is director of the Case Western Reserve University Center for Science, Health and Society, in Cleveland.

The researchers can't prove cause and effect. Still, the findings highlight the critical need for obesity prevention. "There are probably 140,000 cases of obesity-related cancers a year. This is a big issue," Berger said.

Experts generally agree that 13 cancers have clear ties to obesity. The current study found that nine of these 13 cancers are increasing in younger people. The nine cancers, and the percentage of new cases in people from 20 to 44, include:

Breast cancer -- 10.5 percent,

Colon and rectal cancer -- 5.8 percent,

Kidney cancer -- 7.8 percent,

Endometrial cancer -- 7.3 percent,

Thyroid cancer -- 23.9 percent,

Liver cancer -- 2.5 percent,

Gastric cardia (cancer at the top of the stomach) -- 6.2 percent,

Meningioma (cancer in the lining of the brain and spinal cord) -- 16.8 percent,

Ovarian cancer -- 10.6 percent.

Boston oncologist Dr. Jennifer Ligibel said this study is a "really interesting first look at the incidence of obesity and cancer risk in young adults, but there's still a lot of work to be done."

She said the review does a nice job of gathering available evidence. But there's "not a huge body of information yet because weight has increased pretty significantly in young people in a short time, and we don't know the ramifications of that yet," added Ligibel, who is with the Dana Farber Cancer Institute.

Ligibel also chairs the American Society of Clinical Oncology's obesity and energy balance subcommittee. She wasn't involved in the study.

She said it's not clear exactly how obesity might increase cancer risk. "But it's probably not just one factor," she noted.

"Obesity causes higher levels of inflammation. It also causes higher levels of insulin and other growth hormones. Obesity leads to higher levels of sex hormones. Also, there are related factors, including diet. There's a lot we need to learn," she said.

Berger added that epigenetics are likely involved, too. Epigenetics are changes that occur in gene activity without changing the DNA itself.

Those kinds of changes may be lasting, even if someone who was heavy as a child loses weight, Berger said.

He said it's probably similar to what happens with smoking and cancer risk. When people quit smoking, their risk of cancer drops dramatically, but never completely disappears, he explained.

And even though the risk might not go away completely, it's still important to try to lose weight, he said.

"Cutting down obesity impacts cancer risk, as well as the risk of diabetes and heart disease. Losing weight helps," Berger said.

Ligibel agreed, citing studies that showed the risk of cancer was cut by half for people who've had weight-loss surgery.

The study looked at 100 publications worldwide, with data reaching back more than four decades.

The review also points to the need for physicians to keep cancer on their diagnostic radar, even for younger patients. "If you have an obese patient with blood in the stool, evaluate them for colon cancer, even at a younger age," Berger suggested.


A Light Breakfast Might Cut Cost of Pricey Prostate Cancer Drug

Published: March 28, 2018

Source:https://www.cancercompass.com/cancer-news/article/61123.htm

(HealthDay News) -- Here's one way to cut the cost of a $10,000-a-month prostate cancer drug: Take it with food, some researchers suggest.

Investigators said they found that taking Zytiga (abiraterone acetate) with a low-fat breakfast boosts its efficiency. That could make it more convenient and significantly cheaper, the new study suggested.

Zytiga is the standard medicine for prostate cancer that has spread and has progressed despite hormonal therapy. Patients are told to take four 250-milligram pills first thing in the morning, then wait an hour before eating breakfast.

But the small study found that taking one-fourth of the recommended dose with a low-fat breakfast -- for example, cereal with skim milk -- was just as effective. In addition, it enabled patients to cut drug costs by 75 percent.

"The patient gets a simplified schedule, slightly more control over his daily life, the convenience of eating whenever he chooses and the opportunity to share the cost-savings with his insurance company," said study lead author Dr. Russell Szmulewitz.

"Taking this medicine while fasting is wasteful," added Szmulewitz, a prostate cancer specialist at the University of Chicago.

A one-month supply of Zytiga costs $8,000 to $11,000 when bought wholesale, or just over $100,000 each year. Many patients take the drug for two to three years, the study authors noted.

Combining the lower dose -- a single 250-mg pill -- with food did not reduce the drug's effectiveness. Progression-free survival was identical for 34 patients who took the lower dose with food and 34 patients who took the recommended dose without food -- about 8.6 months, the findings showed.

Taking the lower dose with food reduced costs by as much as $300,000 per patient, the researchers said.

"Although it should be validated with a larger trial with more robust clinical endpoints, given the pharmacoeconomic implications, these data warrant consideration by prescribers, payers and patients," Szmulewitz said in a university news release.

The study was published March 28 in the Journal of Clinical Oncology.

Zytiga's per-patient cost of about $10,000 a month is a textbook example of what's called "financial toxicity," said study co-author Dr. Mark Ratain, director of the university's Center for Personalized Therapeutics.

This refers to the economic burden placed on patients by the high cost of care, Ratain explained.

"At least three-quarters of this expensive drug is wasted. It's excreted and flushed away," he added.


The connection between diet, obesity, and cancer: Nutrition experts explore the evidence

Published: March 27, 2018

Source:https://www.sciencedaily.com/releases/2018/03/180327162556.htm

About one third of cancer cases are estimated to be linked to dietary and other modifiable risk factors, especially for obesity-related cancers such as breast, colorectal, ovarian, endometrial, kidney, gallbladder, esophageal, and pancreatic cancers. In this special theme issue of the Journal of the Academy of Nutrition and Dietetics, food and nutrition practitioners and other health professionals take an in-depth look at the relationship between nutrition, obesity, and cancer prevention, treatment, and survival and identify research gaps for future prevention research efforts.

The United States has a high burden of cancer. The American Cancer Society estimates there will be more than 1.7 million new cases diagnosed in 2018 and around 610,000 cancer deaths. Studies strongly suggest that diet is associated with cancer and that obesity increases the risk of many types of cancer as well as several chronic diseases, including type 2 diabetes, cardiovascular disease, hypertension, and chronic inflammation.

Key issue highlights:

Obesity prevalence in the US has tripled over the last 50 years. In 2016, a report by the International Agency for Research on Cancer highlighted that excess body fatness increases the risk for 13 types of cancer. Lead investigator Stephen D. Hursting, PhD, MPH, professor, Department of Nutrition, University of North Carolina at Chapel Hill, and colleagues review the multiple mechanisms underlying the obesity-cancer link. Their detailed review also assesses the dietary interventions that are being implemented in preclinical and clinical trials.

"Obesity-associated metabolic perturbations are emerging as major drivers of obesity-related cancer, including alterations in growth factor signaling, inflammation, and angiogenesis," explained Dr. Hursting. "Preclinical evidence suggests that dietary interventions, such as calorie restriction, intermittent fasting, low-fat diet and the ketogenic diet, have the potential to reverse some of these obesity-associated alterations; however, more clinical data are needed to confirm translation to human subjects."

A group led by Guido Eibl, MD, from the Department of Surgery, David Geffen School of Medicine at UCLA, on behalf of the Consortium for the Study of Chronic Pancreatitis, Diabetes, and Pancreatic Cancer, reviews the current knowledge pertaining to obesity and type 2 diabetes as risk factors for pancreatic ductal adenocarcinoma (PDAC), one of the deadliest cancers. Although the risk factors promoting PDAC development have been known for several decades, their underlying molecular mechanisms and interactions have just recently begun to be explored. The article highlights the risk factors for PDAC development and progression, their interplay and underlying mechanisms, and the relation to diet, and outlines research gaps and opportunities.

High quality epidemiologic studies associate obesity with an increased risk of PDAC, however, there are many unanswered questions. For example, the beneficial effects of weight reduction and bariatric surgery on improving insulin resistance are known, but their role in decreasing PDAC incidence is still essentially unknown.

"Altogether, given the high mortality of PDAC and the expected increase in obesity and diabetes over the next few decades, efforts should be undertaken to mechanistically understand the link between obesity, diabetes, and PDAC. Preclinical animal models are available that will facilitate the study of these important interactions to advance our knowledge, so that the obesity- and diabetes-driven burden of PDAC can be curbed," commented Dr. Eibl.

Consumption of dietary energy density (DED) has been associated with weight gain in adults. DED is the ratio of energy (kilocalories or kilojoules) intake to food weight (grams) and is a measure of diet quality. Cynthia A. Thomson, PhD, RD, professor, Mel and Enid Zuckerman College of Public Health, The University of Arizona, and colleagues present results of an investigation into the association between baseline DED and obesity-associated cancers in over 90,000 postmenopausal women enrolled in the observational study or the calcium and vitamin D trial and hormone replacement therapy trials of the Women's Health Initiative. Investigators found that DED was associated with higher risk of any obesity-related cancer. Of note, the higher risk was restricted to women with normal BMI.

"The demonstrated effect in normal-weight women in relation to risk for obesity-related cancers is novel and contrary to our hypothesis," remarked Dr. Thomson. "This finding suggests that weight management alone may not protect against obesity-related cancers if women favor a diet pattern indicative of high energy density. Higher DED in normal-weight women may promote metabolic dysregulation independent of body weight, an exposure known to increase cancer risk.

DED is a modifiable risk factor. Nutrition interventions targeting energy density as well as other diet-related cancer preventive approaches are warranted to reduce cancer burden among postmenopausal women.

In a pilot intervention among 46 cancer survivors aged 60 years or older, Wendy Demark-Wahnefried, PhD, RD, professor of Nutrition Science, University of Alabama at Birmingham, and colleagues, posed the question of whether a home vegetable gardening intervention was feasible among older cancer survivors, and whether it was associated with improvements in diet and other health-related outcomes. Participants were randomized to receive a year-long vegetable gardening intervention immediately or to a wait-list control arm.

Investigators found the gardening intervention was well accepted, safe, and feasible and also significantly improved reassurance of worth and reduced gains in central adiposity. Data also suggested that it increased vegetable and fruit consumption by approximately one serving per day.

"Results suggest that future larger studies are warranted. A fully powered randomized controlled trial is currently underway and recruiting 426 older cancer survivors across Alabama," noted Dr. Demark-Wahnefried.

Nancy J. Emenaker, PhD, MEd, RDN, LD, and Ashley J. Vargas, PhD, MPH, RDN, both registered dietitian nutritionists from the National Institutes of Health, review the scientific evidence linking diet and cancer. They explain the inconsistencies in the nutrition and cancer scientific literature and the issues that registered dietitian nutritionists (RDNs) face when translating this complex information for patients.

"RDNs are uniquely positioned to provide balanced, evidence-based information from peer-reviewed literature to help at-risk and cancer patients understand the strength of the evidence guiding individual health decisions," observed Dr. Emenaker and Dr. Vargas. "Despite the best efforts of nutrition science researchers, inconsistencies exist across the diet-cancer prevention scientific literature. Clinical trials are the gold standard of research, but the body of scientific data should be compelling before translating scientific findings to our at-risk, presumed healthy patients for disease prevention and patients with a good prognosis undergoing treatment."

"RDNs play such an important role in both cancer prevention and cancer care. Our profession is involved in research to investigate diet-cancer relationships, as well as supporting individuals and communities in making lifestyle changes for cancer prevention and treatment. RDNs are integral in providing quality care by implementing evidence-based interventions," added Linda Snetselaar, PhD, RDN, LD, endowed chair and professor, Department of Epidemiology, College of Public Health, University of Iowa, and Editor-in-Chief of the Journal of the Academy of Nutrition and Dietetics.


Cancer patients' pain eased by simple bedside chart

Published: March 26, 2018

Source:https://www.sciencedaily.com/releases/2018/03/180326090318.htm

Patients with cancer could benefit from a simple bedside system to manage their pain, a study suggests.

The new approach reduces pain levels compared with conventional care, the research with patients shows.

Pain affects half of all people with cancer and an estimated 80 per cent of those with advanced cancer, causing both physical and emotional impact on patients.

Researchers at the University of Edinburgh worked with doctors to develop the Edinburgh Pain Assessment and management Tool (EPAT) -- a pen and paper chart which medical staff use to regularly record pain levels in a simple traffic light system.

Amber or red pain levels -- indicating moderate or severe pain -- prompts doctors to review medications and side effects and monitor pain more closely.

The trial looked at pain levels in almost 2000 cancer patients over five days, following admission to regional cancer centres.

Patients whose care included use of the chart reported less pain during this time, compared with patients with standard care, who did not show an improvement.

Importantly, use of the chart was not linked to higher medicine doses. Authors suggest that it works by encouraging doctors to ask the right questions and reflect on pain medications and side effects more frequently, before patients reach a crisis point.

Researchers say the system is a simple way to put pain management at the forefront of routine care, but caution that more studies are needed to understand how it could work longer term.

The study was published in the Journal of Clinical Oncology and was funded by Cancer Research UK.

Professor Marie Fallon, of the Palliative and Supportive Care Group at the University of Edinburgh, said: "These exciting findings show the important benefits of influencing doctors' behaviours, rather than looking for more complex and expensive interventions. These findings are a positive step towards reducing the burden of pain for patients and making them as comfortable as possible at all stages of cancer."

Martin Ledwick, Head Information Nurse at Cancer Research UK, said: "In most cases it should be possible for cancer pain to be controlled if it is assessed and managed effectively. Any work that encourages medical teams to assess and monitor pain more carefully to help this happen has to be a good thing for patients."


Little known natural treatments for cancer blow away widely held myths

Published: March 24, 2018

Source:https://www.naturalnews.com/2018-03-24-little-known-natural-treatments-for-cancer-blow-away-widely-held-myths.html

A cancer diagnosis is truly one of the most terrifying things a human can ever face. It is understandable that at such a time a person might be drawn to the apparent security of relying on the recommendations of the “qualified” doctor or oncologist who suggests a regimen of chemotherapy and/or radiation as the best chance of beating this terrifying disease.

Nonetheless, it is precisely when receiving such a diagnosis that a person most needs to remain calm and face the true facts, one of which is the fact that conventional cancer treatments do not represent the best course of action.

Many natural health advocates, including Mike Adams of Natural News, have for years been warning that chemotherapy is not only largely ineffective, but often dangerous. This fact has been backed up by several studies, including a recent study by a research team from the Albert Einstein College of Medicine at Yeshiva University. That study found that “chemotherapy, despite decreasing tumor size, increases the risk of metastatic dissemination.” In other words, on the surface, chemotherapy might appear to reduce the physical size of a tumor, but it increases the risk that the cancer will metastasize, or spread elsewhere in the body.

Furthermore, a study published in the journal Clinical Oncology in 2004, admitted that chemotherapy is only effective 2 percent of the time – no matter which type of cancer you’re talking about – and that only refers to people who survive for a five-year period.

This does not mean that patients who have been diagnosed with cancer have no hope of successful treatment. They simply need to be brave enough to look in the right direction for a cure. After all, nature contains all we need to heal ourselves, if only we are willing to dig deep enough to find the answers.

Waking Times recently published a series of articles which outlined scientifically proven cancer treatments, including:

Laetrile (also known as amygdalin or vitamin B17): According to Waking Times, laetrile destroys cancer cells while leaving other cells unharmed. The article explains:

Laetrile is made of 4 parts, two of which are glucose, the third of which is benzaldehyde and the fourth of which is cyanide. … [T]here are many foods including vitamin B12 that contain cyanide, but they are safe since the cyanide remains locked up as part of another molecule. … [C]ancer cells contain an enzyme that healthy cells do not, beta-glucosidase, called the “unlocking enzyme”. This enzyme causes the release of both the benzaldehyde and the cyanide, thus destroying the cancer cell, but cannot occur in a healthy cell, since it doesn’t contain this unlocking enzyme. 

Cannabis: After being vilified for decades, cannabis has come into its own in recent years as a treatment for many illnesses, including cancer. Marijuana contains tetrahydrocannabinol (THC) and cannabinoids (CBD), and several studies have confirmed the ability of these ingredients to fight cancer. For example, a 2010 study published in the journal Molecular Cancer found that “Cannabinoids reduce ErbB2-driven breast cancer progression through Akt inhibition.”

Cesium chloride: Cancer creates an environment which lowers the pH of healthy cells, creating an acidic environment. This destroys the ability of DNA and RNA to control healthy cell division, which allows cancer cells to multiply indiscriminately. Cesium chloride is extremely alkaline, boosting the body’s alkalinity and restoring its natural pH balance. It also interferes with the body’s uptake of glucose, effectively starving the cancer cells.

These are just three of the many, many natural cancer treatments which have a proven track record of successfully beating this insidious disease. So, if you or a loved one has been diagnosed with cancer, don’t feel defeated; just be brave enough to look in the right direction for a cure.


More than 2,500 cancer cases a week could be avoided

Published: March 23, 2018

Source:https://www.sciencedaily.com/releases/2018/03/180323091000.htm

More than 135,500 cases of cancer a year in the UK could be prevented through lifestyle changes, according to new figures from a Cancer Research UK landmark study published today.*

This equates to 37.7% of all cancers diagnosed each year in the UK -- rising to 41.5% in Scotland.

The latest figures, calculated from 2015 cancer data, found that smoking remains the biggest preventable cause of cancer despite the continued decline in smoking rates. Tobacco smoke caused around 32,200 cases of cancer in men (17.7% of all male cancer cases) and around 22,000 (12.4%) in women in 2015, according to the research published in the British Journal of Cancer.

Excess weight is the second biggest preventable cause of cancer. Around 22,800 (6.3%) cases of cancer a year are down to being overweight or obese. This amounts to around 13,200 (7.5%) cases of cancer in women and around 9,600 (5.2%) in men.

Obesity causes 13 types of cancer, including bowel, breast, womb and kidney. And the results suggest that more than 1 in 20 cancer cases could be prevented by maintaining a healthy weight.

The third biggest preventable cause of cancer is overexposure to UV radiation from the sun and sunbeds, which causes around 13,600 cases of melanoma skin cancer a year (3.8% of all cancer cases).

Other preventable causes of cancer include drinking alcohol, eating too little fibre (causing around 11,900 and around 11,700 cases respectively, which is 3.3% each) and outdoor air pollution. While air pollution is to blame for around 3,600 lung cancer cases a year (1% of all cancer cases), it still causes far fewer cases of lung cancer than tobacco.

Sir Harpal Kumar, Cancer Research UK's chief executive, said: "Leading a healthy life doesn't guarantee that a person won't get cancer, but it can stack the odds in your favour. These figures show that we each can take positive steps to help reduce our individual risk of the disease.

"This research clearly demonstrates the impact of smoking and obesity on cancer risk. Prevention is the most cost-effective way of beating cancer and the UK Government could do much more to help people by making a healthy choice the easy choice."

Professor Linda Bauld, Cancer Research UK's prevention expert, said: "These new figures show that the battle to conquer smoking-related cancer is far from over. But the declining numbers of smokers show that prevention strategies are working.

"Obesity is a huge health threat right now, and it will only get worse if nothing is done. The UK Government must build on the successes of smoking prevention to reduce the number of weight-related cancers. Banning junk food TV adverts before the 9pm watershed is an important part of the comprehensive approach needed."

Janet Boak, 55, a grandmother of three from Carlisle, was diagnosed with womb cancer at 51 after she noticed spots of blood four years after her menopause. During surgery to remove two fibroids from her womb, cancer was found. Janet then had a full hysterectomy to remove her womb and cervix. Because the cancer was caught in the earliest stages and hadn't spread, she avoided any further treatment.

Volunteering to take part in some womb cancer research after her treatment, Janet was shocked to find out that the possible contributing factors for womb cancer included being obese and being inactive.

Janet said: "That was me. At almost 20st and wearing up to a size 30, I was huge and most of my weight was around my stomach. I couldn't remember the last time I did any exercise.

"Of course I'd known I needed to lose weight but I hadn't realised just how much I was putting my life at risk."

Janet joined a local slimming group in 2015, changed her diet and started taking exercise.

She said: "The weight gradually fell off and now, over two years on, I've lost more than 6st and wear a size 16. I could barely keep up with my three young grandchildren before but now I'm always running around after them. I even ran Race for Life for Cancer Research UK last year -- something I never imagined I would do.

"Getting cancer was terrifying but it was the wake-up call I needed. I don't know what the future holds but at least I know I'm doing all I can to stay healthy and happy."


Could a Pap Test Spot More Than Just Cervical Cancer?

Published: March 21, 2018

Source:https://www.cancercompass.com/cancer-news/article/61072.htm

(HealthDay News) -- Pap tests have helped drive down rates of cervical cancer, and a new study suggests they also could be used to detect other gynecologic cancers early.

According to the study authors, tissue and fluid collected during a Pap test can detect endometrial and ovarian cancer in women when subjected to genetic testing.

If this new test bears out, it would save thousands of lives each year by catching these cancers at an earlier, more treatable stage, said researcher Dr. Amanda Fader. She is director of the Kelly Gynecologic Oncology Service at Johns Hopkins University School of Medicine in Baltimore.

"The goal here was to be able to detect these cancers through tumor gene mutations that are present in either the bloodstream or fluid collected from the cervix or vagina," Fader said. "If we could detect the cancers earlier or at a pre-cancerous state, there's a potential to not only achieve more cures, but to preserve more fertility in many women."

In a Pap test, doctors collect cells from the cervix using a scraper or brush. The cells are then sent to a lab for analysis.

The researchers behind the new study developed a testing regimen called PapSEEK to see if additional samples collected during a pelvic exam could be used to detect endometrial or ovarian cancer.

PapSEEK searches out "DNA mutations that have already been identified for specific cancers," Fader said. "We tested cervical fluid samples to look at 18 genes that are highly or commonly mutated in endometrial or ovarian cancer."

To see whether the test works, the researchers gathered samples from 1,658 women, including 656 with endometrial or ovarian cancers, as well as just over 1,000 healthy women for the control group.

The PapSEEK test accurately detected 81 percent of endometrial cancers and 33 percent of ovarian cancers, according to the study.

Accurate detection increased to 93 percent and 45 percent, respectively, when researchers used a Tao brush to collect samples. A Tao brush resembles a pipe cleaner, Fader said, and can be used to collect tissue samples closer to potential tumor sites.

In addition, the researchers further improved ovarian cancer detection rates to 63 percent by testing for tumor DNA in a patient's blood, alongside the DNA Pap test.

A larger study to validate the new test is under way, Fader said.

A "hopeful" timeline would produce the data necessary to get the test into practice within two or three years, but it could take longer, Fader noted.

Debbie Saslow, senior director of human papillomavirus (HPV)-related and women's cancers for the American Cancer Society, said validating the test could take much longer.

"This is a really early preliminary set of results that looks promising. But there's still a long way to go to know if this would actually be helpful," Saslow said.

"I'm not saying it's not promising. I'm just saying it'll take a lot more work," a lot more time and a lot more women to know if it would be clinically valuable, she added.

The report was published in the March 21 issue of the journal Science Translational Medicine.


Breast cancer: Obesity may hinder some treatments

Published: March 19, 2018

Source:https://www.medicalnewstoday.com/articles/321251.php

Obesity may be the reason that some cancers become resistant to drugs intended to stop the formation of new blood vessels that fuel tumor growth, according to recent research led by Massachusetts General Hospital in Boston.

In a paper now published in the journal Science Translational Medicine, the researchers explain how obesity and molecular factors linked to it may promote resistance to anti-angiogenic inhibitors in breast cancer.

Anti-angiogenic therapy — which is designed to prevent the growth of blood vessels that feed tumors — is showing mixed results in people with breast and other cancers.

It is also well known that obesity raises the risk of many types of cancer, including breast cancer.

The new study is the first to show a link between these two "observations." It also offers some molecular targets that might improve response to treatment with anti-angiogenic inhibitors.

"Collectively," explains lead study author Dr. Joao Incio, of the Department of Radiation Oncology at Massachusetts General Hospital, "our clinical and preclinical results indicate that obesity fuels resistance to anti-vascular endothelial growth factor therapy in breast cancer via production of several inflammatory and pro-angiogenic factors, depending on the subtype of cancer."

"Targeting these resistance factors," he continues, "may rejuvenate the use of anti-angiogenic therapy in breast cancer treatment."

Angiogenesis and its inhibition

Angiogenesis is a natural process in the body that repairs and grows blood vessels. Some chemical signals stimulate the process and some chemical signals inhibit it. Levels of these are normally kept in balance so that blood vessels are made only when and where necessary.

These processes also play a key role in cancer. Without a dedicated blood supply, tumors cannot grow and spread. However, they do so because they also generate chemical signals that trigger angiogenesis, resulting in the growth of blood vessels that keep them fed with oxygen and nutrients.

Angiogenesis inhibitors are drugs that are designed to interfere with the chemical signals involved in angiogenesis. One of these drugs blocks vascular endothelial growth factor (VEGF), a signaling molecule that triggers growth of new blood vessels when it binds to proteins on cell surfaces.

However, Dr. Incio and his colleagues found that obesity "promotes resistance to VEGF inhibitor therapy" by altering chemical signals in tumors. They note that it increases "interleukin-6 [IL-6] and possibly also fibroblast growth factor 2 [FGF-2] in the tumor microenvironment."

The team also discovered — with the help of "mouse models of cancer with and without obesity" — that resistance to VEGF inhibitors may be overcome by using the "appropriate combination therapy."

Obesity, anti-VEGF therapy in breast cancer

The researchers started their investigation by analyzing the results of a clinical trial that tested the anti-VEGF drug bevacizumab, with and without chemotherapy, in 99 people with breast cancer.

Promising results from early clinical trials had led to the accelerated approval of the drug for the treatment of metastatic breast cancer in the United States. But approval was then withdrawn after subsequent studies found no evidence of benefit to long-term survival.

The trial that Dr. Incio and his colleagues investigated had shown that bevacizumab only benefited a small percentage of people.

When the researchers analyzed the trial data, they found that people whose body mass index (BMI) was 25 or higher — that is, if they fell into the overweight or obese category — had larger tumors when they were diagnosed.

On average, these people had tumors that were 33 percent bigger than those whose BMI was under 25.

In addition, tissue samples from people who had more body fat revealed that their tumors had a smaller blood supply, which is known to reduce the effects of chemotherapy.

Further examination showed that people with a higher BMI had higher circulating levels of two molecules: IL-6, which promotes inflammation, and FGF-2, which promotes angiogenesis.

There was also evidence that these factors were present in fat cells and adjacent cells in the tumors.

The role of IL-6 and FGF-2 in mouse models

In the next stage of the study, the researchers sought to confirm these findings in mouse models of breast cancer, both with and without obesity. They used two models: one of breast cancer that is positive for the estrogen receptor (ER), and the other of triple-negative breast cancer.

They found, in the case of the obese mice, that the tumor microenvironments — which contained many fat cells and had reduced levels of oxygen — responded poorly to anti-VEGF treatment. Morever, at a molecular level, responses differed depending on the breast cancer subtype.

For example, in obese mice with ER-positive breast cancer, the fat cells and some types of immune cell had higher levels of several pro-inflammation and pro-angiogenic molecules — including IL-6.

The researchers found that when they blocked IL-6 in the ER-positive obese mice, the animals' responses to anti-VEGF therapy improved and matched that of the lean mice.

Obese mice with triple-negative breast cancer, on the other hand, showed higher levels of FGF-2 but not of IL-6. In their case, blocking FGF-2 raised their response to treatment to that of the lean mice.

Blocking either of those molecules in lean mice with either type of breast cancer did not improve their response to anti-VEGF treatment.

"This is the first study to propose that markers such as body mass index could help personalize anti-VEGF therapy, with blockade of molecules like IL-6 or FGF-2 for overweight or obese cancer patients."

Dr. Joao Incio

The scientists note that several inhibitors of the two pathways are already available. For example, to inhibit FGF-2 in their experiments, they used the widely used diabetes drug metformin, which has been showing promise in slowing the growth of some cancers.


Mediterranean diet helps prevent cancer, nutrition science study finds

Published: March 18, 2018

Sourcehttps://www.naturalnews.com/2018-03-18-mediterranean-diet-helps-prevent-cancer.html

(Natural News) Everyone may have heard, at some point, a friendly suggestion to “eat your vegetables.” It turns out, that is actually sound advice, when it is part of the Mediterranean Diet (MD), according to research. In a study that appears in Current Nutrition Reports, authors used available information from various studies to provide an overview of the link between MD and cancer formation.

The study offered a glimpse of two operational definitions of MD. The first one, the Mediterranean Dietary Score, assigns a value for each component of MD. Beneficial components are factored in the score, which includes the increased intake of vegetables, fruits and nuts, legumes, unprocessed cereals, fish, and a high ratio of monounsaturated fatty acids to saturated fatty acids. In addition, the dietary score also identifies components that are harmful, such as meat and meat products – including poultry – and certain dairy products.

The second one is a derivative of the dietary score, with some modification on food items and scoring. Some important differences include the following:

Removing potatoes from the vegetable group

Splitting fruits and vegetables into two groups

Excluding the dairy group

Adding whole-grain products in a separate category

Including red and processed meat only in the meat group

The authors also looked at randomized clinical trials (RCTs) and prospective cohorts studies on the effects of MD. The first RCT that showed the relationship between MD and ischemic heart disease was the Lyon Diet Heart study, which revealed that MD has a protective effect against cancer development. The cohort studies, meanwhile, indicated that MD could lessen the risk of overall cancer mortality by 13 percent.

The effects of MD on certain types of cancer were also reviewed in this study. The authors found the diet can reduce the likelihood of breast cancer in postmenopausal women. In other forms of cancer, researchers noted that the diet reduced it by the following percentages: 17 percent for colorectal cancer, 4 percent for prostate cancer, 27 for gastric cancer, 42 percent for liver cancer, 44 percent for esophageal squamous cell carcinoma, and 40 percent for head and neck cancer.

“The Mediterranean Diet’s ability to help prevent cancer stems from the natural anti-cancer phytonutrients found in the food components of the diet,” explained Mike Adams, the Health Ranger, author of Food Forensics. “Stunningly, there are a few doctors and health practitioners still living today who believe there’s no such thing as an anti-cancer nutrient in natural foods. This is the scientific equivalent of believing in the Flat Earth theory, or the cultural equivalent of believing that women shouldn’t vote or that whites and blacks should drink from different water fountains,” Adams explained. “Every informed nutritionist, doctor and scientist knows that many natural foods contain potent anti-cancer compounds. Anyone who denies that is either scientifically illiterate or self-deluded,” Adams added.

In addition, the components of the MD were also individually reviewed to understand their health benefits.

Fruits and vegetables:  Researchers believe that the protective property of fruits and vegetables is due to the presence of flavonoids. In particular, flavonoids possess antioxidant, anti-inflammatory, anti-mutagenic, and anti-proliferative properties.

Fish: Eating copious amounts of fish means that the body has access to n-3 fatty acids, the authors wrote. The fatty acids are anti-inflammatory and may inhibit the development of cancers.

Whole grains: The fiber content of whole grains directly affect a person’s chances of developing colorectal cancer, with increased consumption having positive health outcomes. Reviewed studies also indicated that whole grains are also linked to a reduction of insulin resistance – which greatly benefits those with Type 2 diabetes.

Olive oil: The authors noted that consuming olive oil has decreased the likelihood of breast cancer for women, as well as cancers of the digestive system and the development of neoplasms in the respiratory system. Olive oil also contains polyphenols which target specific cells that may cause cancer.

Alcohol and red wine in moderation: Researchers define “moderate” in the study to less than 30 grams a day for men and 20 g/day for women. A separate study has shown that drinking less than 12.5 grams of ethanol (a component of alcoholic beverages) a day can decrease the risk of dying from cancer.

Red and processed meat: Red and processed meat in MD is not widely consumed and is considered to be unfavorable. One study showed that the consumption of red meat is linked to the development of colorectal tumors.

Dairy products: There are differing results of studies on the effects of milk and dairy products when it comes to cancer development.

Researchers concluded that the Mediterranean diet, characterized by food rich in vegetables, fruits, nuts, legumes, cereals, and fish, lowers the incidence and the development of cancer; thus, reducing the number of deaths associated with the illness.


Coffee May Have Bigger Effect on Your Body Than Thought: Study

Published: March 15, 2018

Source:https://www.cancercompass.com/cancer-news/article/61012.htm

(HealthDay News) -- Coffee has been tied to many health benefits. Now, a small study suggests a daily java habit may affect the body's metabolism more extensively than thought.

The study, of 47 adults, found that heavy coffee consumption -- four to eight cups a day -- altered blood levels of more than 100 metabolites. That refers to a broad range of chemicals that change after eating or drinking.

Many of the effects were expected, researchers said, but a few were surprising.

For example, coffee cut levels of certain metabolites related to the endocannabinoid system -- the same system affected by marijuana. This reduction is the opposite of what happens when you take pot, the researchers said.

What does it all mean? That's not clear.

But many studies have found that coffee drinkers typically have lower risks of various diseases than nondrinkers do, explained Marilyn Cornelis, the lead researcher on the new work.

The possible benefits include lower risks of Parkinson's disease, diabetes, multiple sclerosis and certain cancers.

"But most of those studies are just looking at associations," said Cornelis, an assistant professor of preventive medicine at Northwestern University's Feinberg School of Medicine in Chicago. "They looked at people's self-reported coffee intake and their risk of disease."

This study, she explained, tried to "get more at the mechanisms -- the biology that might be underlying those associations."

The findings, published March 15 in the Journal of Internal Medicine, come from a clinical trial that involved 47 Finnish adults. All were habitual coffee drinkers.

Researchers had them abstain from coffee for one month, then drink four cups per day the next month, and eight cups a day the following month. Blood samples were collected at the end of each month.

In general, coffee consumption triggered many expected changes in metabolism, Cornelis said.

But her team also spotted some previously unknown effects. Besides the endocannabinoid changes, there were shifts in certain metabolites related to the steroid system and fatty acid metabolism. The steroid system includes cholesterol and hormones such as testosterone and estrogen.

Whether there are implications for people's health, however, is unknown.

"We hope that this will be hypothesis-generating," Cornelis said. Future studies, she explained, could dig into the connection between coffee and endocannabinoid metabolites, for example -- to see whether it helps explain why coffee drinkers have lower risks of certain diseases.

