cancer research Archives - Amazing Health Advances

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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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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Genetic Variant linked to Increased Risk of Leukemia in Hispanic/Latino Children

The AHA! Team — Fri, 17 May 2024 08:07:50 +0000

Keck School of Medicine of USC via News-Medical – Acute lymphoblastic leukemia (ALL), the most common childhood cancer, disproportionately affects children of Hispanic/Latino origin in the United States. They are 30-40% more likely to get ALL than non-Hispanic white children, but the exact genetic basis and cause of that increased risk are unknown. (ALL) disproportionately affects children of Hispanic/Latino origin in the United States Now, a study from the Keck School of Medicine of USC has revealed a key genetic variant contributing towards the increased risk, as well as details about the biological basis of ALL. The team used genetic fine-mapping analysis, a statistical method that allows researchers to disentangle the separate effects of genetic variants in a region of the genome. They identified a variant found at a relatively high frequency in people of Hispanic/Latino origin that increases ALL risk by around 1.4 times. The study, funded in part by the National Institutes of Health, was just published in the journal Cell Genomics. “Combined with the fact that around 30% of Hispanic/Latino people in the United States carry this gene variant, but it’s basically absent in people of predominantly European ancestry, we think it’s an important contributor to the increased ALL risk among this group,” said the study’s lead author, Adam de Smith, PhD, an assistant professor of population and public health sciences and a member of the USC Norris Comprehensive Cancer Center at the Keck School of Medicine, as well as a scholar of the Leukemia & Lymphoma Society. The researchers also performed tests to better understand how the variant, located on the IKZF1 gene, which underlies B-cell development, relates to ALL through its influence on the development of B-cells, a type of white blood cell known to be disrupted by the disease. “Together, the analyses in our study provide the statistical, biological and evolutionary insights behind this increased risk, and may ultimately aid scientists working to develop screening tools and therapies for ALL.” -Charleston Chiang, PhD, associate professor of population and public health sciences and associate director of the Center of Genetic Epidemiology at the Keck School of Medicine and study’s co-senior author The genetic basis of leukemia risk To pinpoint the genetic basis of the elevated ALL risk Hispanic/Latino children face, the researchers analyzed genetic data from the California Cancer Records Linkage Project. Their dataset included 1,878 Hispanic/Latino children in California with ALL and 8,411 without the condition; 1,162 non-Hispanic white children with ALL and 57,341 without; and 318 East Asian children with ALL and 5,017 without. The research team focused on the IKZF1 gene, known to relate to ALL but never before linked with ethnic risk disparities. Using genetic fine-mapping analysis, they independently analyzed each position along the gene-;known as a single nucleotide polymorphism (SNP)-;to determine whether having a certain variant increased ALL risk. They found three independent SNPs linked to higher ALL incidence, one of which was present in about 30% of people of Hispanic/Latino origin in the U.S. and less than 1% of people of primarily European origin. Although overall risk for the disease is low across all racial/ethnic groups, children with that gene variant, located at SNP rs76880433, were 1.44 times as likely to develop ALL as children without the variant. The genetic ancestry of most Hispanics/Latinos can be traced to Europe, Africa, and Indigenous America. Further investigation revealed that the risk variant was specifically linked with Indigenous American ancestry and may have become more common in this group because it conferred a selective advantage at some point in human history. Next, the Keck School of Medicine team partnered with co-senior author Vijay Sankaran, MD, PhD, an associate professor of pediatrics at Harvard Medical School and attending physician at the Dana-Farber/Boston Children’s Cancer and Blood Disorders Center, to conduct a series of experiments to better understand how the genetic variant at IKZF1 increases risk for ALL. One experiment analyzed chromatin accessibility, a test which indicates how fully a given gene can be expressed. The researchers found that the risk variant reduced chromatin accessibility, preventing IKZF1 proteins from being fully expressed. Sankaran and his team also conducted experiments with stem cells, finding that “knocking out” the IKZF1 gene caused B-cell development to stall in its early stages. “Looking at all of this together, we think that the risk variant is reducing IKZF1 expression,” de Smith said. “By doing so, it’s keeping B-cells in a more immature state, which would increase ALL risk by giving the cells more chance to develop mutations that could eventually lead to overt leukemia.” Leukemia screening and treatment The new insights about IKZF1 bring researchers one step closer to developing effective screening tools to predict who may develop ALL, but more research is needed. In addition, the findings provide important clues about potential ways to treat the disease, for instance by progressing B-cell development after it stalls. “We also need to understand whether this variant is associated with different patient outcomes, such as the risk of relapse or chances of survival, and why that might be,” de Smith said. He and his colleagues also hope to explore whether the newly identified risk variant helps explain the even higher risk of ALL among Hispanic/Latino adolescents and young adults, who are more than twice as likely to get the disease than people who are non-Hispanic white. About this research In addition to de Smith, Chiang and Sankaran, the study’s other authors are Soyoung Jeon, Jalen Langie, Tsz-Fung Chan, Steven Gazal, Nicholas Mancuso and Joseph Wiemels from the Center for Genetic Epidemiology and the USC Norris Comprehensive Cancer Center, Keck School of Medicine of USC; Lara Wahlster, Susan Black, Liam Cato, Soumyaa Mazumder and Fulong Yu from Boston Children’s Hospital and Department of Pediatric Oncology, Dana-Farber Cancer Institute; Linda Kachuri from the Stanford University School of Medicine; Nathan Nakatsuka from the New York Genome Center; Guangze Xia from the Guangzhou National Laboratory, Guangzhoi, China; Wenjian Yang and Jun Yang from St. Jude Children’s Research Hospital, Memphis; Celeste Eng, Donglei Hu, Esteban Gonzalez Burchard and Elad Ziv from the Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco; Catherine Metayer from the School of Public Health, University of California, Berkeley; and Xiaomei Ma from the Yale School of Public Health. This work was supported by the National Institutes of Health [R01CA262263, R01CA155461, R00CA246076, R35GM142783, R01DK103794, R01CA265726]; the New York Stem Cell Foundation; and the Dana-Farber Cancer Institute Presidential Priorities Initiative. Source: Keck School of Medicine of USC Journal reference: de Smith, A. J., et al. (2024) A noncoding regulatory variant in IKZF1 increases acute lymphoblastic leukemia risk in Hispanic/Latino children. Cell Genomics. doi.org/10.1016/j.xgen.2024.100526. To read the original article click here.

