Podcasts about cancer cells

Medical Disclaimer: The information shared in this podcast, including discussions about diet, nutrition, and other health topics by our guest surgeon, is for informational purposes only. It is not intended as a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of a qualified healthcare provider with any questions about your medical condition, health, or diet. Never disregard professional medical advice or delay seeking it because of something you heard in this podcast. Reliance on any information provided on this podcast is solely at your own risk. The Rose turns 39! Join founders Dorothy Gibbons and Dr. Dixie Melillo as they share stories of hope, dignity, and care for every woman, especially those told there’s no way forward. This special episode honors their legacy, tackles barriers for the uninsured, and reveals why The Rose means a better life for thousands. Support The Rose HERE. Subscribe to Let’s Talk About Your Breasts on Apple Podcasts, Spotify, iHeart, and wherever you get your podcasts. Key Questions Answered 1. Is there hope for patients with advanced breast cancer? 2. What is the hardest conversation Dr. Melillo has had with a patient? 3. What are some challenges faced by patients seeking charity care or financial assistance for breast cancer treatment? 4. How has being a woman influenced their approach to patient care at The Rose? 5. How did personal experiences with poverty influence Dorothy and Dixie’s commitment to healthcare? 6. What is a common misconception about The Rose? 7. What barriers still exist in the healthcare system for uninsured or underinsured women? 8. What role does nutrition play in cancer and medical training? 9. How has The Rose made an impact on the quality of life for its patients? Timestamped Overview 00:00 Breast Health Podcast Insights 03:38 Cancer Program Income Barrier 08:49 Misadventure: Dog, Buick, and Hospital 12:07 Lessons from Unexpected Challenges 13:26 Wig Styling Expertise Shared 16:03 Healthcare Access and Cost Crisis 22:34 Insulin Receptors in Cancer Cells 23:11 Defying Cancer Prognosis with DietSee omnystudio.com/listener for privacy information.

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Clinical researchers are set to launch immune-cell therapy clinical trials aimed at tackling treatment resistance in solid tumour, supported by a €11.9 million grant from the Disruptive Technologies Innovation Fund. The project is being spearheaded by a consortium from LIfT BiSciences, University of Galway, Galway University Hospitals and Hooke Bio. The funding award, announced by Minister for Enterprise, Trade and Employment, Peter Burke T.D., and Minister for Further and Higher Education, Research, Innovation and Science, James Lawless T.D., is the largest single grant awarded by the Disruptive Technologies Innovation Fund to date, with €5.9 million in direct funding going to University of Galway. The consortium will launch the first-in-human clinical trials of a ground-breaking neutrophil-based cancer immune-cell therapy developed by LIfT BioSciences, a client of Údarás na Gaeltachta with an Irish base in An Spidéal, Co. Galway. Neutrophils are part of the first line of defence in the body's immune response. The trial will focus on patients with metastatic cervical and head and neck cancer who have exhausted all standard treatments, including checkpoint inhibitors. Trials, which will be conducted at Galway University Hospitals, are expected to begin in 2026. The grant will support the clinical development of LIfT BioSciences' next-generation cell therapy designed to overcome resistance in solid tumours, known as Immuno-Modulatory Alpha Neutrophils (IMANs). University of Galway will contribute its deep expertise in oncology and cell therapy clinical trials, as well as in translating laboratory research into clinical applications, including predictive biomarkers. Hooke Bio will provide advanced analytical tools to optimise and assess how patients respond to this novel therapy. The study will first establish the safe and effective dose of immune-cell cancer therapy and then combine this treatment with other immune-based therapies to overcome resistance to these cancer treatments observed in some patients. Professor Sean Hynes, Consultant Histopathologist and Translational Cancer Researcher from University of Galway's School of Medicine and Lead Academic of the award said: "In partnership with LiFT BioSciences and Hooke Bio, we are very excited about University of Galway and Galway University Hospital being at the forefront of delivering on new oncological cellular therapies by using neutrophils, the body's own first responders, in the fight against cancer and ensuring patients in the West of Ireland have access to such cutting edge treatments." Professor Fidelma Dunne, Director of the Institute for Clinical Trials at University of Galway, said: "The Institute for Clinical Trials is proud to support this collaboration and look forward to working closely with Disruptive Technologies Innovation Fund partners LifT BioSciences and Hooke Bio, and with academic and clinical colleagues at the University and Galway University Hospital. The programme will bring a new therapy to patients with an unmet critical need. This will be a truly inspirational journey from basic science to a first in human trial as we deliver this novel cell therapy to cancer patients." Dr Michael McCarthy, Consultant Medical Oncologist and Principal Investigator at University Hospital Galway, added: "Cancer remains one of the most complex and dynamic diseases. IMANs have the potential to overcome key limitations of current cancer treatments by activating both the innate and adaptive branches of the immune system. This dual stimulation enables a comprehensive anti-tumour response, representing a transformative advancement in cancer therapy. We are pleased to receive this grant in collaboration with LIfT and Hooke Bio, and we look forward to accelerating the clinical development of this groundbreaking immunotherapy." Dr Andrew Finnerty Manager of the Centre for Cell Manufacturing Ireland at University of Galway, said: "We at the Centre for Cell Manufacturing Ire...