The endocannabinoid system helps regulate a range of body functions, Cornelis noted. These include blood pressure, sleep, appetite and calorie-burning. Coffee has been linked to better weight control, and it's possible, she said, that its effects on endocannabinoids play some role.

She said the effects of coffee were the opposite of what you'd expect with marijuana -- which is a famous trigger of the "munchies."

For now, though, it's hard to know what to make of the findings, said Angela Lemond, a spokesperson with the Academy of Nutrition and Dietetics. She was not involved with the research.

The study was small, Lemond said, and it set up an artificial situation where people went from no coffee to four cups a day, then jumped to eight daily.

"That's going from zero caffeine to about 400 milligrams a day, then 800," Lemond pointed out.

It's not clear, she said, whether the metabolite changes reflect what happens with people's typical coffee-drinking habits.

Right now, Lemond noted, U.S. dietary guidelines say that adults can safely consume up to 400 milligrams of caffeine a day -- or, roughly, what these study participants downed in month two.

But if you do drink that much coffee, you should not load it with cream and sugar, Lemond stressed.

"You also need to look at your total day," she said. "People often don't realize what their caffeine intake is from sources like soda or tea."

Beyond that, Lemond said, people should think about caffeine's impact on their anxiety levels or sleep problems.

If you drink coffee in lieu of sleep, she noted, that's a problem. "So many people are sleep-deprived," Lemond said. "Even if there is a health benefit from coffee, that sleep deprivation will cancel it out."


Cutting Chemo Heart Risks for Breast Cancer Patients

Published: March 12, 2018

Source: https://www.cancercompass.com/cancer-news/article/60973.htm

(HealthDay News) -- Two classes of blood pressure drugs show promise in preventing heart complications caused by chemotherapy for breast cancer, researchers report.

One in four women who receives the chemo drug Herceptin develops potentially dangerous heart problems. However, the drug is highly effective at treating an aggressive form of breast cancer called HER2-positive, the scientists added.

"We don't want to avoid this exceptionally effective treatment just because it might cause damage to the heart," said study chair Dr. Maya Guglin, of the University of Kentucky's Heart and Vascular Institute.

The American Heart Association has warned doctors and patients to consider the heart risks of Herceptin when developing a treatment plan for HER2-positive breast cancer.

Guglin and colleagues found that two classes of drugs -- ACE inhibitors and beta blockers -- did not help protect the hearts of patients who received Herceptin alone.

But they did protect the hearts of patients who also received another chemotherapy drug called doxorubicin before they received Herceptin.

In those patients, heart problems occurred in 37 percent of patients who received ACE inhibitors and 31 percent of those who received beta blockers. That compared with 47 percent of patients who didn't receive either type of drug.

"The data clearly demonstrated that, for patients with HER2-positive breast cancer taking both doxorubicin and Herceptin, adding either an ACE inhibitor or a beta blocker to the treatment regimen can significantly offset the chance of heart problems," Guglin said in a university news release.

While the study offers some clarity about treatment options, Guglin said further research is needed before doctors consider this a new standard of care.

The U.S. National Cancer Institute-funded study was presented Sunday at the annual meeting of the American College of Cardiology in Orlando, Fla. Research presented at meetings is usually considered preliminary until published in a peer-reviewed medical journal.


Curcumin, when given in combination with drugs for lung cancer, reduces drug resistance, increasing their effectiveness

Published: March 10, 2018

Sourcehttps://www.naturalnews.com/2018-03-10-curcumin-in-combination-with-drugs-for-lung-cancer-reduces-drug-resistance.html

(Natural News) Shortness of breath, a hoarse voice, and persistent cough are warning signs you shouldn’t ignore. They’re the most common signs of lung cancer, the second leading type of the disease in the U.S. Patients may acquire resistance to anti-cancer drugs after an average survival period of seven to nine months. The cancer progresses, patients suffer from harmful side effects and take a turn for the worse. It doesn’t help that they and their families spend a fortune on expensive drugs, only to find out that they’re helpless against the Big C.

A study published in the Journal of Traditional Chinese Medicine offers hope for lung cancer patients and their loved ones. It showed how part of the answer lies in nature’s medicine cabinet. Curcumin, the main active ingredient in the unassuming turmeric, combined with anti-cancer drugs, can kill the tumors that cause cancer. It can also prevent the growth of drug-resistant cells to ensure complete recovery.

Cells were treated with curcumin and the anti-cancer drug gefitinib alone. Others were treated with curcumin and the drug combined. Cell growth and death were examined closely. Statistical analysis checked for accuracy the findings.

Nature’s pharmacy

The good news is that results showed that curcumin and gefitinib suppress the multiplication of cancer cells. The said combination can also lower resistance to the anti-cancer drug gefitinib, and win a big part of the battle against the Big C.

What is this little hero called curcumin like? Curcumin is a bright yellow substance found in some plants. It belongs to the ginger family.

Described as a “pharmacy unto itself,” curcumin boasts anti-inflammatory, anti-tumor, and antioxidant qualities, with no side effects at all. It lowers the risk of the biggest killer the world over — heart disease — by improving the way the lining of the blood vessels work. Curcumin also helps the brain by increasing the levels of the growth hormone brain-derived neurotropic factor (BDNF). Brain disorders have been linked to low levels of this hormone.

Nature and science

Curcumin is also boon for those suffering from various aches and pains. It helps lift the burden of arthritis sufferers and those with diverticular disease, irritable bowel (IBS), inflammatory bowel disease, dyspepsia, and peptic ulcer because it protects the stomach lining.

Cancer, and other types of disease for that matter, may no longer mean the death of those who suffer from it. It need not lead to depression, even suicide, among patients who can’t bear the pain and expense the Big C is notorious for. It need not send families with or without the cancer gene in their body to the depths of despair.

The battle against cancer is a battle not only for its many patients and their families. It is a battle mankind needs to wage for its very survival.


Colorectal cancer: The importance of diet

Published: March 9, 2018

Sourcehttps://www.medicalnewstoday.com/articles/321171.php

Colorectal cancer is quite common, especially among the aging population. An important risk factor for colorectal cancer is diet, and dietary choices are also vital during and after treatment. In this Spotlight, we give you an overview of which diets are best, and which are best avoided.

Prevention: What to avoid

Numerous studies have indicated that a diet too rich in red meat is associated with a heightened risk of colorectal cancer. "Red meat" is defined by the World Health Organization (WHO) as "all mammalian muscle meat, including beef, veal, pork, lamb, mutton, horse, and goat."

A review of the evidence supporting this link notes that "consumption of red meat might be related directly to the incidence of [colorectal cancer] or indirectly because a diet high in meat tends to be low in vegetables, fruit, and fiber."

A study of North Italian populations showed that individuals who eat red meat alongside eggs, cheese, and other fatty foods — as well as refined starches — on a frequent basis had an almost twice higher risk of developing rectal or colon cancer than their peers who favored a plant-based diet.

More recent research also revealed that "a daily increase of 100 [grams] of all meat or red meat is associated with a significant 12–17 percent increased risk of colorectal cancer."

In 2015, a report published by the International Agency for Research on Cancer made the news by pointing out that every 50-gram portion of processed meat, such as bacon or salami, eaten every day increases a person's risk of developing colorectal cancer by 18 percent.

This evidence led the WHO to classify processed meats as "carcinogenic to humans."

The damage caused by unwholesome diets made the headlines again in early 2018, when a study published in The BMJ reported that "ultra-processed foods" might increase the risk of developing various types of cancer.

Prevention: What to eat

So, if a high intake of red meat and processed foods contributes to the risk of colorectal cancer, what should be eaten to protect our bodies from this outcome?

According to the ACS, a diet high in fruits, vegetables, and fibers could help to minimize the risk, and many existing studies seem to support this advice.

A study from the Loma Linda University in California found that vegetarian-style diets are linked to a decreased risk of colorectal cancer. The researchers studied four types of plant-based diet. These were:

vegan, or strictly no products of animal origin

lacto-ovo vegetarian, which includes dairy and eggs but no meat

pescovegetarian, which includes fish but no meat

semi vegetarian, which includes meat and fish infrequently

All four of these plant-based diets were deemed to be less likely to lead to cancer than non-vegetarian diets.

One study from last year also suggests that the more colorful your meal the better, and that individuals should focus on integrating a rainbow of fruit and vegetables into their diets.

More specifically, their experiments on the pig model — which provides the closest resemblance to the human body in terms of metabolic processes — indicated that purple potatoes might protect against colon cancer.

That may be because these root vegetables contain compounds that reduce levels of certain pro-inflammatory proteins in the body, and inflammation is known to contribute to colon cancer risk.

Recently, researchers have also isolated a number of elements typical of Mediterranean-style diets that could help to prevent the onset of colorectal cancer.

People with a low risk of developing this condition ate plenty of fruits, vegetables, nuts, and whole grains, as well as fish and poultry, rather than red meat, and they drank little alcohol and soft drinks.

What to eat during and after treatment

According to guidelines from the Dana-Farber Cancer Institute in Boston, MA, people undergoing treatment for colorectal cancer should also favor the "rainbow plate" meals and eat a varied array of fruits and vegetables to support their immune system.

Eating small but frequent portions is another approach that specialists at the Dana-Farber Institute suggest that people following treatment may find useful.

They advise patients to stay hydrated and avoid alcohol and caffeine, explaining that some types of medication may clash with these beverages.

But a previous study conducted by researchers at the Institute — which we covered on Medical News Today — indicated that those undergoing treatment for colorectal cancer had an almost halved risk of cancer recurrence if they drank four cups of coffee, or 460 milligrams of caffeine, per day.

As lead study author Charles Fuchs explains, "We found that coffee drinkers had a lower risk of the cancer coming back and a significantly greater survival and chance of a cure."

Research published last year in JAMA Oncology suggests that a diet high in sources of fiber may improve survival rates for patients with stage one colorectal cancer. Eating whole grains was also linked to a better treatment outcome, the researchers noted.

Another study from last year notes that eating a minimum of 2 ounces (approximately 57 grams) of tree nuts — such as cashews, hazelnuts, walnuts, and pistachios — almost halved the risk of colon cancer recurrence for individuals following stage three cancer treatment. Tree nut consumption also reduced the risk of death following treatment by 53 percent.

As for the risk of developing a second cancer following treatment, the ACS say that it can be reduced by making the same healthful diet choices advised for the prevention of a first cancer. These include maintaining a healthy weight, placing "an emphasis on plant foods" in daily meals, and avoiding alcohol intake.

In fact, Dr. Victor Moreno — from the University of Barcelona in Spain — and colleagues found that lifestyle factors are more important than genetic risk factors when it comes to the development of colorectal cancer.

"This is important, considering that lifestyle, unlike genetic traits, is somewhat modifiable."

First study author Dr. Gemma Ibáñez

This suggests that a "revamp" of personal health choices may go a long way toward supporting positive outcomes.


Higher Vitamin D levels may be linked to lower risk of cancer

Published: March 7, 2018

Source:https://www.sciencedaily.com/releases/2018/03/180307230406.htm

High levels of vitamin D may be linked to a lower risk of developing cancer, including liver cancer, concludes a large study of Japanese adults published by The BMJ today.

The researchers say their findings support the theory that vitamin D might help protect against some cancers.

Vitamin D is made by the skin in response to sunlight. It helps to maintain calcium levels in the body to keep bones, teeth and muscles healthy. While the benefits of vitamin D on bone diseases are well known, there is growing evidence that Vitamin D may benefit other chronic diseases, including some cancers.

But so far, most studies have been carried out in European or American populations, and evidence from Asian populations is limited.

As Vitamin D concentrations and metabolism can vary by ethnicity, it is important to find out whether similar effects would be seen in non-Caucasian populations.

So an international research team, based in Japan, set out to assess whether vitamin D was associated with the risk of total and site specific cancer.

They analysed data from the Japan Public Health Center-based Prospective (JPHC) Study, involving 33,736 male and female participants aged between 40 to 69 years.

At the start of the study, participants provided detailed information on their medical history, diet and lifestyle, and blood samples were taken to measure vitamin D levels.

Vitamin D levels varied depending on the time of year the sample was taken, tending to be higher during the summer and autumn months than in the winter or spring.

After accounting for this seasonal variation, samples were split into four groups, ranging from the lowest to highest levels of vitamin D.

Participants were then monitored for an average of 16 years, during which time 3,301 new cases of cancer were recorded.

After adjusting for several known cancer risk factors, such as age, weight (BMI), physical activity levels, smoking, alcohol intake and dietary factors, the researchers found that a higher level of vitamin D was associated with a lower (around 20%) relative risk of overall cancer in both men and women.

Higher vitamin D levels were also associated with a lower (30-50%) relative risk of liver cancer, and the association was more evident in men than in women.

No association was found for lung or prostate cancer, and the authors note that none of the cancers examined showed an increased risk associated with higher vitamin D levels.

Findings were largely unchanged after accounting for additional dietary factors and after further analyses to test the strength of the results.

The researchers point to some study limitations, for example numbers of organ specific cancers were relatively small. And while they adjusted for several known risk factors, they cannot rule out the possibility that other unmeasured (confounding) factors may have influenced the results, making it difficult to draw firm conclusions about cause and effect.

Nevertheless, key strengths include the large sample size for overall cancer, a long follow-up period and the large number of blood samples analysed.

The authors say their findings support the theory that vitamin D may protect against the risk of cancer, but that there may be a ceiling effect, which may suggest that there are no additional benefits beyond a certain level of vitamin D.

"Further studies are needed to clarify the optimal concentrations [of vitamin D] for cancer prevention." they conclude.


Kids Who Vape Face Toxin Dangers, Study Finds

Published: March 5, 2018

Source:https://www.cancercompass.com/cancer-news/article/60916.htm

(HealthDay News) -- Teenagers who use e-cigarettes expose themselves to cancer-causing toxins, particularly if they choose fruit-flavored products, a new study reports.

Urine tests revealed elevated levels of five different toxins in the bodies of teens who use e-cigarettes (often called vaping). And all of the toxins are known or suspected carcinogens, said lead researcher Dr. Mark Rubinstein, a professor of pediatrics with the University of California, San Francisco.

Teens who used e-cigarettes had up to three times greater amounts of the toxins in their urine than teens who never vape, the researchers found.

"One of the reasons why more teens are using these products is they feel that they are safe and/or safer than smoking," Rubinstein said. "Based on these results, if the teenagers kept using these products over the years, we believe it could be dangerous."

The toxins -- acrolein, acrylamide, acrylonitrile, crotonaldehyde and propylene oxide -- all belong to a class of chemicals known as volatile organic compounds (VOCs).

In particular, fruit-flavored e-cigarettes produced significantly higher levels of acrylonitrile. That's a concern because fruit flavors are most popular among teens and acrylonitrile is a known carcinogen, the researchers said.

"Right now a lot of the flavors being marketed seem to clearly be targeting teens," Rubenstein said. "I think it's difficult to argue that you're marketing these products to adults trying to wean off cigarettes when you're offering flavors like 'unicorn poop' and bubble gum."

Volatile organic compounds are released when e-cigarette liquid is heated to the point when it becomes vapor, Rubinstein said. The liquid contains solvents that are approved food additives, but when heated these additives can form other chemical compounds, including VOCs, he said.

Toxic VOCs also are present in traditional tobacco cigarettes, and in greater quantities. The researchers behind the new study said "dual users" -- teens who alternate between cigarette smoking and e-cigarette smoking -- had up to three times higher levels of five toxins than those who only vape.

Gregory Conley is president of the American Vaping Association, a nonprofit that advocates for e-cigarettes. He said: "The results of this study fall in line with prior literature estimating the cancer risk from e-cigarette use to be orders of magnitude lower than the risk from smoking cigarettes. While it is clear from the data that environmental sources of toxins played a considerable role in the levels measured among all groups, the data nonetheless shows significant reductions in exposure among exclusive e-cigarette users."

But to Dr. Norman Edelman, senior scientific advisor to the American Lung Association, the study results show that e-cigarettes aren't as harmless as some might think.

"Now, it's true that if they smoked combustible cigarettes they would get more of this stuff," Edelman said. "But this does make it quite clear that vaping is not safe."

To investigate chemical exposure from e-cigarettes, the researchers looked at three different groups -- e-cigarette users, "dual users" who also smoke traditional cigarettes, and teens who don't smoke or vape.

The researchers recruited 103 participants with an average age of 16, and analyzed urine samples from all for the presence of potentially dangerous volatile organic compounds.

"They're doing it the right way. They're not measuring what's in the vaped liquid, they're measuring what gets into the kids' bodies, which is really the important question," Edelman said.

All e-cigarettes appear to create VOCs, even those that don't contain nicotine. The VOCs acrylonitrile and acrylamide were found in elevated levels in the urine of teens who said they don't use nicotine-laced e-liquid.

"That was interesting and surprising to us," Rubinstein said. "Although most of the teenagers used the nicotine-containing products, some did not and we were able to find these toxins even in them. That's because the solvents are still in these products, even if there's no nicotine."

Edelman said the study exposes the erroneous assumption that because e-cigarettes are "more safe" than tobacco, they can serve as a substitute for quitting smoking altogether.

"The most safe approach is smoking cessation, and for kids the most safe approach is smoking prevention," Edelman said. "What I'm concerned about is that all this talk about 'more safe' under the rubric of harm reduction is going to make us forget about the importance of smoking prevention and smoking cessation."

The U.S. Food and Drug Administration needs to step up regulation of e-cigarettes, particularly when it comes to teenage use and fruit-flavored products that appear to target teens, Rubinstein said.

"I definitely think there needs to be greater regulation to prevent teenagers from using these products," Rubinstein concluded.


Antibiotics may impact cancer treatment efficacy

Published: March 3, 2018

Source: https://www.sciencedaily.com/releases/2018/03/180303090356.htm

Antibiotic use is known to have a near-immediate impact on our gut microbiota and long-term use may leave us drug resistant and vulnerable to infection.

Now there is mounting laboratory evidence that in the increasingly complex, targeted treatment of cancer, judicious use of antibiotics also is needed to ensure these infection fighters don't have the unintended consequence of also hampering cancer treatment, scientists report.

Any negative impact of antibiotics on cancer treatment appears to go back to the gut and to whether the microbiota is needed to help activate the T cells driving treatment response, says Dr. Gang Zhou, immunologist at the Georgia Cancer Center and the Department of Biochemistry and Molecular Biology at the Medical College of Georgia at Augusta University.

"It likely depends on what types of therapy physicians are giving to patients and how often they also are giving them antibiotics," says Zhou, corresponding author of the study in the journal Oncotarget.

They have some of the first evidence that in some of the newest therapies, the effect of antibiotics is definitely mixed. Infections are typically the biggest complication of chemotherapy, and antibiotics are commonly prescribed to prevent and treat them.

"We give a lot of medications to prevent infections," says Dr. Locke Bryan, hematologist/oncologist at the Georgia Cancer Center and MCG.

"White blood cell counts can go so low that you have no defense against bacteria, and that overwhelming infection can be lethal," says Bryan, a study co-author.

In this high-stakes arena, where chemotherapy is increasingly packaged with newer immunotherapies, Bryan, Zhou and their colleagues have more evidence that antibiotics' impact on the microbiota can mean that T cells, key players of the immune response, are less effective and some therapies might be too.

They report that antibiotic use appears to have a mixed impact on an emerging immunotherapy called adoptive T-cell therapy, in which a patient's T cells are altered in a variety of ways to better fight cancer.

They found that one of the newest of these -- CAR T-cell therapy -- is not affected by antibiotics, likely because it is not so reliant on the innate immune system.

"These infused T cells can pretty much act on their own to kill cancer cells," Zhou says.

With this approach, physicians retrieve T cells from a patient's blood, engineer them to express a tumor-finding receptor -- called chimeric antigen receptor, or CAR -- and give them back to the patient. These patients typically will receive a conditioning chemotherapy regimen, which often includes the common agent cyclophosphamide, or CTX, to intentionally wipe out some of their normal T cells and make room for the engineered super-fighters. This emerging treatment is often used in patients who have failed multiple other treatments, including chemotherapy.

Even long-term antibiotic use does not seem to hinder the efficacy of CAR T-cell therapy against systemic lymphoma in their animal model. While they could see the impact of antibiotics on the microbiota, mice with CAR T-cell therapy continued to respond well to cancer treatment.

But the efficacy of another mode of adoptive T-cell therapy was impacted. This model mimics therapy in which receptors that target the patient's tumor are put onto their T cells. In this case, the researchers transferred tumor-specific CD4+T cells to treat mice with colorectal cancer.

One key difference here is that, unlike the CAR T-cell therapy, these engineered T cells still need help from the innate immune system to fight the tumor, now that they can better target it, Zhou says.

Mice with colorectal cancers that did not receive antibiotics were cured after being treated with the chemotherapy CTX followed by CD4+T-cell therapy. However, with antibiotics on board, this curative effect was lost in three out of five mice three weeks after treatment.

Their studies also confirmed that antibiotic use impacts the efficacy of the widely used CTX, when it's used alone, in this case to treat B-cell lymphoma. In addition to directly killing rapidly dividing cancer cells, CTX gets the attention and help of endogenous T cells, and antibiotics reduced that T-cell response, the scientists report.

Their findings in lab animals confirmed the recent work of others that the altered intestinal microbiota impacts CTX's ability to fight sarcoma, a rare cancer of our connective tissue. Bigger picture, it suggests that some chemotherapy regimens rely on the gut bacteria to stir the immune system to fight cancer, the scientists write.

"It is clear in animal models that if you wipe out the intestinal microbiota, like you do with antibiotics, it will attenuate the chemotherapy efficacy," says Zhou. "There is also emerging clinical evidence showing that for CTX-based chemotherapy, some patients who also get antibiotics for a longer period of time, seem to have less optimal outcomes."

Human studies are needed to see whether antibiotics affect the outcomes of adoptive T-cell therapy and to give clinicians and their patients better information about how best to maneuver treatment, Zhou notes.

The microbiota is comprised of trillions of bacteria, viruses and funguses and the biggest population resides in our gut, where they help us digest food and protect us from other invaders. Anyone who has taken an antibiotic also knows it can wreak havoc with the gut, causing severe diarrhea and other discomfort as it alters the natural -- and healthful -- complement of our microbiota.

While even a single course of antibiotics has been shown to disrupt the microbiota in humans, Zhou has shown in mice that it is protracted use that likely also impacts the immune response. And, when mice, at least, have a weakened immune system their microbiota literally looks different and there is evidence that antibiotics suppress their immune response.

Even with antibiotics out of the equation, there can be conflicting crosstalk between chemotherapy and immunotherapy. If/when chemotherapy hampers the immune response it could obviously impact the efficacy of some immunotherapies. So scientists and clinicians alike also are trying to figure out how best to combine these different therapies, to achieve optimal synergy.

The research was funded by the National Institutes of Health and an American Cancer Society Research Scholar Grant.


Calcium Supplements Tied to Higher Odds of Colon Polyps

Published: March 2, 2018

Source:https://www.cancercompass.com/cancer-news/article/60910.htm

(HealthDay News) -- Could the calcium supplement you take to help your bones be harming your colon?

That's the suggestion from a new study that finds a link between the daily supplement and an increased risk for polyps in the colon.

Polyps are not cancerous, but some can eventually turn into cancer if they're not removed.

Further research is needed to confirm the findings. But if calcium supplements do boost the risk of polyps, "this has important public health implications" for colon cancer prevention and screening, the study authors concluded.

The researchers added that millions of people worldwide take calcium supplements and that any possible risks have to be weighed against potential benefits.

The study was led by Dr. Seth Crockett of the University of North Carolina School of Medicine in Chapel Hill. His team tracked outcomes for 2,000 people, aged 45 to 75, who all had a history of polyps.

The study participants were randomly assigned to take either daily calcium supplements, daily vitamin D supplements, both, or neither for three or five years.

Those who took calcium alone or a combination of calcium and vitamin D were more likely to have polyps six to 10 years after the start of the study, the findings showed.

Women and smokers appeared to be at higher risk when taking calcium supplements, but not vitamin D alone, Crockett's team found.

The researchers also said that while calcium supplements were associated with an increased risk of polyps, calcium obtained solely through food in the diet was not.

Dr. David Bernstein, a gut specialist who wasn't involved in the study, said it does give doctors and patients pause for thought. He's a gastroenterologist at North Shore University Hospital in Manhasset, N.Y.

Bernstein stressed, however, that while polyps were more likely in the supplement users, "no colon cancers were found in the follow-up period" among the study participants.

Still, based on the new findings, Bernstein believes that "vitamin D and calcium supplementation should only be used for an appropriate medical indication."

And for those who do take the supplements for a good medical reason -- for example, weakened bones -- a regular colonoscopy is recommended, Bernstein said.


New approach uses single PET scan to personalize cancer treatment

Published: March 1, 2018

Source:https://www.sciencedaily.com/releases/2018/03/180301103709.htm

Researchers have developed a same-day, noninvasive positron emission tomography (PET)-based imaging approach to assess PD-L1 positive tumors, and the study is presented in the featured article of The Journal of Nuclear Medicine's March issue.

A healthy immune system strikes a delicate balance between eradicating infections and cancers and not overreacting to damage one's own tissue. Immune checkpoints help control the immune response, but tumors exploit these checkpoint pathways by expressing special proteins that evade antitumor immune responses. One major checkpoint inhibitor pathway is the PD-1 pathway, and its ligand is PD-L1.

In this study, the PD-L1 ligand, which enables cancer to evade a person's immune system, has been successfully targeted for the first time with a fluorine-18 (18F)-labeled PD-L1 radioligand. Until now, efforts to predict response to treatments targeting PD-1 or PD-L1 have typically been limited to evaluation of a single patient biopsy sample.

"This approach represents an opportunity for physicians to noninvasively assess all of a patient's tumors for PD-L1 expression with a single PET scan and timely readout," explains David J. Donnelly, PhD, at Bristol-Myers Squibb Research and Development in Princeton, New Jersey. "This may help guide treatment decisions and assess treatment response, to help identify the right treatment for the right patient at the right time and right dose."

For the study, an anti-PD-L1 adnectin (an engineered, target-binding protein) was labeled with 18F to generate 18F-BMS-986192, which was then evaluated in mice bearing bilateral PD-L1(-) and PD-L1(+) subcutaneous tumors. 18F-BMS-986192 was also evaluated for distribution, binding and radiation dosimetry in healthy cynomolgus monkey. The results of the study demonstrate the feasibility of the approach, and the radiation dosimetry estimates indicate that the tracer is safe to administer in human studies. Clinical studies are now underway to measure PD-L1 expression in human tumors.


Nut consumption may aid colon cancer survival

Published: February 28, 2018

Source:https://www.sciencedaily.com/releases/2018/02/180228160438.htm

People with stage III colon cancer who regularly eat nuts are at significantly lower risk of cancer recurrence and mortality than those who don't, according to a new, large study led by researchers at Yale Cancer Center.

The findings were published today in the Journal of Clinical Oncology.

The study followed 826 participants in a clinical trial for a median of 6.5 years after they were treated with surgery and chemotherapy. Those who regularly consumed at least two, one-ounce servings of nuts each week demonstrated a 42% improvement in disease-free survival and a 57% improvement in overall survival.

"Further analysis of this cohort revealed that disease-free survival increased by 46% among the subgroup of nut consumers who ate tree nuts rather than peanuts," said Charles S. Fuchs, M.D., M.P.H., director of Yale Cancer Center and senior author of the study. Tree nuts include almonds, walnuts, hazelnuts, cashews, and pecans, among others. In contrast, peanuts are actually in the legumes family of foods.

"These findings are in keeping with several other observational studies that indicate that a slew of healthy behaviors, including increased physical activity, keeping a healthy weight, and lower intake of sugar and sweetened beverages, improve colon cancer outcomes," said Temidayo Fadelu, M.D., a postdoctoral fellow at Dana-Farber Cancer Institute and lead author of the paper. "The results highlight the importance of emphasizing dietary and life-style factors in colon cancer survivorship."

Additionally, the researchers emphasized, the study highlighted connections between biological mechanisms that worsen disease not just in colon cancer but in certain chronic illnesses such as type 2 diabetes.

Many previous studies have reported that nuts, among other health benefits, may help to reduce insulin resistance, a condition in which the body has difficulty processing the insulin hormone. Insulin resistance leads to unhealthy levels of sugar in the blood and is often a predecessor to type 2 diabetes and related illnesses.

Earlier research among patients with colon cancer has revealed worse outcomes among those with lifestyle factors that heighten insulin resistance, such as obesity, lack of exercise, and a diet with high levels of carbohydrates that quickly raise levels of blood sugar.

"These studies support the hypothesis that behaviors that make you less insulin resistant, including eating nuts, seem to improve outcomes in colon cancer," Fuchs said. "However, we don't know yet what exactly about nuts is beneficial."

Nuts also might play a positive role by satisfying hunger with less intake of carbohydrates or other foods associated with poor outcomes, Fuchs noted.

Patients may not be eating nuts due to concerns about the high fat content. For example, a one-ounce serving of about 24 almonds holds about 200 calories, including 14 grams of fat. "People ask me if increasing nut consumption will lead to obesity, which leads to worse outcomes," he said. "But what's really interesting is that in our studies, and across the scientific literature in general, regular consumers of nuts tend to be leaner."

Dietary changes can make a difference. An earlier analysis of diets in the same patient cohort by Fuchs and his colleagues found a significant link between coffee consumption and reduced recurrence and mortality in colon cancer.

When Fuchs advises his patients about lifestyle choices, "first and foremost I talk about avoiding obesity, exercising regularly and staying away from a high-carbohydrate diet," he said. "Then we talk about things like coffee and nuts. If you like coffee or nuts, enjoy them, and if you don't, there are many other helpful steps you can take."

"Overall, we are working to apply the same rigorous science to the understanding of diet and lifestyles in the colon cancer patient population that we apply to defining new drugs," Fuchs said.


Improved method of treating pancreatic cancer

Published: February 26, 2018

Source:https://www.sciencedaily.com/releases/2018/02/180226131424.htm

A heating and freezing process known as dual thermal ablation can kill pancreatic cancer cells, according to new research from Binghamton University, State University at New York.

The collaborative study, conducted by researchers from academia and industry and funded by grants from the National Cancer Institute, used pancreatic cancer cells to investigate the effect of heating and freezing on cell death. The research was conducted by Robert Van Buskirk and John Baust, professors of biological sciences and directors at Binghamton University's Institute of Biomedical Technology, and Kenneth Baumann, a graduate student studying biology.

"How do we solve the problem of pancreatic cancer when it comes to trying to get rid of the tumor, when chemo and radiation just simply doesn't work?" said Van Buskirk. "The whole idea is, can one come up with a different surgical intervention that's less invasive and more effective?

"In order to figure that out, you can commercially obtain pancreatic cancer cells and grow them on specialized plasticware," Van Buskirk said. "The basic question is, are both freezing and heat in combination more effective than freezing or heat alone? If you freeze pancreatic cancer cells like you do in cryoablation, a lot of them die, but some will survive and regrow. If you heat them, they'll die, but again some will come back. But with dual-thermal ablation, for reasons that we do not yet understand, more die and don't come back. In fact, over time, cells that survive the initial insult continue to die."

"What we've observed is that we are able to achieve complete cell death using a combination of heating and then freezing at temperatures that alone would not be lethal to kill pancreatic cancer cells," said Baumann.

Researchers heated and froze cancer cells and looked at the effect, using various technologies to determine the level of cell death, on regrowth as well as which cell stress pathways were activated.

"Using a variety of assays, we are able to determine the initial level of cell death as well as to what extent the surviving population is able to regrow," Baumann said. "We were also able to determine the specific paths of cell death activated as a result of the dual thermal exposure."

"When cells are disturbed -- which means they are frozen or they see heat -- various cell stress pathways are activated," said Van Buskirk. "The interesting thing about cells, especially cancer cells, is that they will activate pathways to protect themselves. The objective of this line of molecular-based research is to find out which stress pathways are activated in pancreatic cancer cells so that we can better understand why dual-thermal ablation appears to be more effective."

"Current studies are focused on elucidating which stress pathways specifically cause these cells to die or what is keeping them alive. That way, we can optimize this treatment to be as effective as possible against pancreatic cancer," Baumann said.

According to Van Buskirk, modulating these stress pathways is the key to making the heating and freezing ablation process more effective. This could lead to the development of a new way to remove cancerous pancreatic tumors.

In addition to the cell molecular research, several members of the study team are working on developing new catheter technologies to deliver this ablative therapy to patients. "If a very thin catheter can be developed to target the tumor, and if we understand how pancreatic cancer responds to ablation at the molecular level, then we may be able to develop a new therapy to approach something that has been completely unapproachable, the targeted killing of a tumor in a very difficult place: the pancreas," said Van Buskirk.


Fear and hoping: Adding hope to health messages may motivate better behaviors

Published: February 23, 2018

Source:https://www.sciencedaily.com/releases/2018/02/180223092136.htm

While fear about health concerns may grip people, adding a little hope to a message might make people more willing to take preventative actions, according to researchers.

In two studies, hope and self-efficacy -- the belief that a person can help themselves -- significantly predicted intentions to take actions against skin cancer, such as wearing sunscreen or protective clothing.

"With health messages, it's not enough just to tell people, or merely educate them, you need to motivate them, and emotions are really good motivators," said Jessica Myrick, associate professor of communications, Penn State. "We often think of emotions as irrational, but what our research is pointing to is that emotions can help us do the things that will keep us healthy and safe, so it's important to understand the broad scope of emotional responses to different type of messages and messaging components."

According to the researchers, previous work indicated that while fear can grab attention and create awareness about a health problem, it might not necessarily lead to behaviors that could help people tackle the problem.

"There's a lot of interesting work done on fear appeals, but we were wondering, if you're going to tell people how to prevent something scary from happening, that might generate hope," said Myrick. "We don't understand a lot empirically about how shifting from being scared of something in a message to then being told how to fix it, or prevent it, might shift the emotional state from fear to hope."

