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Forest Bathing to Boost Anticancer Immunity

The AHA! Team — Wed, 30 Jul 2025 06:38:14 +0000

Michael Greger M.D. FACLM via Nutrition Facts – Spending time in a forest, or even anticipating it, significantly lowers levels of cortisol (a stress hormone), more so than being in an urban area. Natural killer cells are one of the ways our body fights off cancer, and visiting a forest can induce a significant increase in both their numbers and their activity. I’ve previously shown how exposure to nature can have self-reported psychological benefits, but there was a dearth of data on changes in objective measurements, so I was excited to see this paper on the effects of forest bathing, “a traditional practice characterized by visiting a forest and breathing its air,” on levels of the stress hormone cortisol in the participants’ saliva. The level of cortisol in our saliva is considered an indicator of our stress level, and study participants’ salivary cortisol levels were significantly lower after walking in a forest or even just hanging out in one (“forest watching”), compared to walking or just being in a city, as you can see at 0:49 in my video Boosting Anticancer Immunity with Forest Bathing. However, the same effect was found before they went to the forest, too. Indeed, “forest bathing, in particular forest watching, was associated with significantly lower cortisol levels both before and after this practice if compared with visiting an urban area.” Therefore, it appears that just the thought of spending time in a forest relieves stress. So, “when comparing the effects of forest bathing versus urban visiting, the anticipated placebo effect…may play a more important role in influencing cortisol [stress] levels than the actual experience” of being in the forest. I was ready to dismiss this as just another nebulous psychological effect until I read this: “Studies on the effects of ‘Shinrin-yoku’ [forest bathing] on the immune function showed that visiting a forest can induce a significant increase in the number and activity of natural killer (NK) cells,” one of the ways our body fights off cancer. That got my attention. It all started with this study: Twelve men were taken on a long weekend trip to walk in the forest, and nearly all of them (11 out of 12) showed higher natural killer cell activity afterward. It wasn’t just a little increase either; they had about a 50 percent increase in NK cell activity after the trip compared to before they went to the forest, as you can see at 2:00 in my video. Now, exercise alone can affect immune function, but “there were no significant differences in walking steps before and during the trip.” The study participants were just walking in a forest instead. However, they were taken on a trip somewhere, which introduced other variables, so what about randomizing them to go on a city trip versus a forest trip? If there were some special forest effect, how long would it last? Do you have to walk in the forest every day? Before jumping into all that, let’s first see if it works in women, too. This study had the same kind of set-up, and the same kind of results: a significant boost in natural killer cell activity from walking in the woods. What’s more, this time, the participants were retested a week later, and their natural killer cell activity was still up. When they were retested a month after the trip their levels were back to baseline, as you can see at 2:45 in my video. So, walking in the woods once a week should do it, but the study involved a multi-day trip. Who can go to the forest all weekend, every weekend? How about just a day trip? The title gives it all away: “A Day Trip to a Forest Park Increases Human Natural Killer Activity and the Expression of Anti-Cancer Proteins in Male Subjects.” The same results and the same big jump measured the day after the trip compared to before and with the same staying power, as you can see at 3:08 in my video. And, natural killer cell activity was still boosted a week later. “This suggests that if people visit a suburban forest park once a week on a day trip, they may be able to maintain increased NK activity” and a boost in anticancer immune function. I’m still not convinced, though. How can you attribute the benefit to the forest itself, when all you have are before and after data? To make the case that nature had anything to do with it, you’d need a control group of study participants who took the same kind of trip but went somewhere else instead. And here we go. Again, the study title says it all: “Visiting a Forest, but Not a City, Increases Human Natural Killer Activity and Expression of Anti-Cancer Proteins.” By the end of the forest trip, the participants experienced a boost of 80 percent in NK activity after forest bathing, compared to only a 10 percent bump for the city walkers, as shown below and at 3:58 in my video. Both trips were matched for physical activity, alcohol, and sleep, too— other factors and behaviors that can affect immune function. So, we’ve got confirmation of boosted immunity, but only on the forest trip, “indicating that forest bathing does indeed enhance human NK activity.” Moreover, the researchers found that “the increased NK activity and numbers of NK cells induced by a forest bathing trip lasted more than 7 days, even 30 days, after the trip.” As you can see below and at 4:26 in my video, NK activity was still up a week later and even a bit up a month later. “This suggests that if people visit a forest once a month, they may be able to maintain increased NK activity. This may be important in health promotion and preventive medicine.” Now that we know that forest bathing induces a real effect, the next question is, Why? What is it about forests that give us the boost? (You can imagine Big Pharma wondering if it can be made into a pill.) We’ll find out next. The video I mentioned at the start is Are There Health Benefits of Spending Time in Nature?. Stay tuned for the follow-up post: Why Does Forest Bathing Boost Natural Killer Cell Function?. For other ways to improve immune function, check out related posts below. Key Takeaways Spending time in a forest, or even anticipating it, significantly lowers levels of cortisol (a stress hormone), more so than being in an urban area. Forest exposure is associated with a notable increase (around 50 percent) in NK cell activity, which plays a role in fighting off cancer. After a single forest trip, NK cell activity remains elevated for up to a week, and, in some cases, positive effects last up to a month. A day trip to the forest can be enough to maintain elevated NK cell activity if done weekly or monthly. Studies comparing forest versus city exposure confirm that forest environments uniquely boost immune function, independent of other factors like exercise and sleep. To read the original article click here.