Prostate cancer is the second most diagnosed cancer among men worldwide and remains a leading cause of cancer-related death. While early forms of the disease can usually be treated successfully, advanced cases remain a major challenge. Scientists have now discovered a new potential way to slow the growth of advanced, treatment-resistant prostate cancer. These results were recently published in Volume 16 of Oncotarget by researchers from the University of Cincinnati College of Medicine. Understanding Advanced Prostate Cancer Early-stage prostate cancer can often be treated successfully. Most treatments work by lowering testosterone levels or blocking the hormone from activating the androgen receptor (AR), which drives cancer growth. In some patients, however, the disease progresses to castration-resistant prostate cancer (CRPC). Even with drastic reductions in testosterone levels, the tumors continue to grow at this stage. CRPC is much more difficult to treat, and current therapies such as hormone blockers or chemotherapy typically extend life by only a few months. One reason for this resistance is that cancer cells often switch to a different form of the androgen receptor called AR-V7. This variant remains permanently active, even without testosterone, making hormone-based drugs less effective. Because of this, new treatment strategies that work independently of hormone levels are needed. The Study: Targeting a New Weakness in Prostate Cancer Cells In the study titled “Targeting PCNA/AR interaction inhibits AR-mediated signaling in castration resistant prostate cancer cells,” researchers Shan Lu and Zhongyun Dong from the University of Cincinnati College of Medicine investigated a new way to block CRPC growth. Full blog - https://www.oncotarget.org/2025/07/29/a-new-way-to-target-resistant-prostate-cancer-cells/ Paper DOI - https://doi.org/10.18632/oncotarget.28722 Correspondence to - Zhongyun Dong - dongzu@ucmail.uc.edu Video short - https://www.youtube.com/watch?v=fiJWZ_fKxgs Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28722 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, PCNA, androgen receptor, PCNA inhibitors, AR splicing variants, CRPC To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

Podcasts are better with visuals! → Watch On YouTube Join 50,000+ men getting weekly strategies to build muscle, boost energy, and extend performance, delivered straight to your inbox. → Join the Newsletter We're here to help you build muscle. Download our FREE body part specializations below. → Free Resources   Show Notes/Description In this groundbreaking episode, Ben Pakulski sits down with Dr. Dominic D'Agostino to unpack a revolutionary approach to fighting cancer using metabolic therapy, ketosis, and fasting protocols. Dr. D'Agostino shares over 15 years of cutting-edge research on how ketones, calorie restriction, and metabolic biomarkers can suppress tumor growth, reduce treatment side effects, and potentially prevent cancer altogether. You'll learn how to personalize your glucose-ketone index, why metabolic health is the key to longevity, and what fasting protocols may optimize immunity and resilience. Whether you're focused on performance, prevention, or recovery, this episode is packed with actionable insights that challenge the status quo of modern medicine. Points To Watch Out For How ketones suppress cancer cell growth The glucose-ketone index you should track Fasting as a cancer prevention strategy Why metabolic health is your first defense How ketone therapy boosts immune response About Ben Ben Pakulski is the Chief Performance Officer to elite executives, successful entrepreneurs, and top athletes. With over 25 years of experience, he coaches high achievers to build the physical, psychological, and metabolic resilience required to lead at the highest level. As the creator of the Muscle Intelligence framework, Ben specializes in aligning biology and behavior to drive sustained peak performance. His mission is to redefine what's possible for people in their prime and push the boundaries of human potential. Connect with Dominic Audacious Nutrition Instagram Website