Fear and hope may work together to create more persuasive messages, said Myrick, who worked with Robin Nabi, professor of media effects and health communication, University of California, Santa Barbara.

"We can think of hope and fear as the carrot and the stick," said Nabi. "Either one alone could be effective. But the two together may be an especially winning combination."

In the first study, 341 participants, whose ages ranged from 17 to 72 years old, were recruited from Amazon's online task-completion platform, Mechanical Turk. The participants reviewed and reacted to an article about skin cancer from a web page designed to resemble a page on the health site WebMD.

The article was divided into three sections with the subheads: "How susceptible are most of us to skin cancer?," "How severe is skin cancer?" and "What actions can we take to prevent skin cancer and how effective are those measures?" The subsections of the message reflect factors that can drive persuasive health messaging results, including whether a person feels susceptible to the condition, whether they believe the condition is serious -- severity -- and whether they believe that help exists and that they have access to that help, according to the researchers.

After reviewing the message, the participants reported on emotions they felt about the article, including hopeful, optimistic and encouraged, all emotions that the researchers considered hope states.

Self-efficacy and hope did serve as significant predictors of sun safety intentions, according to the researchers, who published their findings in the journal Health Communication, currently online.

In a second study, 382 undergraduate college students were recruited to watch a melanoma awareness video and then answer a series of questions about the video. A total of 367 students completed a follow-up survey sent a week later to determine if the participants engaged in any sun safety behaviors.

The findings in the second study indicated that hope played a role in adopting sun safety measures and that even a week later, the participants were engaged in those safety behaviors.

Myrick said that adding hope to messages not only may create more persuasive messages -- it also may be more ethical.

"You don't just want to leave people in a state of fear," said Myrick. "You want to give them possible solutions to help."

According to the researchers, future work may look at not just thinking about designing singular messages, but understanding the greater message environment, including how health fears are reported in the media.

"This study is a nice early step in looking at the complex dance between different types of emotions and cognitions so that we can better promote public health," Myrick said. "And maybe this leads to ways to design other health campaigns -- for instance, for influenza vaccination campaigns -- that work in concert with the fear that is generated by news coverage to try to give people some hope and help them remember the things they can do daily -- get a vaccine, wash your hands, and don't go to school when you're sick."


7 Signs of protein deficiency

Published: February 22, 2018

Source:https://www.naturalnews.com/2018-02-22-7-signs-of-protein-deficiency.html

(Natural News) Here’s something you may have heard before: “Protein is the basic foundation of the body.”

Protein provides the building blocks of our muscles and bones, it assists in tissue building and repair, and it’s necessary for natural enzyme and hormone production.

With protein being so vital in most of our bodily functions, it’s no wonder that lacking this building block can cause problems. If you or someone you know is exhibiting any of the following signs, you might be suffering from protein deficiency:

  1. You feel moodier and more anxious: Proteins are long chains of amino acids. These are important molecules that make up a large portion of our tissues and support various biological functions. One such amino acid is tyrosine, which is required for the natural production of dopamine, noradrenaline, and serotonin. All of these hormones play key roles in soothing away tension and bringing about feelings of calm and relaxation.
  2. Your workouts aren’t as efficient: Almost everyone knows that protein is needed for muscle building. What isn’t as widely realized is the fact that it helps sustain our energy levels. Without protein, our bodies will eventually resort to breaking down muscles to keep us going. So on top of contributing to our muscle mass, protein can also help maintain feelings of wakefulness as you go about your workout routine.
  3. You’re unable to concentrate: In addition to reducing feelings of anxiety, dopamine and serotonin can restore mental alertness. Protein is necessary for various neurological functions, which is why you might feel a bit of “brain fog” if you aren’t getting enough of this nutrient.
  4. You have difficulty sleeping: Once again, serotonin is crucial here. This hormone is needed for a good night’s sleep, so a lack of it can result in sleeplessness.
  5. You struggle with weight loss: As was previously mentioned, consuming protein ensures that the body doesn’t have to burn muscle to keep on chugging. This attribute of protein is vital to those attempting to gain muscle mass and those with reasonable weight loss goals. Furthermore, loading up on protein promotes feelings of satiety, making you less likely to seek out something unhealthy to snack on.
  6. You feel gassier than usual: A body that’s bogged down by protein deficiency will often experience compromised natural biological functions. Digestive functions are a good example: not getting enough protein can disrupt enzyme production and make it more difficult to digest certain foods.
  7. You bruise easier but heal slower: Insufficient protein intake has been linked to poor bone health, putting you at a higher risk of bone fractures. If you are injured, you might even encounter quite a few problems during the recovery process. Bones and muscles require protein for optimal recuperation.
  8. There’s no denying that protein is a must-have nutrient that you need for your daily intake. But how do you make sure that you get the right kind of protein? Allow us to make it easier for you. The Health Ranger Store offers a variety of proteins for you to choose from… from whey proteins to hemp proteins, we’ve got them all.
  9. Not only do many of our proteins come from reliable and trusted third-party manufacturers, but they’re all rigorously tested for heavy metals too. We know how much protein matters, which is why we’ve done everything we can to bring you the best.

Zika virus could help combat brain cancer

Published: February 21, 2018

Source:https://www.sciencedaily.com/releases/2018/02/180221122930.htm

Zika virus, feared for causing microcephaly in babies whose mothers were infected during pregnancy by attacking the cells that will give rise to the fetus's cerebral cortex, could be an alternative for treatment of glioblastoma, the most common and aggressive kind of malignant brain tumor in adults.

This discovery was made by researchers at the University of Campinas's School of Pharmaceutical Sciences (FCF-UNICAMP) in São Paulo State, Brazil.

"Zika virus, which has become a threat to health in the Americas, could be genetically modified to destroy glioblastoma cells," said Rodrigo Ramos Catharino, a professor at FCF-UNICAMP and head of the institution's Innovare Biomarker Laboratory.

Through the mass spectrometry analysis of Zika virus-infected glioblastoma cells, scientists also identified the presence of digoxin, a molecule which induced the death of tumoral cells of skin and breast cancer in previous experiments.

Resulting from a Thematic Project supported by the Sao Paulo Research Foundation -- FAPESP , the study is described in an article posted to bioRxiv, a preprint repository for the biological sciences, and accepted for publication by Journal of Mass Spectrometry.

Previous research conducted recently in Brazil and elsewhere points to increased mortality rates for human neural progenitor cells (hNPCs) infected by Zika virus, as well as growth inhibition and morphological abnormalities.

Alterations in these cells, which are precursors of brain cells and become cortical neurons in embryos and fetuses, may be a cause of microcephaly in babies whose mothers have been infected by Zika. Other studies have shown that the virus is capable of moving into brain cells, modifying the regulation of the cell cycle, and inducing their death.

In light of these findings, the researchers at FCF-UNICAMP set out to investigate the effects of Zika virus when it infects glioblastoma cells. To do this, they infected human malignant glioblastoma cells with Zika and recorded microscope images of them 24 hours and 48 hours after infection in order to observe any metabolic alterations (cytopathic effects) caused by inoculation of the virus.

The results of the analysis showed that the glioblastoma cells displayed moderate cytopathic effects 24 hours after infection, such as rounded, swollen cell bodies and formation of syncytia, masses of cytoplasm in which the membrane contains several nuclei.

The most severe cytopathic effects were observed 48 hours after infection, with a larger number of rounded, swollen cells, more syncytium formation and pronounced loss of cell integrity, all of which denote cell death.

"The cytopathic effects of Zika infection on glioblastoma cells were observed most clearly after 48 hours. Cell morphology was almost totally altered during this period," Catharino said.


Tobacco Kills, No Matter How It's Smoked: Study

Published: February 20, 2018

Source:https://www.cancercompass.com/cancer-news/article/60804.htm

(HealthDay News) -- Smokers who think cigars or pipes are somehow safer than cigarettes may want to think again, new research indicates.

The study tracked the health and habits of more than 357,000 Americans from 1985 to 2011.

It found that, compared to people who had never smoked, people who regularly smoked only cigarettes had double the risk of death in that time frame, from whatever the cause. And they had quadruple the odds of dying from a tobacco-linked cancer such as cancer of the lung, bladder, esophagus, pancreas, larynx and mouth.

But people who claimed they smoked only cigars weren't off the hook.

Cigar smokers had a 20 percent elevated odds of death from any cause, and a 61 percent higher risk of death from a tobacco-linked cancer, the researchers reported in the Feb. 19 issue of JAMA Internal Medicine.

Rates for pipe smokers were similarly high: This group had a 58 percent higher risk of dying from a tobacco-linked cancer during the study period, compared to never-smokers.

"In 2015, an estimated 12.5 million people in the United States aged 12 years or older were current cigar smokers," noted the research team, which was led by Carol Christensen, of the U.S. Food and Drug Administration's Center for Tobacco Products.

The study authors also noted that just under 1 percent of Americans said they have smoked some sort of tobacco pipe at least 50 times over their lifetime.

Two medical experts said the study sends an important message, especially to young people who might think one form of smoking is less dangerous than another.

"Combustible tobacco used in any form is a cancer risk, and pipe and cigar smokers cannot be given a pass," said Dr. Len Horovitz, a pulmonary specialist at Lenox Hill Hospital in New York City.

Patricia Folan directs the Center for Tobacco Control at Northwell Health in Great Neck, N.Y.

She noted that "a full-size cigar can contain chemicals the equivalent of one pack of cigarettes, and individuals who switch from cigarettes to cigars frequently unintentionally inhale cigars the way they inhaled cigarettes -- exposing them to large amounts of the hazardous substances in cigar smoke."

There was some good news from the FDA study, however: The risk of death from any cause or tobacco-linked cancers fell once smokers quit.

So, Folan said, "I would not say that cigars are better than cigarettes -- but quitting is." She urged smokers "to ask for help from your health care provider" on kicking the habit.


Family History of Breast Cancer Matters, Even for Older Women

Published: February 19, 2018

Source:https://www.cancercompass.com/cancer-news/article/60795.htm

(HealthDay News) -- Women with a family history of breast cancer remain at higher risk for breast cancer even after age 65, a new study suggests.

The findings could influence screening recommendations for older women, said researchers at Georgetown University Medical Center, in Washington, D.C.

Age is the strongest risk factor for breast cancer. But having a mother, sister or daughter with the disease -- a "first-degree relative" -- can double the risk, the study authors said.

"Family history of breast cancer does not decline as a breast cancer risk factor as a woman ages. The relationship didn't vary based on whether a first-degree relative's diagnosis was made in a woman age 50 or younger, or older than age 50," said study leader Dejana Braithwaite.

This means women with that first-degree family history should consider this risk factor when deciding whether to continue mammography screening as they age, said Braithwaite, an associate professor of oncology at Georgetown.

The researchers examined records on more than 400,000 women included in a breast cancer registry from 1996 to 2012. They looked at family history of breast cancer among women between 65 and 74 and those aged 75 and older.

Overall, a first-degree family history leads to an absolute increase in five-year risk of breast cancer of 1.2 to 10.3 percentage points, the study found.

However, the actual increase depends on age and breast tissue density, the researchers noted. For example, the five-year risk for breast cancer among women 65 to 74 with dense breast tissue jumped from 15 percent among those with no family history of the disease to nearly 24 percent among those with a close relative with breast cancer.

Similar odds were seen among women 75 or older with the same breast density.

"The goal of our work is to provide evidence that helps inform breast cancer screening guidelines for older women," Braithwaite said in a Georgetown news release. "Older women who are in good health and have a first-degree family history may consider a screening mammogram even as they age beyond the screening recommendations for average risk women."

The U.S. Preventive Services Task Force now recommends that women between 50 and 74 have mammography breast cancer screening every two years. The task force says the benefits of screening aren't as clear for women 75 and older.

The American Cancer Society advises all healthy women between the ages of 45 and 54 to have a yearly mammogram. These screenings can occur every two years after 55 if a woman is otherwise healthy, the group advises.

Breast cancer screening guidelines are evolving, said the study's senior author Dr. Karla Kerlikowske.

"As breast cancer screening guidelines change from age-based to risk-based, it is important to know how standard risk factors impact breast cancer risk for women of different ages," said Kerlikowske.


Lung Cancer One of Many Reasons Not to Smoke

Published: February 18, 2018

Source:https://www.cancercompass.com/cancer-news/article/60794.htm

(HealthDay News) -- You already know that smoking causes lung cancer. But tobacco use can lead to other major health problems, too, experts warn.

"Cigarette smoking is probably the single most harmful thing you can do to your health," said Jonathan Foulds, a professor of public health sciences and psychiatry at Penn State College of Medicine.

"It's hard to find a part of the body not affected by it," Foulds said in a college news release.

Besides its link to lung cancer, smoking is also tied to heart attack, stroke, diabetes and other types of cancers, the news release noted.

As for lung cancer, "if you smoke a pack a day or more, your risk of getting lung cancer isn't just one-and-a-half or double that of a nonsmoker. It's 20 times as great," Foulds said.

Moreover, quitting smoking has a bigger effect on reducing heart attack risk than lowering high blood pressure or cholesterol, Foulds said.

It's important to tell your doctors if you smoke, Foulds and other experts say.

"You should let your dentist know if you smoke because he or she can take special care to evaluate you for tongue, head and neck cancers," said Dr. Alexis Reedy-Cooper, a family medicine doctor at Penn State's Medical Center. "Dentists are often the first to detect those."

Smokers also endanger others. Children in homes with a smoker are at increased risk for asthma, ear infections and lung infections. Pregnant women who smoke put their unborn child at risk for complications and premature delivery, Foulds pointed out.

"It's not a question of whether [smokers] should quit -- it is critical that they quit," Foulds said. "Smoking is a risk factor for so many things that it doesn't make sense to wait."

Doctors should talk to patients who smoke about the health benefits of quitting, Foulds and Reedy-Cooper said. They can help them quit through methods such as medication and counseling.


Dad Can Pass on Ovarian Cancer Genes, Too

Published: February 16, 2018

Source:https://www.cancercompass.com/cancer-news/article/60781.htm

(HealthDay News) -- A gene mutation that's passed down from a father is associated with earlier onset of ovarian cancer in daughters and prostate cancer in the father and his sons, a new study suggests.

Previous research had shown that sisters of women with ovarian cancer have a higher risk for the disease than their mother, but the reasons for this were unclear.

"Our study may explain why we find families with multiple affected daughters: Because a dad's chromosomes determine the sex of his children, all of his daughters have to carry the same X chromosome genes," said study author Kevin Eng. He's an assistant professor of oncology at Roswell Park Comprehensive Cancer Center, in Buffalo, N.Y.

Eng's team decided to look at whether genes on the X chromosome passed down from the father might influence a daughter's risk of ovarian cancer.

The researchers examined data about pairs of granddaughters and grandmothers. They also sequenced portions of the X chromosome from 186 women affected by ovarian cancer.

The investigators discovered that women with ovarian cancer linked to genes inherited from their father's mother developed the cancer much earlier than those with ovarian cancer linked to genes from their mother. In addition, the same genes from the father's mother are also associated with higher rates of prostate cancer in fathers and sons.

Further investigation led the researchers to a previously unknown mutation on the X chromosome that may be associated with cases of ovarian cancer that develop more than six years earlier than average.

The findings suggest that a gene on the X chromosome may increase a woman's risk of ovarian cancer, independent of other known risk genes, such as the BRCA genes. But the researchers did not prove that this gene causes ovarian cancer risk to rise.

Further research is needed to confirm the identity and function of this gene, the study authors added.

The study was published Feb. 15 in the journal PLoS Genetics.

"What we have to do next is make sure we have the right gene by sequencing more families," Eng said in a journal news release.

"This finding has sparked a lot of discussion within our group about how to find these X-linked families," Eng said. "It's an all-or-none kind of pattern: A family with three daughters who all have ovarian cancer is more likely to be driven by inherited X mutations than by BRCA mutations."


Cancer: 'Ultra-processed' foods may increase risk

Published: February 15, 2018

Source:https://www.medicalnewstoday.com/articles/320932.php

A large study suggests that increasing consumption of ultra-processed foods — such as soda and sugary drinks, instant noodles, packaged snacks, and some reconstituted meats — may be linked to a proportional rise in cancer risk.

However, in their report of the findings that was recently published in The BMJ, scientists from universities in Paris, France, and São Paulo in Brazil caution that the finding came from an observational study and that more research should now be done to confirm it.

Observational studies are not designed to prove cause and effect — but they can offer insights into links between variables such as diet and disease.

In this case, the researchers analyzed the diet and health of 105,000 middle-aged individuals in the NutriNet-Santé cohort study. The participants gave information about their typical intake of thousands of different foods.

They found that for every 10 percent rise in the proportion of ultra-processed foods consumed, there was a 12 percent higher risk of cancer.

Further analysis revealed an 11 percent rise in the risk of breast cancer but no significant link with increased risk of prostate cancer or colorectal cancer.

"As the global consumption of highly processed foods increases," report Martin Lajous and Adriana Monge, of the National Institute of Public Health in Mexico, in a linked editorial, "understanding the health impact of these foods has become a relevant and timely topic."

Of the new findings, they observe that although they offer "an initial insight into a possible link between ultra-processed foods and cancer [...] we are a long way from understanding the full implications of food processing for health and well-being."

High cancer rates and ultra-processed foods

The latest estimates of worldwide figures suggest that there were 14.1 million new cases of cancer in 2012, and that this number is expected to climb to 24 million by 2035.

In the United States — where cancer is the second most common cause of death — the American Cancer Society (ACS) estimate that there will be around 1.7 million newly diagnosed cases of cancer, and more than 609,000 deaths to the disease, in 2018.

According to the ACS, at least 42 percent of newly diagnosed cases of cancer are preventable. These include 19 percent in which smoking is the main cause and 18 percent that result from a combination of factors, including "poor nutrition."

In their new study paper, the researchers cite evidence that suggests that many countries are shifting toward higher consumption of "ultra-processed foods," or food that has undergone several "physical, biological, and/or chemical processes."

A number of surveys — including some done in the U.S., Europe, Brazil, Canada, and New Zealand — have revealed that 25–50 percent of daily energy intake is from ultra-processed foods such as fizzy drinks, packaged snacks and baked goods, ready meals, sugary cereals, and reconstituted meats.

A need to investigate the link

The researchers suggest that the health consequences of this trend should be studied, because ultra-processed foods have a number of characteristics that could be disease-causing.

For instance, they are higher in added sugar and salt as well as total fat and saturated fat, and they are lower in fiber and vitamins.

Another concern is that, because of contact with packaging materials, ultra-processed foods may become contaminated with potentially harmful substances.

Also, these foods contain additives that, although approved for food use, remain controversial in that some animal and cell studies have suggested that they may cause cancer. These additives include the processed meat additive sodium nitrite and the white food pigment titanium dioxide.

Investigation of the health effects of ultra-processed foods is a relatively new field. Some studies have raised the possibility that they may be linked to higher risk of obesity, high blood pressure, and high cholesterol, but robust evidence is "still very scarce."

The authors write that, to their knowledge, their observational study "is the first to investigate and highlight an increase in the risk of overall — and specifically breast — cancer associated with ultra-processed food intake."

Detailed food classification

For their study, the researchers analyzed data from people who completed questionnaires about the foods that they consumed over 24 hours on at least two occasions. The detail gathered allowed them to measure typical intake of 3,300 different foods.

Cancer incidence was measured over an average of 5 years. Data were taken from information on participant reports and were cross-checked against medical records and national databases.

The researchers categorized the foods into four groups, according to the "extent and purpose of industrial food processing."

Ultra-processed foods are those that, according to the classification system used in the study, undergo the most industrial food processing.

The study paper gives a long list of ultra-processed foods, including: fish nuggets; packaged sweet and savory snacks; packaged breads; meat products that have been reconstituted with the aid of nitrites or other non-salt preservatives; and foods "made mostly, or entirely from sugar, oils, and fats."

Some examples of substances added during industrial processing include flavoring agents, colors, humectants, emulsifiers, and artificial sweeteners. These are often added to "imitate sensorial properties," or to "disguise undesirable qualities."

No cancer link with less processed foods

At the other end of the product spectrum are staple foods such as "fruits, vegetables, pulses, rice, pasta, eggs, meat" that have undergone minimal or no processing. They are typically "fresh or dried, ground, chilled, frozen, pasteurized, or fermented."

In-between lie the less processed foods, which include "canned vegetables with added salt, sugar-coated dried fruits," and meat that has been "preserved only by salting," plus "cheeses and freshly made unpackaged breads."

The study uncovered no significant link between cancer and the consumption of less processed foods, and a lower risk of overall cancer and breast cancer with intake of fresh and minimally processed foods.

While commending the researchers for the detailed data that they analyzed and collected on diet and cancer, as well as for the multiple statistical analyses that they conducted, Lajous and Monge nevertheless note that the "interesting results require replication and further refinement."

They also highlight that while the food classification system used in the research "may be useful for descriptive purposes and for replication," it does not necessarily provide the type of detail that is helpful to consumers and policymakers.

Lajous and Monge conclude:

"Care should be taken to transmit the strengths and limitations of this latest analysis to the general public and to increase the public's understanding of the complexity associated with nutritional research in free living populations."


Warning from the American Heart Association: Breast cancer treatments, such as radiation and chemo, can cause heart failure

Published: February 14, 2018

Source:https://www.naturalnews.com/2018-02-14-warning-from-the-american-heart-association-breast-cancer-treatments-radiation-and-chemo-heart-failure.html

(Natural News) Sometimes the cure is worse than the ailment, the saying goes, and a new warning from the American Heart Associationis shedding light on the quandary many women face when weighing breast cancer treatment against the potential side effects.

According to the group, some of the most popular breast cancer therapies can actually damage the heart significantly. They report that problems like heart failure, valve problems, and abnormal heart rhythms are the most common heart-related side effects of getting cancer therapy. These problems might not appear until a long time after the treatment has come to an end.

The treatments identified as having the greatest risks to heart health include chemotherapy, targeted therapy and radiation. Breast cancer survivors who have a particularly heightened risk of cardiovascular disease include those who are exposed to radiation and chemotherapy that damage the heart and those with a sedentary lifestyle that causes weight gain while they undergo treatment. Those with pre-existing risk factors for heart disease, including unchecked or uncontrolled high cholesterol or high blood pressure throughout their treatment, also have a higher risk.

More than 48 million American women are dealing with cardiovascular disease, and more than four million are currently living with breast cancer. With the leading cause of death for American women being cardiovascular disease, experts are now urging patients and doctors to give serious consideration to the cardiovascular effects of the treatment options on the table.

The immunotherapy drug Herceptin, for example, raises the risk of heart failure, while radiation therapy can block or narrow arteries. Eight treatments with the chemotherapy drug doxorubicin can raise a woman’s risk of heart failure by five percent, while 14 doses raise it by an incredible 48 percent. It has been suggested that administering it more slowly could reduce its impact on the heart. Other cancer drugs have been known to tighten artery muscles and cause abnormal heart rhythms, increasing heart attack risk.

Breast cancer survivors who are older than 65 are actually more likely to die from heart failure and other cardiovascular problems than breast cancer, so it’s a matter that deserves very careful attention when choosing a treatment route.

It is also worth noting that the two conditions have many risk factors in common, such as smoking, family history, poor diet, and age. Moreover, hormone replacement therapy is a risk factor for heart disease as well as breast cancer.

Lifestyle changes can reduce your risks

Just as both illnesses have similar risk factors, it’s also possible to make some lifestyle changes that will reduce your chances of getting them. Speaking to the Associated Press, Ohio State University Ross Heart Hospital’s Dr. Laxmi Mehta said: “More importantly, we see that many of the same things that improve heart health (healthy diet, healthy weight, exercise, not smoking) can also reduce a woman’s risk for breast cancer.”

The American Heart Association recommends that everyone with or without breast cancer adheres to their Life’s Simple 7, a list of behaviors that can keep people healthy overall and reduce breast cancer risk. They are designed to be changes that everyone can make without spending a lot of money. The Simple 7 include being physically active on a regular basis, eating healthy food, reaching and maintaining a healthy weight, maintaining healthy blood pressure, keeping blood sugar in check, avoiding tobacco, and keeping cholesterol at healthy levels.


Obesity associated with longer survival for men with metastatic melanoma

Published: February 12, 2018

Source:https://www.sciencedaily.com/releases/2018/02/180212190944.htm

Obese patients with metastatic melanoma who are treated with targeted or immune therapies live significantly longer than those with a normal body mass index (BMI), investigators report in a study published in Lancet Oncology of 1,918 patients in six independent clinical cohorts.

This effect, referred to as the "Obesity Paradox," principally manifested itself in men, said Jennifer McQuade, M.D., lead author and instructor of Melanoma Medical Oncology at The University of Texas MD Anderson Cancer Center.

"Obese men consistently did much better than men with a normal BMI, with nearly a doubling of overall survival," McQuade said. The researchers found no significant differences in survival between women with normal, overweight or obese BMI.

"The question is what underlying mechanism causes this advantage in obese men, and can we take advantage of it to improve outcomes in patients with melanoma?" McQuade said. "One hint may be the interaction between obesity, sex, and outcomes, which has not been detected before in any cancer."

Women with metastatic melanoma have long been known to have better outcomes compared to men, McQuade noted. In this study obesity overcame that survival disadvantage for men, leading researchers to now look at the possible impact of sex hormones in this effect.

Associations don't prove causation, the researcher's note, but point to new areas to study in greater depth.

"The public health message is not that obesity is good. Obesity is a proven risk factor for many diseases," McQuade said. "Even within our metastatic melanoma population, we would not suggest that patients intentionally gain weight. We need to figure out what is driving this paradox and learn how to use this information to benefit all of our patients."

Obesity is a known risk factor for developing 13 types of cancer according to the World Health Organization and is set to overtake smoking as the leading preventable cause of cancer. The relationship between obesity and survival in patients that already have cancer is not as consistent. Recent studies have shown a similar survival benefit for obese patients with colorectal or kidney cancer.

Obesity expected to be disadvantage

The team expected to find obesity to be harmful for melanoma patients, based in part on research that implicates obesity in activation of a cancer-promoting molecular pathway called IGF-1/PI3K/AKT.

They analyzed the association between body mass index (weight divided by height) and progression-free survival (PFS) and overall survival (OS) in six independent cohorts of patients treated with targeted therapy, immunotherapy or chemotherapy in pivotal trials that led to FDA approval of these drugs.

While advantages in PFS and OS emerged in an overall meta-analysis of the entire group, the survival benefit associated with obesity was restricted to men treated with targeted or immunotherapies, where obese men had a 47 percent decreased risk of death compared to men with normal BMI.

Doubling of overall survival in men

Results from 599 patients receiving combination targeted therapy of dabrafenib (BRAF inhibitor) and trametinib (MEK inhibitor) were:

  • Normal BMI of 18.5-24.9 -- median PFS of 9.6 months, OS of 19.8 months
  • Obese BMI 30 and above -- median PFS 15.7 months, OS 33.0 months

A multivariable analysis that included factors such as age, sex, stage, disease burden, certain mutations and prior treatment showed that obesity still improved PFS and OS compared to normal BMI patients.

The team analyzed results by sex and found significant differences only among men.

  • Normal BMI men -- PFS 7.2 months, OS 16.0 months
  • Obese men -- PFS 12.8 months, OS 36.5 months.

By contrast, women, for example, had overall median survival of at least 33 months, regardless of BMI.

A validation cohort of 240 patients treated with vemurafenib (BRAF inhibitor) and cobimetinib (MEK inhibitor) yielded similar results.

For immunotherapy, in a cohort (330 patients) treated with checkpoint inhibitors blocking either the PD1 check point on T cells or its PD-L1 ligand, results again showed no differences among women, but:

  • Normal BMI men -- PFS 2.7 months, OS 14.3 months
  • Obese men -- PFS 7.6 months, OS 26.9 months

A cohort of patients treated with the immune checkpoint inhibitor ipilimumab (207 patients) showed similar results. There was no effect of obesity found among two cohorts (541 patients) treated only with the chemotherapy dacarbazine.

Possible estrogen connection

The researchers are following up to understand biological factors that might provide an advantage to obese male patients. Obesity is associated with increased inflammation, which could improve the effectiveness of checkpoint blockade drugs that unleash an immune response against cancer.

The sex-specificity of the observed differences points to a potential hormonal mediator. Fat (adipose) tissue produces an enzyme called aromatase that converts male hormones called androgens into estrogens, female hormones. Perhaps this happens enough in obese men to help them clear some type of hurdle toward greater survival, McQuade said. The researchers are collaborating with investigators at the University of Pennsylvania that have found that turning on a very specific type of estrogen receptor on melanoma makes it vulnerable to immunotherapy.

The MD Anderson team also is looking at gene expression, mutations and immune profiling to identify potential differences in melanoma in obese and non-obese patients and developing preclinical models.


Hot tea tied to higher cancer risk for smokers and drinkers

Published: February 06, 2018

Source:http://www.foxnews.com/health/2018/02/06/hot-tea-tied-to-higher-cancer-risk-for-smokers-and-drinkers.html

Drinking scalding hot tea is associated with an increased risk of esophageal tumors in people who also smoke and drink alcohol, two habits that already make many cancers more likely, a Chinese study suggests.

Among Chinese adults who drank at least one beer, cocktail or glass of wine daily, those who also consumed burning hot tea every day were 5 times more likely to develop esophageal cancer than people who drank tea at any temperature less than once a week, the study found.

For current smokers, drinking scalding hot tea every day was associated with roughly twice the risk of esophageal cancer as consuming tea less than weekly.

 “Keeping away from both tobacco and excessive alcohol use is the most important means for esophageal cancer prevention,” said study coauthor Dr. Jun Lv of Peking University Health Science Center in China.

“Under this increased risk of esophageal cancer from smoking and drinking alcohol, if people like drinking very hot tea, the risk of developing cancer will be synergistically higher,” Lv said by email.

But by itself, drinking hot tea doesn’t increase cancer risk, Lv said.

China is among the countries with the highest incidence of esophageal cancer, researchers note in the Annals of Internal Medicine. Because tea drinkers in China, especially men, are more likely to drink alcohol and smoke, previous studies haven’t offered a clear picture or whether burning hot tea might be an independent risk factor for esophageal tumors.

While some prior research has suggested tea may help protect against tumors in the digestive tract, other studies have shown repeated consumption of very hot food or drink might damage the esophagus and help tumors take hold, the researchers note.

For the current study, researchers examined data on 456,155 adults ages 30 to 79 who completed questionnaires about their smoking, alcohol and tea habits.

At the start of the study, none of the participants had cancer. Researchers followed half of the participants for at least 9 years. During the study, 1,731 people developed esophageal tumors.

People who drank scalding hot tea, consumed excessive amounts of alcohol and also smoked had more than five times the risk of esophageal cancer than individuals who didn’t do any of these things.

The study wasn’t a controlled experiment designed to prove whether or how the temperature of tea might impact the risk of esophageal tumors.

Another limitation is that study participants reported on their own smoking and drinking habits, and their reports could be unreliable. Researchers also only had data on tea consumption from one point in time, when people joined the study, making it impossible to know how changing habits might have impacted the cancer risk.

“People probably do not estimate their tea temperature perfectly, and this is one of the main limitations of the study,” said Neal Freedman, author of an accompanying editorial and a researcher with the Division of Cancer Epidemiology and Genetics at the National Cancer Institute in Bethesda, Maryland.

“Drinking tea at a lower temperature should not be considered as a replacement for smoking cessation and limiting alcohol intake,” Freedman said by email. “Nevertheless, accumulating data suggest that drinking very hot tea may also increase the risk of esophageal cancer, and it may be prudent for people who drink very hot beverages to wait until it cools down a bit before drinking, whether or not they also smoke cigarettes or drink alcohol.”


Aging immune system may explain age-related cancer risk increase

Published: February 05, 2018

Source:https://www.sciencedaily.com/releases/2018/02/180205151549.htm

The key to cancer prevention may lie in the immune system rather than genetic mutations, the current focus of most anti-cancer efforts across the world, according to a major new study carried out at the University of Dundee.

Eight million people die of cancer across the world each year. Men are significantly more likely than women to be diagnosed with cancer in their lifetime, and for most cancers the chance of developing the disease rises dramatically with age.

For decades, it has been known that mutations arising either as a result of genetic predisposition, or lifestyle and environmental factors cause cancer. The traditional view is that the way cancer incidence increases with age could be understood and quantified if multiple (typically five to six) mutations in one cell are required to initiate cancer.

The Dundee team, which also features researchers from Heriot Watt University, the University of Edinburgh and the Institut Curie in France, have shown that the declining immune system with age may actually be a stronger reason for the increasing incidence of developing cancer than multiple mutations.

Following the hypothesis that an ageing immune system may result in higher rates of cancer, just as it leads to older people being more prone to other diseases, they looked at data on 2 million cases of cancer over the 18-70 age range. They then developed a mathematical equation for how they would expect cancer incidence to rise in relation to a declining immune system and compared it to the age profiles for 100 different cancers.

Their model fitted the data better than the multiple mutation hypothesis. Because the immune system generally declines more slowly in women than men, they were also able to account for the gender difference in cancer incidence, something that mutations alone cannot easily explain.

This suggests that the immune system, particularly as it declines, may play a far bigger role in the development of cancer than previously thought. If borne out by further studies, this could have significant implications for cancer prevention and treatment across the globe.

"This is still very early days but if we are proven right then you could be talking about a whole new way to treat and prevent cancer," said senior author Dr Thea Newman, formerly Vice Principal of Research and Professor of Biophysics and Systems Biology at Dundee.

"Nearly all of the mainstream research into cancer is based on how we can understand genetic mutations, target them and thereby cure the disease. We're not debating the fact that mutations cause cancer, but are asking whether mutations alone can account for the rapid rise in cancer incidence with age when ageing causes other profound changes in the body."