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Cancers Can Be Detected in the Bloodstream Three Years Prior to Diagnosis

The AHA! Team — Fri, 20 Jun 2025 05:20:22 +0000

Johns Hopkins Medicine via Newswise – The study, partly funded by the National Institutes of Health, was published May 22 in Cancer Discovery. Genetic material shed by tumors can be detected in the bloodstream three years prior to cancer diagnosis, according to a study led by investigators at the Ludwig Center at Johns Hopkins, Johns Hopkins Kimmel Cancer Center, the Johns Hopkins University School of Medicine and the Johns Hopkins Bloomberg School of Public Health. The study, partly funded by the National Institutes of Health, was published May 22 in Cancer Discovery. Investigators were surprised they could detect cancer-derived mutations in the blood so much earlier, says lead study author Yuxuan Wang, M.D., Ph.D., an assistant professor of oncology at the Johns Hopkins University School of Medicine. “Three years earlier provides time for intervention. The tumors are likely to be much less advanced and more likely to be curable.” To determine how early cancers could be detected prior to clinical signs or symptoms, Wang and colleagues assessed plasma samples that were collected for the Atherosclerosis Risk in Communities (ARIC) study, a large National Institutes of Health-funded study to investigate risk factors for heart attack, stroke, heart failure and other cardiovascular diseases. They used highly accurate and sensitive sequencing techniques to analyze blood samples from 26 participants in the ARIC study who were diagnosed with cancer within six months after sample collection, and 26 from similar participants who were not diagnosed with cancer. At the time of blood sample collection, eight of these 52 participants scored positively on a multicancer early detection (MCED) laboratory test. All eight were diagnosed within four months following blood collection. For six of the eight individuals, investigators also were able to assess additional blood samples collected 3.1–3.5 years prior to diagnosis, and in four of these cases, tumor-derived mutations could also be identified in samples taken at the earlier timepoint. MCED tests “This study shows the promise of MCED tests in detecting cancers very early, and sets the benchmark sensitivities required for their success,” says Bert Vogelstein, M.D., Clayton Professor of Oncology, co-director of the Ludwig Center at Johns Hopkins and a senior author on the study. Detecting cancers years before their clinical diagnosis “Detecting cancers years before their clinical diagnosis could help provide management with a more favorable outcome,” adds Nickolas Papadopoulos, Ph.D., professor of oncology, Ludwig Center investigator and senior author of the study. “Of course, we need to determine the appropriate clinical follow-up after a positive test for such cancers.” The study was supported in part by National Institutes of Health grant #s R21NS113016, RA37CA230400, U01CA230691, P30 CA 06973, DRP 80057309, and U01 CA164975. Additional funding was provided by the Virginia and D.K. Ludwig Fund for Cancer Research, the Commonwealth Fund, the Thomas M Hohman Memorial Cancer Research Fund, The Sol Goldman Sequencing Facility at Johns Hopkins, The Conrad R. Hilton Foundation, the Benjamin Baker Endowment, Swim Across America, Burroughs Wellcome Career Award for Medical Scientists, Conquer Cancer – Fred J. Ansfield, MD, Endowed Young Investigator Award, and The V Foundation for Cancer Research. The Atherosclerosis Risk in Communities study has been funded in whole or in part with federal funds from the National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, under contract numbers 75N92022D00001, 75N92022D00002, 75N92022D00003, 75N92022D00004, and 75N92022D00005. To read the original article click here.