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Eating THESE Seeds May Reduce Breast Cancer Mortality, Study Shows

AHA Publisher — Thu, 21 Oct 2021 07:00:47 +0000

Stephanie Woods via NaturalHealth365 – Breast cancer is the second most common cancer in women in the United States, coming just behind skin cancer. It also falls just behind lung cancer as the second leading cause of death in women. An estimated 1 in 8 women will be diagnosed with breast cancer in their lifetime. And, while – conventionally speaking – doctors promote mammograms as a “helpful” diagnostic tools to detect the presence of tumors, they do nothing to decrease the risk of developing breast cancer. Thankfully, nature provided various plants that contain compounds with cancer-fighting properties. One such example is flaxseed, which according to studies may reduce the mortality rate by as much as 70%. High Concentrations of Lignans Make Flaxseed a Cancer-Fighting Superfood Flaxseed is chock full of phytoestrogens called lignans. These plant estrogens act as antioxidants in the body. You can find lignans in many common foods: Beans Pumpkin seeds Broccoli Sesame seeds Grains like oats, wheat, barley, and rye Sunflower seeds While these are all great sources, flaxseed tops them all with amounts that are much, much higher. And it seems that a high concentration of lignans is precisely what is needed when fighting breast cancer. Impressive Research Shows Flaxseed Reduces Tumor Growth A review of research on flaxseed and breast cancer from the University of Toronto highlights some exciting discoveries that could mean very good news for cancer patients. Observational studies showed a reduced breast cancer risk (primarily among postmenopausal women) in connection with the intake of flaxseed, urinary excretion, or serum levels. A 33% to 70% reduction in breast cancer mortality was attributed to lignans. Most animal studies maintaining a diet that is 2.5% to 10% flaxseed, flaxseed oil, or the equivalent amount of lignans reduces the growth of tumors. Clinical trials found that tumor growth in breast cancer patients was reduced after patients were given 25 grams of flaxseed a day for 32 days. That’s not all! Flaxseed boosts brain health as well which helps with mental health issues like depression and anxiety. Flaxseed Protects Women From Breast Cancer in MULTIPLE Ways Science has identified several ways that flaxseed can help protect women from breast cancer: It decreases the proliferation of tumor cells Lignans block the blood supply to the tumor It lowers the risk of metastasis Lignans block estrogen receptors and lower excess estrogen production Study after study shows that flaxseed is not only a powerful cancer fighter, but it can also reduce your risk of cancer. Best of all, it is something you can start adding to your diet today. Here Is How to Incorporate Flaxseeds Into Your Diet Most of the studies found that 2.5 tablespoons of flaxseed, just 25 grams, is effective in fighting cancer. Postmenopausal women can safely have up to 40 grams a day. But how do you do it? Flaxseed isn’t that tasty on its own, but you can still get the benefits by adding it to foods you are already eating such as: Oatmeal Mashed sweet potato Smoothies Salad Yogurt Cereal Soups Muffins Bread Naturally, you should look for organic brown or golden flaxseeds to ensure purity and avoid varieties that may be polluted with agrochemicals. Grinding your flaxseed will make it easier to incorporate into your foods, but when it is ground it does go rancid fairly quickly. You want to grind about a week’s worth of flaxseed at a time and store it in the refrigerator or freezer in an airtight container. It is also recommended that you work up to at least 2 tablespoons but give your body time to get used to all the fiber by incremental increases. Making this small change to your diet could save your life. Sources for this article include: Cancer.org GreenMedInfo.com AICR.org To read the original article click here.