A primary cause of immune system ageing is the shrinking of the thymus gland. This is where T cells, which circulate the body killing dysfunctional cells or foreign agents, are produced.

Thymic involution begins from around the age of one and the thymus roughly halves in size every 16 years, with a corresponding fall in the production of T cells. The researchers found an extremely strong correlation between the chances of certain cancers increasing and the new T cell populations falling.

"The immunosurveillance hypothesis is that cancer cells are continually arising in the body but that normally the immune system kills them before a new tumour is able to establish itself," said Dr Sam Palmer, who initiated the research at Dundee before taking a post at Heriot Watt University.

"The T cells are constantly scanning for cancer cells, looking to destroy them. If they can't find them soon enough or the immune system is weak then the cancer population has the chance to grow. The chances of this happening will increase with age as the thymus is shrinking all the time.

"For our model, we imagined a war between T cells and cancer cells, which the cancer cells win if they grow beyond a certain threshold. We then set this threshold to be declining with age, proportional to T cell production. This simple hypothesis turns out to be able to explain much of the cancer incidence data."

Dr Luca Albergante, formerly of Dundee and now based at the Institut Curie, added, "The increase of cancer incidence with age is slower in women, something which we would naively expect to be effectively gender-neutral. However, the thymus gland shrinks more slowly in women, so we were able to make a prediction on the differential cancer incidence with gender that once again shows our model to be more accurate than the traditional model."

The team tested their model on data from the US-based National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) programme. The results showed that many cancers appear to be very strongly linked to the decline of the immune system, while others are more likely linked to a combination of immune system decline and multiple mutations.

Professor Clare Blackburn of the University of Edinburgh, an expert in thymus biology, said, "We believe that our findings are extremely relevant and show the need to take the immune system even more seriously in cancer research.

"In addition to mutations, this suggests we should also focus on how to boost thymus function in a controlled way, perhaps by transplantation or by controlled regeneration, so we can increase the number of T cells we are making. Of course, we also need to look at whether there may be unintended consequences of doing this, and how to minimise these if they occur."

The interdisciplinary researchers, drawn from the fields of biology, physics and computer science, have published the study in the latest edition of the Proceedings of the National Academy of Sciences.


Exercise May Help Lung Cancer Surgery Go More Smoothly

Published: February 02, 2018

Source:https://www.cancercompass.com/cancer-news/article/60663.htm

(HealthDay News) -- Lung cancer patients can halve their risk of postop complications by taking up an exercise program before their surgery, a new report suggests.

For the study, researchers analyzed reports on 13 clinical trials that included a total of over 800 people who had surgery for cancer. The patients had been treated for cancer of the bowel, liver, esophagus, lung, mouth or prostate.

Among lung cancer patients, engaging in regular exercise before surgery was tied to 48 percent lower odds of postoperative complications. In addition, these patients were released from the hospital about three days earlier than others, the investigators found.

And the more exercise lung cancer patients did, the lower their risk of complications, according to study author Daniel Steffens. He is with the Surgical Outcomes Research Centre at the University of Sydney, in Australia.

However, the researchers could not prove a cause-and-effect relationship. And the link between exercise and surgery for other types of cancer was unclear, mostly because few of the studies looked at other cancers, and the poor quality of evidence, the investigators noted.

The new report was published Feb. 1 in the British Journal of Sports Medicine.

"Postoperative complication is a major concern for patients undergoing [cancer] surgery," Steffens and his colleagues wrote in a journal news release.

The authors said their findings suggest that exercise before lung cancer surgery might be beneficial.

The "findings may also impact on health care costs and on patients' quality of life, and consequently have important implications for patients, health care professionals and policy makers," but further research is needed to confirm this, the team added.

The exercise programs in the study lasted from one to four weeks (an average of two weeks), and the frequency varied from three times a day to three times a week. Workouts included aerobic exercise (such as walking) and weight training.


Prostate cancer: Poor prognosis in men with diabetes

Published: January 31, 2018

Source:https://www.sciencedaily.com/releases/2018/01/180131121339.htm

Men with type 2 diabetes are less likely to develop prostate cancer than patients without diabetes. However, the mortality rate is higher. Researchers of the German Center for Diabetes Research (DZD) from Tübingen and experts of Helmholtz Zentrum München and the Urology Department of Tübingen University Hospital were able to show that in the affected individuals the androgen receptor and the mitogenic forms of the insulin receptor were more strongly expressed. This could explain why patients with diabetes have a poorer prognosis for prostate cancer. The current results were published in the journals Molecular Metabolism and Endocrine Related Cancer.

Prostate cancer and type 2 diabetes are among the most common diseases in men. Although studies indicate that people with diabetes suffer more frequently from cancer, men with diabetes do not increasingly suffer from prostate cancer. On the contrary, meta-analyses of studies have shown that diabetes patients are less likely to develop this carcinoma. However, the mortality rate is higher. This is also confirmed by current research carried out by researchers at the Institute for Diabetes Research and Metabolic Diseases (IDM) of Helmholtz Zentrum München at the University of Tübingen, a partner of the DZD, in cooperation with the Department of Urology at Tübingen University Hospital. The research team recently analyzed the data of patients who had their prostate removed due to cancer. As expected, among them were fewer patients with diabetes than in the general population. However, prostate cancer patients with diabetes were significantly more likely to have metastases in the lymph nodes. In addition, the proportion of patients who are at very high risk according to the guidelines of the National Comprehensive Cancer Network (NCCN) was significantly higher among those with diabetes.

But how do prostate carcinomas differ in men with and without diabetes? What makes prostate carcinoma in patients with metabolic disease so aggressive? The researchers investigated these questions in another study. For this purpose, they analyzed 70 tumor samples from patients without diabetes and 59 samples from patients with type 2 diabetes.

Since male sex hormones (androgens) play an important role in the development of prostate cancer, the scientists investigated the androgen signaling chain. We conducted a gene expression analysis of key proteins and found that in men with diabetes, the androgen receptor (AR) was increased," said Dr. Martin Heni, who led the study at the IDM. The signaling pathway mediated by AR was also more strongly activated.

The scientists identified another difference: "Insulin receptors of isoform A are increasingly expressed in the prostate carcinomas of patients with diabetes," said Dr. Stefan Lutz, first author of the study. These can bind insulin-like growth factors (IGFs). This contributes to increased cell growth and cell division. Normally, adults mainly express the isoform B, which does not bind IGF.

In addition, in patients with diabetes, the steroid biosynthesis in the tumor is also altered. Less protective estrogen receptor ligands are formed.

This further strengthens the androgen signaling pathway in tumors.

Our research provides new insights into why prostate cancer is so aggressive in men with type 2 diabetes," said Dr. Heni, summarizing the results. Prostate carcinoma in men with type 2 diabetes has a poorer prognosis and must therefore be diagnosed and treated earlier and more comprehensively than prostate cancer in nondiabetics," said Professor Arnulf Stenzl, MD, head physician of the Urology Department of Tübingen University Hospital.


Vitamin deficiency 'puts cancer cells into hibernation'

Published: January 29, 2018

Source:https://www.sciencedaily.com/releases/2018/01/180129145837.htm

A new potential therapeutic agent, diphenyleneiodonium chloride (DPI), effectively switches off cancer stem cells, preventing their proliferation, researchers report.

"It's extraordinary; the cells just sit there as if in a state of suspended animation," explains Professor Michael Lisanti, Chair of Translational Medicine and lead investigator.

The discovery is significant because the drug halts the propagation of cancer stem cells without causing the toxic side-effects normally associated with more conventional chemotherapy.

Reporting their laboratory findings in the journal Aging, the team observed that addition of DPI to a mixed population of cells eliminated the tumour initiating cancer stem cells. However, the drug was non-toxic for "bulk" cancer cells, which are not thought to be cancer-forming.

The authors describe how DPI targets more than 90 protein enzymes which feed mitochondria and help generate the cell's energy. Specifically, DPI works as an inhibitor of Vitamin B2 -- Riboflavin -- starving the cells of the energy.

"Our observation is that DPI is selectively attacking the cancer stem cells, by effectively creating a vitamin deficiency," explained Professor Lisanti. "In other words, by turning off energy production in cancer stem cells, we are creating a process of hibernation.

"The beauty of this is that DPI makes the cancer stem cells metabolically-inflexible, so they will be highly susceptible to a many other drugs."

Chemotherapy produces many nasty side-effects, because it helps create toxic free radicals. However, DPI did not increase free radicals.

The Salford team -- which specialises in the discovery new non-toxic therapies -- and has published substantially on the anti-cancer impacts of Vitamin C and antibiotics -- is calling the discovery the start of a new type of chemotherapy, and they even have a name for it 'Mitoflavoscins'.

"In terms of chemotherapies for cancer, we clearly need something better that what we have at present, and this is hopefully the beginning of an alternative approach to halting cancer stem cells," commented Professor Federica Sotgia, a co-author of the study.


Struggling to Quit Smoking? Try These Tips

Published: January 28, 2018

Source:https://www.cancercompass.com/cancer-news/article/60606.htm

(HealthDay News) -- If your New Year's resolution was to quit smoking, it's probably time to consider ways to improve your chances of success.

For starters, list your reasons for wanting to quit, suggest experts from the U.S. Food and Drug Administration. Want to improve your health? Save money? Smell and taste food better?

Those are common reasons smokers cite for wanting to kick the habit -- something that nearly 70 percent of adult smokers say they want to do, according to the FDA.

Reviewing your reasons for wanting to quit can help you when you get the urge to smoke.

Also, don't be too hard on yourself. Quitting smoking can be difficult so you might have to try a few times before you're successful. Research has shown that trying but failing to quit can lead to more attempts in the future, and that it often takes multiple attempts to finally quit smoking.

The agency also notes that there are a number of FDA-approved products that can help you quit smoking.

These include nicotine replacement therapy products. They provide controlled amounts of nicotine, to reduce smoking withdrawal symptoms and cravings. Two types are available by prescription -- a nicotine nasal spray and a nicotine inhaler. Three types can be bought over-the-counter -- nicotine gum, skin patches and lozenges.

Their effectiveness can vary, but these products can double your chances of successfully quitting smoking, according to the FDA.

There are also FDA-approved prescription drug products without nicotine that can help you quit smoking. Just be sure to read and carefully follow the directions for prescribed smoking-cessation products and talk to your doctor if you have questions.Anyone younger than 18 who wants to quit smoking should talk to a health care professional about whether they should use smoking-cessation products, according to the FDA.


Quality of children's sleep may affect eating habits and weight

Published: January 26, 2018

Source:https://www.sciencedaily.com/releases/2018/01/180126085445.htm

Several measures of poor sleep quality were associated with higher body mass index (BMI) in children, according to data presented at the American Association for Cancer Research Special Conference Obesity and Cancer: Mechanisms Underlying Etiology and Outcomes, held Jan. 27-30.

About one in five children between the ages of 6 and 19 is obese, according to recent statistics from the Centers for Disease Control and Prevention. The percentage of U.S. children with obesity has more than tripled since the 1970s, with significant immediate and long-term effects.

"Childhood obesity very often leads to adult obesity," said the study's lead author, Bernard Fuemmeler, PhD, MPH, professor and associate director for cancer prevention and control at Virginia Commonwealth University's Massey Cancer Center. "This puts them at greater risk of developing obesity-related cancers in adulthood."

Fuemmeler explained that previous research has shown that sleep patterns play a role in obesity in adults, but most research exploring the connection between sleep and obesity in children has focused on the duration of sleep, rather than the way quality of sleep or circadian patterns affect eating behaviors and weight.

In this study, Fuemmeler and colleagues enrolled 120 children whose mothers had participated in the Newborn Epigenetic Study, a federally funded project that examines how environmental exposures and nutrition, both pre-birth and during early childhood, affect how genes work. The average age of the children was 8. Researchers controlled for age, sex, race, and maternal education as an indicator of socioeconomic status.

To track the sleep-wake cycle, the children wore accelerometers continuously for 24 hours per day for a period of at least five days. To gauge eating habits, children completed the "eating in the absence of hunger test." Children ate a meal and reported when they were full; the researchers then tracked how much food they ate once they had reached the point of satiety.

The researchers found:

  • Shorter sleep duration, measured in hours, was associated with a higher BMI z-score (body mass index adjusted for age and sex). Each additional hour of sleep was associated with a .13 decrease in BMI z-score, and with a 1.29 centimeter decrease in waist circumference.
  • More fragmented rest-activity rhythms and increased intradaily variability, a measure of the frequency and extent of transitions between sleep and activity, were also associated with greater waist circumferences.
  • Earlier onset of the most active period during daytime, diurnal activity, was associated with higher intake of calories once the children had reached the point of satiety.

Overall, Fuemmeler said, the study results indicate that while sleep duration is important, examining markers of sleep quality may also be useful in designing childhood obesity prevention strategies.

"Today, many children are not getting enough sleep," Fuemmeler said. "There are a number of distractions, such as screens in the bedroom, that contribute to interrupted, fragmented sleep. This, perpetuated over time, can be a risk factor for obesity. Because of the strong links between obesity and many types of cancer, childhood obesity prevention is cancer prevention, in my view."

Fuemmeler said that while further research is necessary to understand more about the way poor sleep affects weight, families would benefit from following guidelines established by the American Academy of Pediatrics.

The study's primary limitation is that it did not include prospective data that might have helped researchers assess whether sleep quality influences weight gain or weight in children affects their sleep. Fuemmeler said that data will be encompassed in future studies.

The study was funded by a grant from the National Institute of Child Health and Human Development.


New Treatments Tackling Tough Lung Cancer

Published: January 25, 2018

Source:www.cancercompass.com/cancer-news/article/60588.htm

(HealthDay News) -- Medical advances have led to "enormous" progress in treatments for the leading type of lung cancer, a new report shows.

Lung cancer kills about 1.6 million people worldwide each year. The type known as non-small cell lung cancer accounts for about 85 percent of lung cancer cases.

"Progress has been enormous in the past 20 years," said Dr. Roy Herbst, chief of medical oncology at Yale Cancer Center and co-lead author of the paper.

Still, many challenges remain, Herbst and his colleagues report Jan. 24 in the journal Nature.

Lung cancer is difficult to detect in the early stages and hard to treat as it progresses. That has made it the leading cause of cancer death.

Non-small cell lung cancer was long treated with surgery followed by chemotherapy or radiation or both.

"Options for treatments have improved in recent years with the advent of two classes of drugs -- molecularly targeted therapies and, more recently, immunotherapies," Herbst said in a Yale news release.

Molecularly targeted drugs attack tumor cells that have mutated genes, such as EGFR, that drive cancer. About one-quarter of patients with non-small cell lung cancer now can be given various targeted drugs, and researchers are working to identify more molecular targets for drugs.

However, patients eventually develop resistance to these drugs, Herbst said.

But another treatment arrived in 2015, when the U.S. Food and Drug Administration approved the first "immune checkpoint blocker" for patients with advanced non-small cell lung cancer. These drugs target mechanisms that prevent the body's immune T-cells from attacking tumors.

Immune checkpoint blockers help about one-fifth of these cancer patients. But as with targeted therapies, most tumors eventually become resistant to immunotherapies, the report says.

New immunotherapies need to be developed, Herbst said.

"We need to move the personalized approach that we've used for targeted therapy to immunotherapy, matching the right patient to the right medicine at the right time," he explained.

Research is also underway to find new ways to detect lung cancer and monitor it as it progresses.

"Overall, we're seeing unprecedented benefits for people with NSCLC [non-small cell lung cancer], but it's a very tough disease," Herbst said.

"We're still only helping 30 or 35 percent of patients," he added. "Our research has to remain novel and innovative. We still have a lot of work to do."


Reducing Your Risk of Cervical Cancer

Published: January 23, 2018

Source:https://health.usnews.com/health-care/for-better/articles/2018-01-23/reducing-your-risk-of-cervical-cancer

January, Cervical Health Awareness Month, serves as an important reminder to speak with your doctor about how to protect yourself against human papillomavirus infection and to screen for cervical cancer. While the American College of Obstetricians and Gynecologists recommends annual gynecological examinations for healthy women, recent recommendations have changed for cervical cancer screening. It's important to be aware of preventative HPV vaccinations as well as the recommended timeline for screenings.

As a gynecologic oncologist at Montefiore Health System in Bronx, New York, I work to educate my patients about cervical cancer and how to decrease their risk of getting this disease. Here are some important questions and answers I use to help reduce the risk of getting cervical cancer. I encourage you to have this conversation with your physician, too.

Who Gets Cervical Cancer?

In the United States, cervical cancer is the third most common type of cancer of the female reproductive system, and the third most common cause of death from cancers of the female genital tract. Your risk of contracting and dying from cervical cancer is higher in countries where there isn't screening for cancer and pre-cancer. Screening tools, such as a Papanicolau test (Pap test) or other equivalent, help decrease cervical cancer deaths by 75 percent in countries with such programs. Sadly, we know that women who have never been screened account for more than half of all women with cervical cancer.

Research shows that the average age for developing cervical cancer in the United States is 48, and the risk for having cervical cancer before age 21 is less than 1 percent. Despite your age, it's important to be aware of the risk factors associated with cervical cancer, including: conditions that impair your immune system (such as HIV, early onset of sexual activity, multiple sexual partners, a high-risk sexual partner who has multiple partners or HPV infection, and history of sexually transmitted infections like Chlamydia or genital herpes.

Finally, cervical cancer is more common in communities with higher poverty levels and among non-white women. If you think you may be at an increased risk for cervical cancer, please discuss your risk factors with your physician, and ask how you can schedule regular screenings and possibly even receive preventative treatments.

What Causes Cervical Cancer?

HPV is responsible for the development of more than 99 percent of cervical cancers. In fact, the connection between HPV and cervical cancer is stronger than the association between smoking and lung cancer. It's important to recognize that HPV infection is very common and affects up to 80 percent of sexually active women in the U.S.

Despite the high prevalence of HPV nationwide, the majority of women who contract HPV will clear the infection and never go on to develop cervical cancer. However, it's believed that persistent infection causes pre-cancerous changes in the cells of the cervix, and if left untreated over a long period of time, this can potentially progress to invasive cancer.

What Can I Do to Reduce My Risk of Cervical Cancer?

In recent years, vaccinations against HPV have been introduced for both adolescent males and females. This vaccination has the potential to make an impactful difference. If 70 percent of the population gets this vaccination, over time, it's predicted to help decrease cervical cancers in the U.S. by over 300,000 cases every year. Currently, countries that have achieved vaccination of over 70 percent have already reported up to 40 percent decreases in development of high-risk pre-cancers.

Who Should Be Vaccinated Against HPV?

The Advisory Committee on Immunization Practices in the United States recommends vaccination of girls and boys aged 11 to 12; however, children as young as 9 can be vaccinated. Females who have not been vaccinated or who did not complete their vaccinations should have "catch-up" vaccinations from the ages of 13 to 26. Standard HPV vaccination has not been shown to help women of older ages or who have already had cervical cancer.

When Should I Get Screened for Cervical Cancer?

Screening for cervical cancer should start for women ages 21 and older who have normal immune systems and who do not have cancer symptoms. Women who are between 21 and 30 should get screened with a Pap test every three years. The most recent guidelines suggest that screening with Pap testing alone is safe for women 30 and older, and that screening intervals can be lengthened to every five years if HPV testing is performed with the Pap test. While these are general recommendations, it is important that each patient be evaluated by her doctor to discuss co-existing conditions, medical history and any history of a compromised immune system or abnormal Pap testing.

While recent advances in testing for the HPV virus have changed recommendations for treatment and screening intervals, it's important to discuss your risks with your physician and not delay HPV vaccinations and cervical cancer screenings. Cervical cancer is a highly preventable and curable disease if caught early enough.


Workouts May Boost Life Span After Breast Cancer

Published: January 22, 2018

Source:https://www.cancercompass.com/cancer-news/article/60529.htm

(HealthDay News) -- Longer survival after breast cancer may be as simple as staying fit, new research shows.

In the new study, regular exercise appeared to reduce breast cancer survivors' risk of heart disease, diabetes and possibly even the odds for breast cancer's return.

One breast cancer specialist said the findings should give survivors hope.

"A common question asked by patients who have recently completed treatment is 'What can I do to prevent this from happening again?' " said Dr. Alice Police. She is regional director of breast surgery at Northwell Health Cancer Institute in Sleepy Hollow, N.Y.

"We now have one more very well done study that supports the idea that exercise -- as opposed to weight loss alone -- is very important in preventing breast cancer recurrences," Police said.

The new research was led by Christina Dieli-Conwright, assistant professor of research, in biokinesiology and physical therapy at the University of Southern California (USC).

Her team tracked outcomes for 100 breast cancer survivors who'd received cancer treatment less than six months before entering the study.

Nearly half of the participants were obese and 77 percent had developed metabolic syndrome. That's a group of health conditions -- high blood pressure, excessive body fat and high blood fat levels -- that raises a person's odds for heart disease.

"Many people don't know the No. 1 cause of death for breast cancer survivors is heart disease, not cancer," Dieli-Conwright noted in a USC news release.

"In breast cancer patients, metabolic syndrome is exacerbated by obesity, a sedentary lifestyle and receipt of chemotherapy," Dieli-Conwright explained.

In fact, she added, women with metabolic syndrome are 17 percent more likely to develop a breast cancer, three times more likely to have breast cancer recurrence, and twice as likely to die from breast cancer, compared to women without the syndrome.

In the new study, women were randomly assigned to either a non-exercise ("control") group or to a group that undertook three one-on-one exercise sessions each week for four months.

The workout program included resistance training with weights as well as moderate-intensity aerobic exercise.

At the end of the four months, rates of metabolic syndrome were 80 percent in the non-exercising group, but they'd dropped to just 15 percent in the exercise group, the findings showed.

In addition, the women in the exercise group lost fat, gained muscle and reduced their risk of heart disease, the investigators reported. Also, among those in the exercise group, blood pressure levels fell by 10 percent and blood levels of "good" HDL cholesterol rose by 50 percent.

The bottom line, according to Dieli-Conwright: "Exercise is a form of medicine."

Police agreed. And while the study couldn't prove that regular workouts might thwart cancer's return, she said the theory makes sense.

"Exercise promotes changes in our bodies that go beyond how we look, and make all of our cells and organs happier so that we can remain cancer free," Police said.

Breast cancer specialist Dr. Stephanie Bernik is chief of surgical oncology at Lenox Hill Hospital in New York City. She said the study is important because "many cancer patients -- especially those undergoing chemotherapy -- become sedentary, and these habits often persist once treatment is completed."

But getting back into a workout routine is key to long-term survival, Bernik said, and "women that eat right and exercise are more likely to have a normal longevity."


Quick Test Could Spot Precursor to Esophageal Cancer

Published: January 19, 2018

Source:https://www.cancercompass.com/cancer-news/article/60521.htm

 (HealthDay News) -- A pill-sized device that you swallow might help detect a change in the esophagus that can lead to a deadly form of cancer, researchers are reporting.

The esophagus is the tube that carries food from your mouth to your stomach. And the change that occurs in the esophagus, known as Barrett's esophagus, usually results from long-term reflux. Barrett's esophagus is considered a precursor to a type of cancer called esophageal adenocarcinoma.

More than 80 percent of people diagnosed with this cancer die within five years. Yet, medical experts say that many of these deaths could be prevented if people were diagnosed earlier with Barrett's esophagus.

However, that usually requires a costly and invasive test, known as an endoscopy, that also requires sedation. According to the researchers, this prevents some people from being screened for the condition.

Screening with the new device could one day change that, the authors of the new study suggest.

"Our goal is early detection," Dr. Amitabh Chak, a professor of medicine and researcher at Case Western Reserve Medical School in Cleveland, said in a university news release.

"Symptoms of Barrett's esophagus, such as heartburn, can also be commonly seen in individuals who have acid reflux disease without Barrett's esophagus. These symptoms can easily be treated by over-the-counter medications so people often don't get tested for Barrett's esophagus, particularly by an invasive test such as endoscopy," Chak explained.

This has meant that, about 95 percent of the time, people haven't known they had Barrett's esophagus until diagnosed with cancer, he said.

To address this issue, the researchers developed the swallowable device. Using it to test for Barrett's esophagus takes five minutes and is more than 90 percent effective in detecting the condition, they said.

The device is about the size of a vitamin pill. It's attached to a thin silicone catheter. Once swallowed, it enters the stomach. Doctors then inject air into the catheter to inflate a small balloon.

The balloon is moved around to swab the lower esophagus near the stomach -- the area where Barrett's esophagus usually develops. The swab collects a sample of cells before it's deflated, pushed back into the catheter and retrieved through the mouth. The cells extracted by the device are then analyzed for abnormalities.

A clinical trial involving 86 people showed the swallowable test was more than 90 percent accurate in detecting those with Barrett's esophagus.

Also, 82 percent of those who had the test reported little or no anxiety, pain or choking during the procedure. About 93 percent said they would do it again.

"We wanted an easier, less costly test that could provide a practical way for screening and early detection of individuals with Barrett's esophagus, who can then be followed closely to prevent development of [esophageal cancer]," Chak said.

A report on the device and the clinical trial results was published Jan. 17 in Science Translational Medicine.


Single blood test screens for eight cancer types

Published: January 18, 2018

Source:https://www.sciencedaily.com/releases/2018/01/180118141803.htm

Johns Hopkins Kimmel Cancer Center researchers developed a single blood test that screens for eight common cancer types and helps identify the location of the cancer.

The test, called CancerSEEK, is a unique noninvasive, multianalyte test that simultaneously evaluates levels of eight cancer proteins and the presence of cancer gene mutations from circulating DNA in the blood. The test is aimed at screening for eight common cancer types that account for more than 60 percent of cancer deaths in the U.S. Five of the cancers covered by the test currently have no screening test.

"The use of a combination of selected biomarkers for early detection has the potential to change the way we screen for cancer, and it is based on the same rationale for using combinations of drugs to treat cancers," says Nickolas Papadopoulos, Ph.D., senior author and professor of oncology and pathology.

The findings were published online by Science on Jan. 18, 2018.

"Circulating tumor DNA mutations can be highly specific markers for cancer. To capitalize on this inherent specificity, we sought to develop a small yet robust panel that could detect at least one mutation in the vast majority of cancers," says Joshua Cohen, an M.D.-Ph.D. student at the Johns Hopkins University School of Medicine and the paper's first author. "In fact, keeping the mutation panel small is essential to minimize false-positive results and keep such screening tests affordable."

The investigators initially explored several hundred genes and 40 protein markers, whittling the number down to segments of 16 genes and eight proteins. They point out that this molecular test is solely aimed at cancer screening and, therefore, is different from other molecular tests, which rely on analyzing large numbers of cancer-driving genes to identify therapeutically actionable targets.

In this study, the test had greater than 99 percent specificity for cancer. "Very high specificity was essential because false-positive results can subject patients to unnecessary invasive follow-up tests and procedures to confirm the presence of cancer," says Kenneth Kinzler, Ph.D., professor of oncology and co-director of the Ludwig Center. The test was used on 812 healthy controls and produced only seven false-positive results.

The test was evaluated on 1,005 patients with nonmetastatic, stages I to III cancers of the ovary, liver, stomach, pancreas, esophagus, colorectum, lung or breast. The median overall sensitivity, or the ability to find cancer, was 70 percent and ranged from a high of 98 percent for ovarian cancer to a low of 33 percent for breast cancer. For the five cancers that have no screening tests -- ovarian, liver, stomach, pancreatic and esophageal cancers -- sensitivity ranged from 69 percent to 98 percent.

"A novelty of our classification method is that it combines the probability of observing various DNA mutations together with the levels of several proteins in order to make the final call," says Cristian Tomasetti, Ph.D., associate professor of oncology and biostatistics, who developed the algorithm. "Another new aspect of our approach is that it uses machine learning to enable the test to accurately determine the location of a tumor down to a small number of anatomic sites in 83 percent of patients."

Although the current test does not pick up every cancer, it identifies many cancers that would likely otherwise go undetected. "Many of the most promising cancer treatments we have today only benefit a small minority of cancer patients, and we consider them major breakthroughs. If we are going to make progress in early cancer detection, we have to begin looking at it in a more realistic way, recognizing that no test will detect all cancers," says Bert Vogelstein, M.D., co-director of the Ludwig Center, Clayton Professor of Oncology and Howard Hughes Medical Institute investigator.

To zero in on the analytes they included in their CancerSEEK test, the research team pulled data from more than three decades of cancer genetics research generated at their Ludwig Center at Johns Hopkins, where the first genetic blueprints for cancer were created, as well as data from many other institutions.

To precisely determine the optimal number of DNA bases to assess in the CancerSEEK test, the researchers used a method based on diminishing returns. "The more DNA bases you assay, the more mutations you are capable of finding, but eventually you reach a point of diminishing returns," explains Cohen. "We designed our test to reflect this point of diminishing returns, including the DNA markers that were useful to detecting the cancers and eliminating those that did not add benefit." The result was a relatively small panel of highly selective DNA markers.

"This test represents the next step in changing the focus of cancer research from late-stage disease to early disease, which I believe will be critical to reducing cancer deaths in the long term," says Vogelstein.

CancerSEEK is noninvasive and can, in principle, be administered by primary care providers at the time of other routine blood work. "This has the potential to substantially impact patients. Earlier detection provides many ways to improve outcomes for patients. Optimally, cancers would be detected early enough that they could be cured by surgery alone, but even cancers that are not curable by surgery alone will respond better to systemic therapies when there is less advanced disease," says Anne Marie Lennon, M.D., Ph.D., associate professor of medicine, surgery and radiology, clinical director of gastroenterology and director of the Multidisciplinary Pancreatic Cyst Program.

The investigators feel that a test that will be used routinely for cancer screening must have a cost in line with or less than other currently available screening tests for single cancers, such as colonoscopy. They envision that the CancerSEEK test will eventually cost less than $500.

Larger studies of the test are currently under way.


More evidence of link between severe gum disease and cancer risk

Published: January 16, 2018

Source:https://www.sciencedaily.com/releases/2018/01/180116111145.htm

Data collected during a long-term health study provides additional evidence for a link between increased risk of cancer in individuals with advanced gum disease, according to a new collaborative study led by epidemiologists Dominique Michaud at Tufts University School of Medicine and Elizabeth Platz of the Johns Hopkins Bloomberg School of Public Health and Kimmel Cancer Center.

The study, published in the Journal of the National Cancer Institute, used data from comprehensive dental exams performed on 7,466 participants from Maryland, Minnesota, Mississippi, and North Carolina, as part of their participation in the Atherosclerosis Risk in Communities (ARIC) study who were then followed from the late 1990s until 2012. During the follow-up period, 1,648 new cancer cases were diagnosed.

The research team found a 24 percent increase in the risk of developing cancer among participants with severe periodontitis, compared to those with mild to no periodontitis at baseline. Among patients who had no teeth -- which can be a sign of severe periodontitis -- the increase in risk was 28 percent. The highest risk was observed in cases of lung cancer, followed by colorectal cancer.

When the researchers did sub-group analyses, they found that participants with severe periodontal disease had more than double the risk of developing lung cancer, compared with no/mild periodontitis. An 80 percent increase in risk of colon cancer observed for participants who were edentulous at baseline, which is consistent with prior findings, and among never smokers, a two-fold higher risk was noted for participants with severe periodontitis, compared to those who had no/mild periodontitis.

"This is the largest study addressing the association of gum disease and cancer risk using dental examinations to measure gum disease prior to cancer diagnosis," said first and corresponding author Dominique Michaud, Sc.D., professor of public health and community medicine at Tufts University School of Medicine. "Additional research is needed to evaluate if periodontal disease prevention and treatment could help alleviate the incidence of cancer and reduce the number of deaths due to certain types of cancer."

Michaud noted that the findings were particularly interesting in light of research, including a recent study in Science, which determined that colorectal cancer tissues contain bacteria that are present in the mouth, including bacteria that have been associated with periodontal disease.

The researchers also uncovered a small increase in the risk of pancreatic cancer in patients with severe periodontitis. Although not significant statistically, the association has been seen in other similar studies, including a number of studies led by Michaud of Tufts.

The research team accounted for the impact of smoking among the participants, since people who smoke are more likely to get periodontal disease, and smoking raises the risk of lung and colon cancers.

"When we looked at data for the people who had never smoked, we also found evidence that having severe periodontal disease was related to an increased risk of lung cancer and colorectal cancer," said Elizabeth Platz, Sc.D., deputy chair of the department of epidemiology at the Johns Hopkins Bloomberg School of Public Health and co-leader of the Cancer Prevention and Control Program at the Johns Hopkins Kimmel Cancer Center.

The ARIC data were especially useful to study because unlike most previous research linking gum disease and cancer risk, periodontitis cases were determined from dental examinations performed as part of the ARIC study rather than participants' self-reports of the disease. The dental exams provided detailed measurements of the depth of the pocket between the gum and tooth in several locations in the mouth. The ARIC data include both Caucasian and African-American participants.

The researchers found no links between increased risk of breast, prostate or blood/lymphatic cancer and periodontitis. The link between periodontitis and increased cancer risk was weaker or not apparent in African-American participants from the ARIC study, except in cases of lung and colorectal cancer. "Additional research is needed to understand cancer-site specific and racial differences in findings," wrote the authors. The researchers caution that the study was limited in size for subgroup analyses, and less common cancers. The findings, however, suggest the need for further study.

Michaud and Platz said the study also points to the importance of expanding dental insurance to more individuals. "Knowing more about the risks that come about with periodontal disease might give more support to having dental insurance in the way that we should be offering health insurance to everyone," Platz said.

Advanced gum disease, also called periodontitis, is caused by bacterial infection that damages the soft tissue and bone that support the teeth. Previous research has shown a link between periodontitis and increased cancer risk, although the mechanism connecting the two diseases is still uncertain.