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6 Ways to Defuse your ‘Cancer Time Bomb’

The AHA! Team — Mon, 10 Feb 2025 06:49:02 +0000

Dr. Veronique Desaulniers via NaturalHealth365 – According to estimates by the American Cancer Society, in 2024, over 2 million new cancer cases and over 600,000 cancer deaths are projected to occur in the United States. Fifty-two years ago, a “war on cancer” was pronounced by President Nixon. Since that declaration, the United States government alone has spent well over $100 billion on cancer research in the hopes of removing the threat of this ticking ‘time bomb.’ But instead, countless lives have been lost as a result of toxic therapies and “experimental drugs” offering false hope. According to estimates by the American Cancer Society, in 2024, over 2 million new cancer cases and over 600,000 cancer deaths are projected to occur in the United States. So, how do we STOP this madness? Christopher Wild, the former director of the International Agency for Research on Cancer, clearly understands the solution to the cancer epidemic. “We cannot treat our way out of the cancer problem. More commitment to prevention and early detection is desperately needed in order to complement improved treatments and address the alarming rise in cancer burden globally.” One out of 3 women and one out of 2 men are destined to develop some form of cancer in their lifetime. So, how do we solve the problem? The answer lies in prevention through education and early detection. Scientists now recognize that we have enormous control over our health by using specific nutrients that can turn our “good genes on” and our “bad genes off.” Six ways that nature can help us diffuse our ‘cancer time bomb’ 1. Decrease cancer-promoting inflammation: Cox-2 is an enzyme responsible for increasing inflammation and promoting cancer. Choosing anti-inflammatory foods and supplements may have a significant impact on reducing inflammation in your body. A few examples are curcumin, clean fish oils, and an extract of cruciferous vegetables called DIM I3C. 2. Prevent DNA damage: Most cancers, including breast cancer, begin with some functional or structural DNA damage, which can trigger a cell to become cancerous. Sometimes a tumor-suppressor gene becomes silenced, or a tumor-promoter gene gets turned on. These nutrients have proven anti-breast cancer effects. Sulforaphane from broccoli sprouts The trace mineral selenium Genistein from fermented (organic, non-GMO) soy Curcumin EGCG found in green tea 3. Block abnormal estrogen production: Toxic aromatase inhibitors block the body’s estrogen production and have serious side effects. If you are concerned with estrogen overload, nature has provided us with natural estrogen regulators that have a protective effect. Lignans from flax seeds bind excess aggressive estrogens and expel them from the body. Melatonin is a cytotoxic hormone that literally puts breast cancer cells to sleep. Pomegranate-derived compounds exhibit anti-proliferative and anti-aromatase activity in breast cancer cells. 4. Trigger cancer cell death: Our normal healthy cells eventually go through a process called ‘apoptosis’ or cell death. Cancer cells turn a deaf ear to the signals that promote cell death. Thus, they keep replicating. Nutrients like curcumin and DIM I3C – from cruciferous vegetables – cause breast cancer cells to self-destruct. 5. Stop the growth of blood vessels that feed tumors: Once tumors develop, they create their own blood supply to feed the tumor. This process is called angiogenesis. Many nutrients can be found in a healthy diet that block this process and cause the cancer cells to “starve.” EGCG from green tea, curcumin, and omega-3 fatty acids from fish and flax are a few examples. 6. Prevent metastasis or spreading of breast cancer: Breast cancer is often associated with metastasis or spread to other organs such as the lungs, liver, and brain. Specific nutrients can actually impair the tumor’s ability to spread by blocking the enzymes that cause the “seeding” of the cancer. Here are a few examples: Sulforaphane from cruciferous vegetables and Broccoli sprouts Curcumin Green tea polyphenols Melatonin The foods and supplements mentioned here are simply the tip of the iceberg. Organic, fresh food, herbs, and spices contain a plethora of anticancer properties. Although Hippocrates had no scientific “proof” that food could heal the body, he innately knew that food was a prescription for health when he stated, “Let food be your medicine.” You CAN defuse your cancer time bomb by being proactive and by making conscious, informed decisions about your health. Editor’s note: Find out how to stop cancer cell growth naturally, own the Stop Cancer Docu-Class created by NaturalHealth365 Programs. Sources for this article include: Wiley.com NIH.gov NIH.gov NIH.gov NIH.gov NIH.gov NIH.gov NIH.gov To read the original article click here.

