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Pomegranates are some of the best foods you can eat to prevent cancer
Published: November 16, 2018
(Natural News) Why do you need to make pomegranates a part of your diet? Apart from being refreshingly delicious, pomegranates are packed with vital nutrients and offer many health benefits, among which is protection from cancer.
Fruits are an essential part of a healthy diet. A significant chunk of their nutritional profile is composed of antioxidants. These are compounds that fight free radicals, which are unstable molecules that tend to accumulate in your body because of factors like natural body processes, your diet, the presence of disease, and your environment.
High concentrations of free radicals in your body lead to oxidative stress, which damages your cells and tissues. The effects of oxidative stress can range from prematurely aging skin to serious diseases, including cardiovascular conditions, neurodegenerative diseases, and cancer.
Antioxidants modify free radicals and turn them into harmless substances your body can either process or expel without incident. In this way, they are an essential part of a substantial protection against cancer.
Pomegranates are rich in antioxidants. One cup of its seeds gives you 30 percent of the recommended daily intake (RDI) for vitamin C, known as one of the most powerful antioxidants in nature. Pomegranate peel and juice also have an abundance of punicalagins. These compounds have antioxidant properties that are three times more potent than those of either red wine or green tea, which by themselves are known for being antioxidant powerhouses.
But the cancer-fighting benefits of pomegranates do not stop with their antioxidant load. A review of the fruit’s value in cancer therapy, published in the journal Pharmacological Research, emphasized its anti-inflammatory, antiproliferative, anti-angiogenic, anti-invasive, and anti-metastatic properties as great reasons it is so effective against cancer.
Inflammation is, under normal circumstances, actually a good thing. As part of your immune response, it tells you that your immune system is up and functional. It becomes problematic when it is prolonged and persistent, becoming a risk factor for cancer and a number of other diseases. The punicalagins and other antioxidant compounds found in pomegranate are linked to reductions in inflammatory activity in breast cancer and colon cancer cells.
Angiogenesis, the formation of new blood vessels, is a key factor in metastasis or the proliferation of cancer cells to other parts of the body. Once cancer has metastasized, it becomes a lot harder to treat, so preventing angiogenesis is an important step in disrupting the disease’s progression. The extracts of pomegranate peel have been confirmed, in a study published in the journal Research in Pharmaceutical Sciences, to have both antiangiogenesis and antiproliferative effects against melanoma.
Pomegranates can also induce apoptosis, or cellular death, according to research published in Growth Hormone & IGF Research. At the end of the day, cancer cells are simply mutated cells. Causing them to undergo the natural process of cellular death by administering substances with apoptotic effects is considered one of the safest ways to kill tumor cells and treat cancer. In the study, pomegranates were shown to cause the deathof prostate cancer cells.
Other health benefits of pomegranates
Here are yet more reasons to eat more pomegranates:
Teenage Obesity May Raise Pancreatic Cancer Risk Years Later
Published: November 14, 2018
(HealthDay News) -- Obesity in the teen years may increase the risk of developing deadly pancreatic cancer in adulthood, researchers report.
The odds for this rare cancer can quadruple due to obesity, the Israeli research team found. Moreover, the risk rises as weight increases, even affecting men in the high normal weight range.
"It's been known for some time that obesity can increase an individual's risk of developing pancreatic cancer, and [this is] an important new finding suggesting that obesity and overweight in adolescence can also impact risk," said Allison Rosenzweig, a senior manager at the Pancreatic Cancer Action Network.
But being overweight or obese doesn't doom you to getting the disease, said Rosenzweig, who had no role in the study.
"Because pancreatic cancer is a relatively rare disease, thought to impact around 55,000 Americans this year, even those at an increased risk have a low likelihood of developing the disease," she said.
Also, because this study looked at retrospective data, it can't prove that excess weight is a cause of pancreatic cancer, only that an association exists.
Pancreatic cancer is the third leading cause of cancer deaths in the United States, with a five-year survival rate below 10 percent, according to the cancer network.
For the new study, researchers led by Dr. Zohar Levi, of Rabin Medical Center in Petah Tikva and Tel Aviv University, collected data on more than 1 million Jewish men and 700,000 Jewish women in Israel. Participants had physical examinations at ages 16 to 19 from 1967 to 2002.
Using the Israeli National Cancer Registry, the researchers identified cases of pancreatic cancer through 2012. Their follow-up revealed 551 new cases of pancreatic cancer.
Compared with normal weight, obesity was associated with a nearly four times higher risk for cancer among men. Among women, the risk was slightly more than four times higher, the researchers found.
Overall, the researchers attributed almost 11 percent of the pancreatic cases to teenage overweight and obesity.
The report was published online Nov. 12 in the journal Cancer.
Dr. Chanan Meydan, of the Mayanei Hayeshua Medical Center in Israel, wrote an editorial accompanying the study. He said weight gain in adolescence may increase inflammation, which damages cells and might raise cancer risk.
"It would be interesting to find whether the inflammatory process in obesity has links to the inflammatory process in malignancy. Are they connected somehow?" said Meydan.
The mechanism behind inflammation is "for the most part, a delicately balanced phenomenon with grave consequences when it's out of balance," he said.
Learning more about how this "switchboard of control" works may help scientists better understand the association between obesity and cancer, Meydan added.
Acid reflux linked with an increased chance of deadly disease such as cancer
Published: November 11, 2018
(Natural News) People who over-eat should rein in their eating habits this new year, warns a study. Researchers from the Tulane University School of Medicine discovered that frequent heartburn in older adults increases the risk of throat, tonsil, and sinus cancer in older people. In the study, the existence of heartburn increased the likelihood of developing the diseases by at least three percent.
Gastroesophageal reflux disease (GERD), which causes heartburn or acid reflux, happens when stomach acids come up the esophagus. This is known to affect 10 to 30 percent of the population, particularly older people and those who are obese. Additionally, medication for acid reflux increases your risk even further, as studies have shown that regularly taking pills can “double your chances” of developing stomach tumors.
With the results, the research team suggests senior adults with the condition be checked for head and neck cancers. According to the authors, GERD is related to “development of malignancy” in the upper digestive tract. This opens up the possibility for early detection and intervention. To note, cancers found in the respiratory system and upper digestive tracts claim 360,000 lives per year.
While most people have experienced acid reflux at some point, it is classified as a mild form of GERD if it happens once every two weeks at least, or moderate to severe if it happens at least once a week.
The group studied data from 13,805 patients aged 66 or older with either cancer of the respiratory system or the upper digestive tract, and compared them to a control group of 13,805 patients without cancer. They discovered a link between GERD and cancer in the larynx (voice box).
“This intuitively makes sense owing to the proximity to the esophagus and the readily exposed mucosa that lines the larynx, resulting in reflux-related tissue injury, mucosal inflammation, and chronic laryngitis,” according to the team.
The findings pointed that GERD was related to the cancer of the throat, tonsils, and parts of the sinuses.
Fast facts on GERD
Most instances of GERD can be modified with changes in lifestyle. Still, be on the lookout for the usual symptoms of the condition:
Acid reflux can be awful if it happens at night, as additional signs include:
Immediately look for a health care provider if GERD is accompanied by severe chest pain, shortness of breath, and pain in the arm or jaw – as this may also be the signs of a heart attack. Additionally, seek medical care if you experience severe and frequent GERD symptoms.
The likelihood of developing GERD is increased for people who are obese or have medical conditions such as a hiatal hernia (swelling of the highest point of the stomach) and connective tissue disorder. GERD can also appear during pregnancy or when the stomach is delayed with emptying.
Factors such as smoking; eating large meals or eating late in the evening; consuming fatty and fried foods; and drinking certain medicine such as aspiring all increase the likelihood of aggravating GERD.
Mammograms Do Save Lives: Study
Published: November 09, 2018
(HealthDay News) -- Women confused by the conflicting advice surrounding the benefits and timing of mammograms will be interested in a new study out of Sweden.
The research, involving more than 50,000 breast cancer patients, found that those who took part in a breast cancer screening program had a 60 percent lower risk of dying from the disease in the 10 years after diagnosis, and a 47 percent lower risk 20 years after diagnosis.
"This is really what we've been waiting for because there has been so much hoopla about mammography not reducing the death rate from breast cancer," said Dr. Lauren Cassell, chief of breast surgery at Lenox Hill Hospital in New York City. She was not involved with the study.
Many people have said it's better treatment, and not screening, that has improved survival, Cassell explained.
"But when you do pick up cancers earlier, patients do better," she said. "We've had a gut feeling that early detection makes a difference, and now we can prove it."
Study co-author Robert Smith, vice president for cancer screening at the American Cancer Society, said, "The advantage of screening is that it offers a woman, if she develops breast cancer, the opportunity to treat that cancer early when the treatment can be less aggressive and when she has more treatment choices."
Finding cancer in an early stage may also avoid aggressive treatments that can diminish quality of life, he added.
"Mammography today, in the setting of modern therapy, confers a substantial benefit to women who attend regular screening," Smith said. "The mortality reductions we observe are principally due to mammography detecting the most aggressive cancers early."
While the findings may seem obvious, the effect of mammograms on survival is something that's been debated in recent years.
The American Cancer Society recommends annual breast cancer screening for women aged 45 to 54, while the U.S. Preventive Services Task Force recommends mammograms every other year for women aged 50 to 74.
The task force says the evidence for earlier screening isn't convincing, but women should make that decision on an individual basis.
Part of the discrepancy is caused by how the evidence is gathered, Smith explained.
Much of the data that has gone into making recommendations came from older studies that weren't able to clearly break out the benefit of early screening on survival, he said.
Early screening finds cancers that wouldn't show symptoms for years, Smith said. Also, survival from breast cancer can get confused with improvements in treatment, making it hard to tease out the benefit of screening, he added.
For the new study, researchers were able to take advantage of highly detailed Swedish data that spanned 52 years. This enabled the researchers to look at data from the late 1950s to the early 1970s, when widespread screening didn't exist, and 39 years later, when widespread screening was available.
What's more, the data for the new study were "individualized" -- so researchers could look at the outcome of every woman in the registry who had breast cancer and whether she was screened or not. This enabled Smith's team to pinpoint the effect of screening on survival.
The researchers also were able to quantify the benefit of screening by looking at deaths after diagnosis.
"The latest study adds to the large body of literature that demonstrates early detection of breast cancer through screening programs saves the most lives," said Dr. Nicole Saphier, director of breast imaging at Memorial Sloan Kettering Cancer Center, Monmouth Regional, in Middletown, N.J.
Breast cancers in women aged 40 to 49 tend to grow faster than breast cancers in older women, she said. "This means mammography and early detection are essential in these women, when the chances of survival are highest," she added.
For the study, Smith and his colleagues collected data on more than 52,400 women aged 40 to 69 in Dalarna, Sweden. All were diagnosed with breast cancer between 1977 and 2015. All the patients received the latest treatment for their stage of cancer, regardless of how it was found.
Dr. Jay Baker is president of the Society of Breast Imaging. In a society news release, he said that, "The conclusion of this study could not be more clear -- modern treatments are important but not solely sufficient. Women who get regular screening mammograms cut their risk of dying of breast cancer by about half."
The Indian gooseberry and chameleon plant contain compounds that kill cancer cells
Published: November 09, 2018
(Natural News) The cost of chemotherapy is often too hard to bear. Even disregarding the physical effects of the dangerous “treatment,” the financial strain alone could force cancer patients to flirt dangerously with despair, or worse, potentially fatal “quick cures.” Yet many people forget that the solution to their condition may be in natural medicine, particularly in certain ethnomedicines found in Asia.
Two such plants were recently validated in a clinical review published in BMC Complementary and Alternative Medicine.
Here, researchers found that the chameleon plant (Houttuynia cordata) and the Indian gooseberry (Phyllanthus emblica) were able to successfully inhibit the growth of cancer cells. MTT assay and flow cytometric analysis of the ethanolic extracts of both plants revealed that compounds found in each induced apoptosis (cell death) and arrested the cell cycle of the cancer. These effects were noted to be dose-dependent.
The team likewise found that these plants displayed low toxicity to non-cancer cells. This means that while they are potent against cancer cells, they did not harm healthy ones.