Scientists have uncovered a promising new strategy to weaken cancer cells' natural defense mechanisms, potentially making chemotherapy more effective. In a study published in Volume 16 of Oncotarget, researchers identified the protein PRDX1 as a key player in helping tumors resist treatment. By targeting this protein, they propose a novel way to combat aggressive, treatment-resistant cancers. Understanding Why Some Cancers Resist Treatment Chemotherapy works by damaging the DNA of cancer cells, forcing them to self-destruct. However, many cancers develop robust repair systems that fix this damage, allowing the tumor to survive and grow. A central component of this repair machinery is a protein called ATM, which acts like a first responder in the cell, detecting DNA damage and coordinating its repair. In ovarian cancer and other aggressive tumors, high levels of ATM have been associated with poor survival rates and resistance to chemotherapy. The Study: How PRDX1 Protects Cancer Cells The study, titled “PRDX1 protects ATM from arsenite-induced proteotoxicity and maintains its stability during DNA damage signaling,” was led by first author Reem Ali and corresponding author Dindial Ramotar from Hamad Bin Khalifa University in Qatar, in collaboration with researchers from the University of Nottingham in the UK. Full blog - https://www.oncotarget.org/2025/07/14/prdx1-identified-as-key-to-chemotherapy-resistance-in-cancer-cells/ Paper DOI - https://doi.org/10.18632/oncotarget.28720 Correspondence to - Dindial Ramotar - dramotar@hbku.edu.qa Video short - https://www.youtube.com/watch?v=suOhF7mPlNQ Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28720 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, redox signaling, homologous recombination, protein interaction, cell cycle, protein modification To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY – July 14, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on June 25, 2025, titled “Hypoxia induced lipid droplet accumulation promotes resistance to ferroptosis in prostate cancer.” In this study, researchers led by Shailender S. Chauhan and Noel A. Warfel from the University of Arizona discovered that prostate cancer cells survive treatment by storing fats in tiny cellular compartments when oxygen levels are low. This process makes the cancer cells less vulnerable to a type of cell death known as ferroptosis. The findings provide new insight into why prostate tumors often resist therapies and suggest potential strategies to improve treatment outcomes. This study focused on ferroptosis, a form of programmed cell death that relies on iron and lipid oxidation to destroy cancer cells. Researchers tested prostate cancer cells under normal and low oxygen conditions and found that hypoxia, or reduced oxygen levels, allowed cancer cells to build up lipid droplets (LD). These structures act as storage units for fats, shielding cancer cells from oxidative damage and preventing ferroptosis from occurring. The researchers found that this adaptation of prostate cancer cells made them less sensitive to ferroptosis-inducing drugs like Erastin and RSL3, even when these drugs were combined for a stronger effect. The team also reported that hypoxia caused significant changes in lipid metabolism, decreasing the availability of specific fatty acids that normally promote ferroptosis. “Transcriptomic analysis revealed that hypoxia significantly reduced the expression of genes related to incorporating polyunsaturated fatty acids into phospholipids (ACSL4, LPCAT3), and parallel lipidomic analysis demonstrated that hypoxia significantly decreased the levels of the ferroptosis-prone lipid class, phosphatidylethanolamine (PE) and increased production of neutral lipid species, cholesteryl ester (ChE (22:5)) and triglycerides (TG(48:1), TG:(50:4), and TG(58:4)).” This research highlights the importance of the tumor microenvironment, particularly oxygen levels, in shaping how cancer cells respond to therapy. By altering their metabolism and storing lipids, prostate tumors may evade treatments designed to trigger ferroptosis. These findings underscore the need to develop new strategies targeting LD dynamics or lipid metabolism to overcome this resistance. Understanding how prostate cancer (Pca) adapts to survive in hypoxic conditions offers a potential avenue for improving therapies. For example, preventing lipid accumulation in cancer cells or releasing stored fats may restore their sensitivity to ferroptosis and improve the effectiveness of current therapies. This approach could have broader implications for treating other solid tumors that share similar metabolic features. DOI - https://doi.org/10.18632/oncotarget.28750 Correspondence to - Noel A. Warfel - warfelna@arizona.edu, and Shailender S. Chauhan - shailenderc@arizona.edu Video short - https://www.youtube.com/watch?v=xFypDT4ALmc Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28750 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, hypoxia, lipid droplets, ferroptosis, resistance, prostate To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

Merck & Co. has acquired Verona Pharma for $10 billion in a deal designed to expand the pharma giant's portfolio of cardio-pulmonary disease treatments. In a step toward virtual cell benchmarking, the Arc Institute has launched the Virtual Cell Challenge to evaluate the ability of transcriptome AI models to generalize to new cell contexts for therapeutic applications. Fujifilm rebrands life science companies to position itself as a drug development leader. Additionally, AAV-OTOF gene therapy shows promise in restoring hearing loss while a new proteomics tool gleams insight into telomere repair. We wrap up our episode with highlights from BIO 2025, as FDA Commissioner Martin Makary, MD, shared his vision for a “New FDA” focused on accelerating drug applications, industry partnerships, and applying AI.Join GEN editors Corinna Singleman, PhD, Alex Philippidis, Fay Lin, PhD, and Uduak Thomas for a discussion of the latest biotech and biopharma news.Listed below are links to the GEN stories referenced in this episode of Touching Base: Merck to Acquire Verona Pharma for $10B, Adding Fast-Growing COPD DrugBy Alex Philippidis, GEN Edge, July 9, 2025 Arc Institute Launces Virtual Cell Challenge to Accelerate AI Model DevelopmentBy Fay Lin, PhD, GEN Edge, June 26, 2025End-to-End: Fujifilm Rebrands Life Sciences Companies, Positioning Itself as Drug Development Cycle LeaderBy Alex Philippidis, GEN Edge, July 8, 2025AAV-OTOF Gene Therapy Trial Restores Hearing in Both Children and Adults By GEN, July 7, 2025 Proteomics Tool Sheds Light on Cancer Cells' Telomere Repair Tactics By GEN, July 7, 2025 Makary Calls for “New FDA” at BIO; Defends Agency's Spring Job CutsBy Alex Philippidis, GEN Edge, June 18, 2025Cell and Gene Therapy Leaders Tell FDA: “Believe in American Solutions”By Kevin Davies, PhD, and Alex Philippidis, GEN Edge, June 5, 2025 Behind the Breakthroughs PodcastHosted by Jonathan D. Grinstein, PhD Hosted on Acast. See acast.com/privacy for more information.