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Novel Antibody May be Key to Better Lung Cancer Treatment

The AHA! Team — Mon, 30 Sep 2024 08:10:14 +0000

Abigail Klein Leichman via Israel21c – Researchers develop synthetic antibody that, when combined with common lung cancer drug, prevents relapse of adenocarcinoma tumors in mouse models. Lung cancer is the leading cause of cancer-related deaths, and the most common form is a non-small-cell type called adenocarcinoma. The main course of treatment today, a kinase inhibitor drug called Osimertinib, is effective for many adenocarcinoma patients. But after a year or more, the cancer usually develops resistance to the drug and the tumor can regrow. Researchers from Israel’s Weizmann Institute of Science just reported their success in developing a novel synthetic antibody that, when combined with Osimertinib, prevents or slows drug resistance and the relapse of adenocarcinoma tumors in mouse models. Lung cancer is the leading cause of cancer-related deaths The results were published in Cell Reports Medicine. “When patients take only the drug, there can be relapse and it’s very bad for the patient because the new tumors are more aggressive,” explains lead author Arturo Simoni-Nieves, a postdoc researcher from Mexico who worked on the project in the lab of Prof. Yosef Yarden, his faculty adviser and incumbent of the Harold and Zelda Goldenberg Professorial Chair in Molecular Cell Biology. “The combination of the antibody and the drug targets two different proteins simultaneously in mouse models and helps us avoid the relapsing of the tumors,” Simoni-Nieves says. This phase of the research project took about three years to complete. “Our next task after testing is understanding the mechanism of how it works. Once we get that information, we can think about trying it with human patients,” says Simoni-Nieves. He expects this step to take another two or three years. Future clinical trials would reveal whether this novel antibody can be developed into a new treatment for lung cancer that not only inhibits the disease but also helps prevent its recurrence. “Osimertinib is the only treatment these patients have so far. Maybe with this antibody we can improve treatment,” says Simoni-Nieves. Osimertinib is the only treatment these patients have so far In addition to Simoni-Nieves and Yarden, the paper has 15 contributing authors, most from the Weizmann Institute as well as two collaborating researchers from the Graduate School of Pharmaceutical Sciences at Osaka University in Japan and three researchers in Italy, from the Department of Medical and Surgical Sciences of the University of Bologna and from the Università Cattolica del Sacro Cuore in Rome. They concluded that their EGFR-AXL antibody “holds therapeutic promise.” The study was supported by Merck KGaA, the Israel Science Foundation, the European Research Council, the Israel Cancer Research Fund and the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation. To read the original article click here.

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New Research Promises Advances to Brain Cancer Treatment

The AHA! Team — Tue, 03 Sep 2024 08:23:36 +0000

Zachy Hennessey via Israel21c – By starving tumors of glucose, researchers may have found an innovative way of selectively killing cancer cells while sparing healthy ones. A team of researchers at Ben-Gurion University has unveiled a novel approach to treating brain cancer by targeting the survival mechanisms of tumor cells under glucose starvation. Their findings, published May 14 in Nature Communications, suggest that accelerating the metabolic processes of tumor cells during glucose starvation could cause them to quickly exhaust their energy supplies and die. Research head Prof. Barak Rotblat, along with co-lead researcher Gabriel Leprivier of the Institute of Neuropathology at University Hospital Düsseldorf, discovered that tumors have less glucose compared to normal tissue. The top priority of cancer cells might be survival rather than growth This observation challenges the belief that cancer cells are primarily focused on rapid proliferation. Instead, the researchers propose that the top priority of cancer cells might be survival rather than growth. Triggering a burst of growth under glucose starvation could lead to the cells running out of energy. Cells regulate their growth based on energy availability, synthesizing fats and proteins when energy is plentiful and halting these processes when energy is scarce to avoid burning out. Tumors are often in a state of glucose starvation. By identifying and disabling the molecular mechanisms that enable their survival under these conditions, the researchers aim to selectively target cancer cells while sparing healthy ones. New research promises advances to brain cancer treatment “We may be able to target just the cancer cells and not regular cells at all, which would be a very promising step forward on the path to personalized medicine and therapeutics that do not affect healthy cells the way chemotherapy and radiation do,” Rotblat explained. The team focused on the mTOR (Mammalian Target of Rapamycin) pathway, which plays a key role in regulating cell growth based on energy levels. They identified a protein within this pathway, 4EBP1, as essential for cells to survive glucose starvation. 4EBP1 inhibits the enzyme ACC1 in the fatty acid synthesis pathway, a mechanism that cancer cells exploit to thrive in low-glucose environments. “Our discovery about glucose starvation and the role of antioxidants opens a therapeutic window to pursue a molecule which could treat glioma [brain cancer],” Rotblat noted. The potential application of this research could extend to other types of cancers. Rotblat’s team is now collaborating with BGN Technologies (BGU’s tech-transfer company) and the National Institute for Biotechnology in the Negev to develop a molecule that will block 4EBP1. This intervention would force glucose-starved tumor cells to continue synthesizing fats, depleting their energy reserves and leading to cell death. The research highlights a new direction in the pursuit of cancer treatments that target cancer cells specifically, offering a potential alternative to conventional treatments such as chemotherapy and radiation that affect healthy cells. To read the original article click here.