We will treat cancer by making it 'slim down'

Published: January 15, 2018

Source:https://www.sciencedaily.com/releases/2018/01/180115121635.htm

For years, attempts have been made to understand the mechanism behind the proliferation of cancer cells: they need metabolites to grow and proliferate as much as a vehicle needs gasoline or electricity to move. However, until now it was not known which metabolites cancer cells actually need. A team of researchers from the Institute of Oncology Research (IOR) at the Università della Svizzera Italiana (USI, Faculty of Biomedical Sciences) led by Prof. Andrea Alimonti has identified one of the mechanisms behind this process, as published in a recent article in the journal Nature Genetics.

From a theory dating back to the early 20th century by Nobel Prize laureate Otto Warburg, it has been believed that, in order to support their growth, cancer cells needed to increase their glucose consumption, without using mitochondrial metabolism. The mitochondrion is an organelle that produces the energy needed for the cell survival, operating as a sort of power station. "Contrary to what was believed for almost a century -- says Prof. Alimonti -- we have discovered that cells in prostate cancer need the mitochondrion, not to produce energy, rather to regulate a specific metabolic process. Specifically, the mitochondrion is able to regulate fat synthesis (lipids) through an enzyme complex called PDC.

The study published by Nature Genetics shows that without the ability to efficiently produce lipids, prostate cancer cells are not able to grow and metastasize, even in the presence of increased glycolysis. "We noticed -- continues Alimonti -- that in prostate cancer cells the activity of the enzyme complex PDC is 10 times that of a normal proliferating cell, and that as a result the cells store several lipids."

It is known that a diet rich in fat can increase the risk of developing prostate cancer, and that obese people are more prone to develop this type of tumour. However, the fact that the metabolism of lipids acts as a fuel to support the tumour has never been clarified in detail and this discovery opens up new and unexpected scenarios in cancer therapy.

"We have identified a number of pharmaceutical compounds that selectively inhibit -- in different experimental models -- the mitochondrial enzyme responsible for the tumour growth, thus limiting fat synthesis and without harming normal cells." "I would like to point out, however -- concludes Alimonti -- that our discovery does not imply that cancer patients must undergo a strict dietary regime, which might in fact hurt them: a reduction of fat in cancer cells can only be obtained by blocking the cancer cells metabolism through specific drugs."

The research was made possible thanks to the contribution of Dr Jinging Chen (IOR) -- first author of the article published on Nature Genetics -- and to Andrea Cavalli of the Institute for Research in Biomedicine (IRB, USI Faculty of Biomedical Sciences), in cooperation with other Swiss, Spanish, and English research centres.

The study has also been made possible thanks to the financial contribution by the European Research Council (ERC), the Swiss National Science Foundation, the IBSA Foundation, the Horten Foundation, and by the J. Steiner Foundation.


Prostate cancer: 'Whole' Mediterranean diet could reduce your risk

Published: January 12, 2018

Source:https://www.medicalnewstoday.com/articles/320600.php

New research finds that closely following a whole Mediterranean dietary pattern — that is, incorporating a high intake of not only vegetables, fruits, and whole grains, but also of legumes, fish, and olive oil — is tied to a lower risk of aggressive prostate cancer.

In a report on their findings that is published in The Journal of Urology, the researchers write that guidelines for preventing prostate cancershould aim to "consider whole dietary patterns instead of individual foods."

Lead investigator Dr. Beatriz Pérez-Gómez, from the Instituto de Salud Carlos III at the University of Alcalá near Madrid, Spain, explains that key elements "such as fish, legumes, and olive oil" should likely be included when suggesting a diet to prevent aggressive prostate cancer.

This is because their results "suggest that a high intake of fruits, vegetables, and whole grains might not be enough."

Prostate cancer occurs because of the uncontrolled growth of cells in the prostate, which is a gland in the male reproductive organs that produces a fluid that forms part of semen. It sits just below the bladder and surrounds the urethra, the tube that urine passes through on its way out of the body.

After skin cancer, prostate cancer is the most common cancer in men in the United States.

Prostate cancer accounts for 1 in 10 cases

The prostate gland is normally the size of a walnut. However, it is not uncommon, as men age, for their prostate to grow bigger, put pressure on the urethra, and cause problems with urine flow.

This condition — known as benign prostatic hyperplasia, or enlarged prostate — is not cancerous. There are also other non-cancerous conditions that can cause changes in the prostate.

In 2017, there were an estimated 161,360 new cases of prostate cancer in the U.S., accounting for nearly 10 percent of all cases of cancer.

Rates of death to the disease have been falling in recent years, and more than 98 percent of men with prostate cancer now survive for more than 5 years after diagnosis.

Various definitions of the Mediterranean diet have emerged since it first came to prominence in health research in the 1960s.

But a common theme is that they emphasize certain key components that include: high intakes of vegetables, fruits, whole cereals, legumes, and olive oil; moderate intakes of fish, meat, dairy, and red wine; and low intakes of eggs and sweets.

'Western, prudent, and Mediterranean' diets

The research examined data from a case-control study of 733 men with prostate cancer and 1,229 healthy men. The average age of the men, who came from seven different parts of Spain, was 66 years.

The study collected a range of data that included not only medical and background information, but also details about their eating habits.

The researchers put the participants into three groups according to which dietary pattern most closely matched their eating habits. The dietary patterns, which are the most common in Spain, were "Western, prudent, and Mediterranean."

In the Western diet, the pattern includes large intakes of fatty dairy foods, processed meats, fast food, refined grains, sweets, sauces, and high-calorie drinks.

The prudent dietary pattern comprises low-fat dairy foods, fruits, vegetables, whole grains, and juices.

Typical features of the Mediterranean pattern defined in this study were high intakes of fish, fruits, vegetables, boiled potatoes, legumes, and olive oil, with low levels of juice intakes.

The researchers categorized each participant within his dietary group according to how closely his eating habits fit with the dietary pattern. Therefore, each dietary pattern had four categories of adherence, ranging from low to high.

In the case of the men diagnosed with prostate cancer, the team categorized the aggressiveness of the disease according to their Gleason score and clinical stage.

Follow Mediterranean diet for reduced risk

Next, they compared the patterns of adherence in the men with prostate cancer and the men who were healthy.

The scientists found that only a "high adherence to the Mediterranean dietary pattern" was significantly associated with a reduced risk of having prostate cancer with aggressive and extensive tumors.

No such link was found in the other dietary patterns, either with aggressive or less aggressive tumors.

The researchers suggest that, subject to other studies confirming their findings, recommending that men closely follow the Mediterranean dietary pattern might be an effective way to reduce the risk of advanced prostate cancer.

"This study adds important evidence to the scarce information regarding the association of diet with [prostate cancer], and highlights the relevance of focusing on global dietary patterns."

Dr. Beatriz Pérez-Gómez


Biomarkers may help predict outcomes in gastric cancer patients who abuse alcohol

Published: January 10, 2018

Source:https://www.sciencedaily.com/releases/2018/01/180110113004.htm

Alcohol consumption has been identified as a modifiable risk factor for cancers such as gastric cancer. A new report in the The American Journal of Pathology sheds light on how specific proteins interact with alcohol, and how that interplay impacts survival and response to platinum-based adjuvant chemotherapy in patients with gastric cancer who may or may not still be drinking. It is the first time that a correlation between a key microRNA-processing modulator, transcription factor IIB-related factor 1 (BRF1), and prognosis of gastric cancer patients has been demonstrated. Investigators also determined that breast cancer susceptibility gene BRCA1/2, and myeloperoxidase (MPO) are more frequent in gastric cancer patients who engage in hazardous or harmful alcohol consumption.

"Alcohol consumption is a known risk factor for gastric cancer, which carries high morbidity and mortality in China. We found that DNA repair-related markers -- BRF1, BRCA1/2, and MPO -- have good prognostic value in gastric cancer patients with or without harmful alcohol consumption habits. Moreover, these proteins are also associated with how effective platinum-based adjuvant chemotherapy will be for gastric cancer patients," explained Hua Wang, MD, PhD, and co-senior author Kangsheng Gu, MD, PhD, both of the Department of Oncology at First Affiliated Hospital of Anhui Medical University, Hefei, Anhui (China).

Researchers analyzed tumor tissue from 77 patients who had undergone surgery for primary gastric adenocarcinoma and 69 tissue samples taken from outside the tumor area. Among them, 66 patients received radical surgery and 57 patients received platinum-based adjuvant chemotherapy. All 77 patients were followed for an average of 18 months, during which time 94% (62/66) experienced disease recurrence. Patients remained free of disease for an average of 14 months (disease free survival, DFS) whereas the median overall survival (OS) was 20 months.

BRF1, BRCA1/2, and MPO were also helpful in predicting which patients would benefit more from platinum-based adjuvant chemotherapy. For example, DFS was extended two-fold or more in patients who underwent chemotherapy and showed negative or low BRCA1/2 expression. For those with negative or low BRCA1, the average disease-free interval was 18 months compared to nine months in the high-expression group. Patients with negative MPO also had a better outcome trend, although it was not statistically significant.

Importantly, investigators found that alcohol continued to have a detrimental effect in patients. High BRF1 expression and MPO-positive inflammatory cell infiltration were more frequent in gastric cancer patients with hazardous or harmful alcohol consumption habits. Abnormal changes in BRCA1 in tissues outside the tumors were more frequent in alcohol abusers. In previous studies, these investigators found similar correlations between BRF1 and alcohol consumption in breast and liver cancer patients.

Understanding the mechanisms of how these proteins interact with alcohol and contribute to carcinogenesis is still being investigated. It is thought that RNA Pol III transcribes genes play a crucial role in alcohol-mediated tumorigenesis. BRF1 regulates RNA Pol III gene transcription, and its overexpression acts though BRCA1 to alleviate inhibition of RNA Pol III transcription. Measurement of MPO is interpreted as a measure of the gastric inflammation and oxidative damage induced by alcohol. BRCA1/2 and MPO also play key roles in DNA damage repair.

"Until now, there have been no good markers to indicate alcohol consumption in gastric cancer tissue," noted Dr. Wang. "Future larger clinical trials are planned to explore the prognostic utility of these biomarkers in gastric and other cancers in patients who consume hazardous quantities of alcohol."


Screening, Treatment Cuts Breast Cancer Deaths in Half

Published: January 9, 2018

Source:https://www.cancercompass.com/cancer-news/article/60426.htm

(HealthDay News) -- Breakthroughs in breast cancer screening and treatment have slashed the percentage of women dying from the disease, a new analysis reveals.

"Advances in screening and treatment are saving lives," said lead researcher Sylvia Plevritis, a professor of radiology and biomedical data science at the Stanford University School of Medicine. "Here's an example that all this investment in research and discovery has had a real benefit. This has translated into making a difference."

Screening and treatment reduced breast cancer deaths by 49 percent in 2012, compared with a 37 percent reduction in 2000, according to the study.

Treatments that target specific types of breast cancer have generated the most scientific advancement and, as such, have taken a larger role in saving lives, the researchers found.

Better cancer treatments accounted for 63 percent of the reduction in breast cancer deaths in 2012, compared with 37 percent due to early detection of cancer through screening, the study findings showed.

Back in 2000, treatment and screening were of equal importance, splitting 50-50 the lives saved from breast cancer, the researchers said.

Hormone therapy now is available to counter breast cancers spurred by estrogen, while the targeted drug Herceptin (trastuzumab) has been a wonder in treating breast cancers caused by genetic abnormalities, explained Dr. Len Lichtenfeld, deputy chief medical officer for the American Cancer Society.

These new treatments, combined with improvements in traditional chemotherapy, are helping more women beat breast cancer, Lichtenfeld said.

The greatest advance in breast cancer screening during the same period was the move to digital mammography, which produces cleaner and better images, he added.

"For the period between 2000 and 2012, there were some advances made in the technology for screening for breast cancer, but there was greater impact made by treatment," Lichtenfeld said.

For the study, Plevritis and her colleagues fed breast cancer monitoring data into a series of six different computer simulations.

Each simulation estimated what the death rate would have been in a given year between 2000 and 2012 without the availability of state-of-the-art screening and treatment, and how much each contributed to the reduction in deaths, Plevritis said.

The computer analysis also looked at how much reduction had taken place within different subtypes of breast cancer.

For example, treatment accounts for about 69 percent of the lives saved in women with cancers driven by both estrogen and genetic abnormalities, while screening is associated with only 31 percent of the mortality decline, the investigators said.

On the other hand, screening still plays a large role in saving the lives of women with so-called "triple-negative" breast cancer, which is not driven by either hormones or genetics. Triple-negative cancers account for about 12 percent of all breast cancer cases, but are nearly twice as common in black women than white women, according to the American Cancer Society.

About 48 percent of the decline in deaths due to triple-negative breast cancer can be chalked up to screening and 52 percent to treatment, similar to the split found in 2000, the researchers said.

"Mammography is an important contributor to the reduction in breast cancer mortality," Plevritis said. "But the overall benefit is greater largely because of the advances in treatment."

Screening remains important because breast cancers detected early are easier to treat, said Dr. Daniel Hayes, clinical director of the University of Michigan breast oncology program.

"Early detection makes the systemic treatment better as well," said Hayes, who's also immediate past president of the American Society of Clinical Oncology. "Most of us who take care of patients still believe rational screening programs are good public health policy. No matter what kind of cancer you have, detecting it early with screening and then treating it substantially reduces your risk of dying from it," he added.

According to Lichtenfeld, "These computer models clearly show that mammography reduces mortality from breast cancer and has made a significant contribution over time. We should not take the message that everything's about treatment. That's not the right message."


Working Night Shift May Raise Women's Odds for Cancer

Published: January 8, 2018

Source:https://www.cancercompass.com/cancer-news/article/60408.htm

(HealthDay News) -- Women who pull the night shift regularly might be at greater risk for a number of cancers, new research suggests.

"Our study indicates that night-shift work serves as a risk factor for common cancers in women," said study author Xuelei Ma. He is an oncologist in the State Key Laboratory of Biotherapy and Cancer Center at West China Medical Center of Sichuan University, China.

"These results might help establish and implement effective measures to protect female night-shifters. Long-term night-shift workers should have regular physical examinations and cancer screenings," Ma said in a news release from the American Association for Cancer Research.

For the new study, the researchers conducted a review of 61 studies involving almost 4 million people from North America, Europe, Australia and Asia, to look for an association between long-term night-shift work and the risk of 11 types of cancer.

The investigators found that working during the wee hours over the long term was associated with a 19 percent greater risk of cancer among women.

Looking at specific types of cancer, Ma and colleagues found the risk of skin cancer jumped 41 percent, the risk of breast cancer increased 32 percent and the odds of developing gastrointestinal cancer was 18 percent higher among women who were long-term night-shift workers. But the study did not prove that night-shift work caused the risk of these cancers to rise.

When the researchers took into account for location, they found that only the night-shift workers from North America and Europe had a greater risk for breast cancer.

"We were surprised to see the association between night-shift work and breast cancer risk only among women in North America and Europe," Ma said. "It is possible that women in these locations have higher sex hormone levels, which have been positively associated with hormone-related cancers such as breast cancer."

The researchers then focused on female nurses who work night shifts and the risk for six different forms of cancer. The findings showed these nurses had a 58 percent higher risk of breast cancer -- a greater increase than any other job included in the study.

In addition, the night-shift nurses had a 35 percent greater risk of gastrointestinal cancer and a 28 percent higher risk of lung cancer than the people who didn't work nights.

"Nurses that worked the night shift were of a medical background and may have been more likely to undergo screening examinations," Ma said. "Another possible explanation for the increased cancer risk in this population may relate to the job requirements of night-shift nursing, such as more intensive shifts."

The researchers also noted that the longer women worked night shifts, the greater their risk of breast cancer. The risk for the disease increased 3.3 percent for every five years of this type of work.

"By systematically integrating a multitude of previous data, we found that night-shift work was positively associated with several common cancers in women," Ma said. "The results of this research suggest the need for health protection programs for long-term female night-shift workers."


Best Ways to Quit Smoking, Cut Your Lung Cancer Risk

Published: January 5, 2018

Source:https://www.cancercompass.com/cancer-news/article/60395.htm

(HealthDay News) -- While there is no sure way to avoid lung cancer, there are steps you can take to reduce your risk.

Smoking contributes to 80 to 90 percent of lung cancer deaths, according to the American Lung Association.

Men who smoke have a 23 times increased risk of lung cancer. And exposure to secondhand smoke causes approximately 7,330 lung cancer deaths among nonsmokers in the United States every year.

So, if you've never smoked, don't start. If you do smoke, try to quit. Talk to your doctor about methods and aids to help you quit. These include nicotine replacement products, medications and support groups, according to UPMC Pinnacle, part of the University of Pittsburgh Medical Center health care system.

To boost your stop-smoking resolve, the health care system recommends the following steps:

·         Set a quit date to solidify your commitment to quitting. Make it a significant date, such as a birthday or anniversary.

·         Prepare for your quit day by getting rid of all tobacco products from your home, car and workplace. Think about things you can do to take your mind off smoking during the first month, when your risk of relapse is high.

·         Give yourself daily reminders about why you want to quit.

·         Create a support system. Find a friend who also wants to quit smoking. If that's not possible, ask family and friends to help keep you on track. Support groups are another option.

·         If you're a nonsmoker, avoid secondhand smoke. If you live or work with smokers, encourage them to quit. If they can't quit, ask them to smoke outside. Avoid areas where people smoke and ask to be seated in the nonsmoking section when you go to restaurants and bars.

·         Have your home checked periodically for seepage of radon gas, especially if you live in an area where radon is a known problem. Your local public health department or local chapter of the American Lung Association can provide more information on radon testing.

·         Avoid known carcinogens. If you work around cancer-causing materials, take measures to protect yourself and follow your employer's posted precautions. For example, if you're given a face mask, wear it. It's also a good idea to talk to your doctor about how to protect yourself at work.

·         Eat plenty of fruits and vegetables. That's far better than taking large doses of vitamin pills, which can do more harm than good.

·         Get regular exercise. If you haven't been active, start slowly.

·         Get lung cancer screenings. That's especially important if you're at high risk. That includes people ages 55-79 who have smoked the equivalent of one pack daily for 30 years. Also included: people 55-79 who have smoked the equivalent of one pack daily for 20 years and who have one additional risk factor, including radon or asbestos exposure, cancer history, strong family history of lung cancer, significant secondhand smoke exposure, chronic obstructive pulmonary disease (COPD) or pulmonary fibrosis.


Mechanism for resistance to immunotherapy treatment discovered

Published: January 4, 2018

Source:https://www.sciencedaily.com/releases/2018/01/180104153444.htm

An urgent question for cancer scientists is why immunotherapy achieves dramatic results in some cases but doesn't help most patients. Now, two research groups from Dana-Farber Cancer Institute have independently discovered a genetic mechanism in cancer cells that influences whether they resist or respond to immunotherapy drugs known as checkpoint inhibitors.

The scientists say the findings reveal potential new drug targets and might aid efforts to extend the benefits of immunotherapy treatment to more patients and additional types of cancer.

The discoveries are detailed in two articles published by the journal Science.

One report, focusing on clinical trial patients with advanced kidney cancer treated with checkpoint inhibitors, is from scientists at Dana-Farber Cancer Institute and the Broad Institute of MIT and Harvard, led by Eliezer Van Allen, MD, of Dana-Farber and the Broad, and Toni Choueiri, MD, director of the Lank Center for Genitourinary Oncology at Dana-Farber.

The second report, identifies the immunotherapy resistance mechanism in melanoma cells, is from a group led by Kai Wucherpfennig, MD, PhD, director of Dana-Farber's Center for Cancer Immunotherapy Research, and Shirley Liu, PhD, of Dana-Farber.

The two groups converged on a discovery that resistance to immune checkpoint blockade is critically controlled by changes in a group of proteins that regulate how DNA is packaged in cells. The collection of proteins, called a chromatin remodeling complex, is known as SWI/SNF; its components are encoded by different genes, among them ARID2, PBRM1, and BRD7. SWI/SNF's job is to open up stretches of tightly wound DNA so that its blueprints can be read by the cell to activate certain genes to make proteins.

Researchers led by Van Allen and Choueiri sought an explanation for why some patients with a form of metastatic kidney cancer called clear cell renal cell cancer (ccRCC) gain clinical benefit -- sometimes durable -- from treatment with immune checkpoint inhibitors that block the PD-1 checkpoint, while other patients don't.

The scientists' curiosity was piqued by the fact that ccRCC differs from other types of cancer that respond well to immunotherapy, such as melanoma, non-small cell lung cancer, and a specific type of colorectal cancer. Cells of the latter cancer types contain many DNA mutations, which are thought to make distinctive "neoantigens" that help the patient's immune system recognize and attack tumors, and make the cancer cells' "microenvironment" hospitable to tumor-fighting T cells. By contrast, ccRCC kidney cancer cells contain few mutations, yet some patients even with advanced, metastatic disease respond well to immunotherapy.

To search for other characteristics of ccRCC tumors that influences immunotherapy response or resistance, the researchers used whole-exome DNA sequencing to analyze tumor samples from 35 patients treated in a clinical trial with the checkpoint blocker nivolumab (Opdivo). They also analyzed samples from another group of 63 patients with metastatic ccRCC treated with similar drugs.

When the data was sorted and refined, the scientists discovered that patients who benefited from the immunotherapy treatment with longer survival and progression-free survival were those whose tumors lacked a functioning PRBM1 gene. (About 41 percent of patients with ccRCC kidney cancer have a non-functioning PBRM1 gene.) That gene encodes a protein called BAF 180, which is a subunit of the PBAF subtype of the SWI/SNF chromatin remodeling complex.

Loss of the PBRM1 gene function caused the cancer cells to have increased expression of other genes, including gene pathway known as IL6/JAK-STAT3, which are involved in immune system stimulation.

While the finding does not directly lead to a test for immunotherapy response yet, Choueiri said, "We intend to look at these specific genomic alterations in larger, randomized controlled trials, and we hope that one day these findings will be the impetus for prospective clinical trials based on these alterations."

In the second report, the scientists led by Wucherpfennig came at the issue from a different angle. They used the gene-editing CRISPR/Cas9 technique to sift the genomes of melanoma cells for changes that made tumors resistant to being killed by immune T cells, which are the main actors in the immune system response against infections and cancer cells. The search turned up about 100 genes which appeared to govern melanoma cells' resistance to being killed by T cells. Inactivating those genes rendered the cancer cells sensitive to T-cell killing. Narrowing down their search, the Wucherpfennig team identified the PBAF subtype of the SWI/SNF chromatin remodeling complex -- the same group of proteins implicated by the Van Allen and Choueiri team in kidney cancer cells -- as being involved in resistance to immune T cells.

When the PBRM1 gene was knocked out in experiments, the melanoma cells became more sensitive to interferon-gamma produced by T cells, and in response produced signaling molecules that recruited more tumor-fighting T cells into the tumor. The two other genes in the PBAF complex -- ARID2 and BRD7 -- are also found mutated in some cancers, according to the researchers, and those cancers, like the melanoma lacking ARID2 function, may also respond better to checkpoint blockade. The protein products of these genes, the authors note, "represent targets for immunotherapy, because inactivating mutations sensitize tumor cells to T-cell mediated attack." Finding ways to alter those target molecules, they add, "will be important to extend the benefit of immunotherapy to larger patient populations, including cancers that thus far are refractory to immunotherapy."


Virus could treat brain tumours by boosting immune system

Published: January 3, 2018

Source:https://medicalxpress.com/news/2018-01-virus-brain-tumours-boosting-immune.html

A virus injected directly into the bloodstream could be used to treat people with aggressive brain tumours, a major new study reports.

Scientists have found that the naturally occurring virus could act as an effective immunotherapy in patients with brain cancer or other cancers that have spread to the brain.

They showed that a type of virus called reovirus could cross the blood-brain barrier to reach tumours, where it replicates and kills the cancer cells.

They also found that the virus was able to 'switch-on' the body's own defence systems to attack the cancer.

The findings are published in the journal Science Translational Medicine.

The study authors, from the University of Leeds and The Institute of Cancer Research in London, believe reovirus therapy could be used in conjunction with other cancer therapies to make them more potent - and a clinical trial is currently underway.

Because the virus infects cancer cells and leaves healthy cells alone, patients receiving the treatment reported only mild flu-like side effects.

Up to now, scientists thought it was unlikely that the virus would be able to pass from the blood into the brain because of the blood-brain barrier, a protective membrane around the brain.

That would have meant that the only way they could get the virus into the brain was to inject it directly into the brain - which is challenging, would not be suitable for all patients, and cannot be regularly repeated.

But the research demonstrated that the virus could be administered through a single-dose intravenous drip.

Nine patients took part in the study which led to the publication of the new research. They had cancers that had either spread to the brain from other parts of the body or were fast-growing gliomas, a type of brain cancer that is difficult to treat, and has a poor prognosis.

All patients were due to have the tumours removed surgically. But in the days before the surgeons operated, the patients were given the virus drip.

Once the tumours were removed, samples were taken and analysed for signs that the virus had been able to reach the cancer, sometimes deep within the brain. In all nine patients, there was evidence that the virus had reached its target.

The researchers also found that the presence of reovirus stimulated the body's own immune system, with white blood cells or 'killer' T-cells being attracted to the tumour site to attack the cancer.

Tissue samples from patients who had surgery but not the virus therapy served as a control.

When compared with the control samples, the tissue taken from the people who had received the reovirus had higher levels of interferons, proteins that 'switch-on' the body's immune system.

Dr Adel Samson, co-lead author and medical oncologist at the Leeds Institute of Cancer and Pathology, at the University of Leeds, said: "This is the first time it has been shown that a therapeutic virus is able to pass through the brain-blood barrier, and that opens up the possibility this type of immunotherapy could be used to treat more people with aggressive brain cancers.

"This study was about showing that a virus could be delivered to a tumour in the brain. Not only was it able to reach its target, but there were signs it stimulated the body's own immune defences to attack the cancer."

Co-lead author Alan Melcher, Professor of Translational Immunotherapy at The Institute of Cancer Research, London, said: "Our immune systems aren't very good at 'seeing' cancers—partly because cancer cells look like our body's own cells, and partly because cancers are good at telling immune cells to turn a blind eye. But the immune system is very good at seeing viruses.

"In our study, we were able to show that reovirus could infect cancer cells in the brain. And, importantly, brain tumours infected with reovirus became much more visible to the immune system.

"This small-scale clinical trial allowed us to ask a crucial biological question about cancer immunotherapy and gain insights which can now be tested further, both in the laboratory and in the clinic.

"Now we know we can get reovirus across the blood-brain barrier, we have begun clinical studies to see just how effective this viral immunotherapy can be at extending and improving the lives of patients with brain tumours, who currently have very limited treatment options available to them.

Clinical trial already underway

The findings of the research based on the initial nine-person study are already being applied in a clinical setting.

In a world first, a new trial has started where patients will be given reovirus in combination with the standard treatment of radiotherapy and chemotherapy which follows surgery.

One patient with a form of brain cancer called glioblastoma is already receiving the combined therapy. In the months following removal of the tumour, he will receive a total of 16 doses of virus alongside chemotherapy and radiotherapy.

Although the earlier trial demonstrated that the reovirus was reaching the cancer cells after just a single dose, doctors have decided to give it repeatedly to patients because of the way it 'kick starts' the body's own defences.

The trial is being led by Susan Short, Professor of Clinical Oncology at the University of Leeds. She said: "The presence of cancer in the brain dampens the body's own immune system. The presence of the reovirus counteracts this and stimulates the defence system into action.

"Our hope is that the additional effect of the virus on enhancing the body's immune response to the tumour will increase the amount of tumour cells that are killed by the standard treatment, radiotherapy and chemotherapy."

She added: "Brain cancer is a devastating disease. For a long time, there have not been many new developments that we could offer patients but the research that is happening at the University Leeds and elsewhere is beginning to offer a new approach."

The Leeds-led trial will identify if the combined therapy can be tolerated by patients and whether it is toxic. But Prof Short says the longer term aim, in wider partnership with other UK research centres, is to see if the virus makes the standard treatment more effective.

Sarah Lindsell, chief executive of The Brain Tumour Charity which co-funded the research, said: "Brain tumours cost too many lives. The only way to change that is through research. This news from the University of Leeds and the Institute of Cancer Research will be welcomed by all of those who know only too well the devastation caused by this cruel disease."

According to figures from Cancer Research UK, almost 11,000 new cases of primary brain cancers are diagnosed in the UK each year. Only 14 percent of patients survive for 10 years or more years following a diagnosis of a primary or malignant brain tumour.


6 Steps to a Healthier You

Published: January 2, 2018

Source:https://www.cancercompass.com/cancer-news/article/60371.htm

(HealthDay News) -- As one year ends and another begins, people often assess their habits and lifestyle, and consider changes that could improve their health.

But what, exactly, should you do?

Here are six steps you can take to enhance your well-being, according to doctors from the University of California, Los Angeles (UCLA):

1. Keep a personal health calendar.

"In our busy lives, we hardly pay attention to our health, and most health issues start with subtle symptoms that we fail to follow," Dr. Aparna Sridhar said in a UCLA news release. She's an assistant professor of obstetrics and gynecology at the university's David Geffen School of Medicine.

"In fact, most patients with illness cannot pinpoint when symptoms started and if there was any association with life events," Sridhar said. "By maintaining a health calendar and jotting down symptoms, medications and mood changes, patients will be able to identify abnormalities sooner and seek care."

2. Eat more fruits and vegetables.

"A number of chronic diseases, including obesity, diabetes, cardiovascular diseases and stroke, have an identified association with diet," UCLA dietitian Dana Hunnes said in the news release. She's senior dietitian at the Ronald Reagan UCLA Medical Center.

"If each of us shifts to a more plant-based diet -- filled with vegetables, whole grains, legumes, nuts, seeds, fruits and other produce -- we can not only potentially lower our risk for these diseases, but we can also be healthier and potentially live longer," Hunnes said. She noted that diets low in animal protein are also linked with greater longevity.

3. Cook at home rather than eat out.

"People who cook at home eat a healthier, more nutritionally dense diet," said Erin Morse, chief clinical dietitian at UCLA Health. "With obesity escalating and contributing to other serious health issues -- like diabetes, heart disease and high blood pressure -- cooking at home is a vastly underutilized tool patients can use to achieve their nutrition goals."

Morse noted that the food served at restaurants usually has less fiber and a lot more salt, sugar, fat and processed carbohydrates than home-cooked meals.

4. Support healthy gut bacteria.

"For better health overall, you not only need to feed your own human cells, but you also need to feed all the microbes that live on you and inside you -- including the gut microbiome," Dr. Zhaoping Li, director of the UCLA Center for Human Nutrition, said in the news release.

"The best foods for these microbes are plant-based foods and drinks," she said.

5. Don't underestimate the benefits of healthy lifestyle changes.

"Certain lifestyle choices are far more integral to your health than any doctor's visit," said Dr. John Mafi. He's an assistant professor of medicine at the David Geffen School of Medicine at UCLA.

"To promote general well-being, mom's advice isn't far off: Eat mostly fresh vegetables, fruits and whole grains; get at least seven or eight hours of sleep per night; reduce your work stress; make time to exercise and get outdoors; and spend quality time with close friends and family," Mafi said.

"The research behind each of these activities clearly demonstrates their benefits to your health," he added.

6. Don't neglect your sinus passages.

"Patients with allergies and sinus problems should be rinsing their sinuses regularly with saline, a surprisingly effective method for controlling symptoms that accomplishes several things," said Dr. Marilene Wang. She's a professor of head and neck surgery at the David Geffen School of Medicine.

Rinsing clears particles and other irritants -- like pollen and smog -- from the nose and sinus passages, Wang said. This can help ease troubling symptoms, including congestion and swelling.

Rinsing the sinuses also thins the mucus and moisturizes the inside of the nose. Nasal membranes "can be very inflamed and sensitive from allergies and infections," she said.

Most drug stores sell sinus rinse kits without a prescription.


Head and neck cancer: Acid reflux may raise risk in seniors

Published: December 30, 2017

Source:https://www.medicalnewstoday.com/articles/320446.php

New research investigates whether the common acid reflux is a risk factor for head and neck cancer in elderly people.

Dr. Edward D. McCoul, at the Tulane University School of Medicine in New Orleans, LA, and colleagues led the new study.

Their findings were published in JAMA Otolaryngology: Head & Neck Surgery.

As they say, cancers of the upper aerodigestive tract (UADT) include malignancies of the larynx, tonsils, and sinuses, among others. Worldwide, these cancers account for more than 800,000 yearly diagnoses of cancer and more than 360,000 yearly deaths.

In the United States, it is estimated that 62,000 people develop head and neck cancers every year, which include oral cavity and larynx malignancies.

There are several factors that are potentially accountable for these cancers, write Dr. McCoul and colleagues, including the use of alcohol and tobacco, viral infections, and chronic inflammation of the upper airways.

But existing studies that have examined the link between the gastroesophageal reflux disease — commonly known as acid reflux or heartburn — and UADT cancers have yielded mixed results.

Additionally, this association has not yet been studied in the elderly U.S. population. So, Dr. McCoul and colleagues set out to examine it.

In the U.S., it is estimated that acid reflux affects as much as 20 percent of the population. Adults with obesity and the elderly are particularly prone to the condition, studies show.

Acid reflux may raise laryngeal cancer risk

To study the link between head and neck cancers and acid reflux, the researchers examined data on 13,805 people aged 66 and above who had been diagnosed with UADT cancer, as well as 13,805 age- and sex-matched healthy controls.

Dr. McCoul and team obtained the data from the Surveillance, Epidemiology, and End Results (SEER)-Medicare database.

The cancer patients — 3,418 of whom were women — had been diagnosed with "malignancy of the larynx, hypopharynx, oropharynx, tonsil, nasopharynx, and paranasal sinuses." In fact, over 60 percent of the patients had laryngeal cancer.

The study revealed a strong association between acid reflux and cancer of the throat, tonsils, and paranasal sinuses.

Of these, "The strongest association between [acid reflux] and the presence of malignancy was seen in the larynx," write the study authors.