Broadcast from KSQD, Santa Cruz on 7-03-2025: Dr. Dawn responds to an email about vitamin D and statin interactions, explaining how statins may prevent vitamin D's longevity benefits by interfering with CoQ10 production. She references a study showing vitamin D preserved telomeres and prevented aging over 3-4 years, but benefits disappeared in statin users. For borderline high LDL, she recommends testing for large versus small particles and oxidized LDL rather than treating with statins or red yeast rice. Red yeast rice may also block CoQ10 production, potentially negating vitamin D benefits. She discusses the critical problem of overmedication in elderly patients through a story of a 75-year-old taking 21 prescription drugs who improved dramatically when reduced to eight medications. Multiple specialists practicing standard care in isolation create dangerous polypharmacy without coordination. HIPAA privacy laws prevent medication sharing between providers, while electronic medical records remain siloed and incompatible. England's pilot program will provide whole genome screening for every newborn within 10 years, assessing hundreds of disease risks and enabling personalized medicine. While beneficial for identifying genetic disorders and drug metabolism variations like 2D6 mutations affecting tamoxifen effectiveness, Dr. Dawn expresses concern about government surveillance implications. Unlike voluntary phone tracking, this represents involuntary comprehensive genetic monitoring of citizens unable to provide informed consent. She describes alarming research showing cancer cells steal mitochondria from nerve cells by extending tubes and sucking out energy-producing organelles. This behavior helps cancer cells survive the hostile journey through bloodstream during metastasis. Turbocharged cancer cells with stolen mitochondria generate more energy and survive better when subjected to physical stress mimicking bloodstream travel. Dr. Dawn explores the parasitic amoeba Entamoeba histolytica, which causes intestinal disease but can become invasive, liquefying organs through tissue destruction. The parasite kills cells without eating them immediately, then consumes fragments and displays stolen cellular proteins on its surface to fool the immune system, potentially leading to CRISPR-based treatments or targeted drugs. She discusses converting plastic waste into acetaminophen using modified E. coli bacteria. Researchers chemically degrade PET plastic into precursor molecules, then use bacterial enzymes to complete synthesis into paracetamol with 92% efficiency. This transforms environmental waste into globally important medication, though she notes acetaminophen risks for regular drinkers due to toxic liver metabolites. MIT research reveals that AI writing assistance reduces brain engagement, memory, and sense of authorship. Students using ChatGPT showed lower neural connectivity in memory, attention, and executive function networks over four months. AI users retained less information and struggled to quote from their own essays. Dr. Dawn compares this to physical atrophy, emphasizing that cognitive challenge strengthens neural pathways like exercise strengthens muscles. She warns about fluoroquinolone antibiotics causing aortic aneurysm ruptures, in addition to known risks of tendon ruptures and retinal detachment. People with dilated aortas, hypertension history, or smoking should avoid these drugs entirely. This represents new information that wasn't widely known among primary care physicians, highlighting the importance of continuing medical education. Research shows celecoxib (Celebrex) cuts colon cancer recurrence rates in half for patients with circulating tumor DNA, but provides no benefit without detectable residual disease. This anti-inflammatory drug appears to impair cancer's ability to thrive in metastatic conditions. The finding supports using circulating tumor DNA testing to identify who needs targeted therapy rather than treating everyone. Dr. Dawn concludes with surprising research showing chronic inflammation during aging occurs only in industrialized societies. Studies comparing indigenous communities from Bolivian Amazon and Malaysia with populations from Italy and Singapore found inflammatory cytokines increase with age only in industrialized groups.

Un team di ricercatori dell'IFOM, dell'Università di Torino e dell'Università degli Studi di Milano, in collaborazione con il Memorial Sloan Kettering Cancer Center di New York, l'Ospedale San Raffaele e l'Istituto di Candiolo, ha individuato una strategia innovativa per rendere i tumori del colon-retto sensibili all'immunoterapia, combinando due chemioterapici specifici. La scoperta, resa possibile grazie al sostegno dell'European Research Council (ERC) e della Fondazione AIRC, è stata pubblicata sull'autorevole rivista scientifica Cancer Cell e apre nuove possibilità terapeutiche per il tumore al colon-retto. A Obiettivo Salute il commento del prof. Alberto Bardelli, Direttore Scientifico di IFOM e Professore Ordinario del Dipartimento di Oncologia dell'Università di Torino, coordinatore dello studio.