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Study Opens the Way for a Potential New Cure for Children with Hard-to-Treat Neuroblastoma

AHA Publisher — Mon, 11 Jan 2021 08:00:58 +0000

University of Gothenburg via News-Medical Net – Researchers at the University of Gothenburg now suggest a possible cure for children with hard-to-treat forms of neuroblastoma using a new combination of drugs. In a new study in the journal Cancer Research, they describe how a two small molecule-based drug combination likely inhibit the tumor’s growth. Neuroblastoma is the most common form of childhood cancer, derived from the peripheral nervous system, i.e., the part of the nervous system that is not the brain or spinal cord. The disease can occur in the chest, neck, abdomen and adrenal glands and can also spread to the spine. Symptoms include general aches, anemia and skeletal pain. The average age of children at diagnosis is 17 months, and it is rarely diagnosed over the age of five. The milder form of neuroblastoma can, in some cases, self-heal, while the more aggressive form is the deadliest form of childhood cancer. Treatment is successful in less than half of these cases. A Long Noncoding RNA Molecule Influences Tumor Suppressor Gene Expression Central molecule in the study is the p53 gene. The p53 gene is often mutated in other cancer forms but rarely in neuroblastoma. When it is not mutated, p53 codes for a protein that inhibit the growth of cancer. This study shows that how the expression levels of a long non-coding RNA molecule influences the function of p53 protein. Interestingly, this long non-coding RNA increases p53 function in the nucleus to make tumor cells more susceptible to cytostatic treatment.” (Chandrasekhar Kanduri, Professor, Medical genetics specialized in RNA epigenetics, University of Gothenburg) Two Small Molecule-Based Drug Combination for Neuroblastoma The RNA molecule NBAT1 changes the function of the protein CRM1, which transports p53 from nucleus to cytoplasm. NBAT1 also helps in keeping the p53 protein in the nucleus to increase p53 controlled gene expression. Based on these findings, the research group tested a new treatment that combines the drugs Selinexor and Nutlin-3a. Both drugs are currently undergoing clinical trials for cancer treatments but not for neuroblastoma. Selinexor restores p53’s ability to inhibit cancer growth and Nutlin-3a inhibits the breakdown of p53. “The combination treatment blocks the protein export function of CRM1, which leads to p53 accumulation in the cell nucleus. This treatment increases p53 dependent functions, such as DNA damage and cell death. We think that combining these two drugs with current treatment strategies may allow us to cure hard-to-treat neuroblastomas.” The results are promising, but they are based on preclinical studies of cancer cell lines and mouse models (xenografts) and more research is needed before the findings can be translated into treatment. These laboratory results have been partly validated with the neuroblastoma patient data, obtained in collaboration with the researchers at Karolinska Institutet. Thus, this study has clearly opened the way for a potential new treatment strategy for high-risk neuroblastoma patients. To read the original article click here.

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New Immunotherapy Shows Promise Against Rare Childhood Cancer