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New Treatment Extends Lives of People With Most Common Type of Liver Cancer

AHA Publisher — Thu, 14 May 2020 07:00:43 +0000

University of California, Los Angeles (UCLA), Health Sciences via Newswise – For the first time in over a decade, scientists have identified a first-line treatment that significantly improves survival for people with hepatocellular carcinoma, the most common type of liver cancer. Researchers found that the combination of atezolizumab, an immunotherapy drug that boosts the body’s natural defenses, and bevacizumab, an anti-angiogenesis drug that inhibits the growth of tumors’ blood vessels, improved overall survival and reduced the risk of death by 42%. It also decreased the risk of the disease worsening by 41%, and the percentage of patients whose cancer shrank or disappeared more than doubled. Results from the clinical trial were published today in the New England Journal of Medicine, and the combination is currently being reviewed for approval under the U.S. Food and Drug Administration’s Real-Time Oncology Reviewpilot program. “The therapy is a real game-changer for people diagnosed with this aggressive disease,” said the study’s principal investigator and lead author, Dr. Richard S. Finn, a professor of medicine at the David Geffen School of Medicine at UCLA and director of the signal transduction and therapeutics program at the UCLA Jonsson Comprehensive Cancer Center. “We now have a new therapy that not only improves survival for people with the disease, which is very challenging to treat, but that helps them live longer while maintaining a high quality of life.” Currently, people diagnosed with advanced liver cancer have limited treatment options, and the prognosis for survival is poor. Clinical treatment advancements have been few and far between. Until now, no new first-line therapy has been shown to improve survival since the drug sorafenib was approved in 2007. Both atezolizumab and bevacizumab are monoclonal antibodies — specialized drugs that attach themselves to specific proteins and disable them — and they have already been used alone and in combination with other therapies to treat other cancers. Atezolizumab targets a protein produced by cancer cells that shuts down the immune system’s infection-fighting T cells, preventing them from attacking the cancer. Bevacizumab interferes with a tumor’s blood supply, preventing the cancer from growing and spreading through the body. “By using these two drugs with different mechanisms of action together, we have increased the number of patients who respond to this treatment and have increased the duration of these responses as compared to the standard treatment, sorafenib,” said Finn. The trial included 501 people, aged 18 and over, from multiple centers worldwide, who had advanced metastatic or unresectable hepatocellular carcinoma. Two-thirds of participants were randomly assigned to receive the atezolizumab and bevacizumab combination, while one-third received sorafenib. Twelve months after the start of treatment, the rate of survival with the combination was 67.2%, compared with 54.6% for the group on sorafenib. “Liver cancer is one of the few cancers that is growing in incidence and death rate,” Finn said. “That’s why it’s so important that we now have something in the front-line setting – after more than a decade – that markedly improves survival in this very challenging disease.” According to the American Cancer Society, liver cancer incidence rates have more than tripled, and death rates have more than doubled, since 1980. Some 800,000 people are diagnosed with this cancer each year, and it is a leading cause of cancer deaths worldwide, accounting for more than 700,000 deaths annually. UCLA Health has a comprehensive liver cancer program with a multidisciplinary team to bring the latest treatments to people with all stages of liver cancer. Tecentriq (atezolizumab) and Avastin (bevacizumab) are registered trademarks of Genentech, a member of the Roche Group. To read the original article click here.