The rate of cancer and cancer malignancy differ greatly among mammalian species. The placental – maternal interface is also highly variable between placental mammals. This lecture will discuss recent advances that suggest that there is a causal connection between the evolution of placental biology and the biology and rate of cancer malignancy. Series: "CARTA - Center for Academic Research and Training in Anthropogeny" [Humanities] [Science] [Show ID: 40694]

The rate of cancer and cancer malignancy differ greatly among mammalian species. The placental – maternal interface is also highly variable between placental mammals. This lecture will discuss recent advances that suggest that there is a causal connection between the evolution of placental biology and the biology and rate of cancer malignancy. Series: "CARTA - Center for Academic Research and Training in Anthropogeny" [Humanities] [Science] [Show ID: 40694]

The rate of cancer and cancer malignancy differ greatly among mammalian species. The placental – maternal interface is also highly variable between placental mammals. This lecture will discuss recent advances that suggest that there is a causal connection between the evolution of placental biology and the biology and rate of cancer malignancy. Series: "CARTA - Center for Academic Research and Training in Anthropogeny" [Humanities] [Science] [Show ID: 40694]

The rate of cancer and cancer malignancy differ greatly among mammalian species. The placental – maternal interface is also highly variable between placental mammals. This lecture will discuss recent advances that suggest that there is a causal connection between the evolution of placental biology and the biology and rate of cancer malignancy. Series: "CARTA - Center for Academic Research and Training in Anthropogeny" [Humanities] [Science] [Show ID: 40694]

The rate of cancer and cancer malignancy differ greatly among mammalian species. The placental – maternal interface is also highly variable between placental mammals. This lecture will discuss recent advances that suggest that there is a causal connection between the evolution of placental biology and the biology and rate of cancer malignancy. Series: "CARTA - Center for Academic Research and Training in Anthropogeny" [Humanities] [Science] [Show ID: 40694]

The rate of cancer and cancer malignancy differ greatly among mammalian species. The placental – maternal interface is also highly variable between placental mammals. This lecture will discuss recent advances that suggest that there is a causal connection between the evolution of placental biology and the biology and rate of cancer malignancy. Series: "CARTA - Center for Academic Research and Training in Anthropogeny" [Humanities] [Science] [Show ID: 40694]

William Lowry, Ph.D., discusses manipulating metabolic pathways in hair follicle stem cells to inhibit tumorigenesis. By blocking glycolysis and glutamine lysis simultaneously, they observed tumor regression, highlighting the complex interplay between metabolism and cancer. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 39256]

William Lowry, Ph.D., discusses manipulating metabolic pathways in hair follicle stem cells to inhibit tumorigenesis. By blocking glycolysis and glutamine lysis simultaneously, they observed tumor regression, highlighting the complex interplay between metabolism and cancer. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 39256]

William Lowry, Ph.D., discusses manipulating metabolic pathways in hair follicle stem cells to inhibit tumorigenesis. By blocking glycolysis and glutamine lysis simultaneously, they observed tumor regression, highlighting the complex interplay between metabolism and cancer. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 39256]

William Lowry, Ph.D., discusses manipulating metabolic pathways in hair follicle stem cells to inhibit tumorigenesis. By blocking glycolysis and glutamine lysis simultaneously, they observed tumor regression, highlighting the complex interplay between metabolism and cancer. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 39256]

William Lowry, Ph.D., discusses manipulating metabolic pathways in hair follicle stem cells to inhibit tumorigenesis. By blocking glycolysis and glutamine lysis simultaneously, they observed tumor regression, highlighting the complex interplay between metabolism and cancer. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 39256]

William Lowry, Ph.D., discusses manipulating metabolic pathways in hair follicle stem cells to inhibit tumorigenesis. By blocking glycolysis and glutamine lysis simultaneously, they observed tumor regression, highlighting the complex interplay between metabolism and cancer. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 39256]

Statistics show that 1 in 3 people will receive a cancer diagnosis in their lifetime...     But the good news is that your body holds a powerful built-in defense: natural killer (NK) and T cells that help identify and destroy abnormal cells before they can spread.     On today's show, I'll share why these immune cells are your first line of defense against cancer and how simple diet, lifestyle, and supplement strategies can help boost their activity naturally.     So join me on today's Cabral Concept 3401 to learn how to activate your natural killer, anti-cancer cells.     Enjoy the show and let me know your thoughts!   - - - For Everything Mentioned In Today's Show: StephenCabral.com/3401 - - - Get a FREE Copy of Dr. Cabral's Book: The Rain Barrel Effect - - - Join the Community & Get Your Questions Answered: CabralSupportGroup.com - - - Dr. Cabral's Most Popular At-Home Lab Tests: > Complete Minerals & Metals Test (Test for mineral imbalances & heavy metal toxicity) - - - > Complete Candida, Metabolic & Vitamins Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Complete Stress, Mood & Metabolism Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Complete Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Complete Omega-3 & Inflammation Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - Get Your Question Answered On An Upcoming HouseCall: StephenCabral.com/askcabral - - - Would You Take 30 Seconds To Rate & Review The Cabral Concept? The best way to help me spread our mission of true natural health is to pass on the good word, and I read and appreciate every review!  