It was hypothesized that these effects can be attributed to the presence of several phenolic acids, namely gallic, p-hydroxybenzoic, vanillic, syringic, p-coumaric, ferulic, and sinapinic acids.
The results of the study suggest the fermented broth of the chameleon plant or the fruit of the Indian gooseberry can be used as an alternative means to treat or prevent cancer.
Fighting the “Big C” using food
Overwhelming evidence links food to health. What you eat and how you do so directly influences how you feel, what you can do, and how vulnerable you are to disease.
Cancer is a scary medical issue to consider, but you can prevent it from happening to you by choosing to diligently follow healthy lifestyle habits. This includes skipping the burgers, chips, and cakes.
Dr. Colleen Doyle, the director of nutrition and physical activity for the American Cancer Society, notes that while “there’s no one food that will reduce your risk of this disease, it’s the synergy between many nutrients [emphasis added] – vitamins, minerals, phytochemicals, antioxidants – that’s likely to give you the most protection.”
Here are some foods that have incredible cancer-fighting properties.
Berries are excellent sources of polyphenols, antioxidants that reduce and repair damage to the cells. They also boost your immune system.
A study performed by a team from the David Geffen School of Medicine at the University of California found that black raspberries and strawberries, in particular, were the most effective in inducing cell death in cancer lines linked to the colon, oral, and breast variety. This may have something to do with a unique phytochemical called ellagic acid found in these specific berries.
Grapes contain resveratrol, a powerful antioxidant and anti-inflammatory. Studies have shown that deep purple and red grapes show the most potential in inhibiting tumor growth.
We recommend that you eat your resveratrol rather than drink it. Red wine does contain this compound, but the alcohol content found in the beverage may actually increase your risk of cancer.
The bright red color of this superfood is thanks to an antioxidant called lycopene. Data suggest that lycopene can protect cells from damage and kill off those that aren’t growing properly. They are especially useful in guarding against skin cancer as lycopene has been studied to negate the negative effects of UV light.
Cancers are vampires — so do yourself a nerdy favor and battle the disease with this yummy (though stinky) superfood. Garlic contains unique antioxidant phytochemicals that intervene in several steps of the cancer process.
To reap the full benefits of garlic, try eating them raw and as part of a homemade salad.
Blood cancers can be treated safely and naturally with cinnamon
Published: November 07, 2018
(Natural News) Cinnamon does more than add a pleasant and appetizing aroma to your favorite dishes – it can also help treat certain cancers. A study published in the Journal of Herbal Medicine found that cinnamon has the ability to modify the growth of and kill blood cancer cells.
Myeloma is a type of blood cancer. Another name for it is multiple myeloma. It’s not as rare as other types of cancer, accounting for only 2.1 percent of all cancer deaths in the U.S. in 2018. Myeloma, however, is a dangerous disease, leaving only 50.7 percent of patients alive five years after getting diagnosed with the disease.
The authors of the study looked at cinnamon as a possible natural alternative treatment for myeloma. Cinnamon’s anti-inflammatory properties are well-established – the researchers wanted to know if the spice had anti-proliferative and anti-angiogenic effectsas well.
They obtained human myeloma cell line RPMI 8226 and treated it with cinnamon bark powder extract. The authors noted that at a concentration of 72 micrograms per milliliter (mcg/mL), cinnamon caused a 50 percent inhibition of cell growth rate in the treated cancer cells compared to untreated controls.
The extract also prevented the formation of new blood vessels that may increase the tumor cells’ ability to spread or metastasize. It was further observed that the extract caused the fragmentation of cancer cell DNA, inducing apoptosis or cellular death.
Observations 24, 48, and 72 hours after treatment confirmed that the effects of cinnamon were time-dependent. DNA fragmentation was at its highest at the 72-hour mark compared to the 24- and 48-hour marks.
The researchers concluded that cinnamon may be an anti-cancer herbal medicine because of its ability to inhibit angiogenesis, prevent inflammation, and induce apoptosis in myeloma tumor cells.
The many health effects of cinnamon
Cinnamon has been used as a natural medicine about as long as it has been used as an aromatic spice. Here are some of the reasons it’s good for the body:
The Sooner You Quit Smoking, the Better
Published: November 06, 2018
(HealthDay News) -- Despite the well-known dangers of smoking, the sizable benefits of quitting may be overlooked, a new study suggests.
"These findings underscore the benefits of quitting smoking within five years, which is a 38 percent lower risk of a heart attack, stroke or other forms of cardiovascular disease," said study author Meredith Duncan, from Vanderbilt University Medical Center in Nashville.
"The bottom line is if you smoke, now is a very good time to quit," Duncan said in an American Heart Association news release.
Her team also found that it takes more than 15 years from the time you quit until your cardiovascular disease risk returns to the level of those who never smoked -- so the sooner you quit, the better.
Cigarette smoking in America is declining and leaving a growing population of former smokers. Earlier studies have hinted that the risk for heart disease lessens within a few years after quitting, but these studies haven't looked closely at smoking history, including changes in smoking habits.
In this study, Duncan and her colleagues analyzed data on the lifetime smoking histories of nearly 8,700 people who took part in the Framingham Heart Study.
At the beginning of the study, none of the participants suffered from cardiovascular disease. Over 27 years, researchers compared the risk for heart disease among people who never smoked with those who quit.
They found that more than 70 percent of heart disease occurred in current or former smokers who smoked at least 20 pack-years -- smoking one pack a day for 20 years.
But smokers who quit within the last five years cut their risk for cardiovascular disease by 38 percent, compared with people who continued to smoke. Moreover, it took 16 years after quitting for the risk of cardiovascular disease to return to the level of never smokers, the researchers found.
The findings are to be presented Sunday at the American Heart Association's annual meeting, in Chicago. Such research is considered preliminary until published in a peer-reviewed journal.
How Necessary Is HPV Cervical Cancer Screening for Women After Age 55?
Published: November 02, 2018
(HealthDay News) -- Testing for human papillomavirus (HPV) has become the standard of care in screening for cervical cancer. But now, Canadian researchers say it may become unnecessary in women aged 55 or older who have one negative result with the test.
The DNA-based HPV test is highly accurate in detecting 14 high-risk strains of the virus that causes the majority of cervical cancers.
In the new study, researchers first gathered data on more than 200,000 women living in British Columbia. They then created a mathematical model that estimated the lifetime risk of cervical cancer in older women, all of who had not been vaccinated against HPV.
The result: Just one negative HPV DNA test at the age of 55 suggested that a woman has a very low risk (less than 1 percent) of cervical cancer, and continued screening with this type of test would provide little benefit, according to the study.
However, the researchers said that regular screening with the traditional -- and cheaper -- Pap test up to age 75 may still prevent some cervical cancers. But even in that case, benefits would decline with age.
"Our results suggest that for countries that use HPV testing as part of their screening, it might be possible to stop screening earlier than we are currently doing, provided women have a negative HPV test," said study author Talia Malagon, of McGill University in Montreal.
But one obstetrician/gynecologist said it's too soon to make firm recommendations.
"I caution readers to use this data as a reason to stop performing cervical cancer screening after age 55," said Dr. Adi Davidov, who directs Ob/Gyn care at Staten Island University Hospital in New York City.
"Firstly, this study uses mathematical modeling, which may not be accurate," he said. "In addition, many patients are already skipping their annual gynecology visit because of newer recommendations of less frequent cervical cancer screening. If women stop seeing their gynecologist at age 55, I worry that other serious conditions will be left undiagnosed."
The new findings were published Nov. 1 in The Lancet Oncology journal.
Right now, most guidelines say cervical cancer screening -- done with either with the Pap test or HPV DNA test -- can be stopped after ages 65 to 69. However, there's been a lack of high-quality evidence to support this recommendation, the researchers said.
"Cervical cancers are caused by infections with oncogenic [cancer-causing] HPV types," Malagon explained in a journal news release. For decades, doctors have turned to the Pap test "to detect the precancerous lesions caused by HPV, which can then be treated before they ever progress to cervical cancer," she added.
The Pap test has saved thousands of lives, but "it is far from perfect because it does not always detect the precancerous lesions which develop into cancer," Malagon said.
"We have known for some time that directly screening instead for the HPV types that cause cervical cancer performs just as well, if not better, than [the Pap test] for screening in women below the age of 60," she said.
What hasn't been known is whether an older woman who tests negative on an HPV screen can safely stop screening, as happens for some older women whose Pap tests come back negative.
The new study might help clear up that question, Malagon said.
She cautioned that the study "does not necessarily suggest that all screening should stop at age 55, since the benefits of continued screening depend on the type of screening used. For countries that still use [Pap test] screening, screening at older ages should further reduce the risk of cervical cancer," she noted.
Furthermore, "our study did not include any cost-effectiveness analysis, which will be a useful next step to inform policy decisions before any change in guidance is considered," Malagon said.
Dr. Jill Rabin helps direct Women's Health Programs at Northwell Health in New Hyde Park, N.Y. She called the findings "interesting," but offered several caveats.
She said factors that might cause "latent" HPV to go undetected -- things like stress or certain medical conditions -- might be in play for some older women, rendering continued HPV screening valuable.
Furthermore, one rare but potentially deadly form of cervical cancer, called adenocarcinoma of the cervix, does not rely on HPV and "most likely will go undetected until its later stages if a regular routine examination is not performed," Rabin noted.
She also agreed with David that cervical cancer screening has long been a "gateway" to better gynecologic care generally.
"My concern is if they stop coming for Pap tests, they will miss an examination which may help uncover other medical and gynecological issues, such as breast, uterine, ovarian and colon cancer," Rabin said.
Even low levels of heavy metals exposure can raise your risk of cancer and multiple organ damage
Published: October 31, 2018
(Natural News) Heavy metals are all around us. You might not see them, but they are widely distributed throughout the environment thanks to their many agricultural, technological, medical, and industrial applications. You might think that if you don’t come into direct contact with these metals, your risk must be minimal, but studies show that even low levels of exposure to heavy metals increase your risk of organ damage and cancer.
The toxicity of heavy metals depends on many factors. While the dose, chemical species and method of exposure all play a role on the heavy metal’s end, there is also an individual risk element depending on your genetics, age, gender and nutritional status. However, researchers have identified a few priority metals that are of concern to everyone on account of their high toxicity: lead, mercury, arsenic, chromium and cadmium.
Researchers from Jackson State University estimate that several million people around the world are subject to chronic arsenic exposure. In places like India, Mexico, and Taiwan, the groundwater is highly contaminated with arsenic, and it also exists in the air. Most people’s biggest source of exposure is diet. This is very concerning because arsenic has been linked in epidemiological studies to problems like vascular disease, neurological disorders, diabetes, and cancer. Exposure to this metal affects all the organs.
Cadmium occurs naturally in the Earth’s crust, but its use in industrial applications like batteries, alloys and pigments is very concerning. The most common methods of exposure to this metal are through ingesting food and inhaling air or cigarette smoke that contains it. Chronic exposure to low levels of the metal has been linked to osteoporosis and emphysema. It has long been linked to lung cancer as well as that of the stomach, prostate, liver and kidney.
Chromium exposure comes from its use in wood preservation, industrial welding, pigments, leather tanning and chrome plating. Although it’s an essential nutrient that helps with metabolism, exposure to higher amounts is very dangerous. For those who aren’t exposed to it at work or due to their proximity to manufacturing plants, ingestion of food and water containing it is the most common form of exposure. It usually targets the lungs, but it is also shown to cause multi-organ toxicity, asthma, and respiratory tract cancer; those who have greater contact with it are subject to even more serious conditions.
Most people are already familiar with how toxic lead can be thanks to public awareness campaigns and the reduction of the heavy metal to a large degree from many industrial uses. Nevertheless, a quarter of homes with more than one child younger than six in the U.S. still have significant amounts of lead in dust, paint, or soil. In fact, lead poisoning is still a common pediatric health problem. It is also found in many people’s drinking water thanks to decaying infrastructure and pipes.
Lead concentrations of just one part per billion can be problematic. Lead exposure has been linked to diminished intelligence, speech problems, attention disorders, social problems, and stunted growth in children, while adults may note spontaneous miscarriage or lower sperm count from low levels of exposure. At higher exposure levels, people might experience brain or kidney damage, blood problems, and gastrointestinal disease.