AHA Publisher — Mon, 30 Nov 2020 08:00:55 +0000

University College London via EurekAlert – A novel CAR T-cell therapy developed by researchers at UCL and designed to target cancerous tumours, has shown promising early results in children with neuroblastoma, a rare form of childhood cancer. For this proof-of-principle study, researchers at the UCL Great Ormond Street Institute for Child Health (GOS ICH) and the UCL Cancer Institute modified the patient’s own T-cells (a type of immune cell), equipping them to recognise and kill neuroblastoma tumour cells. Twelve children with relapsed or refractory (where the disease does not respond to treatment) neuroblastoma were treated as part of the Cancer Research UK-funded phase I clinical trial. The research, published in Science Translational Medicine, is one of the first studies to demonstrate CAR T-cells achieving rapid regression against a solid cancer (non-blood cancer). Although the beneficial effects only lasted a short while, the study provides important evidence that this specific CAR T-cell treatment could be used as a future treatment for children with solid cancers. Neuroblastoma is a rare type of cancer that mostly affects babies and young children and develops from specialised nerve cells (neuroblasts) left behind from a baby’s development in the womb. Up to 100 children in the UK are diagnosed with neuroblastoma each year. Current treatment for children with an aggressive type of neuroblastoma includes surgical removal, chemotherapy with stem-cell transplant, radiotherapy and antibody therapy. Despite this intensive treatment long-term survival is between 50-60 per cent. In CAR T-cell therapy, a type of immunotherapy, T-cells are engineered to contain a molecule called a chimeric antigen receptor (CAR) on their surface which can specifically recognise cancerous cells. For this study the patients’ own T-cells were modified with a CAR to target the GD2 surface protein, which is highly abundant on almost all neuroblastoma cells, but found at very low levels in healthy cells. Researchers found that when using a sufficient dose* of the modified CAR T-cells, this treatment induced rapid reduction in tumour size in some of the patients treated. These effects were transient. Importantly, in all patients the CAR T-cells did not cause any harmful side effects in healthy tissues that express the GD2 molecule. Lead author, Dr Karin Straathof, Research group leader at UCL GOS ICH and Consultant Paediatric Oncologist at Great Ormond Street Hospital NHS Trust said: “It’s encouraging to see the anti-tumour activity induced by these modified T-cells in some of the patients on this study. “While the anti-tumour activity seen was only transient, it provides an important proof-of-principle that CAR T-cells directed at the GD2 molecule could be used against solid cancers in children. “New treatments are needed for high-risk neuroblastoma and with more research we hope to develop this further into a treatment that results in lasting responses and increases the number of patients that can be cured.” Senior author, Dr Martin Pule (UCL Cancer Institute) said: “Targeting of solid cancers by CAR T-cells is dependent on their infiltration and expansion within the tumour microenvironment, and thus far fewer clinical responses have been reported. “The rapid regression in neuroblastoma cells is promising, particularly as this activity was observed in the absence of neurotoxicity which occurs with antibody-based approaches that target GD2.” Dr Pule added: “Targeting neuroblastoma with GD2 CAR T-cells appears to be a valid and safe strategy but requires further modification to promote CAR T-cell longevity.” Dr Sue Brook, medical advisor at Cancer Research UK, said: “Children who have hard to treat cancers like neuroblastoma have limited treatment options open to them, especially when the cancer returns. “The early results for the GD2 CAR-T treatment look promising, especially due to the initial safety data. However more work is needed on making the response last longer, and we are looking forward to seeing the next steps in its development.” The research team are preparing for their next clinical study in collaboration with Autolus, a clinical-stage biopharmaceutical company developing next-generation, programmed T-cell therapies for the treatment of cancer. This study will evaluate AUTO6NG, which builds on this approach utilising the same GD2 CAR alongside additional programming modules designed to enhance efficacy and persistence. To read the original article click here.

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Cancer Treatment: A Researcher Makes Breakthrough Immunotherapy Discovery

AHA Publisher — Fri, 01 Nov 2019 07:00:24 +0000

University of Montreal via EurekAlert – “Our work has identified a new T-cell protein that interacts with the key receptor that detects and responds to cancer antigens…” Dr Christopher E. Rudd, a researcher at the Centre de recherche de l’Hôpital Maisonneuve-Rosemont (CR-HMR) and Université de Montréal, has discovered a new cell therapy approach that boosts the immune response of T lymphocytes to malignant tumours. The results of the study have just been published in the respected journal Nature. “Our work has identified a new T-cell protein that interacts with the key receptor that detects and responds to cancer antigens,” says Prof. Rudd. “We have used those findings to develop a new form of immunotherapy in which hyperactivation of T cells enables them to penetrate and attack tumours. This discovery demonstrates that modulation of the identified protein can activate the immune system and lead to destruction of the cancer cells.” To date, the effectiveness of the new form of immunotherapy against leukemia and some skin cancers has been demonstrated in animals. The next stage will be clinical trials with human subjects. “This discovery is a scientific breakthrough that will have significantly enhance the immune system’s effectiveness in eliminating cancer cells,” says Dr. Denis-Claude Roy, scientific and medical director of the Center of Excellence in Cellular Therapy and CR-HMR. Eventually, this approach could also improve the effectiveness of the new CAR?T cell therapy currently being used at Hôpital Maisonneuve-Rosemont. To read the original article click here.