William Lowry, Ph.D., discusses manipulating metabolic pathways in hair follicle stem cells to inhibit tumorigenesis. By blocking glycolysis and glutamine lysis simultaneously, they observed tumor regression, highlighting the complex interplay between metabolism and cancer. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 39256]

BUFFALO, NY - June 4, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on May 20, 2025, titled “Targeting PCNA/AR interaction inhibits AR-mediated signaling in castration resistant prostate cancer cells." In this study, authors Shan Lu and Zhongyun Dong from the University of Cincinnati College of Medicine investigated how interfering with a protein interaction could reduce prostate cancer growth. Their study based on prostate cancer cells shows that blocking the link between PCNA, a protein important for DNA repair, and the androgen receptor (AR), which drives prostate cancer growth, can slow down cancer cell multiplication. This discovery could lead to a new treatment for patients with advanced prostate cancer, particularly those no longer responding to hormone therapy. Prostate cancer is one of the most common cancers in men. Many patients eventually become resistant to hormone treatment. In this advanced stage, called castration-resistant prostate cancer (CRPC), tumors continue to grow by using either the full-length androgen receptor (AR-FL) or altered versions called AR variants (AR-Vs). This study shows that the interaction between AR and PCNA helps both AR-FL and AR-Vs remain active, supporting cancer cell survival and growth. The researchers identified a new region in the AR that binds to PCNA. They developed a small peptide, R9-AR-PIP, to mimic this region and block the AR-PCNA connection. They found that this peptide reduced AR's ability to bind DNA and lowered the levels of key genes involved in cancer cell growth. Importantly, the peptide was effective against both types of AR, including the variant forms that are especially challenging in CRPC. “We identified a second PIP-box (PIP-box592) in the DNA binding domain of AR and found that dihydrotestosterone enhances the binding of full-length AR (AR-FL) but not a constitutively active variant (AR-V7) to PCNA.” They also tested a small molecule, PCNA-I1S, which interferes with PCNA's ability to move to the cell nucleus and interact with AR. This molecule showed similar effects as the peptide, reducing AR activity and stopping cancer cell growth. Together, these findings suggest that targeting PCNA/AR interactions could be a promising strategy to fight CRPC, especially in patients with limited treatment options. One key result was that both the peptide and the small molecule reduced the levels of cyclin A2, a protein that helps cells divide and is often overexpressed in CRPC. Since this protein is linked to patients' poor outcomes, its reduction could be especially beneficial. This study improves our understanding of how prostate cancer continues to grow even after hormone treatments fail. By blocking a crucial helper of the androgen receptor, researchers have uncovered a new way to potentially slow or stop the disease. Further studies in animal models are needed, but this approach could lead to more effective treatments for men with advanced prostate cancer. DOI - https://doi.org/10.18632/oncotarget.28722 Correspondence to - Zhongyun Dong - dongzu@ucmail.uc.edu Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28722 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, PCNA, androgen receptor, PCNA inhibitors, AR splicing variants, CRPC To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

Statistics show that 1 in 3 people will receive a cancer diagnosis in their lifetime...     But the good news is that your body holds a powerful built-in defense: natural killer (NK) and T cells that help identify and destroy abnormal cells before they can spread.     On today's show, I'll share why these immune cells are your first line of defense against cancer and how simple diet, lifestyle, and supplement strategies can help boost their activity naturally.     So join me on today's Cabral Concept 3401 to learn how to activate your natural killer, anti-cancer cells.     Enjoy the show and let me know your thoughts!   - - - For Everything Mentioned In Today's Show: StephenCabral.com/3401 - - - Get a FREE Copy of Dr. Cabral's Book: The Rain Barrel Effect - - - Join the Community & Get Your Questions Answered: CabralSupportGroup.com - - - Dr. Cabral's Most Popular At-Home Lab Tests: > Complete Minerals & Metals Test (Test for mineral imbalances & heavy metal toxicity) - - - > Complete Candida, Metabolic & Vitamins Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Complete Stress, Mood & Metabolism Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Complete Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Complete Omega-3 & Inflammation Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - Get Your Question Answered On An Upcoming HouseCall: StephenCabral.com/askcabral - - - Would You Take 30 Seconds To Rate & Review The Cabral Concept? The best way to help me spread our mission of true natural health is to pass on the good word, and I read and appreciate every review!  