Mercury is so ubiquitous in our environment that it is impossible to avoid it entirely. However, one of the biggest sources of exposure to mercury in humans comes from dental amalgams, which is something that can be easily avoided. Consumption of mercury-contaminated fish is also a major source. Mercury is toxic to the nervous system, and it can also damage the digestive, nervous, respiratory and immune systems.
Many Mistakenly Believe Alternative Therapies Can Cure Cancer
Published: October 30, 2018
(HealthDay News) -- Despite evidence to the contrary, four in 10 Americans believe alternative therapies can cure cancer, a new survey finds.
Research shows that cancer death rates are much higher among patients who use only alternative therapies than among those who receive standard cancer treatments, according to the American Society of Clinical Oncology (ASCO).
The group's second annual National Cancer Opinion Survey also found that many Americans oppose limiting cancer patients' access to opioid painkillers (such as OxyContin) and support the use of medical marijuana by cancer patients.
The high cost of cancer also emerged as a major concern among Americans.
"This survey serves as a barometer of the American people's views on important cancer-related issues," said ASCO President Dr. Monica Bertagnolli.
"It's revealed a number of critical areas we urgently need to address -- from correcting widespread misinformation about cancer treatments, to ensuring patients have access to the pain medication they need, to alleviating the financial distress both patients and their loved ones experience too frequently," Bertagnolli said in a society news release.
The online survey, conducted in July and August, included almost 4,900 U.S. adults aged 18 and older. About 1,000 have or have had cancer.
The survey found that 39 percent of respondents -- including a high number of cancer patients and family caregivers -- believe cancer can be cured using just alternative therapies, such as enzyme and oxygen therapy, diet, vitamins and minerals.
According to ASCO Chief Medical Officer Dr. Richard Schilsky, "There's no question that evidence-based cancer therapy is necessary to effectively treat the disease."
He added: "The vast majority of alternative therapies either haven't been rigorously studied or haven't been found to benefit patients. When patients are making critical decisions about which cancer treatments to undergo, it is always best to follow the evidence from well-designed research studies."
Younger people -- between 18 and 53 -- were more likely to put their faith in alternative therapies, the survey revealed.
A recent study in the Journal of the National Cancer Institute underscored the danger of such thinking: The death rate from common cancers for people who receive only alternative medicine treatments is 2.5 times higher than for patients who receive standard treatments, such as surgery, radiation, chemotherapy, immunotherapy and hormone-based therapies.
Other findings from the ASCO survey:
"Patients are right to be concerned about the financial impact of a cancer diagnosis on their families. It's clear that high treatment costs are taking a serious toll not only on patients, but also on the people who care for them," Schilsky said.
"If a family member has been diagnosed with cancer, the sole focus should be helping them get well," Schilsky said. "Instead, Americans are worrying about affording treatment, and in many cases, they're making serious personal sacrifices to help pay for their loved ones' care."
Why nutrition-based therapy works better than chemotherapy for treating cancer
Published: October 29, 2018
(Natural News) Two thousand years ago, Hippocrates said that food should be the medicine. Recent developments mirror that ancient saying when it comes to cancer therapy. An Indian study indicated that nutritional therapy possessed certain advantages over chemotherapy as a means of treating the disease.
Cancer comes in many forms that attack various parts of the body. Whatever its appearance or location, it always involves the runaway growth of cells that invade and infect healthy cells.
Most cancers are treated using chemotherapy. Synthetic drugs are applied to the tumorous region to stop the growth of cancer cells or kill them outright.
These anti-cancer drugs are expensive and painful to apply. They also have serious side effects that often undermine the already fragile health of patients.
Researchers have sought out alternative means of treating the increasing number of cancer cases in the world. They set their sights on plants, which have provided both food and medicine since the dawn of time.
Plants have provided a number of natural compounds that show great promise for treating cancer. Three out of every five approved drugs comes from a plant or another natural source.
Fighting cancer with the right nutrition instead of toxic chemicals
Nutritional therapy is a promising means of treating all kinds of disease. It places emphasis on preventing the disease from ever taking root in the body by ensuring proper, balanced nutrition.
Studies have shown connections between the onset of cancer and the diet of patients. The low consumption of whole grains is considered to be a significant factor in the development of cancer.
The “green medicines” used by nutritional therapy are less likely to have adverse effects on the body due to their organic and natural origin. In comparison, chemotherapy drugsare synthetic chemicals that are not normally found in nature, so there is a much higher chance of them causing adverse effects or getting rejected by the body.
The nutrition-based approach to fighting cancer can, therefore, be described to be chemopreventive. It relies on natural compounds that can provide both chemo-preventive effects and the significant amounts of nutrition needed by cancer patients.
Instead of bypassing the immune system of the body to directly attack the disease, it strengthens and supports the immune system so that the body has a much better chance of avoiding illness or recovering from an ailment.
Research on these natural compounds takes more time and effort compared to those covering chemotherapy and radiation therapy. It is more difficult to identify the specific dietary ingredient that is responsible for preventing cancer from spreading or developing in the first place.
Consuming functional foods boosts the immune response against cancer
Nutritional therapy works by improving digestion and nutrient absorption. It uses functional foods that are packed with nutrients such as phytochemicals.
The bioactive compounds in functional food serve to stimulate the immune system. If the immune system is unbalanced, the natural substances guide it back to its normal state.
Many epidemiological studies have taken note of the reduced risk of contracting cancer for people who consumed large amounts of fruits, vegetables, and whole grains. Such diets are also responsible for preventing heart disease.
The results of these and other studies have increased interest in nutritional therapy. Modern tools are being used to evaluate the therapeutic effects of functional foods used in diet-based treatments.
The review concluded that nutritional therapy could one day achieve viability as a treatment for lifestyle diseases, which include heart disease and obesity as well as cancer.
Study explains why tall individuals are more prone to cancer
Published: October 26, 2018
For most cancers, risk increases dramatically with age. But what about the effect of having more cells in the body? Might taller people be more prone to cancer because they have more cells?
Yes, according to Leonard Nunney, an evolutionary biologist at the University of California, Riverside, who examined data from four large-scale surveillance projects on 23 cancer categories. Each of these cancer studies established that tall individuals are at an increased risk of cancer, with overall risk increasing by about 10 percent per 10 centimeter (4 inch) increase in height.
Other researchers have proposed that that factors acting early in life -- nutrition, health, social conditions -- independently influence height and cancer risk. But Nunney, a professor of biology, challenges this hypothesis.
"I tested the alternative hypothesis that height increases cell number and that having more cells directly increases cancer risk," he said. "The data strongly supported this simple hypothesis. For most cancers, the size of the height effect is predictable from the height-related increase in cell number."
Study results appear in the Proceedings of the Royal Society B.
When Nunney performed a comparison of the observed effect of height on the risk of specific cancers for both women and men, he found that the effect of being tall on the risk of thyroid and skin cancer was high in women; for men, skin cancer stood out.
"Tall individuals are at increased risk of almost all cancers," he said. "But skin cancers -- such as melanoma -- show an unexpectedly strong relationship to height. This may be because the hormone IGF-1 is at higher levels in taller adults."
IGF-1 is a growth factor that is particularly important in early development, Nunney explained, but IGF-1 has also been linked to a higher rate of cell division in tall adults.
"If your cells divide more often, then that adds to your cancer risk," he said. "If skin cells are dividing more rapidly in tall people due to high levels of IGF-1, then this could account for the increased risk for melanoma."
Of the 18 cancers scored in both sexes, Nunney found only four showed no significant increase with height in either sex: pancreas, esophagus, stomach, and mouth.
"It is possible that these cancers are more strongly associated with environmental factors," he said. "It is possible, too, that in these tissues cell numbers do not scale with body size -- but this seems unlikely."
Nunney explained that two factors cause increased cancer risk: one is having more cells; the other is having more cell divisions.
"If you double the cells, you double the cancer risk," he said. "If you double the number of cell divisions, you more than double the cancer risk. Living a long time is the worst thing to do if you want to avoid cancer. But then what's the alternative?"
Men are taller than women on average, which may account for why men get more cancer than women.
"About a third of this effect can be accounted for by men having more cells," Nunney said. "But something else is going on to explain the rest."
Breeds of dogs also demonstrate cancer's link to height, he added.
"Smaller dogs get less cancer than bigger breeds of dogs."
Next, Nunney plans to explore how different cancers are being prevented in the body by looking at big long-lived animals.
"If all else is equal, large, long-lived animals should experience higher incidence of cancer than small, short-lived animals," he said. "After all, larger animals have more cells, more divisions, and more mutations. But they show no such tendency to be more cancer prone. This is called Peto's paradox, and I argue it can be resolved through adaptive evolution, namely, that species subject to selection for larger body size and greater longevity evolve additional layers of cancer suppression. I'm interested in exploring how as a species gets bigger and lives longer, it evolves additional barriers to cancer."
Three proteins may play key roles in female fertility and cancer biolog
Published: October 25, 2018
Three proteins regulate each other with surprising twists and turns in female mouse eggs, a finding that may play an important role in female fertility and cancer biology, according to Rutgers-led research.
The unexpected complexity in how these proteins regulate one another does not occur in any other healthy cell type, said study senior author Karen Schindler, an associate professor who specializes in infertility research in the Department of Genetics at Rutgers University-New Brunswick.
The three proteins are Aurora kinase A (AURKA), AURKB and AURKC, and the research is published in the journal Current Biology.
"Our research could provide a way to diagnose and perhaps treat certain types of infertility that end in early miscarriage," said Schindler, who works in the School of Arts and Sciences. "This work also impacts cancer biology research because we suspect that the inter-protein regulation that occurs in eggs also occurs in certain types of aggressive cancers. Therefore, the findings could be useful in thinking about precision medicine treatments for cancer patients."
Schindler, an internationally recognized expert in female gamete (egg) biology, said she specializes in infertility research because she's fascinated by the surprisingly high frequency of infertility worldwide. One in six couples struggle to start a family in the U.S. alone, she noted.
The next steps for reproductive biology include studying the genomes of infertile patients to see if mutations in their genes represent a significant percentage of the patient population with poor outcomes in an in vitro fertilization (IVF) clinic, Schindler said. The next steps for cancer biology include carefully evaluating cancers that have all three proteins and finding ways to harness their interactive regulation into a cancer therapeutic.
Scientists at the Academy of Sciences of the Czech Republic and the Spanish National Cancer Research Centre contributed to the study.
New kind of compound shows early promise against prostate cancer
Published: October 23, 2018
A new type of molecule blocks the action of genes that drive the growth of therapy-resistant prostate cancer, a new study finds.
"Rather than continue making compounds that are just like older drugs, the focus of our work has been to rethink the definition of what a drug-like molecule can be," says corresponding author Susan K. Logan, PhD, associate professor in NYU Langone's Department of Urology.
A joint research team from NYU School of Medicine and New York University found that their "cyclic peptoids" reduced the growth of prostate cancer cells in cultures by 95 percent compared to untreated cells. The experimental drugs also blocked a key, related growth signal in live animal tests.
"We designed our peptoids specifically to hit targets that are currently 'undruggable,'" such as those causing treatment-resistant prostate cancer," adds co-senior author Kent Kirshenbaum, PhD, professor in NYU's Department of Chemistry.
According to the team's report, published online October 23 in Nature Communications, the study compounds blocked growth by interfering with the interaction between the protein beta-catenin and T-cell factor (TCF) transcription factors -- proteins that turn on genes that make cells multiply.
Although the genes are critical for early development of prostate tissue, this gene activity is normally dialed down in adulthood, unless changes re-activate it, which can lead to cancer.
Unlike many existing drugs, the new compounds do not target androgen hormonal signals known to encourage prostate cancer. Most patients treated with anti-androgen drugs see their cancer growth resume within months, so the field has sought additional therapeutic strategies. Many efforts have focused on abnormal Wnt protein signals that occur in 20 percent of the most treatment-resistant prostate tumors, but none have made it to the clinic.
Wnts can cause the buildup of the protein beta-catenin in cell nuclei, where it turns on genes. Leading up to the new study, the research team had spent years designing a new class of rugged, adjustable, protein-like compounds called peptoids that are just large enough to engage with the broad, flat surfaces used by beta-catenin to interact with TCFs.