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Neurons Promote Growth of Brain Tumor Cells

AHA Publisher — Sat, 28 Sep 2019 02:48:35 +0000

German Cancer Research Center via EurekAlert – Glioblastomas invade the healthy brain in a diffuse pattern like a fungal network. As a result, they cannot be completely removed by surgery, and they also survive intensive chemotherapy and radiotherapy. Glioblastomas are thus among the most dangerous tumors in humans; the average survival time is 15 months following the initial diagnosis. Joint press release by Heidelberg University Hospital and the German Cancer Research Center In a current paper published in the journal “Nature”, Heidelberg-based researchers and physicians describe how neurons in the brain establish contact with aggressive glioblastomas and thus promote tumor growth / New tumor activation mechanism provides starting points for clinical trials. Neurons transmit their signals to each other via synapses, fine cell projections with terminals that contact another neuron. Researchers and physicians at Heidelberg University Hospital, Heidelberg Medical Faculty, and the German Cancer Research Center (DKFZ) have now discovered that neurons in the brain form these kinds of direct cell-to-cell contacts with tumor cells of aggressive glioblastomas too, thus transmitting impulses to the cancer cells. The tumor benefits from this “input”: The activation signals are probably a driving force behind the tumor growth and the invasion of healthy brain tissue by tumor cells, as Frank Winkler, Thomas Kuner, and their teams discovered using special imaging methods. But there is also some good news: Certain substances can block the signal transmission in animal experiments. The results have just been published online in the journal “Nature”. Networks of Neurons and Tumor Cells Glioblastomas invade the healthy brain in a diffuse pattern like a fungal network. As a result, they cannot be completely removed by surgery, and they also survive intensive chemotherapy and radiotherapy. Glioblastomas are thus among the most dangerous tumors in humans; the average survival time is 15 months following the initial diagnosis. In 2015, the team led by Frank Winkler, head of the Research Group Experimental Neurooncology in the Clinical Cooperation Unit Neurooncology, discovered a cause of this resistance to treatment: The glioblastoma cells are connected to one another through long cell protrusions. They communicate through these connections, exchange substances that are relevant for their survival, and thus protect themselves from treatment-related damage. The current findings add a further piece of the puzzle to our understanding of this type of cancer: “The tumor cells are not only interconnected in the brain like neurons; they also receive direct signals from them,” explained Winkler, whose research group is affiliated with the University Hospital and the DKFZ. The researchers observed the growth of human glioblastomas that they had transferred to mice, and studied cell cultures with human neurons and tumor cells, and tissue samples from patients. To do so, they used a wide range of modern microscopy methods, which provide detailed three-dimensional images of the connections – only micrometers large – between neurons and tumor cells as well as showing their molecular structure and signals within the cells. Electrical recordings from tumor cells revealed electrical currents generating from the synaptic connections, which form the starting point for further processing of these signals in the tumor cells. “We were able to show that signal transmission from neurons to tumor cells does in fact work like stimulating synapses between the neurons themselves,” added Thomas Kuner, Director of the Department of Functional Neuroanatomy at the Institute for Anatomy and Cell Biology, where the synaptic connections were first discovered by Varun Venkataramani. “This project began with an observation in basic research. In close cooperation with our clinical partners, it has led to conceptually new insights which will allow new treatment approaches to be developed using targeted translational research.” A Fatal Mechanism – But One That Opens Up New Avenues for Treatment How exactly activation of the tumor cell ultimately leads to increased tumor growth and invasion of healthy areas of the brain by the glioma cells has yet to be clarified. It is clear that this mechanism can be blocked in animals, however. Possible methods include a significant reduction of brain activity (for example under general anesthesia), pharmacological interventions that interrupt binding of the neurotransmitters on the AMPA receptor, or blocking the AMPA receptor using genetic engineering. In all these cases, tumor spread became slower in animal experiments. “This mechanism is therefore an extremely interesting approach for drug development and future drug treatments,” neurooncologist Winkler emphasized. “Suitable substances have in fact already been approved that block the AMPA receptor and are used to treat other neurological diseases. These substances are promising candidates for clinical trials.” “The new results not only show what makes glioblastomas so aggressive, but also how they could be stopped. That is highly relevant from a translational point of view and paves the way for clinical studies,” commented Wolfgang Wick, Medical Director of the Neurology Department at Heidelberg University Hospital and head of the Clinical Cooperation Unit Neurooncology at DKFZ. “We are also extremely pleased that the work of our junior researcher Varun Venkataramani, who also works in clinical practice, has been acknowledged by a publication in such a prestigious journal as, Nature’.” The relevance of the results from Heidelberg has been confirmed by a paper from Stanford University, California, USA: Michelle Monje and her research team also found synaptic connections between neurons and tumor cells in currently untreatable pediatric brain tumors and also observed the treatment effects reported by the Heidelberg-based researchers. Both papers are being published in “Nature” simultaneously. To read the original article click here.

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