They go on to summarize the key findings:

"These data suggest that elderly patients with [acid reflux] in the United States are 3.47, 3.23, 2.88, and 2.37 times as likely as those without [acid reflux] to be diagnosed with laryngeal, hypopharyngeal, oropharyngeal, and tonsillar cancers, respectively."

Strengths and limitations of the study

The researchers acknowledge both some of the strengths and some of the weaknesses of their study.

"This longitudinal population-based study," the authors write, "is the first to examine the association between [acid reflux] and the development of UADT malignancies in an elderly population in the United States 66 years and older."

Also, the fact that this was a population-based study with a large sample recruited from a database renowned for its accuracy is a further strength of the study, making the findings generalizable to the elderly U.S. population.

However, the SEER-Medicare database is also known to have some limitations. For one thing, it does not include data about tobacco and alcohol use, which are known risk factors for UADT cancer.

Finally, the research cannot establish a causal relationship, as it is purely an observational study. In this regard, further studies are needed to examine causality, write the researchers, as well as to test the findings in a younger cohort.


Food preserving chemicals linked to hormone disruption and obesity, according to new study

Published: December 29, 2017

Source:https://www.naturalnews.com/2017-12-29-food-preserving-chemicals-linked-to-hormone-disruption-obesity.html

(Natural News) Most people are aware that the chemicals found in food preservatives are rather unhealthy. Even those who continue to eat such foods generally realize on some level that they are not doing their bodies any favors. However, a new study shows that such chemicals are not just toxic; they could also be the reason people are piling on the pounds.

Animal studies have pointed to the link between preservatives in breakfast cereals and other foods and obesity in the past, but this is the first time such findings have been confirmed in humans. In a study published in the Nature Communications journal, researchers from Cedars-Sinai Medical Center used a new protocol to test the effects of endocrine disruptor chemicals on humans.

Three chemicals commonly found in everyday life were tested in the study. The first, butylhydroxytoluene (BHT), is an antioxidant that is added to many popular breakfast cereals and other foods in order to keep the fats in them from becoming rancid and to protect their nutrients. It’s so toxic that it’s banned from food in several European countries, but it can still be found in American cereals.

The second chemical studied, perfluoroctanoic acid (PFOA) is a polymer that is used in carpeting and cookware, along with many other products. The compound tributyltin (TBT), which is found in paints and often makes its way to water, where it accumulates in seafood, was also studied.

According to the researchers, each of the chemicals studied damaged the hormones that send communications between the brain and the gut, and when all three are present, their effect is heightened. Among the three chemicals studied, BHT had the most negative effect.

For their study, the researchers took blood samples from adults and introduced reprogramming genes that converted the cells to induced pluripotent stem cells. These stem cells were then used to grow epithelium tissue, which is what lines the human gut and the neuronal tissues in the hypothalamus, the part of the brain responsible for regulating metabolism and appetite.

Next, they exposed these tissues to the three chemicals individually and in combination to observe what occurred. The chemicals were observed disrupting the networks that help signaling hormones make their way safely out of cells, and they also damaged the cellular structures responsible for converting food and oxygen into energy, the mitochondria.

Interference with signals to stop eating when full

Their findings indicate that exposure to these chemicals on a regular basis can affect the signals the digestive system sends to the brain to tell people that their hunger has been satisfied and they should stop eating. It is when this signaling system stops working properly that people continue eating even though they are full, thereby gaining weight.

With more than a third of American adults now considered obese, this is useful information that can help guide food decisions in those looking to lose some weight. Moreover, the new testing system could offer a very useful, affordable and safe method for evaluating how the many chemicals in our environment affect our health.

Over 80,000 chemicals are currently registered for use in America in everyday items ranging from food and personal care items to lawn care products and household cleaners. The U.S. Department of Health and Human Services’ National Toxicology Program states that the effects of a lot of these chemicals on human health are unknown.

Ethical issues surrounding the exposure of human subjects to substances that could be harmful are a big obstacle when it comes to testing chemical safety, so this new approach could prove significant in helping to properly assess the chemicals people are exposed to on a regular basis.


Can e-cigarettes help smokers quit?

Published: December 29, 2017

Source:https://www.sciencedaily.com/releases/2017/12/171229135258.htm

As e-cigarettes become more popular, fewer people are taking up smoking traditional cigarettes. But can e-cigarettes, an electronic nicotine delivery system, help people quit smoking altogether? That was the focus of a recent study led by a Hollings Cancer Center researcher.

The study found that smokers who are willing to use e-cigarettes tend to smoke less and have increased quit attempts, said Matthew Carpenter, Ph.D., a tobacco control and addiction expert at the cancer center at the Medical University of South Carolina (MUSC).

"Combustible cigarettes are the most harmful form of nicotine delivery. Alternative delivery of nicotine, through e-cigarettes, could significantly reduce harm and the risks of cancer and other diseases to smokers," he said.

In the pilot study, funded by the National Institutes of Health, Carpenter evaluated e-cigarettes in terms of usage, product preference, changes in smoking behaviors and nicotine exposure. Sixty-eight smokers were evaluated: 46 were randomized to use e-cigarettes however they wished, and 22 were randomized to a control group.

Those in the e-cigarette group were given a device with either high or low doses of nicotine. Everyone was followed over a period of four months. The study was published in Cancer Epidemiology, Biomarkers & Prevention in November and is one of the few randomized studies in the U.S. to examine the effects of e-cigarettes and quit attempts.

Results showed that when smokers were given e-cigarettes without any accompanying instructions or requirements for use, uptake was strong, and many participants went on to purchase their own e-cigarettes. This suggests that e-cigarettes might give smokers a suitable alternative to combustible cigarettes. Those who used e-cigarettes smoked less and were more likely to quit smoking, as compared to those in the control group.

"The results are consistent with trials done outside the U.S.," Carpenter said. "Many people rated the e-cigarettes similar to their usual product, which further suggests that these products might promote switching. Anything that gets smokers off combustible cigarettes is a good thing."

Of the two e-cigarette models used in the study, the more powerful device, with a higher dose of nicotine, showed stronger outcomes. People using e-cigarettes throughout the study smoked an average of 37 percent fewer cigarettes, showing a positive effect when making the switch and potentially serving as a tool to help smokers quit.

That's good news for Carpenter and his colleagues at the Hollings Cancer Center. Smoking is the leading cause of cancer and has a negative impact on the effectiveness of cancer treatments. People who quit smoking, regardless of their ages, have substantial gains in life expectancy compared with those who continue to smoke.

Carpenter cautions that while e-cigarettes may help people smoke less or even quit, they are not for everyone. "It is important to protect non-smokers, particularly adolescents and young adults, from starting any nicotine-containing product. This is something we need to really guard against."

E-cigarettes are sometimes seen as a gateway to conventional cigarettes, the most harmful form of nicotine delivery. Studies have shown that e-cigarettes offer significantly less exposure to harmful toxicants, as compared to traditional cigarettes. "We know e-cigarettes are safer than traditional cigarettes, but that doesn't mean e-cigarettes are completely safe." says Carpenter.

More than 1,500 varieties of e-cigarettes are now available, including different looks, high-tech power settings and many flavors, which can make them more appealing to kids. Newer devices can be customized in many ways that will draw in more smokers, but that means they also can entice kids, he said.

"We've gotten very good at the public health messaging of conventional smoking and prevention efforts for adolescents, but now kids see a new technology-based product that is supposedly safer, flavored and isn't a cigarette. These are all these things that raise our alarm bells for adolescents, and, in fact, e-cigarettes are more popular than conventional cigarettes among youth."

E-cigarettes were only recently regulated by the Food and Drug Administration. Largely manufactured overseas, the quality control process varies, he says. Without enough information to answer the long-term public health issues of e-cigarettes, researchers like Carpenter are aware of the importance of further studies on the latest tobacco trends. Combustible cigarettes have been around for many decades. E-cigarettes have not, and the science has a lot of questions left to answer, he said.


New understanding of why cancer cells move

Published: December 28, 2017

Source:https://www.sciencedaily.com/releases/2017/12/171228100918.htm

A University of Hawai'i Cancer Center researcher has identified how some cancer cells are made to move during metastasis. The research provides a better understanding of how cancer spreads and may create new opportunities for cancer drug development.

Metastasis causes the deaths of 90 percent of cancer patients. The spread of cancer by metastasis is driven by a set of mutant proteins called oncogenes which cause cancer cells to multiply uncontrollably and promotes their ability to move. How oncogene activity specifically directs the increased movement and metastasis is highly complex and remains largely unknown.

Joe W. Ramos, PhD, deputy director of the UH Cancer Center and collaborators focused on investigating how these oncogenes and related signals lead to dysregulation of normal processes within the cell and activate highly mobile and invasive cancer cell behavior.

The findings, published in Proceedings of the National Academy of Sciences (PNAS), define a mechanism in which the oncogenes turn on a protein called RSK2 that is required for cancer cells to move. Ramos and colleagues found that the RSK2 protein forms a signaling hub that includes proteins called LARG and RhoA. They show that turning on this signaling hub activates the movement of the cancer cells. These results significantly advance understanding of how cancer cells are made to move during metastasis and may provide more precise targets for drugs to stop cancer metastasis in patients where there are oncogenic mutations.

"These new data are very exciting. Blocking cancer invasion and metastasis remains a central challenge in treating patients. We anticipate that this research may lead to new therapeutic opportunities for brain tumors, melanoma, and breast cancer among others. We are currently focused on these opportunities and developing new compounds to target this signaling hub," said Ramos.

The work was done in collaboration with Michelle L. Matter, PhD, UH Cancer Center researcher in the Cancer Biology Program.


Pet Dogs May Speed Human Brain Cancer Trials

Published: December 26, 2017

Source:https://www.cancercompass.com/cancer-news/article/60332.htm

Man's best friend may help scientists learn more about a deadly brain cancer in people.

Both dogs and humans can develop glioblastoma. Half of people diagnosed with this type of brain cancer live fewer than 14 months, even after treatment with surgery, radiation and chemotherapy.

Sen. John McCain is being treated for glioblastoma and Sen. Ted Kennedy died from the disease in 2009.

Dogs currently have few treatment options for the cancer. Typically, they are euthanized shortly after diagnosis.

A new five-year research project at the University of Minnesota will include pet dogs with glioblastoma. The goal is to find ways to improve treatment of dogs with this type of cancer, said Dr. Liz Pluhar, a professor of veterinary surgery, and her colleagues.

That could lead to new information about glioblastoma that could prove useful in human clinical trials, according to the researchers.

Previously, this team experimented with vaccines made from a dog's own tumor cells and with gene therapy. While both approaches prolonged survival for many dogs, the cancer eventually returned.

This new project will include at least 30 pet dogs with glioblastoma. It seeks to increase understanding of the disease and improve the effectiveness of vaccination and gene therapy.


Multifunctional protein contributes to blood cell development

Published: December 22, 2017

Source:https://www.sciencedaily.com/releases/2017/12/171222090310.htm

Like an actor who excels at both comedy and drama, proteins also can play multiple roles. Uncovering these varied talents can teach researchers more about the inner workings of cells. It also can yield new discoveries about evolution and how proteins have been conserved across species over hundreds of millions of years.

In a new finding, a team of investigators from the Salk Institute has uncovered in mouse cells a previously unknown job for a protein called nup98. In addition to helping control the movement of molecules in and out of the nucleus of the cell, they found that it also helps direct the development of blood cells, enabling immature blood stem cells to differentiate into many specialized mature cell types. Further, they discovered the mechanism by which -- when perturbed -- this differentiation process can contribute to the formation of certain types of leukemia. The findings are published in Genes & Development.

"This research was really a tour de force," says Martin Hetzer, Salk's Chief Science Officer and the study's senior author. "Tobias Franks, my postdoctoral researcher at the time and the paper's first author, used an approach that combined genomics, proteomics, and cell biology. This model wasn't easy to study, and he developed some very clever techniques in the lab to answer these questions."

For years, Hetzer's lab has focused on a class of proteins called nucleoporins (nups for short), which are part of the nuclear pore complex. This complex regulates traffic between the nucleus of the cell, where the genetic material is located, and the cytoplasm, which contains other cellular structures. There are about 30 proteins in the nucleoporin family, and they carry out a number of different functions in addition to forming the nuclear pore. Several of them are known to act as transcription factors: This means they help to regulate when and how genes get translated into proteins.

The finding that nup98 has this additional function was not entirely unexpected. Earlier research from Hetzer's lab had found that it plays a role in gene regulation in other cell types. But the team didn't know about its function in hematopoietic (blood) cells.

In addition, until now the mechanism of how nup98 regulates transcription was not known. The investigators found that it acts through a link with a protein complex called Wdr82-Set1/COMPASS, which is part of the cell's epigenetic machinery. "This epigenetic process helps to control when genes are transcribed into proteins and when transcription is blocked," says Hetzer, who also holds the Jesse and Caryl Phillips Foundation Chair.

Another thing that was different about this study is that it was done in mouse cells rather than simpler model organisms like yeast and fruit flies. "This is the first mechanistic insight of how one of these nup proteins works in mammals," Hetzer adds. "We have only touched the surface here in uncovering how this evolutionarily conserved mechanism works in mammalian cells." Future work in his lab will extend the study of nup98 to primates and humans.

While Hetzer has no immediate plans to pursue their findings as an avenue for developing leukemia drugs, he says it's likely that others may pick up on this aspect of the research. Disruption of the cell differentiation process that contributes to leukemia results from a single gene fusion, when two parts of chromosomes that are not meant to act on each other become linked. He says that cancers driven by a single genetic change like this have proven easier to block with drugs than cancer driven by multiple genetic alterations.


Chronic Heartburn Tied to Higher Odds for Head, Neck Cancers

Published: December 21, 2017

Source:https://www.cancercompass.com/cancer-news/article/60321.htm

(HealthDay News) -- Millions of American seniors suffer the discomfort of chronic acid reflux. Now, new research suggests the condition might raise their odds for even more dangerous foes -- head and neck cancers.

The research can't prove cause-and-effect, and the odds of any one person with chronic heartburn developing one of these relatively rare cancers remains low, experts noted.

But the study of nearly 28,000 Americans over the age of 65 did show a heightened risk.

Overall, a history of gastroesophageal reflux disease (GERD) -- the clinical term for chronic heartburn -- was linked to nearly triple the odds of developing cancers of the voice box (larynx); about a 2.5 greater odds for cancers of the pharynx (top of the throat); a doubling of risk for cancers of the tonsils; and a 40 percent higher odds for cancers in the sinuses.

Head and neck cancers of the respiratory and upper digestive tracts cause more than 360,000 deaths worldwide each year, the researchers noted.

The new study was led by Dr. Edward McCoul, of the Ochsner Clinic Foundation in New Orleans, and published Dec. 21 in the journal JAMA Otolaryngology Head & Neck Surgery.

One gastroenterologist said the findings aren't surprising, given what's known about the effect of acid reflux on sensitive tissues.

"Reflux material from the stomach can rise high in to the esophagus, the food tube between the mouth and the stomach," explained Dr. Anthony Starpoli. He said the same juices "can invade the throat, sinus passages and the lungs, causing [chronic] inflammation."

The link between GERD and another tumor type, esophageal cancer, is already well-known, said Starpoli, associate director for esophageal endotherapy at Lenox Hill Hospital in New York City.

In the new study, McCoul's team tracked data from 13,805 U.S. seniors who'd had cancers of the respiratory and upper digestive tracts between 2003 and 2011. Their medical histories were then compared to the same number of similarly aged people without cancer.

While the study found an association between GERD and head-and-neck cancers, McCoul's team stressed that the data they sourced did not include information about each patient's smoking and drinking history. Both of those habits are major risk factors for head and neck cancers, the study authors noted, so more investigation is needed to tease out the findings.

Dr. David Hiltzik directs otolaryngology at Staten Island University Hospital in New York City. Reading over the findings, he agreed that the study wasn't designed to prove cause-and-effect.

But Hiltzik believes chronic heartburn remains a potential carcinogen and needs to be treated when it occurs.

"We know clinically that acid reflux causes problems throughout life in these areas in the head and neck," he said. "This study reinforces the fact that we need to address these issues early and perhaps more aggressively. I believe patients should be more aware of how their daily diet and behavioral habits can have serious long-term effects."


How gum disease affects your overall health: Bacteria from your mouth enters your blood, then contributes to diseases such as cancer

Published: December 21, 2017

Source:https://www.naturalnews.com/2017-12-21-how-gum-disease-affects-your-overall-health-bacteria-from-your-mouth-enters-your-blood-contributes-to-diseases-such-as-cancer.html

(Natural News) Here’s something to make you check your teeth today: Bacteria in the mouth have long been known to cause various diseases in other parts of the body. While saliva may serve as the first line of defense against unwanted contaminants, some bacteria may be tougher to break down. A study from the Federal University of Santa Maria in Brazil found that gum disease caused by certain bacteria increases the risk of breast cancer in women by up to three times.

Some bacteria cause bad breath, while others can cause inflammation in the mouth. When these bacteria infiltrate the gums, they may pose the risk of entering the circulatory system, and travel to other parts of the body. These bacteria also cause periodontitis, a severe gum infection that damages soft tissues and destroys the teeth. Periodontitis can cause your gums to loosen up and result in tooth loss. Moreover, these bacteria can infect other soft tissues in the body such as breast tissue.

The study, led by Dr. Nigel Carter of the Oral Health Foundation, enlisted 201 women, 67 of which had breast cancer. Individual information was gathered, such as medical history and lifestyle habits, including smoking and alcohol consumption. All of the participants were evaluated for gum inflammation. The findings of the study, published in the Journal of Community Dentistry and Oral Epidemiology, stated that the women with severe gum infections were three times more likely to have breast cancer. Dr. Carter’s research is important because it creates another point of view in identifying the cause of diseases, in this case, starting in the mouth. The researchers involved in the study call for more studies to be done to be able to associate oral diseases with whole body diseases fully.

It’s good to have pearly white teeth and fresh-smelling breath, but taking care of your mouth, teeth, and gums, may be more beneficial than you think. Practicing good oral hygiene not only provides you with higher self-esteem but also helps prevent diseases such as breast cancer and heart disease. Preventing oral diseases and infections is one of the easiest methods in keeping healthy. Here are some tips to guide you towards excellent oral health.

Book an appointment – Visit your dentist one to two times annually for a check-up. Dentists can help identify if you have infections or inflammations that need to be treated. Furthermore, you can also get an oral prophylaxis, or oral cleansing, to remove tartar and plaque build-up on your teeth and inside your gums. This way, the bacteria that cannot be removed with a regular toothbrush may be eliminated.

Brush, brush, brush – Your mom always told you to brush your teeth at least three times a day. It may be a hassle at times, but you’ll benefit from it anyway. Make sure to use natural toothpaste (you can make your own) as much as possible. Fluoride, which is found in almost all commercial toothpaste, is a health risk and must be avoided as much as possible. Also, replace your toothbrush every three to four months.

Don’t forget the tongue– Most people focus only on brushing the teeth, but don’t forget your gums and tongue too! No matter how much you scrub those pearly whites, bacteria may still reside on your tongue and in the crevices of your gums, so make sure to focus on those as well.

Strings attached – After brushing your teeth (and gums and tongue), get some floss and work your way in between those teeth. Toothbrush bristles are often too thick to fit in between teeth, and this would be the job of the floss. You’ll find satisfaction in removing that stubborn food debris from yesterday’s dinner.

Eat your fruits and vegetables – This is as natural as you can get – fruits and vegetables are rich in vitamins and minerals that keep disease-causing bacteria away. Citrus fruits, such as oranges and lemons are acidic and can disintegrate bacteria that your saliva can’t. Furthermore, the fibers in these fruits and vegetables help clean the surface of your teeth, your gums, and your tongue. Don’t forget to munch on an apple today!


Cancer Survivors Often Face Another Hurdle: Faster Aging

Published: December 19, 2017

Source:https://www.cancercompass.com/cancer-news/article/60286.htm

(HealthDay News) -- Treatments that help people beat cancer also can cause them to age prematurely and die sooner, Mayo Clinic researchers report.

Cancer survivors naturally age faster than others who haven't had cancer, and are more likely to develop long-term health problems related to aging while they're still relatively young, the study authors said.

These ailments can include hormone and gland disorders, heart problems, brittle bones, lung scarring and new cancers. Survivors also are more likely to become frail as the years pass.

Childhood cancer survivors' estimated life expectancy is 30 percent lower than that of the general population, and they are three to six times more likely to develop a second cancer, the researchers noted.

With the number of cancer survivors growing, the medical profession needs to start paying more attention to how to keep these people healthy throughout their now-extended lifetimes, said senior researcher Dr. Shahrukh Hashmi. He is an assistant professor of medicine at the Mayo Clinic in Rochester, Minn.

"We are now beginning to see the gravity of a multitude of complications among cancer survivors," Hashmi said. "There is an essential and immediate need for formal cancer survivorship programs to prevent complications in millions of cancer survivors."

Currently there are about 30 million cancer survivors worldwide, but researchers predict that about 19 million new cancer diagnoses will be made every year by 2025. Many of those people will survive their cancer, only to face long-term health consequences.

According to Dr. Charles Shapiro, director of cancer survivorship programs at the Tisch Cancer Institute at Mount Sinai, in New York City, "We're now struggling with our own success. This only comes up as a product of how well we're doing in terms of cancer mortality and increasing the population of survivors. Now we have to deal with the consequences. Sure, you're alive and that's great, but there are consequences."

Harsh chemotherapy and radiation therapy kill off cancer cells, but they also damage normal healthy tissues, Hashmi and colleagues explained. This diminishes the body's natural resilience.

Other drugs used in cancer treatment also appear to contribute to accelerated aging. These drugs can include steroids, hormone therapy and targeted cancer treatments.

The study authors said a wide-ranging review of scientific evidence found that:

  • Chemotherapy, radiation therapy and other cancer treatments cause aging at a genetic and cellular level, prompting DNA to start unraveling and cells to die off sooner than normal.
  • Bone marrow transplant recipients are eight times more likely to become frail than their healthy siblings.
  • Long-term steroid treatment is associated with an increased risk of cataracts, brittle bones, nerve damage, impaired wound healing and diminished immune response.
  • Cancer drugs have been associated with hearing loss, reduced thyroid levels, high blood pressure, heart failure, muscle weakness, arthritis, infertility, constipation, and kidney and liver diseases.
  • Radiation therapy has been linked to dementia, memory loss, hardened arteries and secondary cancers.
  • The hormone drug Tamoxifen, used against breast cancer, has been associated with cataracts.

And, Shapiro added, women who receive chemotherapy are more likely to go into early menopause.

There's now a movement afoot to reduce the amount of treatment needed to beat cancer, as a means of either avoiding or easing these aging effects, Hashmi and Shapiro said.

Studies and clinical trials are evaluating ways to de-escalate treatments for cancers like lymphoma, Shapiro said.

Cancer survivors also can help themselves by adopting a healthier lifestyle, Hashmi advised -- quitting smoking, limiting alcohol consumption, eating right and exercising regularly.

"Taking these steps will help reduce the chances of new cancer development and the development of heart disease," Hashmi said.


Health officials warn that cell phones cause brain cancer, headaches, low sperm count and impaired memory

Published: December 18, 2017

Source:https://www.naturalnews.com/2017-12-18-health-officials-warn-that-cell-phones-cause-brain-cancer-headaches-low-sperm-count-and-impaired-memory.html

(Natural News) Figures indicate that you likely use a cell phone on a daily basis, since 95 percent of all Americans do so. And statistics indicate that most of our children now have one of these devices by the age of 10. That must mean they’re safe, right?

Unfortunately not. And though it has been scientifically proven that cell phones are harmful, health departments all over the country have been loath to speak out against them, leaving an uninformed public vulnerable to serious health problems.

Back in 2011, the World Health Organization’s International Agency for Research on Cancer (IARC) warned:

The WHO/International Agency for Research on Cancer (IARC) has classified radiofrequency electromagnetic fields as possibly carcinogenic to humans (Group 2B), based on an increased risk for glioma, a malignant type of brain cancer1, associated with wireless phone use.

Now, the California Department of Public Health (CDPH) has issued a very watered-down warning about the safety of cell phones, but only after being virtually forced to do so by Joel Moskowitz, director of the Center for Family and Community Health at UC Berkeley’s School of Public Health.

Dr. Moskowitz has been fighting since 2009 to get the CDPH to release information about the dangers of cell phone radiation. For years, they have been sitting on a document entitled “Cell phones and health,” which was commissioned seven years ago and has been revised several times, but was not released until Moskowitz forced the issue by taking the matter to the courts.

The document states clearly:

Health officials are concerned about possible health effects from cell phone EMFs because some recent studies suggest that long-term cell phone use may increase the risk of brain cancer and other health problems.

Susie Steimle, reporting for CBS affiliate KPIX, notes, “The research suggests cell phones could increase our risk for brain cancer and tumors, low sperm count, headaches, and impaired memory, hearing and sleep.”

While cell phone stores in Berkeley began warning their customers about these dangers over a year ago, the CDPH is only now warning people not to sleep with their cell phones under their pillows, and to never carry them in their pockets, but to rather store their mobile devices in their purses or leave them at home.

Nonetheless, when asked whether the CDPH now views cell phones as dangerous, its representative, Dr. Karen Smith, was quick to respond, “Not at all. Our position is that the science is evolving.”

Whatever that means.

Dr. Moskowitz is singularly unimpressed with the CDPH’s attempts at protecting the public.

“Currently we’re not doing a good job in regulating the radiation from these devices,” he said. “In fact, we’re doing an abysmal job. People are being injured and harmed by the delay in having this information accessible to them.”

The CDPH’s own investigation found that people diagnosed with certain forms of brain cancer are more likely to have used cell phones in the preceding decade, and that the cancers usually occurred on the side of the head that their cellphones were most often used on.

Nonetheless, as a society we have become incredibly dependent on our mobile phones, and it is unlikely that people will suddenly stop using them, so what are some safety tips to keep in mind when using these devices?

1. Spend as little time on any given conversation as possible; even a two-minute conversation disrupts brain activity for an hour.

2. Text rather than phoning;

3. Get a newer cell phone that emits less radiation;

4. Use a headset whenever possible;

5. Avoid using your mobile phone in an elevator or any other metal enclosure, including your car;

6. More radiation is emitted when your cell phone battery is low, so keep it charged; and

7. Wait until the phone is answered before physically putting your cell phone to your ear.


What does hair loss have to teach us about cancer metastasis?

Published: December 15, 2017

Source:https://www.sciencedaily.com/releases/2017/12/171215135115.htm

Understanding how cancer cells are able to metastasize -- migrate from the primary tumor to distant sites in the body -- and developing therapies to inhibit this process are the focus of many laboratories around the country. Researchers at the Medical University of South Carolina (MUSC) have identified one mechanism that regulates signaling events leading to cell migration and metastasis. In the October 24, 2017 issue of Science Signaling, they showed that primary cilia act as a focal point to transmit growth signals. Furthermore, they identified a specific ceramide species (produced by ceramide synthase 4 [CerS4]) that disrupts the ability of cells to form this focal point.

"We think this could be one way cancer cells actually migrate from one place to another to induce metastasis," says Besim Ogretmen, Ph.D., senior author for this study, director of the Developmental Cancer Therapeutics Program at the Hollings Cancer Center and professor of Biochemistry and Molecular Biology at MUSC.

The Ogretmen laboratory studies the signaling lipid ceramide and its role in many biological pathways, including cancer biology. Ceramides are made in cells by a family of six ceramide synthase enzymes. To identify how these different enzymes function, the Ogretmen laboratory generated mice that lacked each of these enzymes. Interestingly, mice lacking CerS4 had alopecia, a condition in which hair is lost from some or all parts of the body.

How does hair loss relate to cancer? It turns out that keratinocytes, or skin cells, migrate through the outer skin to maintain hair follicles. In the absence of CerS4, the keratinocytes are hyperactive and migrate too much, thereby disrupting the hair cycle. Ogretmen reasoned that, although this phenotype was unanticipated, the increased migration seen in these keratinocytes may also occur in cancer cells.

"Some unexpected phenotypes in animal models can actually lead to something very important in cancer biology that we didn't expect. In this case, hair loss told us something about cancer metastasis and how that can be regulated," says Ogretmen.

The recent findings from the Ogretmen laboratory indeed showed that ceramide affected cell migration, which is tightly controlled. When the cytokine transforming growth factor beta (TGF-beta) is sensed by the TGF-beta receptor, the receptor concentrates within the primary cilia of cells. The cell then changes the proteins it makes to allow the cell to migrate. Ceramide produced by CerS4 binds to Smad7, a cellular protein that can bind the TGF-beta receptor. The binding of ceramide to Smad7 prevents the TGF-beta receptor from concentrating in the cilia. Ultimately, ceramide prevents the cell from making the proteins necessary for migration.

Having identified a signaling pathway in cells, the researchers next wanted to determine if this pathway was important in cancer patients. The Ogretmen laboratory screened previously reported microarray data sets of several human tumor tissues (metastatic head and neck squamous cell carcinoma, melanoma, and renal cell carcinoma) and showed that, in these samples, only the levels of CerS4 were significantly decreased. Furthermore, using preclinical models, they showed that tumor cells that lost CerS4 expression had an increased incidence of metastasis to distant organs. This increased metastasis could be mitigated when the cell made more Smad7, which inhibited the TGF-beta receptor.

For many years, it was thought that the breadth of ceramide synthases present in cells represented redundant functions for this family of enzymes. This report suggests that this idea needs reframing, since only the ceramide generated from CerS4 regulates migration that is mediated by the TGF-beta receptor.

Future studies are aimed at developing a better model to study tumor development and metastasis in the context of CerS4. There is a mouse strain that develops primary mammary tumors, but those tumors do not form metastases. By decreasing the expression of CerS4 in these mice, the Ogretmen laboratory hopes to better define the way in which CerS4 regulates cell migration and metastasis. Furthermore, these mice would provide an excellent model to test novel therapies aimed at preventing metastasis.

However, there are several limitations to this approach. Targeting the TGF-beta receptor could have detrimental effects on other tissues of the body. Additionally, Bardet-Biedl syndrome is a metabolic disease in which trafficking of proteins within the cilium is blocked. Therefore, targeting the formation of the cilium could prove problematic. Together, it is critical when treating metastasis that the therapy be as specific as possible.

"Unfortunately, most cancer drugs have targets but those targets might be toxic when you inhibit them in other parts of the body. That's why I think the mechanistic studies are so important to try to only target the TGF-beta receptor signaling in the primary cilia but not in other parts of the body," says Ogretmen.


Even smokers may benefit from targeted lung cancer treatments

Published: December 13, 2017

Source:https://www.sciencedaily.com/releases/2017/12/171213120042.htm

Smokers are less likely than non-smokers to have lung cancers caused by targetable genetic changes. But a study published this week in the journal Clinical Cancer Research shows that when they do, smokers benefit just as much as non-smokers from targeted treatments.

"A smoker or former smoker with a targetable alteration has the same probability of benefiting from targeted therapy as a never-smoker with a targetable alteration," says Dara Aisner, PhD, investigator at the University of Colorado Cancer Center and molecular pathologist at CU School of Medicine.

Aisner participated in the study as a member of the Lung Cancer Mutation Consortium (LCMC), a group of 16 research institutions collaborating to explore the genetic drivers of lung cancer. Over the course of data collection, the LCMC enrolled 1,367 lung cancer patients, of which 904 had testing for at least one of 14 cancer-related genes. The current study explored the outcomes of smokers and non-smokers who were treated with targeted therapies against EGFR, ALK, or ROS1.

No matter a patient's smoking history, when one of these targetable genetic alterations was present, matching the alteration with the appropriate targeted therapy was associated with a survival benefit of 1.5 years, compared with patients (smokers and non-smokers) without these alterations.

"Historically, the recommendations have always said that you shouldn't use someone's smoking history to decide whether that person's lung cancer should receive broad molecular profiling. This strengthens the science behind those recommendations," Aisner says.

Aisner also points out that not every patient -- smoking or non-smoking -- will see this benefit from targeted treatments. Regardless of smoking status, some patients will see little benefit, while others may see much more benefit than the average 1.5 years increase over patients who do not receive targeted therapies.

While smokers with targetable genetic changes are equally likely to benefit from targeted treatments, their cancers are less likely to hold these changes. KRAS is the most commonly mutated gene in lung cancer patients with smoking history, found in about 30-40 percent of these cases. Unfortunately, KRAS mutation is currently without an effective targeted treatment. However, KRAS mutation is found in only 6 percent of non-smoking lung cancer patients.

This means that doctors are less likely to find actionable targets when genetically testing a smoker's lung cancer than they are when testing a non-smoker's cancer. It is an open question whether this may bias oncologists against offering genetic testing to lung cancer patients who smoke, despite the fact that guidelines recommend genetic testing regardless of smoking history.

"To my knowledge, nobody's ever looked at whether smokers who have a targetable alteration do as well as non-smokers with these alterations. You might think that comorbidities and other lifestyle factors that tend to accompany smoking might make it seem as if they do less well on these therapies, but our data show that's not the case," Aisner says.

"Essentially, no matter if you do or do not smoke, if your lung cancer holds a targetable alteration, you have the same chance of benefiting from targeted treatments," Aisner says.


New study finds smokeless tobacco causes mouth cancer, with more than half off all cases occurring in Asia

Published: December 12, 2017

Source:https://www.naturalnews.com/2017-12-12-new-study-finds-mouth-cancer-always-comes-from-smokeless-tobacco-use-with-more-than-half-off-all-cases-occurring-in-asia.html

One thing you can rely on about tobacco: It’s bound to give you cancer if you put it in your body.

Most of you may think that statement only applies to smoking tobacco. However, a study in Myanmar puts chewing tobacco in the same category. A recent study has discovered that almost all cases of mouth cancer in the country can be linked to the betel quid – with all patients having chewed betel during their lifetime.