Further, the researchers knew their compound must be engineered, not just to include the right chemical components, but also to fold into a desired three-dimensional form. The researchers "stapled" together the ends of a linear peptoid molecule to form a loop-like, or cyclic, structure. This form resembled the protein hairpins that TCFs depend on to interact with beta-catenin. The stapling stiffened the peptoid such that it could occupy and block the docking site that TCFs would otherwise use.
A new generation of computer simulation tools enabled the team to see early on how drug candidates might fit into their protein target. After this virtual testing, the team then synthesized the compounds for experiments in nutrient-filled, artificial environments called spheroids, where cancer cells grow in three dimensions. Spheroids are more lifelike than in two-dimensional petri dish cultures.
In these experiments, cyclic peptoids reduced treatment-resistant prostate cancer cell growth by roughly 95 percent when compared to untreated cancer cells over 22 days, which compared to just 40 percent growth reduction in cells treated with the unstapled version of the peptoid. The compounds also decreased androgen hormonal signaling, suggesting a dual anti-cancer effect, say the authors.
The researchers also wanted to show that their lead compound could block beta-catenin signals in a live animal. They chose zebrafish, in which rare genetic changes (mutations) that let beta-catenin build up are known to keep eyes from forming. In repeated experiments in fish with such mutations, the team found that that their looping peptoids -- by blocking overactive beta-catenin, a TCF interaction similar to those affecting human prostate cancer -- rescued eye development.
Furthermore, the treatment showed no toxicity in zebrafish at the rough equivalent of a dose that may work clinically in humans. Moving forward, the team will soon test their peptoids on human prostate cancer cells grown in mice. In addition, tests are planned to see if the compound can block the beta-catenin, a TCF interaction known to encourage growth in colon and breast cancers.
Envisioning the design of a new drug class required a multi-disciplinary effort. Logan is an expert in prostate cancer, and helped to choose beta-catenin as the cyclic peptoid target. Study author and androgen expert Michael J. Garabedian, PhD of NYU Langone's Department of Microbiology has long collaborated with the team of chemists at NYU, led by senior study author Kent Kirshenbaum, who designed the peptoids.
First author Jeffrey Schneider was the MD/PhD student in Dr. Logan's lab who did much of the experimental work on the project; and co-first author, Tim Craven of NYU's Department of Chemistry designed the active cyclic peptoid. Craven is a student in the lab of Richard A. Bonneau, PhD, at the NYU Center for Genomics and Systems Biology.
Holger Knaut, PhD, an assistant professor at Skirball Institute of Biomolecular Medicine at NYU Langone, led the zebrafish work. Other study authors include Amanda Kasper, PhD, and Michael Haugbro of NYU's Department of Chemistry; Chi Y. Yun, of Skirball Institute of Biomolecular Medicine; and Erica Briggs from NYU Langone's Department of Urology.
This work was supported by National Institutes of Health grants CA112226, T32GM007308, 5T32CA009161, and NS069839, and by a National Science Foundation grant, CHE-1507964. Additional support came from NYU Department of Biology's Fleur Strand Fellowship and NYU Graduate School of Arts and Science-funded Horizon Fellowship in the Natural and Physical Sciences.
Love Organic Foods? Your Odds for Some Cancers May Fall
Published: October 22, 2018
(HealthDay News) -- Paying extra for those pricey organic fruits and vegetables might pay off: New research suggests eating them might help you dodge a cancer diagnosis.
People who consumed the most organic foods had a 25 percent lower cancer risk compared with those who ate the least, the study found.
Specifically, eating more organically grown foods was linked to a 34 percent reduced risk of postmenopausal breast cancer, a 76 percent decreased risk for all lymphomas and an 86 percent reduced risk for non-Hodgkin lymphoma, said lead researcher Julia Baudry. She is a scientist with the Center for Research and Epidemiology and Statistics at the Sorbonne Paris Cite.
"If our findings are confirmed, organic food consumption may contribute to cancer prevention," Baudry said, though the study did not prove they directly caused cancer risk to drop.
And people shouldn't stop eating fruits and vegetables if they can't afford more expensive organically grown options.
Filling your diet with fruits and vegetables is known to reduce your risk of chronic disease and cancer, regardless of whether or not they're organic, Baudry and other experts said.
Mark Guinter, a postdoctoral fellow with the American Cancer Society, said, "More importantly than anything is making sure you consume your fruits and vegetables, avoid your red and processed meat, and eat whole grains. Those are established relationships with cancer, replicated in multiple populations."
Guinter added that "if people are interested in changing their diets or buying foods that are known to help prevent their cancer risk, those would certainly be avenues to take rather than simply buying organic."
For this study, Baudry and her colleagues analyzed data from nearly 69,000 people taking part in an ongoing French study of the associations between nutrition and health.
The participants all filled out questionnaires regarding their consumption of organic products. These included fruits and vegetables, dairy, meat and fish, eggs, breads and other foods.
They also filled out annual questionnaires regarding the status of their health, including instances of cancer, and were followed for 4.5 years on average.
The researchers found an association between eating organic foods and lower cancer risk, even after taking into account other risk factors for cancer.
"We did consider a variety of factors that may be involved in the relationship," Baudry said, "such as sociodemographic, socioeconomic and lifestyle factors, as well as family history of cancer, or healthier diet in terms of nutrients and food consumption. Controlling for these factors did not substantially modify the findings."
Organic foods are grown without pesticides, fertilizers and other chemicals. Studies have shown that people who eat organic foods have lower levels of pesticide residue in their urine, she noted.
"Exposure to pesticide has been associated with higher cancer risk" in previous studies, Baudry said.
Specifically, Guinter said, this study supports results from a British study that also found an association between organic food consumption and lower risk for non-Hodgkin lymphoma.
"Whenever you see a result that's replicated like that, you find it a little more believable. There's good biologic plausibility behind it," Guinter explained.
According to Dr. Frank Hu, chair of nutrition at the Harvard T.H. Chan School of Public Health, animal studies have shown that pesticides can increase DNA damage, which can increase risk of cancer. Chemicals also can disrupt the endocrine system.
But, Guinter and Hu said, there's not enough human evidence yet upon which to base any new dietary recommendations.
People should eat right and maintain a healthy weight through diet and exercise to prevent cancer, Hu said. Cutting back on alcohol also will help.
"Basically, increasing consumption of fruits and vegetables, whether conventional or organic, can improve overall diet quality and reduce your risk of chronic disease, including cancer," said Hu, senior author of an editorial accompanying the new study.
Why some cancers affect only young women
Published: October 19, 2018
Among several forms of pancreatic cancer, one of them affects specifically women, often young. How is this possible, even though the pancreas is an organ with little exposure to sex hormones? This pancreatic cancer, known as "mucinous cyst," has strange similarities with another mucinous cancer, affecting the ovaries. By conducting large-scale analyses of genomic data, researchers at the University of Geneva (UNIGE) and at the University Hospitals of Geneva (HUG), Switzerland, in collaboration with colleagues from the United States have provided an answer: both tumours originate from embryonic germ cells. While still undifferentiated, these cells migrate to the reproductive organs. On their way, some can mistakenly stop in other organs, bringing a risk of tumour that may occur 30 years later. By allowing a better classification of these mucinous tumours, this study, to be read in the Journal of Pathology, paves the way for a more appropriate and personalized management aligned with the tumour's origin.
Mucinous tumours of the ovary and pancreas affect young women -- between 30 and 40 years of age. They take the form of a large cyst, a kind of ball filled with liquid. Rare -- they account for about 3% of ovarian and pancreatic cancers -- they are usually treated by surgery. Taken in time, the cancerous cyst is completely removed. However, in 15% of cases, the cyst breaks before surgery; the cancer cells spread into the peritoneum, giving rise to metastases that are highly resistant to chemotherapy. In such cases, the survival prognosis of patients does not exceed one year.
"Initially, this work was based on clinical observation," says study leader Dr. Intidhar Labidi-Galy, a researcher at the Translational Research Centre in Onco-haematology at the UNIGE Faculty of Medicine and a physician at the HUG. "As a specialist in ovarian cancer, I came across an article detailing the genetic profile of mucinous tumours of the pancreas. To my great surprise, they had the same genetic alterations as mucinous tumours of the ovary, although these two organs have no direct relationship with each other. Dr. Kevin Elias, assistant professor of obstetrics and gynecology at Brigham's and Women's Hospital, Boston, USA and first author of the paper, identifies the close links between the two tumours: "We found the same genetic mutations, the same types of victims -- young women, often smokers -- and, even more surprisingly, ovarian tissue in pancreatic cysts."
A common origin
Why is a non-gynaecological cancer almost exclusively female? What is the link between the ovary and the pancreas? "It is only during embryogenesis that these organs are really close. At the very beginning of pregnancy, the embryo possesses primordial germ cells -- in a way, precursors of gametes, oocytes or spermatozoa -- which, between 4 and 6 weeks of pregnancy, makes a long migration in the human body. They pass behind the future pancreas and arrive in the outline of the gonads, around the 7th week of pregnancy. Most likely, some of these germ cells stop on the way," says Dr. Labidi-Galy.
Using public databases, Kevin Elias and Petros Tsantoulis from UNIGE, together with Intidhar Labidi-Galy and co-leader Ronny Drapkin from University of Pennsylvania have developed a transcriptomic profile -- which identifies gene expression levels in a tissue -- of primordial germ cells at 6, 7, 11, 16 and 17 weeks of pregnancy, as well as of tumoral and healthy ovarian and pancreatic cells.
The researchers then compared these data, on one hand with the pancreas and on the other hand with the ovary, by studying for each of these two organs the profile of healthy tissues, mucinous tumours and other types of tumours. Their results are clear: in both cases, the transcriptomic profile of the mucinous tumour is far away from the supposed tissue of origin (ovary or pancreas), but very close to the primordial germ cells. This proves that these tumours are closer to the primordial germ cells than to the organ in which they developed.
Unexpected stops during migration
These results indicate that a stop in cell migration that occurred accidentally during the embryonic life of these women may, decades later, be expressed as cancer, depending on their other risk factors (e.g. smoking) and where in the body these primordial germ cells have settled. Indeed, while the scientists have examined the pancreas and ovary, similar cases have been reported everywhere on the migration line of germ cells, particularly in the liver or peritoneum.
"Our results will not change the surgical management of these patients, but may lead us to reflect on chemotherapy protocols. These rare tumours are a bit like the orphan diseases of cancers, for which there are no standard treatments. By linking them to other cancers, we hope to identify treatments that would be effective. For each mutation, what is the best treatment? We are here at the heart of personalized oncology: knowing your enemy in every detail makes it easier to fight him," concludes Dr. Labidi-Galy.
Increased mortality in children with inflammatory bowel disease
Published: October 18, 2018
Children who develop inflammatory bowel disease (ulcerative colitis or Crohn's disease) have an increased risk of death, both in childhood and later in life, a study from Karolinska Institutet in Sweden published in the journal Gastroenterology reports. It is therefore important that patients who are diagnosed as children are carefully monitored, argue the researchers behind the study.
The researchers identified patients with inflammatory bowel disease (IBD) such as ulcerative colitis and Crohn's disease between the years 1964 and 2014 via the Swedish patient register. Using these data, they compared mortality rates in about 9,400 children who developed IBD with those of other children.
Their results show that children who developed IBD before the age of 18 have a three to five-fold higher mortality rate than people without IBD, both during childhood and into adulthood. This translates to a 2.2-year reduction in life expectancy in individuals monitored up to the age of 65.
"It should be remembered that we're talking small differences in number of deaths," explains lead author Ola Olén, consultant and researcher at Karolinska Institutet's Department of Medicine in Solna. "Most young people with IBD do not die earlier than their peers, but a few individuals with a severe case of IBD and serious complications such as cancer greatly elevate the relative risk."
The most common cause of death was cancer, while fatalities due to IBD itself accounted for the largest relative increase in mortality.
"Individuals who are diagnosed in childhood need to be monitored carefully," says Dr Olén. "Those who might especially benefit from being closely monitored to avoid fatal intestinal cancer are children with ulcerative colitis, who also have the chronic liver disease primary sclerosing cholangitis."