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Dozens of Potential Anti-Cancer Drugs Netted in Massive Screening Study

AHA Publisher — Sun, 02 Feb 2020 08:00:16 +0000

Dana-Farber Cancer Institute via Newswise – A variety of existing drugs for treating conditions such as diabetes, inflammation, alcohol abuse, and arthritis in dogs can also kill cancer cells in the lab, according to a study by scientists at Dana-Farber Cancer Institute and the Broad Institute of MIT and Harvard. Newswise — BOSTON – Nearly 50 existing non-cancer drugs were found to kill some cancer cell lines in the lab and researchers were surprised at the high yield of compounds active against cancer cells. Some of the compounds might in due course be tested in clinical trials, while others could help jump-start new drug development. Scientists reported their findings in the new journal Nature Cancer, saying they found an “unexpectedly high rate of anti-cancer activity” among 4,518 drugs that were tested against 578 laboratory cancer cell lines spanning 24 tumor types. Most of the drugs tested were not originally developed or used in oncology (cancer treatment). Using a massive search strategy designed to identify drugs that could be repurposed as cancer treatments or as candidates for cancer drug development, the scientists identified 49 non-cancer drugs that selectively killed cancer cells and whose activity against cancer could be predicted using molecular biomarkers. They reported that another 103 compounds with less selectivity against the cancer cell lines were also identified. “It is conceivable that some non-oncology drugs could be brought directly to clinical trials for testing in cancer patients,” said the authors, led by Steven Corsello, MD, of Dana-Farber, the study’s first author and the founder of the Broad’s Drug Repurposing Hub. However, they said, it is likely that the potential drug candidates will require further study and modification before being introduced into clinical studies. “We thought we’d be lucky if we found even a single compound with anti-cancer properties, but we were surprised to find so many,” said Todd Golub, MD, chief scientific officer and director of the Cancer Program at the Broad, Charles A. Dana Investigator in Human Cancer Genetics at Dana-Farber, and professor of pediatrics at Harvard Medical School. The new work is the largest study yet to employ the Broad’s Drug Repurposing Hub, a collection that currently comprises more than 6,000 existing drugs and compounds that are either FDA-approved or have been proven safe in clinical trials (at the time of the study, the Hub contained 4,518 drugs). The study also marks the first-time researchers screened the entire collection of mostly non-cancer drugs for their anti-cancer capabilities. Some of the compounds killed cancer cells in unexpected ways. “Most existing cancer drugs work by blocking proteins, but we’re finding that compounds can act through other mechanisms,” said Corsello. Some of the four-dozen drugs he and his colleagues identified appear to act not by inhibiting a protein but by activating a protein or stabilizing a protein-protein interaction. For example, the team found that nearly a dozen non-oncology drugs killed cancer cells that express a protein called PDE3A by stabilizing the interaction between PDE3A and another protein called SLFN12 — a previously unknown mechanism for some of these drugs. Most of the non-oncology drugs that killed cancer cells in the study did so by interacting with a previously unrecognized molecular target. For example, the anti-inflammatory drug tepoxalin, originally developed for use in people but approved for treating osteoarthritis in dogs, killed cancer cells by hitting an unknown target in cells that overexpress the protein MDR1, which commonly drives resistance to chemotherapy drugs. The researchers were also able to predict whether certain drugs could kill each cell line by looking at the cell line’s genomic features, such as mutations and methylation levels, which were included in the CCLE database. This suggests that these features could one day be used as biomarkers to identify patients who will most likely benefit from certain drugs. For example, the alcohol dependence drug disulfiram (Antabuse) killed cell lines carrying mutations that cause depletion of metallothionein proteins. Compounds containing vanadium, originally developed to treat diabetes, killed cancer cells that expressed the sulfate transporter SLC26A2. The observations in the study may represent starting points for new drug development. “The genomic features gave us some initial hypotheses about how the drugs could be acting, which we can then take back to study in the lab,” said Corsello. “Our understanding of how these drugs kill cancer cells gives us a starting point for developing new therapies.” This collaboration involved the Broad’s Center for the Development of Therapeutics, the PRISM team, the Cancer Data Sciences team, and the labs of Todd Golub and Matthew Meyerson, MD, PhD, of Dana-Farber and the Broad. The work was funded in part by SIGMA (Carlos Slim Foundation, Slim Initiative in Genomic Medicine for the Americas), the National Institutes of Health, the Conquer Cancer Foundation (Conquer Cancer Foundation of the American Society of Clinical Oncology), and the Next Generation Fund at the Broad Institute of MIT and Harvard. To read the original article click here.