Chewing betel is a habit that is closely related to smoking and drinking alcohol (both of which can also increase the likelihood of developing cancer), which often starts during adolescence.

The World Health Organization (WHO) estimates 250 million users of smokeless tobacco are in Southeast Asia, where Myanmar is located.

Consequently, this region also holds the highest incidence of mouth cancer, with over 95,000 cases each year. The disease is noted to be prevalent in poverty-stricken areas, as these have a greater exposure to smokeless tobacco.

“According to previous studies the incidence of oral cancer, also called mouth cancer, in Southeast Asia has been disturbingly high for many years,” lead author and oncologist Dr. Khin Khin Nwe reports. “It has also been shown that smokeless tobacco use is common in this region – for example in Myanmar more than 50 percent of men use betel quid.”

The study looked into the lifestyles and behaviors of patients who suffer head and neck cancer in order to determine the factors that may have been responsible for the disease. The sample was derived from 307 cancer patients who visited Toungoo Hospital in 2016. Out of the total, 67 people had head and neck squamous cell cancer (HNSCC) and were included in the study. These included 41 males and 26 females with an average age of 59.2 years old for men and 58.7 years old for women. The most common type of cancer noted was in the oral cavity, followed by the larynx, lip and nose.

The participants were then asked about their habits regarding betel quid chewing, smoking and drinking. The highest response was chewing betel alone at 30 percent, followed by a combination of the three habits. All cases of mouth cancer were betel quid chewers, with some cases combining either alcohol or smoking to both.

“Chewing of betel quid has been common in Southeast Asia, including Myanmar, for a long time and our study shows that it is a public health problem,” Nwe concludes. “Efforts are needed to increase awareness of the risks of betel quid chewing so that adolescents do not start the habit and adults are encouraged to quit. This may help to prevent head and neck cancer.”

The National Cancer Institute (NHI) defines smokeless tobacco as tobacco that is not burned. This is introduced into the body through chewing and sucking. There are two main kinds of smokeless tobacco: chewing tobacco (such as betel quid) which is put in the oral cavity, and snuff (a finely cut or powdered tobacco) which is then inhaled or is put inside the mouth to rest.

Aside from cancer, the use of smokeless tobacco can increase the risk of heart disease, gum disease, to name a few. The substance contains nicotine, which is highly addictive. A stark difference between people who smoke tobacco over those who chew it is the chemical’s effect. Persons who chew tobacco absorb tobacco directly into the bloodstream, where it can reach the brain and it can stay in the blood longer than that of smokers.

Finally, smokeless tobacco is NOT an alternative to smoking. Need help with kicking the habit? Check out StopSmoking.news for more ways to start living healthy.


Use of chemotherapy for early stage breast cancer declining, study says

Published: December 11, 2017

Source:https://www.sciencedaily.com/releases/2017/12/171211090725.htm

A study of nearly 3,000 women with early stage breast cancer indicates a recent, significant decline in the use of chemotherapy despite the lack of any change in national treatment recommendations or guidelines, according to researchers at the Stanford University School of Medicine and the University of Michigan.

The findings reflect a growing acknowledgement by oncologists and patients that for some women, the harms of chemotherapy may outweigh its potential benefits. The study also revealed that physicians are more likely to turn to tumor genomic testing when a patient expresses a treatment preference that doesn't match her physician's recommendations.

"For patients with early stage breast cancer, we've seen a significant decline in chemotherapy use over the last few years without a real change in evidence," said Allison Kurian, MD, associate professor of medicine and of health research and policy at Stanford. "This likely reflects a change in the culture of how physicians are practicing, and a move toward using tumor biology to guide treatment choices rather than solely relying on clinical measures."

Kurian is the lead author of the study, which will be published online Dec. 11 in the Journal of the National Cancer Institute. Steven Katz, MD, MPH, professor of medicine and of health management and policy at the University of Michigan, is the senior author.

"Our study shows how breast cancer is a model for how doctors have driven advances in personalized medicine into the exam room to reduce overtreatment," said Katz.

Surveying women, oncologists

The researchers surveyed 5,080 women treated for early stage breast cancer between 2013 and 2015 in Georgia and Los Angeles. Among them, 2,926 had stage-1 or -2 breast cancers that were positive for estrogen receptor expression and negative for human epidermal growth factor receptor-2 expression. (Receptor expression status is often used to guide treatment recommendations for women with breast cancer.)

After categorizing the women based on the involvement of neighboring lymph nodes, the researchers asked them whether their oncologists had recommended chemotherapy and whether they had received it. The researchers also surveyed 504 of the oncologists treating these early stage breast cancer patients about how they decided whether to recommend chemotherapy for the patients.

Kurian and her colleagues found that from 2013 to 2015, there was a decrease from 34.5 percent to 21.3 percent in chemotherapy use in study participants. During the same period, the participants reported a decline in chemotherapy recommendations by their oncologists from 44.9 percent to 31.6 percent.

Chemotherapy use in patients with no lymph node involvement declined from 26.6 percent to 14.1 percent; in patients with lymph node involvement, it declined from 81.1 percent to 64.2 percent.

Finally, 67.4 percent of oncologists surveyed indicated they would order tumor genomic testing to estimate a lymph node-positive woman's risk of cancer recurrence if the woman disagreed with her doctor's recommendation to receive chemotherapy. In contrast, only 17.5 percent would order the test if the patient and doctor were in agreement about her course of treatment.

"We believe this study indicates that physicians are attempting to be more selective in their recommendations and to spare patients toxicity when possible," said Kurian. "As personalized medicine becomes more widely available, doctors are using test results as part of their dialogue with patients about their preferences and overall treatment goals. But the long-term outcomes of these recent changes in chemotherapy use are uncertain."


Simple blood test may predict recurrence of breast cancer

Published: December 08, 2017

Source:https://www.sciencedaily.com/releases/2017/12/171208095544.htm

A simple blood test that detects tumor cells circulating in the blood shows promise as a new way to predict high or low risk of a breast cancer relapse. This is according to data presented today at the 40th annual San Antonio Breast Cancer Symposium. A proof-of-concept study by the ECOG-ACRIN Cancer Research Group (ECOG-ACRIN) measured the prevalence of circulating tumor cells (CTCs) in blood samples from patients cancer-free five years or more after diagnosis, then associated CTC presence with a later recurrence.

"Late recurrence five or more years after surgery accounts for at least one-half of recurrences of breast cancer, and there are no tests that identify who is at highest risk. We found that in women who were cancer-free five years after diagnosis, about 5 percent had a positive CTC test," said lead researcher Joseph A. Sparano, MD, vice chair of the ECOG-ACRIN Cancer Research Group, Philadelphia, and associate director for clinical research at Montefiore Medical Center, Albert Einstein Cancer Center, New York.

"More importantly ...," Dr. Sparano continued, ." ..we also found that a positive test was associated with a 35 percent recurrence risk after two years, compared with only 2 percent for those with a negative CTC test."

The concept is to explore the use of the CTC blood test in a new way. Currently, the test is FDA-approved for use by physicians to monitor response to treatment in patients with advanced breast, colon or prostate cancer, but not early stage cancer. A rise in the number of circulating tumor cells in the blood in patients with advanced disease may indicate trouble before it shows up on a scan. In this study, the research team evaluated this test in a different setting -- individuals alive and cancer-free about five years after their diagnosis and potentially cured, but still at risk for having a recurrence of their disease.

"Our ultimate goal is to use blood tests like this to tailor treatment in a way that minimizes recurrence risk for those at high risk, and spare treatment for those at low risk who may be unlikely to benefit from it," Dr. Sparano said. "The findings of this analysis provide strong evidence to further evaluate this new risk assessment approach using CTC and other blood-based tests in this setting."

The test was done on a single blood sample provided by 547 breast cancer patients who had been diagnosed more than five years prior and treated as part of a large ECOG-ACRIN breast cancer treatment trial, E5103. This group of patients had stage two or three breast cancer, and the cells in their tumors were HER2-negative.

Many women in E5103 remain cancer free and are being followed for their breast cancer status as part of standard care. Dr. Sparano and colleagues set up a biobank and invited these patients to contribute additional specimens for future research into the reasons for late recurrence. The biobank was established by ECOG-ACRIN and the Coalition of Cancer Cooperative Groups with funding from the Breast Cancer Research Foundation, National Cancer Institute, and Susan G. Komen.


Acupuncture May Ease Pain Tied to Breast Cancer Care

Published: December 07, 2017

Source:https://www.cancercompass.com/cancer-news/article/60209.htm

(HealthDay News) -- Some common breast cancer medications can trigger joint pain, but new research suggests acupuncture may ease that side effect.

The finding could be a win-win for breast cancer patients, said one oncologist who reviewed the study.

"Acupuncture has been around for thousands of years and has no real downside," said Dr. Lauren Cassell, chief of breast surgery at Lenox Hill Hospital in New York City.

"If something so simple as acupuncture can improve upon these symptoms and the patients' quality of life, we will have more women becoming compliant in taking their medication, and one would expect improved outcomes," Cassell added.

The new study was led by Dr. Dawn Hershman, who heads the Breast Cancer Program at NewYork-Presbyterian/Columbia University Medical Center, also in New York City.

Hershman's team tracked outcomes for 226 postmenopausal women with early stage breast cancer who were taking drugs called aromatase inhibitors.

These drugs -- which include Arimidex, Femara and Aromasin, among others -- are often used to treat women with estrogen-sensitive breast tumors, Hershman said.

But she added that "many patients suffer from side effects that cause them to miss treatments or stop treatment altogether. We need to identify strategies to control these side effects, the most common of which is debilitating joint pain and stiffness."

Hershman's team wondered if the ancient practice of acupuncture might help. Of the patients in the study, 110 received true acupuncture, 59 were given fake acupuncture (needles placed at ineffective spots on the body), and another 57 were placed on a waiting list.

The patients in the true and fake acupuncture groups underwent twice-weekly sessions for six weeks, followed by one session a week for six more weeks.

After six weeks, patients in the true acupuncture group reported much lower pain scores than those in either the fake acupuncture or waiting list groups, Hershman's team reported.

The study was scheduled for presentation Thursday at the annual San Antonio Breast Cancer Symposium, in Texas.

The finding may mean that women with pain related to aromatase inhibitor use might stick to their meds longer if acupuncture eases their joint pain, "but we need to conduct further studies to determine if this is indeed the case," Hershman said in a meeting news release.

In the meantime, the findings suggest that "health care practitioners should discuss the possibility of acupuncture with patients experiencing aromatase inhibitor-related joint pain and stiffness, because it has the potential to improve their quality of life," Hershman said.

Dr. Cynara Coomer directs the Florina Rusi-Marke Comprehensive Breast Center, at Staten Island University Hospital in New York City. Reading over the findings, she agreed that "the integration of Western and Eastern medicine is an important path to explore" in breast cancer care.

And with an opioid-addiction crisis sweeping the United States, "it is important for physicians to find other means of pain control for our patients," she added.

"This is yet another study that reveals the benefits of acupuncture in treating pain," Coomer said.


4 out of 5 cases of cancer among blacks can be prevented with vitamin D

Published: December 05, 2017

Source:https://www.naturalnews.com/2017-12-05-4-out-of-5-cases-of-cancer-among-blacks-can-be-prevented-with-vitamin-d.html

(Natural News) In a recent video lecture, the Health Ranger explained the many ways in which blacks are being targeted for genocide. The shocking YouTube video titled “The Science Agenda to Exterminate Blacks” describes a variety of “tactics that seek to eliminate blacks from our planet,” including the revelation that many cases of cancer could easily be prevented by addressing the rampant vitamin D deficiency seen in black communities.

As Mike Adams, also the director of CWC Labs, contends, “Every black person in Chicago, in Detroit, New York and the U.K. could prevent cancer — about four out five cancers, by the way — with nothing but vitamin D.” Adams notes that vitamin D deficiency is especially common in people with darker, more melanin-rich skin.

In the past, it’s been reported that some 75 percent of black people living the United States suffer from vitamin D deficiency. And this deficiency comes with a host of other issues; namely, an increased risk of cancer. Further, vitamin D deficiency can also make cancer more aggressive — so not only are vitamin D deficient people more likely to have cancer, it’s more likely that their cancer will be harder to treat as well.

Prostate cancer is a perfect example of this. Mike Adams touches on this disparity in his video, noting that prostate cancer rates for black men in the U.K. are considerably higher than for other races — and their cancer is typically more aggressive. Harvard Prostate Knowledge, the brainchild of Harvard Medical School and Harvard Health Publications, also touches on research that shows vitamin D deficiency can play a role in the incidence and aggressiveness of prostate cancer.

“New findings suggest that prostate tumors in particular can become highly aggressive when a man’s vitamin D levels are too low. A report in the journal Clinical Cancer Research showed that the lower the vitamin D level, the more aggressive the prostate cancer,” the organization explains.

Writing for Live Science, author Christopher Wanjek also reported on a meta-analysis which showed that disparities in cancer rates between races can be attributed to vitamin D deficiency. Wanjek stated that “the researchers found that low vitamin D is independently associated with each of the cancer types for which an unexplained health disparity exists between African-Americans and white Americans.” Numerous cancers were linked to the vitamin D disparity: Bladder, breast, colon, endometrial, lung, ovarian, pancreatic, prostate, rectal, testicular, and vaginal cancer, as well as Hodgkin’s lymphoma and melanoma.

Other studies have demonstrated a link between people of color and cancer incidence. For example, a study of over 1,000 men showed that black men are approximately 74 percent more likely to develop prostate cancer. Further, the researchers also found that the prostate cancer mortality rate was higher in black men also.

It is abundantly clear that many types of cancer can be attributed to vitamin D deficiency — it is also evident that vitamin D deficiency strongly affects minority communities and that there are very real health consequences associated with this deficiency. Yet, as Mike Adams contends, very little is being done to address the fact that vitamin D deficiency is hurting black people around the world. Indeed, these communities are being denied access to valuable health information — information that could keep cancer at bay.

Vitamin D is also known as the sunshine vitamin; and as Adams notes, sunshine is practically free. Even if you need a supplement, it surely costs less than conventional cancer treatments.


Mouth bacteria linked to esophageal cancer

Published: December 1, 2017

Source:https://www.medicalnewstoday.com/articles/320232.php

An analysis of microbes sampled from the mouths of more than 120,000 people has found that two types of bacteria that lead to gum disease are also linked to higher risk of esophageal cancer.

The study — led by NYU Langone Health's Perlmutter Cancer Center in New York, NY — also reveals that some types of mouth bacteria are linked to lower risk of esophageal cancer.

Reporting in the journal Cancer Research, the researchers note that they ruled out potential effects from smoking, alcohol, and body mass index (BMI) when they analyzed the data.

Senior investigator of the study Jiyoung Ahn, an associate professor and epidemiologist at NYU School of Medicine, believes that the findings will take us closer to establishing the causes of esophageal cancer.

She says that this is "because we now know that at least in some cases disease appears consistently linked to the presence of specific bacteria in the upper digestive tract."

'Urgent need' for new prevention strategies

Esophageal cancer is a cancer that starts in the cells of the esophagus, the tube of muscular tissue that moves food from the mouth to the stomach, and which is commonly referred to as the food pipe, or gullet.

The disease accounts for around 1 percent of all diagnosed cancers in the United States, where every year about 16,940 people find out that they have the disease and 15,690 die of it. The cancer is more common in men than in women.

Because the lining of the esophagus has two main types of cell, there are two main types of esophageal cancer: esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma (ESCC). The new study investigated both EAC and ESCC.

Unfortunately, because most people do not discover that they have esophageal cancer until the disease is advanced, only between 15–25 percent of them survive more than 5 years.

"Esophageal cancer is a highly fatal cancer," says Prof. Ahn, "and there is an urgent need for new avenues of prevention, risk stratification, and early detection."

Oral microbiota and links to cancer

The human mouth is home to hundreds of species of bacteria and other single-celled organisms. These "oral microbiota" occupy various habitats in the mouth, such as the gums, teeth, tonsils, tongue, cheeks, and palates.

Studies have shown that the composition of oral microbiota changes with different habits — such as heavy alcohol use, smoking, and diet — and also in response to disease, such as gum (or periodontal) disease and gastric reflux.

There is also evidence that some types of oral microbiota that cause gum disease are linked with cancer of the head and neck.

Prof. Ahn and colleagues note that — mainly as a result of studies that use data from one point in time — there is a long-held view that the composition of oral microbiota influences the risk of developing EAC and ESCC.

But the new study, which followed healthy patients for a decade, is the first to identify, from the hundreds of different types, which specific mouth bacteria are linked to risk of EAC and ESCC.

Some bacteria raise esophageal cancer risk

For their analysis, the team analyzed the microbiota in oral wash samples taken from more 122,000 people who took part in two national studies. The participants were followed for 10 years, during which researchers noted who developed esophageal cancer.

The team compared the genetic information of the mouth microbiota — the "oral microbiomes" — of the participants who developed esophageal cancer with that of equivalent participants who did not develop the disease.

They found that the presence of Tannerella forsythia was tied to higher risk of EAC, and that "abundance" of Porphyromonas gingivalis was tied to higher risk of ESCC.

In contrast, they also identified two types of bacteria — Streptococcus and Neisseria — that were linked to a lower risk of esophageal cancer.

The second of these, Neisseria, is known to play a role in the breakdown of toxic substances in tobacco smoke and is found in greater abundance in the oral cavities of nonsmokers than smokers.

"Our study indicates that learning more about the role of oral microbiota may potentially lead to strategies to prevent esophageal cancer, or at least to identify it at earlier stages."

Prof. Jiyoung Ahn


5 Things You Should Know About Cervical Cancer

Published: December 1, 2017

Source:https://www.cancercompass.com/cancer-news/article/60171.htm

(HealthDay News) -- A little knowledge can go a long way in the fight against cervical cancer.

In fact, the more women know about the disease, the greater their chances of being able to prevent it, say cancer experts from the City of Hope, a cancer treatment and research center in California.

Death rates from cervical cancer have fallen by more than 50 percent in the past four decades as women have learned more about their risk and as increasing numbers have had Pap tests, which help doctors screen for the disease, the experts noted.

However, because this cancer often comes with no early warning signs, City of Hope urges women to protect their health by learning five things about cervical cancer:

1. The most common cause is human papillomavirus (HPV). Roughly 99 percent of cervical cancers are caused by this sexually transmitted infection. The most common strains of the virus, HPV 16 and HPV 18, are responsible for about 70 percent of all cases of the disease. Roughly 14 million new HPV infections are detected each year. Some clear up, but infections that persist can lead to serious health problems.

2. Cervical cancer is often preventable. The U.S. Food and Drug Administration has approved three HPV vaccines. The first was Gardasil, approved in 2006, to protect against HPV 16 and HPV 18. In 2009, the FDA approved Cervarix. A third vaccine, Gardasil 9, which was shown to be 97 percent effective in preventing cervical, vulvar and vaginal cancer and protecting against additional types of high-risk HPV strains, was approved in 2014. It's recommended that young men and women, 9 to 26 years old, be vaccinated against HPV.

3. Lesbians and bisexual women are less likely to be screened for cervical cancer. City of Hope suggests this may be due to fear of discrimination, bad experiences with doctors in the past, and misinformation about cervical cancer.

4. All women 21 and older should get regular exams and screenings. This should include an annual pelvic exam and a periodic Pap test, considered a routine screening for cervical cancer. For a Pap test, cells are collected from the cervix so they can be examined for any abnormalities. Women in their 20s should get a Pap test every three years as long as their results remain normal. Women 30 to 64 years old should get a Pap test every five years as long as their results remain normal.

5. Warning signs of cervical cancer may be scarce. Cervical cancer may cause bleeding, but many women experience irregular periods so this may not seem unusual. Often, the disease does not cause pain or other obvious warning signs, making screening that much more important. Women who suspect a problem should not ignore their symptoms and seek a medical evaluation.


Targeted treatment could prevent spread of pancreatic cancer, heart damage

Published: November 30, 2017

Source:https://www.sciencedaily.com/releases/2017/11/171130170215.htm

Researchers at the University of Cincinnati (UC) College of Medicine have shown that a new targeted treatment could benefit patients with certain pancreatic tumors by preventing spread of the cancer and protecting their heart from damage -- a direct result of the tumor. Higher levels of serotonin among other tumor secretions can cause injury to the valves of the heart over time, leading to cardiac impairment -- a condition referred to as cardiac carcinoid disease -- in these patients.

These findings, reported in the November 2017 issue of Molecular Cancer Therapeutics, could lead to another targeted treatment for patients and prevent the onset of additional complications from their cancer.

"Pancreatic neuroendocrine tumors -- pancreatic NETs, pNETs or islet cell tumors -- are tumors that form from the abnormal growth of neuroendocrine cells in the pancreas," says lead author Hala Elnakat Thomas, PhD, research assistant professor in the Division of Hematology and Oncology, Department of Internal Medicine, and member of the Cincinnati Cancer Consortium and UC Cancer Institute's Pancreatic Cancer Center. "Most pancreatic NETs are functional, meaning they produce hormones. The overproduction of certain hormones results in a number of symptoms termed carcinoid disease which may impact the patients' quality of life if not managed appropriately."

She says mutations in key players of the mTOR pathway, a molecular pathway present and active in several types of cancer, have been identified in pNETs.

"Inhibiting mTOR signaling using everolimus, a targeted therapy, known as a rapalog, for patients with lung and gastroenteropancreatic NETs, has been approved by the FDA. A rapalog inhibits the mTOR protein by preventing it from activating some signals," she says. "However, patients eventually experience progression of cancer on this treatment, highlighting the need for additional therapies. In this study, we focused on pancreatic NETs (pNETs) and thought that treatment of these tumors upon progression on rapalog therapy, with an mTOR kinase inhibitor (mTORKi), could overcome a number of resistance mechanisms in tumors and delay cardiac carcinoid disease."

Elnakat Thomas' team and colleagues including Jack Rubinstein, MD, a member of the Heart, Lung and Vascular Institute and an associate professor within the UC College of Medicine, performed preclinical studies using human pNET cells injected into animal models to determine tumor progression and cardiac function in those treated with a rapalog alone or switched to the mTORKi (CC-223) when cancer progression was noticed.

"Our results showed that in the majority of pNETs that progress on rapalog therapy, it is possible to reduce disease progression when switching instead to an mTORKi, such as CC-223," Elnakat Thomas says. "The mTORKi also may lead to additional cardiac benefit by decreasing valvular fibrosis (damage) when compared with placebo or just the rapalog. The mTORKi also inhibit mTOR but they do it differently than rapalogs, and they are stronger inhibitors of signals, so the inhibition is more complete with an mTORKi than a rapalog. This data warrants further testing of the long-term cardioprotective benefit of an mTORKi in neuroendocrine tumor patients prone to carcinoid syndrome. Altogether, these results are timely as an mTORKi therapy called sapanisertib is currently in phase II clinical trial testing in pNET patients with metastatic cancer or tumors that are not reacting to treatment and cannot be surgically removed."


6 Percent of Cancers Caused by Excess Weight, Diabetes

Published: November 28, 2017

Source:https://www.cancercompass.com/cancer-news/article/60153.htm

(HealthDay News) -- Here's a seriously good reason to watch your diet: Excess weight and diabetes cause nearly 6 percent of cancers worldwide, a new study reports.

"Both obesity and diabetes are preventable causes of cancer for which intervention is possible at multiple levels -- in individuals, communities, health care systems, and policy," said Dr. Graham Colditz, of Washington University School of Medicine in St. Louis.

"More prompt actions are needed to help people maintain a healthy body weight throughout the life course, starting at an early age," Colditz wrote in an editorial accompanying the study.

Diabetes and obesity cause biological changes, such as high sugar levels, chronic inflammation and disrupted sex hormones. Over time, these can lead to cancer, the British researchers explained.

For the report, they analyzed health data from 175 countries. They concluded that 5.6 percent of new cancer cases in 2012 were caused by high body mass index (BMI) and diabetes. BMI is an estimate of body fat based on height and weight.

Overweight and obesity led to about 4 percent of cancer cases, and diabetes caused 2 percent, the study found.

Type 2 diabetes -- by far the most common form of the disease -- is linked to being overweight and sedentary.

Most of the cancer cases caused by diabetes and obesity were in wealthy Western countries, followed by East and Southeast Asian countries, according to the study.

The results were published Nov. 28 in The Lancet Diabetes & Endocrinology.

It's estimated that 422 million adults worldwide have diabetes and more than 2 billion adults are overweight or obese, the researchers said in background notes.

With these cancer risk factors increasing, efforts should focus on prevention and screening, said study lead author Dr. Jonathan Pearson-Stuttard of Imperial College London.

"It is important that effective food policies are implemented to tackle the rising prevalence of diabetes, high BMI and the diseases related to these risk factors," Pearson-Stuttard said in a journal news release.

According to Colditz, the "global burden of cancer due to high BMI and diabetes will continue to increase unless the prevalences of these conditions fall."


Is It Time to Scrap the Pap Test?

Published: November 27, 2017

Source:https://www.cancercompass.com/cancer-news/article/60134.htm

(HealthDay News) -- If you're a woman who's been given the all-clear after one or more combination tests for cervical cancer, you can probably wait five years between screenings, a new large study suggests.

The combination of tests for cervical cancer includes a test to detect the human papillomavirus (HPV) and the test commonly known as the Pap test. HPV is a virus that causes almost all cases of cervical cancers. The Pap test looks for abnormal changes in cells in the cervix that indicate cancer or precancerous changes.

Currently, women are advised to have these two tests every five years if they've had negative results in the past, according to the authors of the new study. Or, women can opt to have a Pap test every three years.

But "women who've had one or more negative HPV tests are at extremely low risk of cervical cancer or precancer, [and] this paper shows we can safely extend the screening interval to five years," said study first author Philip Castle. He's a professor in the department of epidemiology and population health at the Albert Einstein College of Medicine in New York City.

Castle said that not all medical groups agree that the screening interval should be five years.

"There's a natural tension between the medical and public health sides," he said. "Oncologists see the few failures that come from longer screening, but on the public health side, it's clear you can't get to perfect and that there are harms related to screening, so we need to reach a balance."

One big concern on the medical side is that women might mistake longer intervals for cervical cancer screening to mean that they don't need to see their ob-gyn every year, said Dr. Mitchell Kramer, chair of obstetrics and gynecology at Huntington Hospital in Huntington, N.Y.

"It's important for women to come for their regular exam each year," Kramer said. "We do a breast exam and make sure women are getting the other cancer screenings they need, as well as look at other issues or problems related to sexual function and bowel and bladder function."

The study included nearly 1 million women who received cervical cancer screenings from the Kaiser Permanente health care system in northern California. The screenings took place from 2003 to 2014.

The odds of cervical cancer dropped with each five-year combination of test results that showed no HPV and no abnormal cells from the Pap tests. Even without the Pap results, the HPV test detected a similar drop in the risk of cervical cancer, suggesting the HPV test alone might be OK, the study authors said.

Castle explained that most women who get infected with HPV acquire the infection within 10 years of first beginning sexual activity. So, if a woman has had multiple negative HPV tests done at five-year intervals, "the chances of developing invasive cervical cancer is exceedingly small because it's extremely rare for a new infection to be acquired in older women," he said. "Age is a modifier here. Older women tend to be in more stable relationships."

Having multiple partners, or having a partner who has multiple partners, increases the risk for HPV infection, according to the U.S. Centers for Disease Control and Prevention. The CDC also notes that it usually takes decades for an HPV infection to develop into cervical cancer.

But not everyone is convinced that it's acceptable to wait five years between tests.

"I'm hesitant to sign on and advocate for five years just yet," Kramer said. "On occasion, there are still women that may have picked up HPV, and longer intervals might miss those patients. I'm more comfortable with three years."

Castle again pointed to finding a balance. "No matter how much we screen, we'll never get to zero risk," he said.


In addition to preventing cancer, vitamin D now found to prevent Rheumatoid Arthritis, too

Published: November 25, 2017

Source:https://www.naturalnews.com/2017-11-25-in-addition-to-preventing-cancer-vitamin-d-now-found-to-prevent-rheumatoid-arthritis-too.html

(Natural News) The wonders of vitamin D never cease to amaze. Its ability to help prevent cancer has already been established, and we also know it’s great for fighting off depression and metabolic syndrome and improving your overall health. Get ready to add another superpower to this vitamin’s list: A new study has shown that it can also prevent rheumatoid arthritis.

Affecting around 1.3 million American adults and one percent of the world’s population, rheumatoid arthritis develops when the immune system attacks the healthy tissue in your body accidentally, normally in your joints.

This autoimmune disease is characterized by painful inflammation and swelling. It can affect several joints at once, with sufferers often complaining of pain in their wrists, hands and knees. In the early stages, it causes inflammation in the lining of the joint, but it damages the joint itself as it progresses. For some people, this can cause not only persistent pain but also problems with balance and even deformities.

Researchers from the University of Birmingham and University College London analyzed the blood and joint fluid taken from patients suffering from rheumatoid arthritis. Given the potent anti-inflammatory action of vitamin D, the researchers wanted to find out how it would work at the site of the active disease. Past studies focused on immune cells that had been isolated from blood.

This study was the first one to use immune cells that were taken from the blood as well as the inflamed joints of 15 rheumatoid arthritis sufferers between the ages of 40 and 85. This joint fluid, which is known as synovial fluid, is a sticky and thick liquid that serves as a lubricant, reducing the friction between bones when they meet at joints. The blood samples from the rheumatoid arthritis sufferers and the control group without the illness were matched by age and gender.

After testing how the immune cells in the various samples reacted to vitamin D, the researchers discovered that different types of immune cells had different responses.

Good for prevention, but higher doses needed for treating the disease once it sets in

Their findings support the idea that proper levels of vitamin D could help to prevent not only rheumatoid arthritis but also other inflammatory diseases. At the same time, however, taking vitamin D supplements does not seem likely to help those who already have the illness because their immune cells appear to already be desensitized. The researchers theorized that current sufferers might benefit from much higher vitamin D doses or other types of treatment that could bypass or correct the vitamin D insensitivity noted in the immune cells found within the joint.

Next, the researchers would like to find out precisely why rheumatoid arthritis makes immune cells insensitive to vitamin D and how it can be prevented. They’d also like to investigate whether similar effects can be seen in other inflammatory conditions.

Vitamin D is essential for healthy muscles, bones, and teeth. A global study that was published this year showed it can reduce a person’s risk of flu, colds and infections like pneumonia. Deficiencies are shockingly common, and some experts are also calling for the recommended daily intake of the vitamin to be raised.

Spending time in the sun is one of the best ways to encourage your body to produce more vitamin D. Around 15 to 30 minutes a day depending on your skin tone is enough, but you’ll want to skip the sunscreen; sunblock with SPF 30 can reduce your body’s ability to produce the vitamin by 99 percent.

You can also get it from supplements or foods like oily fish, although it’s difficult to get enough of this vitamin from diet alone.


Scientists discover how common alcohol found in wine can kill cancer tumors

Published: November 23, 2017

Source:https://www.naturalnews.com/2017-11-23-scientists-discover-how-common-alcohol-found-in-wine-can-kill-cancer-tumors.html

(Natural News) A new jelly-like implant filled with pure alcohol may show potential in addressing tumor growth and subsequent cancer onset, a study reveals. A team of researchers at the Duke University in North Carolina have developed the new implant in hopes of confining cancer cells by exposing them to pure alcohol. The scientific community believes that doing so is an effective way of eliminating cancer cells, but has previously cautioned that alcohol exposure may also inadvertently affect healthy tissues.

The research team has engineered the implant by mixing ethanol with ethyl cellulose. The experts explain that ethanol is a form of pure alcohol that makes up 12 to 14 percent of wine, while ethyl cellulose is a substance made from wood pulp or cotton and is commonly used as a thickening agent in both the food and pharmaceutical industries. The resulting mixture forms the jelly-like implant, which readily dissolves inside the body.

The scientists then implanted the gel into seven mice with malignant tumors in the mouth to examine its efficacy. The tumor size is subsequently measured after eight days. The results show that all the malignant tumors in mice disappeared. In contrast, only four out of seven mice that received alcohol injections alone have shown clinically significant improvements. According to the research team, the new implant works by slowly releasing small amounts of ethanol into the area of the tumor instead of flooding the site with alcohol.

“Overall, our results suggest that this enhanced version of ethanol ablation could be useful in the treatment of a number of malignancies. Notably, breast cancer is the leading cause of cancer-related deaths in low-income countries…Given the general lack of accessibility to surgery or alternative tumor treatments in developing countries and the promising results presented in this study, enhanced ethanol ablation is a promising method to meet the unmet clinical need of rising cancer mortality that challenges healthcare systems in developing countries,” the researchers report online in the Scientific Reports journal.

However, the research team is quick to point out the limitations of the study and has highlighted the need for further research to better investigate the implant’s potential.

“Although we have demonstrated the efficacy of enhanced ethanol ablation in the treatment of squamous cell carcinomas in the hamster cheek pouch, there are several limitations to this study. First, the use of a chemically-induced tumor model…precluded the possibility of any long-term monitoring of tumor recurrence. Second, a single animal tumor model was utilized. Further study in other tumor models is needed to investigate such recurrence, and demonstrate therapeutic efficacy more broadly,” the researchers add.

Study explains how red wine can stem cancer cells

A 2014 study supports the potential of red wine in boosting cancer treatment and preventing the onset of both head and neck cancer.  A team of health experts at the University of Colorado has examined the correlation between alcohol intake and increased cancer risk in people with a rare genetic disease called Fanconi anemia. According to the experts, people with the genetic disorder are born without the ability to repair DNA cross links and are therefore more susceptible to DNA damage and cancer. 

The research team has observed that a genetic facilitator of cancer onset in patients is basically similar to the cancer-causing mechanism of alcohol. According to the researchers, partially-metabolized alcohol is to blame for the increased risk of cancer in patients. The health experts note that drinking hard alcohol is a surefire way to increase the risk as it often remains in the body and produces partially-metabolized alcohol.