IBD in adults has previously been linked to shortened life expectancy. IBD is often thought to have a more aggressive disease course in children than in adults and has been associated with several types of cancer. However, it has been unclear how life expectancy is affected by childhood-onset IBD and if the mortality rate has changed since the introduction of modern drugs.
"IBD therapy has improved greatly since the 1960s," says Dr Olén. "For one thing, we often now use new types of immunomodulating drugs. However, we couldn't see that mortality rates have gone down since their introduction."
Diets Rich in Fish Oil Could Slow the Spread and Growth of Breast Cancer Cells
Published: October 16, 2018
Omega-3 fatty acids, such as those typically contained in fish oil, may suppress the growth and spread of breast cancer cells in mice. This is according to a new study in the journal Clinical & Experimental Metastasis, which is published under the Springer imprint. According to lead author, Saraswoti Khadge of the University of Nebraska Medical Centre in the US, fatty acids stopped further delayed tumors from forming, and blocked the cancerous cells from spreading to other organs in mice. The researchers speculate that this might be because of the way in which omega-3 fatty acids support the body's immune and anti-inflammatory systems.
Two groups of adult female mice were fed a liquid diet for which the calorie count and percentage of fat that each contained were the same. The notable difference was that one diet contained plant oils rich in omega-6 polyunsaturated fats, and the other diet contained fish oil rich in omega-3 fatty acids. The mice were then injected with 4T1 breast cancer cells that cause aggressive tumors to develop in the breast. These cells are known to spread spontaneously to other parts of the body, such as bones, the lungs and liver, but less frequently to the heart, kidneys and ovaries. The mice were autopsied and studied 35 days after the breast cancer cells were injected.
Khadge and her colleagues found the chance that the breast cancer cells would take hold in the breast glands of the adult female mice was significantly lower in those on the omega 3-diet. Tumors took significantly longer to start developing in these mice, and this had an influence on their size. After 35 days, the tumors detected in their breasts were 50 per cent smaller than those that developed in the omega 6-group. The likelihood of the cancerous cells growing and spreading to other organs in the omega-3 group was also lower and these mice survived longer than those on the omega-6 diet. Indeed some of the omega-3 fed mice appeared to never develop breast cancer.
More T-cells were found in the tissue of the mice in the omega-3 group than in the omega-6 group, and these correlated with dying tumor cells. This is important because T-cells are white blood cells that play a role in strengthening the immune system against tumors. The mice fed an omega-3 diet also had less inflammation. According to Khadge this could mean that a diet rich in omega-3 fatty acids helps to suppress the type of inflammation that can trigger the rapid development and spread of tumors as well as promote T-cell responses to tumors.
"Our study emphasizes the potential therapeutic role of dietary long-chain omega-3 fatty acids in the control of tumor growth and metastasis," explains Khadge, who emphasizes that this does not mean that an omega-3 diet could summarily prevent breast cancer tumors from forming altogether.
This study is based on dietary consumption during adult life. Its findings are in line with previous studies that showed how eating fish oil based diets during pregnancy and as a child markedly suppresses the development and spread of breast cancer.
Health Tip: Considering Genetic Testing For Cancer?
Published: October 13, 2018
(HealthDay News) -- Of all cases of cancer, only 5 to 10 percent are thought to be strongly related to an inherited gene mutation, the American Cancer Society says.
While most people do not need to have predictive genetic testing, the society says testing is worth considering if you have:
A number of close relatives -- such as parents or siblings -- with cancer, especially with the same kind of cancer or stemming from the same genetic mutation.
A close family member with more than one type of cancer.
A family member who developed cancer at a younger-than-expected age.
A family member with a relatively rare cancer, such as breast cancer in a male.
If you and family members are of a certain ethnic background.
If you have a physical symptom of an inherited cancer, such as having colon polyps.
A compound found in many medicinal herbs shown to prevent cancer, blood vessel growth
Published: October 12, 2018
(Natural News) Angiogenesis, the process of forming new blood vessels, begins even before humans are born. Although important to sustaining life, angiogenesis also plays a significant role in the metastasis or proliferation of cancer cells. Because of this, stopping the process is vital to delaying the progression of cancer. As part of their quest for a safe and universally effective treatment for the disease, researchers seek natural substances that inhibit angiogenesis. Oridonin, a compound found in many medicinal herbs, is one such substance, says a study published in the journal BMC Complementary and Alternative Medicine.
The anti-tumor activity of oridonin is well-established, but information regarding its antiangiogenic effects is scarce. The researchers wrote that previous experiments on the compound did indicate its ability to inhibit the growth of capillary networks in tumors.
To test for possible antiangiogenic properties, the researchers conducted an in vitro experiment involving human umbilical vascular endothelial cells (HUVECs) and an in vivo inquiry into the embryonic vasculogenesis and postnatal regeneration of zebrafish.
Endothelial cells make up the endothelium that lines blood vessels. The researchers found that when administered with oridonin, these cells ceased their proliferation, migration, invasion and tube formation. Furthermore, the compound induced apoptosis, the process of normal cellular death. In short, oridonin caused the HUVECs to die out.
In vivo, the administration of oridonin prevented angiogenesis during the embryonic development of zebrafish. Angiogenesis was also inhibited in tail regeneration tests. Analysis showed that the compound reduced the levels of vascular endothelial growth factors, the proteins that stimulate the development of new blood vessels. In contrast, oridonin increased the levels of the gene TP53, which is expressed in the body’s bid to suppress the growth of tumors.
The researchers confirmed the antiangiogenic capabilities of oridonin which give it its antitumor and antimetastatic activities.
Natural ways to suppress cancer
Cancer is not easy to treat, but consuming the right diet can help. Here are some of the best anti-cancer foods one needs to have:
Obesity Doubles Odds for Colon Cancer in Younger Women
Published: October 11, 2018
(HealthDay News) -- While rates of colon cancer have declined among people 50 and older, they're on the rise for younger Americans. Now, new research suggests widening waistlines may be one reason why.
In the study, women aged 20 to 49 who were overweight or obese had up to twice the risk for colon cancer before age 50, compared with normal-weight women.
"Our findings really highlight the importance of maintaining a healthy weight, beginning in early adulthood, for the prevention of early onset colorectal cancer," said study co-author Yin Cao. She's an assistant professor of surgery at Washington University in St. Louis.
Even though obesity has been floated as a possible reason for rising colon cancer rates among the young, "we were surprised by the strength of the link," Cao said in a university news release.
The study wasn't designed to prove cause and effect, only an association. But one colon cancer expert wasn't surprised by the finding.
Dr. Jeffrey Aronoff, a colorectal surgeon at Lenox Hill Hospital in New York City, noted that obesity has long been a risk factor for colon cancer in people over 50. "I do believe that a healthy lifestyle, which includes diet, exercise," may help curb even younger people's odds for the disease, he said.
In the new study, Cao and her colleagues collected data on more than 85,000 U.S. women ages 25 to 44 who took part in a large, ongoing study.
Women who were heavy as teens and gained weight in early adulthood had an increased risk of colon cancer before age 50, the researchers found.
In fact, they estimated that about 22 percent of early onset colon cancers could have been prevented if those who were diagnosed had maintained a healthy weight. Across the whole American population, that could represent thousands of cases of early onset colon cancer that might be prevented.
The risk of early onset colon cancer for overweight and obese women was the same regardless of whether or not the woman had a family history of the disease.
Cao and her team members cautioned that the study cannot prove that increased weight causes early onset colon cancer, only that the two are associated. It is possible that weight is just a marker for other risk factors, such as diabetes or metabolic issues like high blood pressure or higher cholesterol, which have also been on the rise.
And the researchers stress that despite the rise in colon cancer among people under 50, it remains relatively rare, at about 8 cases per 100,000 people. Still, because screening for colon cancer usually starts at 50, those who develop it younger are often diagnosed when the disease is in its late stages and more difficult to treat.
That's why the American Cancer Society recently lowered its recommended age at which most people should have a first screening colonoscopy. The new guidelines advise that screening begins at 45, not 50 as in the previous guidelines.
Colon cancer expert Dr. Sherif Andrawes directs endoscopy at Staten Island University Hospital in New York City. He said the study "is very important and confirms a recent observation among clinicians and experts in the field."
And Andrawes said there's another reason to urge Americans to get screened for colon cancer earlier.
"A bigger concern is those younger patients with cancer present symptomatic at diagnosis -- which may reflect aggressive disease and an advanced stage at onset of discovery, which leads to overall worse outcomes in a younger individual," he said.
And what about the risk for young obese men? According to Cao's team, one limitation of the study is that it included mostly white women, so more research is needed to see if these associations hold for men and other populations.
Being obese can cause breast cancer cells to become more aggressive
Published: October 10, 2018
(Natural News) Obesity has been linked to numerous health problems like cardiovascular diseases and cancer. A recent study observed that there is a link between obesity and metastasis.
Previous studies have shown that obese individuals are more at risk of cancer. Obesity is a condition where there is an accumulation of body fat and a person’s body weight exceeds the ideal weight by at least 20 percent. This causes an expansion of adipose tissue that leads to the release of adipocyte cytokines known as adipokines. These adipokines serve as signals that help the adipose tissue perform its role in regulating cell function, as well as the prevention and spread of disease. Some examples of adipokines are: leptin, TGF-beta, adiponectin, and tumor necrosis factor.
Two major causes of breast cancer deaths in women are tumor recurrence and metastasis, which occur even after the original tumor has been surgically removed. This is why removing the tumor does not necessarily cure cancer.
In this study, conducted by researchers from Helmholtz Zentrum München, Technische Universität München (TUM), and Heidelberg University Hospital, it was determined that the rate of metastasis is altered by a change in energy metabolism. This alteration is brought about by an increase in cytokine levels, specifically TGF-beta and leptin, brought about by obesity. As a result, the function of the lipogenic enzyme Acetyl-CoA-carboxylase 1 (ACC1) in fatty acid synthesis is impaired. When ACC1 is inhibited, the fatty acid precursor acetyl-CoA accumulates and turns on specific gene switches that activate gene programs involved in metastasis. In addition to this, the release of these adipokines has also been linked to chronic inflammation where tumor cell motility, invasion, and epithelial-mesenchymal transition is favored.
This study provides further insight into the link between obesity and metastasis. Now that the molecular mechanism behind has been determined, the next step is to find out therapeutic interventions for these mechanisms.
In one experimental model, the researchers used antibodies to block the leptin receptors involved in the pathway. This led to a reduced metastasis of breast cancer cells.
According to the researchers, “Blocking the signaling pathways and switching off the metastasis-related genes could be a therapeutic target.”
Overall, this study emphasizes what people have known for a long time: Obesity is dangerous to a person’s health.
How to naturally lose weight
In order to avoid the repercussions of obesity on cancer, it is best to maintain a healthy weight. Here are some suggestions on how to naturally lose weight:
Don't Overlook Heart Care After Cancer Diagnosis
Published: October 09, 2018
(HealthDay News) -- Patients with the heart rhythm disorder atrial fibrillation are less likely to see a cardiologist or fill prescriptions for blood-thinning drugs if they've had cancer, a new study finds.
A-fib is an irregular, often rapid heart rate. Failure to take anti-clotting drugs can put these patients at increased risk of stroke, the researchers said.
"Overall, our data suggest that suboptimal [anti-clotting] care exists in A-fib patients who have a history of cancer," said study author Dr. Wesley O'Neal. He's a cardiology fellow at Emory University School of Medicine in Atlanta.
The analysis of data from 380,000 A-fib patients found that 17 percent had a history of cancer.
During just over a year of follow-up, those with a history of cancer who did see a cardiologist were more likely to fill their prescriptions for blood thinners, had a reduced risk of stroke, and did not have an increased risk of bleeding.
They also were more likely to be hospitalized, which may be due to more aggressive treatments, according to the study.
The results were published Oct. 8 in the Journal of the American College of Cardiology.
"The decision to initiate [anti-clotting] therapy or refer to a cardiology provider should be individualized to the patient, but our data suggest that cardiology providers positively influence outcomes among these patients," O'Neal said in a journal news release.