Cancer is normal development spun out of control. It is the great plasticity and power of development, without the overarching controls that guide normal development toward an integrated adult form. Instead, whenever a newly developed kind of tissue acquires the ability to survive, grow, and resist control, there is nothing to stop it. That may be why normal adult cells are often terminally differentiated into a restricted cellular program. And it may be why wound healing, which releases the restricted cellular program and powerfully plastic tissue remodeling, is so tightly regulated and, when dysregulated, so often associates with cancer. With regard to evolutionary history, humans develop differently from their ape ancestors, and their lifestyle causes them to suffer different kinds of tissue damage. Those differences in development and wound healing likely led to new aspects of cancer disease over human history. Series: "CARTA - Center for Academic Research and Training in Anthropogeny" [Humanities] [Science] [Show ID: 40691]

Cancer is normal development spun out of control. It is the great plasticity and power of development, without the overarching controls that guide normal development toward an integrated adult form. Instead, whenever a newly developed kind of tissue acquires the ability to survive, grow, and resist control, there is nothing to stop it. That may be why normal adult cells are often terminally differentiated into a restricted cellular program. And it may be why wound healing, which releases the restricted cellular program and powerfully plastic tissue remodeling, is so tightly regulated and, when dysregulated, so often associates with cancer. With regard to evolutionary history, humans develop differently from their ape ancestors, and their lifestyle causes them to suffer different kinds of tissue damage. Those differences in development and wound healing likely led to new aspects of cancer disease over human history. Series: "CARTA - Center for Academic Research and Training in Anthropogeny" [Humanities] [Science] [Show ID: 40691]

Cancer is normal development spun out of control. It is the great plasticity and power of development, without the overarching controls that guide normal development toward an integrated adult form. Instead, whenever a newly developed kind of tissue acquires the ability to survive, grow, and resist control, there is nothing to stop it. That may be why normal adult cells are often terminally differentiated into a restricted cellular program. And it may be why wound healing, which releases the restricted cellular program and powerfully plastic tissue remodeling, is so tightly regulated and, when dysregulated, so often associates with cancer. With regard to evolutionary history, humans develop differently from their ape ancestors, and their lifestyle causes them to suffer different kinds of tissue damage. Those differences in development and wound healing likely led to new aspects of cancer disease over human history. Series: "CARTA - Center for Academic Research and Training in Anthropogeny" [Humanities] [Science] [Show ID: 40691]

Cancer is normal development spun out of control. It is the great plasticity and power of development, without the overarching controls that guide normal development toward an integrated adult form. Instead, whenever a newly developed kind of tissue acquires the ability to survive, grow, and resist control, there is nothing to stop it. That may be why normal adult cells are often terminally differentiated into a restricted cellular program. And it may be why wound healing, which releases the restricted cellular program and powerfully plastic tissue remodeling, is so tightly regulated and, when dysregulated, so often associates with cancer. With regard to evolutionary history, humans develop differently from their ape ancestors, and their lifestyle causes them to suffer different kinds of tissue damage. Those differences in development and wound healing likely led to new aspects of cancer disease over human history. Series: "CARTA - Center for Academic Research and Training in Anthropogeny" [Humanities] [Science] [Show ID: 40691]

Cancer is normal development spun out of control. It is the great plasticity and power of development, without the overarching controls that guide normal development toward an integrated adult form. Instead, whenever a newly developed kind of tissue acquires the ability to survive, grow, and resist control, there is nothing to stop it. That may be why normal adult cells are often terminally differentiated into a restricted cellular program. And it may be why wound healing, which releases the restricted cellular program and powerfully plastic tissue remodeling, is so tightly regulated and, when dysregulated, so often associates with cancer. With regard to evolutionary history, humans develop differently from their ape ancestors, and their lifestyle causes them to suffer different kinds of tissue damage. Those differences in development and wound healing likely led to new aspects of cancer disease over human history. Series: "CARTA - Center for Academic Research and Training in Anthropogeny" [Humanities] [Science] [Show ID: 40691]

Cancer is normal development spun out of control. It is the great plasticity and power of development, without the overarching controls that guide normal development toward an integrated adult form. Instead, whenever a newly developed kind of tissue acquires the ability to survive, grow, and resist control, there is nothing to stop it. That may be why normal adult cells are often terminally differentiated into a restricted cellular program. And it may be why wound healing, which releases the restricted cellular program and powerfully plastic tissue remodeling, is so tightly regulated and, when dysregulated, so often associates with cancer. With regard to evolutionary history, humans develop differently from their ape ancestors, and their lifestyle causes them to suffer different kinds of tissue damage. Those differences in development and wound healing likely led to new aspects of cancer disease over human history. Series: "CARTA - Center for Academic Research and Training in Anthropogeny" [Humanities] [Science] [Show ID: 40691]