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Discovery of Potent Immune Cell That Can Destroy Multiple Types of Cancer

AHA Publisher — Tue, 28 Jan 2020 08:00:14 +0000

Angela Betsaida B. Laguipo, BSN via News-Medical Net – The immune system is the body’s defense against harmful pathogens that may enter the body. Immune cells, such as white blood cells and macrophages work hand in hand to fight off disease-causing microorganisms, including cancer. A team of scientists at Cardiff University may have discovered a new type of immune cell that can kill most cancers, which may be dubbed as a major breakthrough in treating potentially-fatal cancers. The discovery was previously believed to be impossible, but thanks to an accidental discovery in the laboratory, the researchers found a new type of T-cell that can potentially combat cancer. The study is published in the journal Nature Immunotherapy. What They Found Since the body’s immune system targets foreign bodies, it also fight cancer cells. Immunotherapy is used to target cancer cells, but in some instances, it works only for some types. It’s usually made of white blood cells and some organs and tissues from the lymph system. For years, doctors used a treatment dubbed as CAR-T therapy, which involves getting the patient’s own immune cells and genetically modifying them. In this method, the T cells are then returned to the body where they start to hunt and kill cancer cells. However, this treatment only targets some types of cancer cells, such as bone marrow and blood cancers, but was not effective for solid tumors, which account for a majority of cancer cases. Since the scope of efficacy is limited, scientists are looking for other ways the immune system naturally attacks tumors, hoping to find something that can kill multiple cancer cells all at once. T-cell Receptor (TCR) and Cancer Cells The novel T-cell is believed to have the ability to distinguish cancer cells from healthy ones. It carries a never-before-seen receptor that latches on to most human cancers while ignoring healthy cells in the body. The surface molecule, MR1, where the new T-cell attaches to, is also found in almost all cells in the body. But they may present differently on cancer cells, permitting a single TCR to be able to effectively target many types of tumors. In laboratory studies, the researchers found that the immune cell equipped with the new receptor was revealed to kill skin, lung, colon, blood, bone, breast, kidney, ovarian, prostate, and cervical cancer. “The development of a ‘one size fits all’ type of immunotherapy, which could target different types of cancer cells and does not need to be manufactured for each individual patient, is an exciting prospect. This research represents a new way of targeting cancer cells that is really quite exciting, although much more research is needed to understand precisely how it works. It is still early days and we are a while off from confirming whether this approach will definitely work in patients,” Dr. Alasdair Rankin, Director of Research and Policy at the blood cancer charity Bloodwise, said. Novel Treatments The researchers believe that the new breakthrough could pave the way for the formulation of new and effective therapy to combat cancer. Though the discovery is still young, it serves as a stepping stone for other researchers to build on the new approach to study it further and start on both animal and human studies. “So far, the power of these immune cells to kill cancer cells has been tested in a lab dish and in mice. At the moment, this is very basic research and not close to actual medicines for patients. But in the long term, the hope is that this type of immune cell could be the basis of new immune therapies, either by infusing these cells directly into patients or by unleashing their capacity to act. There is no question that is a very exciting discovery, both for advancing our basic knowledge about the immune system and for the possibility of future new medicines,” Prof Daniel Davis, Professor of Immunology, University of Manchester, who was not involved in the study, said. To read the original article click here.

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Tips for Beating Cancer: Activate Your Body’s 5 Health Defense Systems