With cancer survivors in the United States expected to number more than 20 million by 2026, more attention must be paid to their long-term health needs, according to an accompanying journal editorial.
High doses of vitamin C aggressively kill cancer cells, research confirms
Published: October 07, 2018
(Natural News) If you’ve heard that high doses of vitamin C can kill cancer, there’s a good chance you’ve also heard some official-sounding organizations claiming that there is no science to back this up. However, new research shows that high doses of vitamin C can indeed fight cancer, underscoring the findings of countless other studies like it that are widely ignored by the medical industry.
Detractors choose to focus on those studies that showed it didn’t work, conveniently ignoring the fact that many of the studies that were inconclusive in this regard simply weren’t testing big enough doses to unlock its effectiveness.
Research carried out at the University of Iowa confirms that vitamin C does kill cancer cells selectively without damaging normal cells. One study showed that the vitamins can reduce mutations that cause cancer in mice, while another study showed it can kill as much as 50 percent of human lymphoma cells.
Another study, this one from the Perlmutter Cancer Center, found that injecting mice with high doses of vitamin C stopped leukemia cancer stem cells from humans from growing, probably by telling the faulty stem cells in bone marrow to die. A different study found that adding vitamin C via IV to typical chemotherapy drugs extended the average survival times of pancreatic cancer patients from 5.65 months to 12 months.
Then there’s the University of Kansas study that injected high doses of vitamin C into ovarian cells from humans. They found that the vitamin targeted the ovarian cancer cells without harming healthy cells, and they went on to repeat the study on mice and human subjects.
These findings wouldn’t be surprising to the researchers who worked on a review that was published in the Puerto Rico Health Sciences Journal in 2008. After looking at studies that used extremely higher amounts of vitamin C intravenously, they concluded that it can be effective against tumors, although they said that its efficacy could not be judged when it was administered orally.
Even though the authors called for further research into vitamin C’s cancer-fighting power, nothing was done about it at the time. After all, chemotherapy has been so profitable for the medical and pharmaceutical industries, and it would be hard to profit off of something as cheap, widely available, and unpatentable as vitamin C .
IV may not be the only way to deliver high doses of vitamin C
Some people have been getting these treatments on their own at alternative cancer clinics, but it’s not widely accepted. In addition, those who are wary of IVs find it extremely difficult to get the high blood concentration needed for this treatment to work its magic when they take it orally.
Now, however, there is a new form of vitamin C that could change everything. Liposomal vitamin C can create vitamin C levels in the blood that are 100 to 500 times greater than those normally achieved by oral ingestion, making it easier for people to fight cancer.
Liposomal vitamin C is encapsulated in lecithin, which shields it from digestive enzymes that would normally break it down. It makes its way through the digestive system with ease and is absorbed by the intestines before being transported into the liver, where it is released into the bloodstream.
This approach does away with the waste and gastric upset seen with conventional vitamin C tablets while maintaining high blood concentrations. Whether it will one day make its way into the mainstream and give riskier treatments like chemotherapy a run for their money remains to be seen, however.
Does Aspirin Help Prevent Liver Cancer?
Published: October 05, 2018
(HealthDay News) -- Take two aspirins and reduce your risk of liver cancer? New research suggests this weekly routine might help.
The researchers found that taking two or more standard-dose (325 milligram) pills a week was associated with a 49 percent lower risk of liver cancer.
"Regular use of aspirin led to significantly lower risk of developing [liver cancer], compared to infrequent or no aspirin use. And we also found that the risk declined progressively with increasing aspirin dose and duration of use," said lead study author Dr. Tracey Simon. She's a research fellow in gastroenterology at Massachusetts General Hospital in Boston.
It should be noted, however, that the study did not prove that aspirin reduced liver cause risk, just that there was an association.
For the study, researchers analyzed long-term data from more than 45,800 women and 87,500 men in the United States.
The investigators reported that aspirin's protective effect increased over time. Risk of liver cancer was 59 percent lower among those who took aspirin regularly for five years or more.
The risk reduction declined after people stopped taking aspirin, however. And it disappeared altogether eight years after aspirin was discontinued, the findings showed.
Regular use of acetaminophen (Tylenol) or nonsteroidal anti-inflammatory drugs like ibuprofen (Motrin, Advil) was not linked to reduced risk of liver cancer, according to the study. The results were published Oct. 4 in JAMA Oncology.
The findings support results from previous studies, the researchers said.
However, Simon said additional research is still needed. "Since regular aspirin use carries the risk of increased bleeding, the next step should be to study its impact in populations with established liver disease, since that group is already at risk for primary liver cancer," she said in a hospital news release.
Liver cancer is relatively rare, but it has increased in the United States over the past 40 years. Also, liver cancer death rates have risen faster than those of any other cancer, the researchers noted.
Senior study author Dr. Andrew Chan pointed out that "aspirin use is already recommended for prevention of heart disease and colorectal cancer in certain U.S. adults." Chan is the hospital's chief of clinical and translational epidemiology unit.
"These data also add to a growing list of cancers for which aspirin appears to have anti-cancer activity," he said in the news release.
This could be a rationale for more patients to discuss an aspirin regimen with their doctors, Chan said.
Could Diet Affect Breast Cancer Risk?
Published: October 03, 2018
(HealthDay News) -- Like the human gut, the breast gland has a "microbiome" that's influenced by diet, new animal research suggests.
Although the findings are preliminary, scientists hope their work might someday improve the treatment and prevention of breast cancer.
"Being able to shift the breast microbiome through diet may offer a new approach to preventing breast cancer or at least reducing the risk," said the study's lead author, Katherine Cook. She's an assistant professor at Wake Forest University School of Medicine in Winston-Salem, N.C.
For the study, the researchers fed female monkeys a high-fat Western diet or a plant-based Mediterranean diet for 2.5 years. They noted this is the rough equivalent of eight human years.
The monkeys who were fed the Mediterranean diet ended up with a different mix of bacteria in their breast tissue from those fed the Western diet -- a roughly 10-fold increase in mammary gland lactobacillus, the researchers found.
There's some evidence that this type of bacteria may help inhibit breast cancer tumor growth, the study authors said. The monkeys on the Mediterranean diet also had more bile acid in the metabolites in their breast tissue, which could also reduce breast cancer risk, the researchers said.
A Mediterranean style of eating emphasizes lots of plant-based foods, such as fruits and vegetables, whole grains, legumes and nuts. Its followers use herbs and spices instead of salt, and also limit red meat.
"We were surprised that diet directly influenced microbiome outside of the intestinal tract in sites such as the mammary gland," Cook said in a university news release. "However, we are just at the early stages of understanding how dietary effects on the microbiome might be used to protect women from breast cancer."
Much more research is needed, the researchers said. Also, it's possible that the results seen in lab studies on animals won't be replicated in humans.
Type 2 Diabetes Tied to Raised Risk of Tumors, Cancer Deaths
Published: October 02, 2018
(HealthDay News) -- Type 2 diabetes is associated with an increased risk of developing cancer and dying from certain forms of the disease, a new study suggests.
However, the researchers noted, the absolute increased risk is low.
"Our findings do not suggest that everyone who has diabetes will go on to develop cancer in later life," said study leader Hulda Hrund Bjornsdottir, from the Swedish National Diabetes Register.
Her team analyzed data gathered between 1998 and 2014 from more than 450,000 people in Sweden with type 2 diabetes and more than 2 million people without diabetes who were followed for an average of seven years. The study focused on 12 types of cancer.
The study couldn't prove cause-and-effect. However, compared to those without type 2 diabetes, people with the blood sugar disease had a 231 percent higher risk of liver cancer, a 119 percent higher risk of pancreatic cancer and a 78 percent higher risk of uterine cancer.
In addition, those with diabetes had an increased risk of penile cancer (56 percent higher), kidney cancer (45 percent higher), gallbladder and bile duct cancer (32 percent higher), and stomach cancer (21 percent higher). They also had a 20 percent higher risk of colorectal cancer and bladder cancer, and a 5 percent higher risk of breast cancer.
The research was to be presented Tuesday at the annual meeting of the European Association for the Study of Diabetes, in Berlin.
The findings don't necessarily mean that diabetes somehow causes cancer, Bjornsdottir stressed. Instead, "diabetes and cancer share certain risk factors that might contribute to these associations, including obesity, smoking and diet," she explained in a meeting news release.
When the investigators looked at the results over a 10-year period, they found there was a 38 percent greater increase in new cases of pancreatic cancer and a 30 percent greater increase in lung cancer incidence among people with type 2 diabetes than among those without the blood sugar disease.
The researchers also found that among patients with type 2 diabetes, death rates were 29 percent higher for prostate cancer, 25 percent higher for breast cancer and 9 percent higher for colon cancer, when compared with people without diabetes.
"With the number of people with type 2 diabetes doubling over the past 30 years, our findings underscore the importance of improving diabetes care," Bjornsdottir said.
Now, with diabetes tied to cancer risk, "the importance of a healthy lifestyle is clearer than ever," she added.
More than 415 million people worldwide have diabetes -- about one in 11 adults -- and the number is expected to rise to 642 million by 2040, the study authors noted.
New cancer vaccine shows early promise for patients with HER2-positive cancers
Published: September 30, 2018
Treatment with a HER2-targeted therapeutic cancer vaccine provided clinical benefit to several patients with metastatic HER2-positive cancers who had not previously been treated with a HER2-targeted therapeutic, according to data from a phase I clinical trial presented at the Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival, held Sept. 30-Oct. 3.
Among 11 evaluable patients who had received more than the lowest dose of the vaccine, six (54 percent) had clinical benefit. One patient with ovarian cancer had a complete response that lasted 89 weeks, one patient with gastroesophageal cancer had a partial response that lasted 16 weeks, and four patients (two with colon cancer, one with prostate cancer, and one with ovarian cancer) had stable disease.
"Immunotherapy marshals the exquisite specificity of the immune system to destroy cancer, and some types may have potentially fewer side effects than traditional chemotherapy," said Jay A. Berzofsky, MD, PhD, chief of the Vaccine Branch at the Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. "We are using a vaccine approach to generate an immune response to HER2, which is found at high levels on and drives the growth of several types of cancer, including breast, ovarian, lung, colorectal, and gastroesophageal cancers.
"Our results suggest that we have a very promising vaccine for HER2-overexpressing cancers," continued Berzofsky. "We hope that one day the vaccine will provide a new treatment option for patients with these cancers."
The patients' vaccines are individually customized by Berzofsky and colleagues using their own immune cells isolated from their blood. The blood-derived immune cells are modified in several ways in the laboratory. The final product, which is administered intradermally (between the layers of the skin), comprises patient-derived dendritic cells genetically modified with an adenovirus to produce parts of the HER2 protein.
Preclinical studies, which were previously published in the AACR journal Cancer Research, showed that this type of vaccine could eradicate large, established tumors as well as lung metastases in mice.
In the dose escalation portion of the phase I clinical trial, patients were injected with the vaccine on weeks 0, 4, 8, 16, and 24 after enrollment in the study. Among the six patients who received the lowest dose of the vaccine, 5 million dendritic cells per injection, no clinical benefit was seen. Among the 11 patients who received either 10 million or 20 million dendritic cells per injection, six had clinical benefit.
Adverse reactions were predominantly injection-site reactions that did not require treatment. No cardiotoxicity was seen.
"Based on the current safety and clinical benefit data, the dose of the vaccine was increased to 40 million dendritic cells per injection and the trial opened to patients who have previously been treated with a HER2-targeted therapeutic, including patients with breast cancer," said Berzofsky.
"Moving forward, we would like to investigate whether we can increase the proportion of people who benefit from treatment with the vaccine by combining it with checkpoint inhibitor therapy," he added.
According to Berzofsky, the main scientific limitation of the study is that it is a relatively small, phase I clinical trial with no placebo control. However, the approach is sufficiently promising to warrant additional trials.
What you eat can prevent, manage, or treat cancer and diabetes
Published: September 28, 2018
(Natural News) Researchers from Northwestern Polytechnical University in China and the University of Agriculture Faisalabad in Pakistan discovered that a diet’s composition affects the gut microbiota. In particular, certain diets can modulate it, which, in turn, can lead to either beneficial or adverse outcomes in a person’s health. The findings of the study, which was published in Food Science and Human Wellness, came from a comprehensive analysis of previous reports that have linked certain diets and gut microbiota.