However, the scientists note that the lowest cancer incidence are seen in those who regularly drank red wine. “In red wine, there’s something that’s blocking the cancer-causing effect of alcohol… resveratrol takes out the cells with the most damage — the cells that have the highest probability of being able to cause cancer,” researcher Robert Sclafani told Science Daily online.


Women prefer getting mammograms every year

Published: November 22, 2017

Source:https://www.sciencedaily.com/releases/2017/11/171122151037.htm

Women prefer to get their mammograms every year, instead of every two years, according to a new study being presented next week at the annual meeting of the Radiological Society of North America (RSNA).

"Women understand that yearly mammograms have been shown to save lives and do not consider previously reported 'harms' to be as important as getting screened," said study author Ghizlane Bouzghar, M.D., chief radiology resident at Einstein Medical Center in Philadelphia.

For years, the standard recommendation among most medical groups was that women at average risk of breast cancer undergo screening mammography annually beginning at age 40. However, in 2009, the U.S. Preventive Services Task Force (USPSTF) issued a controversial recommendation that women at average risk be screened biennially, or every two years, beginning at age 50. This recommendation, reaffirmed in 2016, was based in part on the "harms" associated with screening mammography.

These "harms," as defined by the USPSTF, include diagnosis and treatment of noninvasive and invasive breast cancers that would otherwise not have become a threat to a woman's health and the unnecessary biopsies and associated anxieties resulting from false-positive results.

Others argue that while reducing over-diagnosis and false positives are a priority, the benefits of early detection far outweigh the negative factors associated with the perceived harms. Absent from the debate has been one notable opinion: that of the women being screened.

"The USPSTF associates annual screening mammography with 'harm' and recommends biennial screening mammography instead," Dr. Bouzghar said. "However, there is no study to date that looked at women's preference regarding annual versus biennial screening mammography, and whether women think that biennial screening causes less, equal or more anxiety."

Dr. Bouzghar and colleagues at Einstein set out to determine whether women preferred annual or biennial screening and to investigate whether or not reported harms of mammography influenced this preference.

The research team surveyed 731 women (mean age 59) undergoing screening and diagnostic mammograms at Einstein from December 2016 to February 2017. Women were asked whether an abnormal mammogram or breast biopsy causes emotional harm, whether screening every two years was associated with less or more anxiety, and whether they preferred to have a screening mammogram every other year or every year.

Variables such as the patient's age, race, family and personal history of breast cancer, prior biopsies and abnormal mammograms, and underlying anxiety disorder were also included.

Of the women surveyed, 71 percent preferred getting screened every year. A family history of breast cancer and prior breast biopsy were the only two variables to have an additional positive influence on annual screening preference.

"Many women are much better educated about the value of screening mammography than they are given credit for," Dr. Bouzghar said. "I also think that some of the USPSTF's concerns about the 'harms' were somewhat paternalistic, and in 2017 women are more empowered about many things, including their healthcare."


Chemo brain starts during cancer's progression, not just after chemotherapy

Published: November 21, 2017

Source:https://www.sciencedaily.com/releases/2017/11/171121095143.htm

The memory and thinking problems experienced by cancer survivors, known as "chemo brain" or "chemo fog," are not just the result of chemotherapy treatment, they may start as tumors form and develop, suggests a Baycrest-led study.

Researchers found that female mice with a form of breast cancer demonstrated impaired performance on learning and memory tests before chemotherapy drugs were administered, according to recent findings published in the journal Neuroscience.

"Our work isolated that the cancer is responsible for some of the memory and thinking complaints experienced by cancer survivors, and that drug therapy adds to the problem," says Dr. Gordon Winocur, lead author on the study, senior scientist at Baycrest's Rotman Research Institute and psychology professor at Trent University and the University of Toronto. "Both factors independently affect brain function in different ways, which can lead to the development of other psychological disturbances, such as anxiety and depression."

After chemotherapy, as many as 65 per cent of patients with breast cancer report memory lapses, difficulty concentrating, taking longer to complete tasks and difficulty multitasking. Patients with other types of cancer have reported similar problems.

Through the study, researchers were also able to pinpoint three different brain changes caused by the progression of cancer and the drugs used in treatment.

1. As the tumor develops, the body's immune system responds by releasing cytokines to inhibit the cancer's development. Researchers discovered that the body's reaction causes inflammation in the brain's nervous system, which impacts its function.

2. Chemotherapy was found to limit the production of new brain cells in regions responsible for memory function, which leads to a loss of memory.

3. The combination of tumor growth and chemotherapy led to shrinkage in brain regions that are important for learning and memory.

"Our research found that the cancer and chemotherapy cause three separate, but related brain changes," says Dr. Winocur. "Understanding the nature of the cognitive impairment and the underlying biological mechanisms are essential to the development of an effective treatment for chemo brain. Our work shows that a targeted approach addressing all three issues is necessary to successfully treat the condition."

The study was conducted on female mice, half of them with cancer and the other half without. Scientists first administered a series of learning and memory tests to all the mice to investigate the impact of the tumor on brain function. After the initial data was collected, the mice either received the chemotherapy drugs, methotrexate and 5-fluouracil, or a saline solution. The mice were then retested on the same trials and some additional ones. Once testing was complete, brain images, tissue and blood samples were used to analyze changes to brain structure and cytokine activity (proteins released by the immune system to help fight off infections or diseases).

Researchers found that prior to treatment, mice with tumors performed worse on learning and memory tests compared to their normal counterparts. After chemotherapy, the performance of cancerous mice worsened and the non-cancerous mice also showed signs of cognitive impairment.

"People are living longer thanks to more effective chemotherapy and cancer treatments," says Dr. Winocur. "Addressing chemo brain will help improve a patient's quality of life since these side effects can lead to emotional and mental health issues that affect a person's ability to function in society."

These findings lay the foundation for the development of targeted treatments. In previous work, Dr. Winocur demonstrated that drugs used to treat memory and thinking problems in Alzheimer's disease and physical exercise can offset chemo brain's impact. As next steps, Dr. Winocur will investigate these effects in cancer survivors who complain of chemo brain following chemotherapy.


Heavier Women May Need Mammograms More Often

Published: November 20, 2017

Source: https://www.cancercompass.com/cancer-news/article/60096.htm

(HealthDay News) -- Women who are overweight or obese may need to be screened for breast cancer more frequently, new Swedish research suggests.

The reason? Overweight or obese women are at greater risk of having breast cancer detected after the tumor has grown large -- over 2 centimeters -- than their slimmer counterparts, the study found.

Heavier women also have a worse prognosis when their breast cancers are detected between regular cancer screenings (known as interval cancers) than normal weight women, the findings showed.

"It seems overweight women would need shorter time intervals between screenings than other women, but our study was not designed to quantify how much," explained Dr. Fredrik Strand, a radiologist at the Karolinska University Hospital.

The study included more than 2,000 women from Sweden. All were aged 55 to 74, Strand said. All were diagnosed with invasive breast cancer between 2001 and 2008. The average BMI was 25.6. BMI is a rough estimate of body fat based on height and weight measurements.

A BMI between 18.5 and 24.9 is considered normal. A BMI of 25 to 29.9 is overweight, and over 30 is considered obese.

A 5-foot 6-inch woman with a normal BMI would weigh between 118 and 150 pounds. For that same woman, overweight would be about 155 to 180 pounds. Obesity would begin around 186 pounds, according to the U.S. National Heart, Lung, and Blood Institute.

The researchers wanted to learn what factors -- in a country with universal access to breast cancer screening -- might have played a role in these women having large tumors when diagnosed either at the time of screening or during the interval between screenings. For this study, the interval between screenings was up to two years, Strand said. In the United States, the interval is usually around 12 months, the researchers noted.

The study found that a BMI above 25 and having denser breast tissue were linked to higher odds of a large tumor when diagnosed with breast cancer during a screening. Only BMI was associated with having a large tumor for interval cancers.

Women with a BMI above 25 with interval cancers had a worse prognosis than thinner women. Strand said a worse prognosis was defined as the cancer coming back, the cancer spreading, or death from the cancer.

The study findings might be even stronger if done in a U.S. population, he added, because people in the United States tend to be heavier than they are in Sweden.

Dr. Laurie Margolies, chief of breast imaging at Mount Sinai Health System in New York City, said the study adds "another piece of evidence that might end the confusion about when to get a mammogram. Women should be screened every year."

Both experts noted that the findings need to be replicated. And Margolies said she'd like to see the study done with a U.S. population.

Strand is to present his study on Nov. 29 at the Radiological Society of North America annual meeting, in Chicago. Findings presented at meetings are typically viewed as preliminary until they've been published in a peer-reviewed journal.


How a poorly explored immune cell may impact cancer immunity and immunotherapy

Published: November 17, 2017

Source: https://www.sciencedaily.com/releases/2017/11/171117141801.htm

The immune cells that are trained to fight off the body's invaders can become defective. It's what allows cancer to develop. So most research has targeted these co-called effector T-cells.

But a new study takes a step back and considers: What if the problem isn't with the effector T-cells but starts higher up the cellular chain?

And so researchers looked at naïve T-cells -- a type of immune cell that hasn't yet been triggered to fight. Naïve T-cells differentiate into the fighter effector T-cells.

"People didn't realize the problem may not only be directly from the effector cells themselves, but may also stem from a defect in the naïve cells. We found naïve cells already have a problem in patients who have cancer. If the naïve cells are functionally impaired, the effector cells cannot be healthy," says study author Weiping Zou, M.D., Ph.D., the Charles B. de Nancrede Professor of Surgery, Pathology, Immunology and Biology at the University of Michigan.

Naïve T-cells are not well understood in cancer, in part because the effector T-cells have direct control over tumor immunity. So that's where researchers have focused their attention. Also, naïve T-cells are rare in the tumor microenvironment -- the traditional battlefield between cancer and immune cells.

The new study, published in Science Immunology, finds that tumor metabolism impacts naïve T-cells. The tumor cells use a lot of glucose. When the glucose is metabolized, it produces lactate -- and lactate turns out to be very bad for naïve T-cells. Once the tumor produces a certain level of lactate, it causes damage to the naïve T-cells, including cell death.

Currently, efforts to predict response to cancer immunotherapy focus on memory and effector T-cells. The new research suggests another path.

"Yes, you do see problems in effector T-cells, but you have to keep in mind that to begin with, the naïve T-cells are functionally impaired by the tumor metabolism," Zou says.

Researchers will look for ways to manipulate the metabolism to try to recover the function of the naïve T-cells in the hopes that it can make immunotherapy more effective. Some early phase clinical trials are testing a way to target the lactate pathway. Researchers hope this could provide a rationale for combining immunotherapy with a therapy to regulate metabolism.

"When you have more healthy naïve T-cells to begin with, hopefully you will get more healthy effector T-cells, which will overcome some of the resistance we see with immunotherapy," Zou says.


Should You Be Screened for Lung Cancer?

Published: November 16, 2017

Source: https://health.usnews.com/health-care/patient-advice/articles/2017-11-16/should-you-be-screened-for-lung-cancer

The goal of cancer screening in people who have no symptoms is to catch cancer early, when it's most treatable. Most screening recommendations for breast, cervical and colon cancer (the types of cancer for which there are widely used screening tests) are for people who are at average risk of developing these diseases. In contrast, only people with a history of heavy smoking, who are therefore at high risk, undergo lung cancer screening.

Lung cancer screening has become more common since the results of the National Lung Cancer Screening Trial, a randomized, multi-centered study, were published in the New England Journal of Medicine in 2011, says Dr. Edwin Jackson, a pulmonologist at the Ohio State University Comprehensive Cancer Center. The NLCST found that screening heavy smokers with low-dose helical CT scans was better than chest X-rays for finding early cancers.

"The conditions do not get any better for screening than for lung cancer," says Dr. H. Gilbert Welch, a professor of medicine at the Dartmouth Institute for Health Policy & Clinical Practice. "Lung cancer is far and away the most common cause of cancer death in this country, more than the next four cancers combined. Screening works better if you find a group who is really at high risk for the disease." Welch says this is easy with lung cancer. You find people who have a history of heavy smoking.

Should You Be Screened?

Individuals between the ages of 55 and 77 who have a 30-pack year history of smoking and are current smokers, or have quit within the past 15 years, are eligible for annual CT scans for lung cancer screening. (To gauge pack years, multiply the number of packs of cigarettes you smoked daily by the number of years you smoked.) Even if you qualify for screening, however, it does not necessarily mean you should be screened.

"The more nuanced part [of the should-I-be-screened question] is can patients tolerate what a positive screening test will advise us to do?" Jackson says. In other words, is an individual able to undergo a biopsy or curative surgery if the screening test is positive? Individuals with other health conditions, such as advanced heart failure or COPD, may not be strong enough to tolerate surgery. For them, screening might not make sense.

This is where shared decision making comes in, Jackson says. "We talk to our patients about the risks and benefits of lung cancer screening. One of the risks will be the workup following a positive screening test [for example, a biopsy], which can cause more harm than good." Another downside, he says, is the risk of developing a secondary cancer from annual screening with radiation.

Welch says lung cancer screening produces a lot of false positive results (about 25 percent of screens are positive). This means something that's not cancer shows up on the scan. These findings may require additional procedures or more frequent imaging. Only about 1 in 25 positive screening results is actually cancer, Jackson says. The rest are usually harmless nodules. Another downside to screening, Welch says, is overdiagnosis, or finding cancers that never would have become symptomatic.

Does Lung Cancer Screening Save Lives?

Yes, but not as many as you might think. Jackson says the number of cancers doctors actually find with lung cancer screening is very low. Most people will either have a negative screen or a false positive. Therefore, the number of deaths prevented because of screening is also low. The NLCST found that people screened with low-dose helical CT had a 15 to 20 percent reduced risk of dying from lung cancer over seven years (17.6 deaths per 1,000 people screened with CT scan versus 20.7 deaths per 1,000 screened with a chest X-ray).

However, Jackson says, a side benefit of screening is that it provides an opportunity to offer evidenced-based therapies for smoking cessation. "One of the best ways to get out of the screening pool is to have stopped smoking for more than 15 years," he says. "As you stop smoking, every year your risk of lung cancer goes down." At Ohio State, where Jackson practices, he says they use the time between completing the actual CT scan and when the radiologist delivers the results to talk about smoking cessation and offer products and strategies to help people quit. About 50 percent of those who go through this process stop smoking. "These are pretty strong numbers for smoking cessation," Jackson says.

The Bottom Line

Welch says smokers who are eligible for screening need to educate themselves about the benefits and harms of lung cancer screening and make a choice that's right for them. He adds: "It's just not the most important thing to do." Instead, people should stop smoking, walk regularly and eat well. Welch says that in our drive for early detection of cancer – any cancer – we've distracted people from more important interventions, like pursuing a healthy lifestyle. "We have this idea that we can test ourselves to health. That is not true," he says.

"A negative screen is not a license to smoke," Jackson adds. "People should not see this as a clean bill of health. Look at a negative screen as a fresh start, a time to stop smokingand further decrease your risk of developing lung cancer in the future."


How to Do a Skin Cancer Body Check

Published: November 15, 2017

Source: https://www.cancercompass.com/cancer-news/article/60050.htm

(HealthDay News) -- Every year, about 5 million Americans are treated for skin cancer -- an abnormal growth of skin cells that most often develops on areas exposed to the sun.

You can spot early signs by regularly checking your skin for changes.

Everyone is susceptible to skin cancer. However, people who have light skin that burns easily, red hair, and/or blue eyes have a higher risk.

Three types of skin cancer account for nearly all cases: basal cell and squamous cell carcinomas and, the most dangerous, melanoma.

Follow the A-B-C-D-E method to help you know when a growth needs to be evaluated by your doctor.

Here's what to look for when evaluating skin growths:

Asymmetry: The two halves of the growth don't match.

Border: The edges are irregular or poorly defined.

Color: You see various shades of tan, brown, black or even white, red or blue.

Diameter: Melanomas are often the size of a pencil eraser or smaller.

Evolving: You spot a growth that's changing in size, shape or color.

To fully examine your body, start by looking straight ahead into a mirror. Check your face and torso. Next, raise your arms to see your right and left sides. Then look at your arms, including underarms, hands and palms. Check the front and back of your legs and feet as well as your soles and between your toes. Use a hand mirror to check the back of your neck.

Finally, examine your scalp, parting your hair as you move across your head.

Be sure to have your doctor give your skin the once-over during your annual wellness exam, and see a dermatologist for any suspicious growths.


HPV testing is better than the Pap test at detecting cervical cancer

Published: November 14, 2017

Source:https://www.sciencedaily.com/releases/2017/11/171114091315.htm

A new paper in the Journal of the National Cancer Institute finds that testing for cervical cancer using HPV testing in addition to the Pap smear is unlikely to detect cancer cases that wouldn't be found using HPV testing alone.

The main goal of cervical screening programs is to detect and treat precancer before cancer develops. Cytology-based screening, known as the Pap test or Pap smear, is used to detect abnormal cells. The Pap test can also find noncancerous conditions, such as infections and inflammation.

Cervical cancer screening guidelines have changed dramatically over the last 15 years, following introduction of testing for the dozen high-risk human papillomavirus (HPV) types that cause virtually all cervical cancer and its precursors. Despite more research into HPV, and the introduction of preventive HPV vaccines, screening will remain important and comprise many millions of tests annually for decades to come. But improved screening methods have also introduced some confusion, even controversy.

HPV testing is more sensitive than the Pap test for detecting precancer. The HPV test captures the known cancer causing viruses, but there are gynecologists who believe that there may be unknown cancer causing viruses and so continue to do the Pap smear (plus HPV testing).

However, reports of rare HPV-negative, Pap-test-positive cancers are motivating continued use of both tests (cotesting) despite increased testing costs. An HPV test, in which doctors test a cervicovaginal specimen for the presence of the nucleic acids of carcinogenic types of HPV, is more sensitive than the Pap test (a microscopic examination of exfoliated cells) for detection of precancers. Thus, if a single screening method were chosen to complement HPV vaccination, primary HPV testing likely would gradually supplant the Pap test.

In the US, an interim guidance issued by a committee of experts from several clinical societies recommended primary HPV testing every three years, the same as the Pap test. Alternatively, current guidelines recommend cotesting but, in recognition of the additional reassurance provided by this approach compared with the Pap test alone, the screening interval is extended to every five years. Draft guidelines from the US Preventive Services Task Force recently recommended either primary HPV testing every five years or the Pap test every three years for women 30 to 64, and did not recommend cotesting.

The accumulated evidence supports inclusion of HPV testing in screening; thus, the main choice moving forward is between cotesting and primary HPV testing alone.

Researchers were searching for realistic performance data to quantify the additional benefit of the Pap test component of cotesting, as the costs of intensive screening of all women using two screening tests are substantial.

In January 2003, just prior to US FDA approval of HPV and Pap test cotesting in mid-2003 and interim guidelines in 2004, Kaiser Permanente Northern California, a large integrated health care organization, introduced three-year cotesting in women aged 30 years and older. Kaiser Permanente has now screened over a million women by cotesting. This remains the most extensive experience of HPV testing incorporated into routine screening in the world.

Researchers here quantified the detection of cervical precancer and cancer by cotesting compared with HPV testing alone at Kaiser Permanente, where 1,208,710 women have undergone triennial cervical cotesting since 2003. Screening histories preceding cervical cancers (n=623) and precancers (n=5,369) were examined to assess the relative contribution of the Pap test and HPV test components in identifying cases.

The analysis found that HPV testing identified more women subsequently diagnosed with cancer and precancer than the Pap test. HPV testing was statistically significantly more likely to be positive for cancer at any time point, except within 12 months. HPV-negative/ Pap test-positive results preceded only small fractions of cases of precancer (3.5%) and cancer (5.9%); these cancers were more likely to be regional or distant stage than other cases.

Given the rarity of cancers among screened women, the contribution of the Pap test to screening translated to earlier detection of at most five cases per million women per year. Two-thirds (67.9%) of women found to have cancer up to 10 years of follow-up at Kaiser Permanente were detected by the first cotest performed.

The researchers conclude that the added sensitivity of cotesting versus HPV alone for detection of treatable cancer affected extremely few women.


Effective therapy against glioblastoma by attacking telomeres

Published: November 13, 2017

Source:https://www.sciencedaily.com/releases/2017/11/171113123806.htm

The Telomere and Telomerase Group at the Spanish National Cancer Research Centre (CNIO) has shown that it is possible to block the growth of human and murine glioblastoma in mouse models by blocking the TRF1 protein; an essential component of the telomere-protective complex known as shelterin. The study, published in Cancer Cell, describes a new and promising way to combat this type of brain tumour, considered one of the most lethal and difficult to treat, by attacking its ability to regenerate and divide immortally.

The average life expectancy of patients with glioblastoma is about 14 months. This brain tumour (which is the most common) can evade and overcome the limited therapeutic options that exist today to treat it. It is particularly known for its ability to regenerate, because, the tumour contains a subset of cells with characteristics that are similar to stem cells, called glioblastoma stem cells (GSCs), one of these cells is capable of reproducing the entire tumour.

These GSCs cells are the cornerstone of glioblastoma and one of its identifying features. One of their characteristics is that they have very high levels of the telomeric protein TRF1, which in addition to being essential for protecting telomeres, is required to maintain the capacity of these cells to regenerate the tumour.

"We know that TRF1 is expressed particularly in stem cells, so we thought it would be interesting to see what would happen in tumours that had a strong tumour stem cell nature if we blocked TRF1," explains Maria A. Blasco, head of the Telomeres and Telomerase Group and senior author of the paper. Glioblastoma is clearly a type of tumour that could benefit from blocking TRF1 owing to the ability of its glioma stem cells to regenerate the tumours after current treatments.

BLOCKING TRF1 REDUCES TUMOUR GROWTH

"The first thing we saw was that TRF1 is highly overexpressed in both mouse and human glioblastomas, which indicated that by blocking it we could perhaps impair its growth," says Leire Bejarano, a member of Blasco's group and first author of the paper.

Consequently, Blasco, Bejarano and colleagues started working with mouse models. They removed TRF1 during the initiation of the tumour, as well as blocked it once the glioblastomas had already formed. "Both strategies -- said Bejarano -- led to a significant increase in the survival rate of the mice with glioblastomas." In the first case, the increase in survival was of 80% and in the case of already-existing tumours the increase in survival was of 30%.

By studying the mechanisms by which TRF1 inhibition limited tumour growth, they found that inhibiting TRF1 caused a reduction in the proliferation and in the stem properties of glioma stem cells. This was in turn triggered by an increase in DNA damage at telomeres, which resulted from the destruction of glioblastoma telomeres. In the end, they prevented the tumour cells from continuing to multiply.

After the success in the mouse models, they began to work with human tumour cells. This required grafting glioblastoma stem cells derived from human patients into mice and treating them with a series of compounds developed at CNIO that inhibit TRF1 and which mechanism of action has been described recently by the same CNIO group. When compared with the animals treated with TRF1 inhibitors with those treated with a placebo, those treated with the TRF1 inhibitor displayed a reduction in the growth and size of the tumours, accompanied by an 80% decrease in tumour TRF1 levels and an increase in the survival rate.

A NEW THERAPEUTIC WINDOW

In addition to the anti-tumoural properties observed, blocking TRF1 appears to be safe because did not affect the olfactory and neuromuscular functions, nor the memory, of the mice. This strengthens the idea that we now have a new therapeutic window to inhibit TRF1 in this type of brain tumour.

"It has a major therapeutic effect on glioblastoma," says Blasco. "We see that inhibiting TRF1 is an effective strategy for treating glioblastoma both by itself and in combination with current radiation and temozolomide therapies," explained the authors, who also collaborated with the Seve-Ballesteros Foundation Brain Tumour Group at CNIO, headed by Massimo Squatrito, the CNIO drug dicovery Experimental Therapeutics Programme, directed by Joaquin Pastor, and the CNIO Confocal Microscopy Unit, led by Diego Megías.

The next step -- which they are already working on -, is to verify the effectiveness of the TRF1 inhibitors developed at CNIO in combination with other drugs that are already being used in the clinic.


Even light drinkers at risk of cancer

Published: November 11, 2017

Source:https://www.medicalnewstoday.com/articles/320021.php

I enjoy the occasional glass of wine, and I wouldn't consider this level of drinking to be harmful to my health. But it appears I'm wrong; that seemingly innocent glass of pinot could be increasing my risk of cancer.

If you think I'm being dramatic, you're probably among the 70 percent of Americans who don't realize that alcohol consumption is a significant risk factor for cancer.

As a writer for a medical news website, I'm well aware that drinking can increase cancer risk. I'm also aware of the studies suggesting that moderate alcohol consumption has health benefits.

It's highly likely that I subconsciously use the latter as an excuse for my occasional glass of wine: "It's good for me, so why not?!"

But, as a new statement from the American Society of Clinical Oncology (ASCO) — which was recently published in the Journal of Clinical Oncology — reveals, even light drinking could be putting my health at risk.

"Alcohol," write the study authors, "is causally associated with oropharyngeal and larynx cancer, esophageal cancer, hepatocellular carcinoma, breast cancer, and colon cancer. Even modest use of alcohol may increase cancer risk, but the greatest risks are observed with heavy, long-term use."

ASCO's conclusions come from a review of more than 150 studies looking at the link between alcohol and cancer.

What is more, the authors report that around 5.5 percent of new cancer cases and around 5.8 percent of cancer deaths worldwide are directly related to alcohol intake.

'People don't associate drinking with cancer'

Only 38 percent of people in the United States are actively cutting back on their alcohol intake as a way of reducing cancer risk.

"People typically don't associate drinking beer, wine, and hard liquor with increasing their risk of developing cancer in their lifetimes," notes Dr. Bruce Johnson, president of ASCO. But maybe it's time that we did.

"[...] limiting alcohol intake is a means to prevent cancer," adds lead statement author Dr. Noelle K. LoConte, an associate professor of medicine at the University of Wisconsin in Madison.

"The good news is that, just like people wear sunscreen to limit their risk of skin cancer, limiting alcohol intake is one more thing people can do to reduce their overall risk of developing cancer."

Dr. Noelle K. LoConte

As part of the statement, ASCO put forward some recommendations that they believe could help to reduce alcohol intake in the U.S. These include increasing the price of alcohol, raising alcohol tax, introducing stricter regulations on the sale of alcohol to minors, and incorporating alcohol control strategies in cancer prevention plans.

The statement also highlights the importance of oncologists in informing us about the cancer risks associated with alcohol intake.

"Oncology providers," write the authors, "can serve as community advisors and leaders and can help raise the awareness of alcohol as a cancer risk behavior."

Yes, ASCO's recommendations could help to reduce alcohol consumption across America, but I am a firm believer that cutting back on the booze starts with oneself.

Cutting back to cut cancer risk

Earlier this year, I took part in Dry January, a public health campaign designed to encourage people to abstain from alcohol for 1 month.

I was sure that denying myself that glass of pinot would be challenging, but I was surprised at how little I missed it.

That said, my abstinence from alcohol did not last beyond 1 month, and I suspect that this was the case for many others who participated in Dry January. I was reintroduced to Mr. Pinot at a friend's birthday party in February, and it was then that I tagged myself as a "social drinker."

By definition, a social drinker is a person who predominantly consumes alcohol in a social setting, but not to excess levels.

If I'm honest, I can't see myself abstaining from alcohol long-term; I enjoy a drink with my friends. However, given that even modest alcohol intake has been linked to cancer and other health problems, maybe we could all benefit from cutting back on the drink.

Cancer is one of America's biggest health burdens. In fact, just last year, more than 1.6 million new cancer cases were diagnosed in the U.S., and more than 595,000 people died from the disease.

I don't want to add to these statistics. So, the next time I'm out with friends and debating that extra drink, I'll be asking myself, "Is that glass of wine really worth risking my health?"

If you're looking to limit your alcohol intake, the National Institute on Alcohol Abuse and Alcoholism provide some useful tips.


Cancer immunotherapy uses melanin against melanoma

Published: November 10, 2017

Source:https://www.sciencedaily.com/releases/2017/11/171110142352.htm

Researchers have developed a melanin-enhanced cancer immunotherapy technique that can also serve as a vaccine, based on early experiments done in a mouse model. The technique is applied via a transdermal patch.

"Melanin is a natural pigment that can efficiently transform absorbed sunlight energy into heat," says Zhen Gu, corresponding author of a paper on the work and an associate professor in the joint biomedical engineering program at North Carolina State University and the University of North Carolina at Chapel Hill. "We demonstrated that melanin, which is found at high levels in melanoma, can actually be used to help treat melanoma. We do this by shining near infrared (IR) light on a therapeutic skin patch, which promotes the systemic immune response that fights cancer."

"There are a lot of immune cells in the skin, and the fundamental concept here is to train the body's immune system to respond effectively to the presence of melanoma cells -- which could both limit the likelihood of developing tumors and help the body fight off tumors that are already established," says Yanqi Ye, lead author of the work and a Ph.D. student in the joint biomedical engineering program.

The new technique starts with a lysate -- a tumor puree, made up of ruptured melanoma cells. The lysate is used to fill an array of microneedles, embedded in a polymeric transdermal patch. By itself, the lysate is inactive and harmless. But when the patch is applied to the skin, the largest immune organ of the body, the immune system knows that, whatever the lysate is, it shouldn't be there. This triggers an immune response, and that response allows the immune system to "remember" the melanoma lysate, improving its response time and efficiency should it encounter melanoma again.

Because melanoma contains high levels of the pigment melanin, the lysate-filled microneedles are fairly dark in color. They absorb light. The researchers take advantage of that in their new technique, shining near IR light onto the transdermal patch. The light is then largely absorbed by the melanin in the microneedles, which quickly raises the temperature of the skin where the patch is applied.

The local heat causes a fever-like environment in the skin and promotes the release of lysate from the microneedles, effectively attracting and activating immune cells. The increased temperature also contributes to the locally increased blood and lymphatic flow that facilitates the migration of immune cells. This increased immune response amplifies the ability of the body to remember -- and respond to -- the lysate, better protecting against incursions of melanoma.

To test the patch's potential as a vaccine, the researchers used three groups of mice: one group got the patch and was exposed to IR light; one group got the patch, but was not exposed to IR light; and one group got an empty patch. The mice had the patch on for five days. Ten days after the patch was applied, mice were injected with active melanoma cells.

Within one month, all of the mice who received the empty patch had died from melanoma. The lysate patch by itself, without exposure to near IR light, provided little protection: only 13 percent of the mice survived. Meanwhile, 100 percent of the mice that got the lysate patch and IR light survived after two months- and 87 percent of them had no tumors.

To further test the patch's therapeutic properties, researchers performed a similar experiment. Except this time, all of the mice had already developed two tumors -- one on each side of the body. The patch was placed on the tumor on the left side of their bodies.

Mice that received the lysate patch and IR light saw significant decreases in tumor volume for both tumors, though the tumor on the left (the one directly under the patch) shrank more. The patch by itself, without IR light, limited tumor growth -- particularly on the left -- but did not eradicate it.

"This demonstrates that the technology could have potential in targeting both cancer metastasis and primary tumors," says Gianpietro Dotti, coauthor of the study and a professor in the University of North Carolina School of Medicine.

The researchers then ran similar experiments using lysate made from two other cancers -- breast cancer and a second form of melanoma with limited melanin. In both cases, the researchers added melanin to the lysate to make it more light absorbent. The results were similar to those from the first form of melanoma: patches used in conjunction with near IR light got the most promising results.

"These results are encouraging, but we are in the early stages of development," Gu says. "The next step would be a large animal study to further evaluate the safety and efficacy of the technique. And while it is much too early to estimate cost, we think that the treatment could be scaled up and would be affordable."


Low-Fat Diet May Cut Pancreatic Cancer Risk for Overweight Older Women

Published: November 9, 2017

Source:https://www.cancercompass.com/cancer-news/article/59976.htm

(HealthDay News) -- A low-fat diet may lower older women's risk of pancreatic cancer, a new study suggests.

The study included more than 46,000 overweight and obese women between the ages of 50 and 79 who ate high-fat diets when they joined a clinical trial between 1993 and 1998.

Some were assigned to eat less fat and more vegetables, fruits and grains (the intervention group). Others followed their normal diet (the comparison group). This continued until 2005.

After 15 years of follow-up, 92 cases of pancreatic cancer were identified in the intervention group and 165 in the comparison group. That translates to a rate of 35 cases per 100,000 in the intervention group and 41 per 100,000 in the comparison group, the researchers said.

The study was published online recently in the Journal of the National Cancer Institute.

"Based on previous observational studies, we knew diet may play a role in the risk for pancreatic cancer in both men and women," said study first author Dr. Li Jiao. She is an associate professor of medicine-gastroenterology at Baylor College of Medicine in Houston.

But no clinical trials have investigated whether changing diet can modify the risk, she added in a college news release. Instead, the researchers behind the new study analyzed data from the Women's Health Initiative, a major research project focused on health issues for postmenopausal women.

The analysis showed that "a low-fat diet was particularly effective in reducing pancreatic cancer risk in overweight and obese postmenopausal women," Jiao said.

A low-fat diet was not found to lower the disease risk for women whose weight was normal, however. The researchers said that merits further study.

In addition, Jiao said the findings may not apply to men.


Misregulated protein breakdown promotes leukemias and brain cancer

Published: November 8, 2017

Source:https://www.sciencedaily.com/releases/2017/11/171108132040.htm

An enzyme that is responsible for the breakdown of specific amino acids in food plays a key role in the development of leukemias and brain cancer, scientists from the German Cancer Research Center (DKFZ) in Heidelberg have now reported in Nature. The researchers have hence discovered a surprising link between energy metabolism and the so-called epigenetic code. These labels in the DNA of cancer stem cells determine the activity of genes and, thus, many cellular functions. The authors think that blocking this enzyme is a promising possibility to combat cancer.

Acute myeloid leukemia (AML) is an aggressive type of blood cancer