AHA Publisher — Fri, 20 Dec 2019 08:40:49 +0000

William W. Li, MD via Dr. Axe – Tips for beating cancer should always include dietary components, but all too often, this part of cancer treatment is ignored. We turned to William Li, MD, world-renowned doctor and author of the New York Times bestseller Eat to Beat Disease: The New Science of How Your Body Can Heal Itself to learn more about his thoughts on using food to activate our bodies’ innate healing abilities. Q: Could you share a list of the top surprising foods linked to cancer? A: There’s a laundry list of foods that increase risk for cancer, and these include some disturbingly common foods such as processed meat, which is classified as a carcinogen by the World Health Organization, and grilled meats. Grilling meat produces polycyclic aromatic hydrocarbons (PAH). These are carcinogens that form when oils from the meat drip into the flame and smoke. The rising smoke deposits the carcinogens right on the meat. High grilling temperatures also convert amino acids and proteins in meat into toxic heterocyclic amines (HCA). And if you don’t carefully clean the grill surface and leave the black char, the next time you put food on the grill, you are coating it with carcinogens. Q: We often hear that the body “wants to be well” and has an incredible capacity to heal itself. Why, do you think, don’t more oncologists talk about food choices when a person is diagnosed with cancer? A: The body is hardwired with health defense systems that work to help us resist diseases, including cancer, from the time we are born to our last breath. These health defenses, which I describe in my book Eat to Beat Disease, are: • Angiogenesis • Our regenerative system • Our microbiome • DNA protection • Our immune system These systems help our body heal itself. However, when they are weakened or damaged, cancer can develop. Oncologists aren’t trained to look at health defenses — they are trained to diagnose and treat the cancers that have evaded them. The treatments involve surgery, drugs and radiation — food is not part of their traditional toolbox. And all doctors have little to no education or training when it comes to nutrition. All of this is changing because oncologists are beginning to recognize the impact of food in cancer treatment. For example, a study by oncologists of 826 patients with Stage III colon cancer undergoing treatment found that those who ate two servings of tree nuts each week had a 57 percent improvement in survival. Another oncology study of 249 patients with various cancers who were being treated with immunotherapies found that those who did not respond were lacking a healthy bacterium in the gut microbiome called Akkermansia. The only way to grow Akkermansia is by consuming foods like pomegranate, cranberries and mangoes. This is emerging evidence that food can collaborate with medicine to improve cancer treatment. Oncologists are starting to pay attention. Q: If someone is newly diagnosed with cancer, what are the most important foods to start working into the diet right away? A: Everyone is different, and it’s important to individualize diet based on a person’s needs. For example, someone with diabetes tolerates foods differently from someone with celiac disease. But, there are some general principles for using food as medicine, especially when it comes to cancer. We know cancers grow blood vessels to feed themselves, so it’s important to eat foods that can starve cancer by cutting off these bad blood vessels. These are called antiangiogenic foods, which include: soy, tomatoes, green tea, oily fish, berries and brassica vegetables. We also know that cancers are especially dangerous because they contain cancer stem cells, which can keep cancers coming back after treatment. New research shows that cancer stem cell-killing foods exist, including purple potatoes, green tea, coffee and walnuts. We know a strong immune system can help wipe out cancer cells. Immune-boosting foods include: broccoli sprouts, blueberries and chili peppers. Eating prebiotic foods that contain fiber, like mushrooms and beans, can feed healthy gut bacteria, which helps lower inflammation and improve immunity. Other microbiome-boosting foods include fermented foods like kimchi, sauerkraut and yogurt. Knowing your health defenses, and which foods boost them, is key for using diet to fight cancer. But remember, food is not a cure, so diet is an important part of the toolbox along with modern treatments, like immunotherapy or antiangiogenic therapy. Q: Is there anything else you’d like to add? A: There are some foods that people should really think twice about consuming, because they disrupt the health defenses that help you avoid cancer. These are: processed meat, sugar sweetened beverages, artificial sweeteners, and ultra-processed foods. These foods are everywhere, and part of the typical American diet, but consuming them regularly should be considered a risk. Your health defenses can be boosted or lowered by different foods. Choose the ones that boost your health. William W. Li, MD, is an internationally renowned physician, scientist and author of the New York Times bestseller Eat to Beat Disease: The New Science of How Your Body Can Heal Itself. His groundbreaking work has led to the development of more than 30 new medical treatments and impacts care for more than 70 diseases including cancer, diabetes, blindness, heart disease and obesity. His TED Talk — Can We Eat to Starve Cancer — has garnered more than 11 million views. Dr. Li has appeared on Good Morning America, CNN, CNBC and the Dr. Oz Show, and he has been featured in USA Today, Time Magazine, The Atlantic and O Magazine. He is president and medical director of the Angiogenesis Foundation. More information can be found at: www.drwilliamli.com and on social media @drwilliamli To read the original article click here. For more articles from Dr. Axe click here.

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