Gut microbiota – those microorganisms that hang around a person’s gastrointestinal (GI) tract – is an indicator of how we interact with the world. In an article published in Biochemical Journal, it is described as “one of the largest interfaces between the host, environmental factors, and antigens in the human body” – and for good reason: On average, at least 60 metric tons of food pass by the GI tract in a person’s lifetime, which is composed of both harmful and beneficial microbes.
There are a lot of factors that affect the composition of gut microbiota, with most studies pointing out to diet as one of the leading factors. However, more recent studies have started to look at the correlation between food and gut microbiota as it affects the overall health of the host, and some findings report microbial communities to be vital in the development of a person.
“A disturbance in the interaction between nutrition, metabolism, and microbiome may constitute an important factor in the deregulation of normal host homeostasis,” the authors wrote. “Such disturbances in the structure and function of microbiota have been found to be related to the development of various diseases.”
For this study, they looked at how specific diets impact the gut microbiota. In essence, a basic human diet is composed of protein, fat, and carbohydrates, collectively called macronutrients. A certain diet, therefore, adjusts the ratio of these macronutrients in order to address a certain need. In particular, a diet that is high in protein produces amino acids, ammonia, and short fatty acids after proteolytic bacteria in the gut process it. However, high concentrations of ammonia are positively linked to the development of malignant growths.
The authors also looked at the impact of certain forms of fiber in the gut. Cellulose, for example, is not completely degraded in the GI tract; instead, it undergoes bacterial fermentation – along with other complex carbohydrates – which stimulates the growth of beneficial microbes such as bifidobacteria and lactobacilli.
The effects of certain dietary components were also noted in the study, particularly on how it influences the gut microbiota and the host’s overall health.
Modern Western diets, which have less fiber and vegetables, may have adverse effects on gut microbiota as some microbial species are lost. Conversely, those who have a high-fiber, low-fat diet adds more beneficial microbes to the gut and contains a smaller amount of pathogenic bacteria.
The Mediterranean diet, which contains fruits, grains, monounsaturated fat, vegetables, and polyunsaturated fats, has lower levels of Bacillaceae, Proteobacteria, and acute phase C-reactive proteins. Bacterial populations of Clostridium and Bacteroidetes, however, were higher. In addition, vegetarian diets showed increased levels of Faecalibacterium prausnitzii, Clostridium clostridioforme, and Bacteroides Prevotella, but Clostridium cluster XIVa species were lower.
In the study, the authors indicate that having a healthy gut microbiota is associated with the prevention of conditions like cancer, obesity, Type 2 diabetes, cardiovascular diseases, and Parkinson’s disease.
The authors deduced a link between diet and gut microbiota, and how it can affect a person’s overall health; however, further research is still needed to understand its exact process.
“There is still a substantial gap in our understanding of how diet modulates the microbiota and how microbiota modulates the immunity of the host,” the researchers wrote in the study. “New tools and new approaches are needed for further investigations, as the modulation of the [gastrointestinal tract] microbiota represents a promising new method for the prevention, management, and treatment of various diseases.”
Scientists find that a popular Chinese herbal medicine is effective in eliminating colon cancer cells
Published: September 26, 2018
(Natural News) Coix lacryma-jobi var. ma-yuen (Rom.Caill.) Stapf, also known as adlay, adlay millet, or Job’s tears, has been identified by previous studies as having anti-proliferative effects on lymphoma, lung cancer, and colon cancer. A study published in the journal BMC Complementary and Alternative Medicine investigated the anti-cancer effects of Coix lacryma-jobi var. ma-yuen Stapf sprout extracts (CLSE) on colorectal cancer cells.
The results convinced the researchers that CLSE may be used to treat patients with colon cancer because of its ability to suppress the cancer cells’ migration, invasion, and adhesion, as well as the growth of new blood vessels.
Protein produced in gut could stave off deadly bone marrow transplant complication
Published: September 24, 2018
Researchers at Mount Sinai have discovered that an antimicrobial protein found in the gut can stave off a common and highly lethal side effect of bone marrow transplants, according to a study published in the Journal of Clinical Investigation in September.
The protein, regenerating islet-derived 3-alpha (REG3α), is made by cells in the lining of the gastrointestinal tract. It plays a role in a complication of bone marrow transplants called graft-versus-host-disease (GVHD), in which the donated bone marrow's immune cells attack the patient's gastrointestinal tract.
This study shows that GVHD causes increased serum levels of REG3α throughout the body while, paradoxically, decreasing the production of the protein in the gastrointestinal tract as GVHD worsens.
The Mount Sinai researchers showed that mice that could not make the protein did not survive GVHD, but also found that adding REG3α to human gastrointestinal cell lines prolonged their survival, confirming its unexpected function. These findings demonstrated that REG3α, previously only considered a biomarker for GVHD, can have a role in saving patients from the disease.
While patients suffering from GVHD are normally given immune suppressants, this research suggested that enhancing the immune system with REG3α is a better strategy and may also be helpful for illnesses such as inflammatory bowel disease that also involve the immune system in the gastrointestinal tract.
"There is a way to treat immune disorders of the gastrointestinal tract by enhancing the immune system rather than suppressing it, as we do now," said lead researcher James Ferrara, MD, Ward-Coleman Chair of Cancer Medicine and Director of the Hematologic Malignancies Translational Research Center at The Tisch Cancer Institute at the Icahn School of Medicine at Mount Sinai and Co-Director of the Mount Sinai Acute GVHD International Consortium (MAGIC). "These results show a new function for the lining of the gastrointestinal tract protecting itself, leading to a new class of drugs."
Alternative therapies for breast cancer
Published: September 22, 2018
(Natural News) When you think of breast cancer, surgery and chemotherapy probably come immediately to mind. Many patients often end up undergoing one or both of these treatments, and the prospect of going under the knife or being injected with chemicals can be scarier to some people than the diagnosis itself. However, some patients are finding success with other options that rarely get mentioned in medical appointments because they don’t make their doctors any money. Here are some alternatives that are worth exploring in addition to or instead of traditional treatment.
Vitamins and minerals can have an effect on the cancer in many cases. Some of the vitamins and minerals that alternative doctors say can make a difference include vitamin E, vitamin B complex, calcium, zinc, magnesium, essential fatty acids, and coenzyme Q10.
The vitamin that tends to get the most attention when it comes to cancer is vitamin C. Researchers have shown that high doses of vitamin C can kill cancer cells. However, it works best when it is administered intravenously, bypassing the usual gut metabolism to create blood levels that are as much as 500 times higher than those achieved by oral administration. This concentration is needed for the vitamin to attack cancer cells, studies show.
Don’t overlook the importance of diet
While not everyone will see success with IV vitamin C therapy or even be willing to try it in the first place, the fact remains that vitamins can make a big difference to your health and immunity, which is extremely important when you’re fighting cancer or trying to prevent it. That’s why a healthy diet rich in organic vegetables and fruit should be the first change that anyone makes upon being diagnosed with breast cancer. It’s also important to avoid foods that are high in sugar – or even cut it out entirely if possible.
Another alternative treatment for breast cancer that is gaining some traction is saffron. A recent review in the Journal of Nutrition and Intermediary Metabolism revealed that some of the compounds found in saffron have incredibly powerful anticancer effects, killing cancer cells without damaging normal ones. Like vitamin C, however, high doses are needed to gain the effects.
Other treatments worth considering
There are lots of other approaches that people are using to supplement or replace conventional breast cancer treatment. For example, shark cartilage therapy blocks the creation the new blood vessels, starving tumors. Metabolic therapy uses approaches like detoxification, colon cleansing, and an anti-cancer diet of enzymes, whole foods, and vitamins.
Another area that deserves serious consideration is mind-body therapy. The reason that treatments like chemotherapy and surgery often fail is because on their own, they completely ignore how the mind and the body work together to maintain optimum health. Relaxation techniques, meditation and yoga are all excellent ways to reduce the stress hormones in the body that can make cancer worse. Massage therapy can help increase the protective white blood cells in breast cancer patients while taking the edge off of pain and anxiety.
Some people find that approaches like art or music therapy are also useful for relieving the pain, anxiety and stress that accompany cancer. Patients can even take the mind-body notion one step further by turning to treatments like hypnosis and biofeedback. Acupuncture can also help relieve the symptoms not only of cancer itself but also the side effects of treatment. These treatments usually work best in conjunction with other treatments rather than on their own.
It’s important to research all your options when it comes to breast cancer treatment. Even if you ultimately decide that you feel better going the conventional route, there are lots of valid alternative treatments that could increase your chances of success and mitigate the side effects.
5 Facts Every Woman Should Know About Ovarian Cancer
Published: September 19, 2018
(HealthDay News) -- The early symptoms of ovarian cancer are often confused with less serious issues, making successful treatment less likely, a cancer expert warns.
Ovarian cancer is called a "silent killer." That's because many women are diagnosed too late, said Dr. David Fishman of NewYork-Presbyterian Queens Hospital in New York City.
"Ovarian cancer takes the lives of far too many women, because of misdiagnosis, and a lack of awareness that all women are at risk of developing ovarian cancer," said Fishman, director of gynecologic oncology at the hospital.
It's important for women to know their risk of developing this deadly disease, and to recognize its earliest warning signs, Fishman said.
More than 250,000 women around the world are diagnosed with ovarian cancer every year, and 140,000 die from it, according to a hospital news release.
Fishman offered the following five facts about this type of cancer that every woman should know:
Obesity and vitamin D deficiency may indicate greater risk for breast cancer
Published: September 19, 2018
Vitamin D is already well known for its benefits in building healthy bones. A new study supports the idea that it also may reduce cancer risk as well as breast cancer mortality, especially in women with a lower body mass index. Study results are published online today in Menopause, the journal of The North American Menopause Society (NAMS).
Breast cancer remains the most common cancer in women worldwide and is the leading cause of death from cancer in women. Reproductive risk factors such as early onset of puberty, late menopause, later age at first pregnancy, never having been pregnant, obesity, and a family history have all been shown to be associated with breast cancer development. The role of vitamin D concentration in the development of breast cancer, however, continues to be debated.
This study involving more than 600 Brazilian women suggests that vitamin D may reduce cancer risk by inhibiting cell proliferation. Study results appear in the article "Low pretreatment serum concentration of vitamin D at breast cancer diagnosis in postmenopausal women."
Researchers involved in the study concluded that postmenopausal women had an increased risk of vitamin D deficiency at the time of their breast cancer diagnoses, associated with higher rates of obesity, than women of the same age group without cancer. Similar studies also have previously demonstrated a relationship between vitamin D and breast cancer mortality. Women in the highest quartile of vitamin D concentrations, in fact, had a 50% lower death rate from breast cancer than those in the lower quartile, suggesting that vitamin D levels should be restored to a normal range in all women with breast cancer.
"Although published literature is inconsistent about the benefits of vitamin D levels and breast cancer, this study and others suggest that higher levels of vitamin D in the body are associated with lowered breast cancer risk," says Dr. JoAnn Pinkerton, executive director of NAMS. "Vitamin D may play a role in controlling breast cancer cells or stopping them from growing. Vitamin D comes from direct sunlight exposure, vitamin D3 supplements, or foods rich in vitamin D."
New blood test detects early stage pancreatic cancer
Published: September 17, 2018
Pancreatic cancer is currently very difficult to detect while it is still resectable. A new blood test developed by researchers at Lund University in Sweden, Herlev Hospital, Knight Cancer Center and Immunovia AB, can detect pancreatic cancer in the very earliest stages of the disease. The results have been published in the Journal of Clinical Oncology.
Due to diffuse symptoms, pancreatic cancer is usually diagnosed very late in the disease progression. Therefore, despite pancreatic cancer representing less than 3% of all cancer cases, more people currently die from it than breast cancer. By 2030, pancreatic cancer is expected to be the second deadliest type of cancer in the world.
"Our test can detect pancreatic cancer with 96% accuracy at stage I and II, while there is still the possibility of successful surgical intervention. There is currently no cure and few treatment options for advanced pancreatic cancer, which is the late stage when pancreatic cancer is usually diagnosed," explains Carl Borrebaeck, professor at the department of Immunotechnology at Lund University.
The study used samples from patients in both Denmark and the US, at different stages of the disease.
The blood test is developed on a so-called antibody microarray that consists of hundreds of recombinant antibody fragments. These antibody fragments are specific for a number of immune-regulatory proteins, cancer-associated antigens, and so on.
Since the immune system is the first to respond to threats like complex diseases, such as cancer, autoimmune diseases and infections, the microarray was designed to mirror this early response. This provides information about the development of tumours long before being visible on CT or detected by ctDNA. From those hundreds of markers, 29 markers were selected to detect pancreatic cancer with 96% accuracy at stage I and II.
In the future, the screening method could be used to screen people who are at a higher risk of developing pancreatic cancer, such as those with a hereditary risk, newly onset diabetes patients and patients with chronic inflammation of the pancreas.
The next step has already been initiated, which is a large US prospective study for high risk individuals.
High-fat diet found to stimulate cell growth in the colon, increasing risk of colon cancer
Published: September 16, 2018
(Natural News) A high-fat diet can make the cells of your intestinal lining prone to cancer, according to a study published in Nature. These results bolster the long-standing claim stating that obesity and a high-fat, high-calorie diet are salient factors for many types of cancer.
The paper, titled “High-fat diet enhances stemness and tumorigenicity of intestinal progenitors”, illustrates how a high-fat diet affects the structure and function of the intestine in mammals. It specifically includes in the study intestinal stem cells and non-intestinal stem cells — focusing on the cells’ capacity to create and initiate tumors.
“The new study of mice suggests that a high-fat diet drives a population boom of intestinal stem cells and also generates a pool of other cells that behave like stem cells — that is, they can reproduce themselves indefinitely and differentiate into other cell types,” says co-lead author Semir Beyaz. The behavior exhibited by these cells, he says, is what brings about intestinal tumors.
To verify the correlation between stem cells and cancer linked to obesity, mice were fed with a diet consisting of 60 percent fat for a period of nine months to a year. In comparison, Americans usually consume anywhere between 20 to 40 percent of fat in their diet.
Researchers found that mice fed the high-fat diet packed 50 percent more body mass and developed more intestinal tumors compared to mice that were fed normally. The intestinal cells from the mice were then isolated and grown in a culture dish, in which researchers discovered that cells from mice under the high-fat diet brought about “mini-intestines” at a more rapid pace than the mice that were fed normally. Consequently, they also identified that mice under the high-fat diet produced progenitor cells, which are differentiated daughter of stem cells, that exhibit behavior similar to stem cells. Similarities include an extended lifespan as well as the ability to generate mini-intestines outside of its body.
Upon further study of the mice under the high-fat diet, researchers also established a presence of a hyperactivated nutrient-sensing pathway. The pathway known as the fatty acid sensor PPAR-delta functions by enabling a metabolic process to convert fat instead of carbohydrates and sugars to energy when exposed to a high-fat diet. PPAR-delta is also found to activate a gene set essential to stem cell identity. Future studies will target narrowing down possible cancer drugs that will address tumors stemming from obesity.
The study bolsters previous research which claims that obese people are more likely to have colorectal cancer, as well as those which have indicated that intestinal stem cells are the most likely to acquire mutations resulting to colon cancer. The stem cells, which last a lifetime, live in intestine linings known as the epithelium. The stem cells, in turn, create all of the different cell types that compose the epithelium.
“The epidemiological link between a high-fat diet and colorectal cancer has been reported for many years, but the underlying mechanisms were not known,” Beyaz says. “Our study for the first time showed the precise mechanisms of how a high-fat diet regulates intestinal stem cell function and how this regulation contributes to tumor formation.”
Aside from Yilmaz, an assistant professor of biology and member of Massachusetts Institute of Technology‘s (MIT) Koch Institute for Integrative Cancer Research, the research was co-authored by David Sabatini, M.D., Ph.D. of the Whitehead Institute. In addition, MIT post-doctoral student Miyeko Mana and MIT visiting scientist Jatin Roper were lead authors.
Look for Early Signs of Thyroid Cancer, Experts Urge
Published: September 15, 2018
(HealthDay News) -- Cases of thyroid cancer are on the rise in the United States, and experts want you to know how people at high risk for the disease can detect it early.
According to the American Cancer Society, 54,000 new cases will be diagnosed in the United States in 2018. And three out of four of these cases will be women. But anyone can get the disease. Symptoms can occur earlier in women, who are typically diagnosed in their 40s or 50s, while men commonly are diagnosed in their 60s or 70s.
"While the majority of thyroid cancers arise without a family history, if you have a family history of thyroid cancer, you should have any new lump or mass in your neck evaluated by your physician," said Dr. Brett Miles. He is co-chief of the division of head and neck oncology at the Icahn School of Medicine at Mount Sinai in New York City.
Also, people with a history of Hashimoto's thyroiditis, radiation exposure to the neck, or familial colon polyps are at increased risk, he added.
"A good rule of thumb is that swollen lymph nodes or lumps in your neck that do not go away after about three to four weeks should be evaluated," Miles said in a Mount Sinai news release.
Thyroid cancer facts:
Thyroid cancer is a tumor or growth in the thyroid gland in the front of the neck.
Several types of thyroid cancer exist. The most common is papillary carcinoma, which is curable, especially if caught early.
Important risk factors include: A family history of thyroid cancer; a history of radiation exposure to the head, neck or chest; or a diet low in iodine.
Regular follow-up care is an essential part of treatment.
Symptoms of thyroid cancer include:
A lump or enlarged lymph nodes in the neck.
Neck pain or tightness.
Hoarseness, persistent cough.
Difficulty swallowing or breathing.
A thyroid exam every three years if you are 20 to 39 years of age.
A thyroid exam every year if you are 40 or older.
Avoid unnecessary exposure to radiation.
Have checks often if you've been exposed to radiation of the head, neck or chest, and have a family history of thyroid cancer.
Do a thyroid neck self-exam, looking for asymmetries or protrusions below the Adam's apple.
Most thyroid cancer patients do not have any symptoms when they are diagnosed, said Dr. Raymond Chai, an assistant professor of otolaryngology at the Icahn School of Medicine at Mount Sinai.
"These cancers are often only identified during routine physical examination by a physician," Chai said. "It's important to note the vast majority of early stage thyroid cancers can be successfully treated, and that's why early detection is critical," he added.
Severe periodontitis associated with an increased risk of lung, colorectal, pancreatic cancers
Published: September 14, 2018
(Natural News) Having severe periodontal disease may increase the risk of developing certain types of cancer, according to a long-term study published in JNCI: Journal of the National Cancer Institute. Medical professionals explained that the condition, more commonly known as advanced gum disease, is usually caused by bacterial infection that damages the soft tissue and bone that support the teeth. Previous studies demonstrated a link between gum disease and cancer onset, but the mechanism behind the connection remained unclear.
A team of health experts led by epidemiologists at the Tufts University School of Medicineand the Johns Hopkins Bloomberg School of Public Health pooled data from the Atherosclerosis Risk in Communities (ARIC) study as part of the research. The cohort included up to 7,466 participants from various U.S. states — such as Maryland, Minnesota, Mississippi and North Carolina — who were followed up from the late 1990s until 2012. The cohort was composed of Caucasian and African-American participants.
The research team measured the probing depth and gingival recession at six sites on all teeth to determine the severity of periodontal disease in patients. Likewise, the experts used two-sided statistical tests to determine the patients’ cancer risk. The participants’ smoking history was also taken into account, given its link to periodontal disease onset.
Severe periodontal disease elevates colorectal, lung cancer risk
The results showed that 1,648 patients developed cancer, while 547 died of the disease during a median follow-up of 14.7 years. Likewise, the study revealed that the overall cancer risk was 24 percent higher in patients with severe periodontal disease compared with those who had mild periodontal disease and otherwise healthy controls. The findings also showed that the risk rose to 28 percent in patients with no teeth. In addition, data from subgroup analysis found an 80 percent increased risk of colorectal cancer in patients who were edentulous at baseline.
Patients with severe periodontal disease were also twice as likely to develop lung cancer than those who had no/mild periodontitis. The research team added that the risk of lung cancer was more significant in patients who did not smoke. Moreover, the findings demonstrated that severe periodontal disease was associated with a slight increase in pancreatic cancer risk.
However, the scientists added that the overall risk of cancer was weaker or not apparent among black participants, except for lung and colorectal cancers. The research team also did not observe a correlation between severe periodontal disease and increased risk of breast, prostate or blood/lymphatic cancer. The scientists added that the findings highlight the importance of expanding dental insurance to more patients.
“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. 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,” researcher Elizabeth Platz told Science Daily online.
The researchers readily acknowledged the study’s limitations and noted that the findings might warrant further investigation.
“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. 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,” first author Dominique Michaud said.
Going Vegetarian to Cut Colon Cancer Risk
Published: September 11, 2018
(HealthDay News) -- There's no disputing the fact that regular colonoscopies, now suggested to start at age 45 for those with an average risk of colorectal cancer, can help prevent the disease by finding -- and removing -- precancerous growths.
And a study of 77,000 adults published in JAMA Internal Medicine found that you can also lower your risk of this cancer by making changes in your diet right now, whatever your age.
Doctors know that eating red and processed meats raises the risk of colorectal cancer, while eating fiber-rich foods lowers it. The JAMA findings got more specific about different types of diets.
On average, eating vegetarian may lower colon cancer risk by 19 percent and rectal cancer by 29 percent compared to non-vegetarians -- people who eat meat at least once a week. Besides eating less meat, the vegetarians in the study ate fewer sweets, snacks, refined grains and high-calorie beverages and more fruits, vegetables, whole grains, beans and nuts.
However, the protective effects vary with the type of vegetarian diet, the researchers said.
By the study's numbers:
Pesco-vegetarians: Eating fish and seafood, but avoiding other meats lowers colorectal cancer risk by 43 percent.
Lacto-ovo vegetarians: Avoiding meat, but eating eggs and/or dairy products lowers colorectal cancer risk by 18 percent.
Vegans: Avoiding all meat, eggs and dairy lowers colorectal cancer risk by 16 percent.
Semi-vegetarians: Eating meat less than once a week lowers colorectal cancer risk by 8 percent.
Research can't yet explain exactly how eating vegetarian helps. But one theory says it could be because vegetarians often follow other healthy behaviors, such as exercising and not smoking, which also reduce cancer risk.
Walking: Still the Starting Line for Fitness
Published: September 06, 2018
(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
(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
(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
(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
(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.
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
(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
(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):
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
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
(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
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
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
(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
(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:
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
(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
(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
(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
(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
(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
(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
(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
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
(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
(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
(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.
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.
Blood test can predict optimal treatment for advanced prostate cancer, study finds
Published: July 24, 2018
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
(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.
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
(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:
Study Confirms Added Cancer Risk for Diabetics, Especially Women
Published: July 20, 2018
(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
(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
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
(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:
Natural solution for damage done by chemo: Omega 3s found to treat wounds from inflamed mucous membranes in cancer patients
Published: July 13, 2018
(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
(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
(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
(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
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
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
(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
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
(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
(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
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
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.
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.
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
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
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
(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
(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
(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
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
(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:
Breaking through a tumor's defenses
Published: June 7, 2018
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
(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
(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
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
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
(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
(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
(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
(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
(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
(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
(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
(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
(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
(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
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
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
(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
(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
(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:
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:
New insights into the origins of mutations in cancer
Published: May 01, 2018
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
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
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
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
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
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
(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
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
(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
(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:
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
(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
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
(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:
Want to Help Beat Colon Cancer? Live Healthy
Published: April 12, 2018
(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
(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
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
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
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
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
(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
(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:
Childhood Obesity May Be Driving More Cancers in Young Adults
Published: March 29, 2018
(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
(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
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
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
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
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
(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
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
(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
(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
(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
(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.
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
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
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
(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
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
(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
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
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
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
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
(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:
Zika virus could help combat brain cancer
Published: February 21, 2018
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
(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
(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
(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
(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
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
(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
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:
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.
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:
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
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
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
(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
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
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
(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
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:
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
(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
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
(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
(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
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
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
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
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
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
(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
(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
(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
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 a