In this episode of the Epigenetics Podcast, we talked with Ani Deshpande from Sanford Burnham Prebys about his work on epigenetic regulation and developing small molecules through high throughput screens for AML. Throughout our discussion, we delve into Dr. Despande's journey into the field of biology and science, tracing his evolution from a literature enthusiast in Mumbai to a dedicated cancer researcher. He reflects on his formative experiences during his PhD at Ludwig Maximilian University in Munich, where she developed murine models for refractory acute myeloid leukemia (AML). We examine these models' contributions to therapeutic discovery and understanding the intricate mechanisms underscoring AML's complexities. Transitioning to his postdoctoral work at Scott Armstrong's lab in Boston, Dr. Despande shares his insights on the importance of epigenetic regulators, such as DOT1L, in leukemias, and how they can serve as strategic therapeutic targets. His ambitious pursuit of translational research is further highlighted through his efforts in developing a conditional knockout mouse model and his collaborative work utilizing CRISPR technology to refine our understanding of epigenetic regulation in cancer pathogenesis. Moreover, we engage in a conversation about the challenges and opportunities that arise when establishing his lab at Sanford Burnham Prebys. Dr. Despande candidly discusses the delicate balance between pursuing topics of genuine interest versus adhering to grant fundability, underlining the tension researchers face in the current scientific landscape. His emphasis on the critical need for innovation within lab settings serves as a motivational call for emerging scientists to venture beyond the established templates that often inhibit groundbreaking discoveries. We conclude our dialogue with an exploration of his recent projects, which involve targeting specific epigenetic modifiers and how his lab's findings can contribute to greater understanding and potential treatments for not only AML but also other pediatric cancers driven by gene fusions. Dr. Despande's insights into the integration of modern technologies, such as CRISPR libraries, exemplify his commitment to pushing the boundaries of cancer research. In addition to discussing his scientific contributions, we touch upon Dr. Despande's foray into podcasting (The Discovery Dialogues), shedding light on his motivation to bridge the communication gap between scientists and the broader public. He articulates his desire to demystify scientific discoveries and promote awareness about the intricate journey of research that lays the groundwork for medical advancements. This multidimensional discussion not only highlights his scientific achievements but also emphasizes the importance of effective science communication in fostering public understanding and appreciation of research.   References Deshpande AJ, Cusan M, Rawat VP, Reuter H, Krause A, Pott C, Quintanilla-Martinez L, Kakadia P, Kuchenbauer F, Ahmed F, Delabesse E, Hahn M, Lichter P, Kneba M, Hiddemann W, Macintyre E, Mecucci C, Ludwig WD, Humphries RK, Bohlander SK, Feuring-Buske M, Buske C. Acute myeloid leukemia is propagated by a leukemic stem cell with lymphoid characteristics in a mouse model of CALM/AF10-positive leukemia. Cancer Cell. 2006 Nov;10(5):363-74. doi: 10.1016/j.ccr.2006.08.023. PMID: 17097559. Deshpande AJ, Deshpande A, Sinha AU, Chen L, Chang J, Cihan A, Fazio M, Chen CW, Zhu N, Koche R, Dzhekieva L, Ibáñez G, Dias S, Banka D, Krivtsov A, Luo M, Roeder RG, Bradner JE, Bernt KM, Armstrong SA. AF10 regulates progressive H3K79 methylation and HOX gene expression in diverse AML subtypes. Cancer Cell. 2014 Dec 8;26(6):896-908. doi: 10.1016/j.ccell.2014.10.009. Epub 2014 Nov 20. PMID: 25464900; PMCID: PMC4291116. Sinha S, Barbosa K, Cheng K, Leiserson MDM, Jain P, Deshpande A, Wilson DM 3rd, Ryan BM, Luo J, Ronai ZA, Lee JS, Deshpande AJ, Ruppin E. A systematic genome-wide mapping of oncogenic mutation selection during CRISPR-Cas9 genome editing. Nat Commun. 2021 Nov 11;12(1):6512. doi: 10.1038/s41467-021-26788-6. Erratum in: Nat Commun. 2022 May 16;13(1):2828. doi: 10.1038/s41467-022-30475-5. PMID: 34764240; PMCID: PMC8586238.   Related Episodes Targeting COMPASS to Cure Childhood Leukemia (Ali Shilatifard) The Menin-MLL Complex and Small Molecule Inhibitors (Yadira Soto-Feliciano) MLL Proteins in Mixed-Lineage Leukemia (Yali Dou)   Contact Epigenetics Podcast on Mastodon Epigenetics Podcast on Bluesky Dr. Stefan Dillinger on LinkedIn Active Motif on LinkedIn Active Motif on Bluesky Email: podcast@activemotif.com

Is your daily diet secretly fuelling chronic disease? Dr. William Li reveals the shocking truth about what you're really eating. Dr. William Li is a world-renowned medical scientist specialising in chronic disease and blood vessel growth. He is Founder & President of the Angiogenesis Foundation, and his groundbreaking research has led to 44 medical treatments that target over 70 diseases. He is also the bestselling author of ‘Eat To Beat Your Diet'. He explains:  The number one common food that feeds cancer cells The surprising link between salt and accelerated aging How poor sleep is connected to belly fat The hidden health risks of microplastics in your diet How sugar quietly fuels chronic diseases 00:00 Intro   02:28 What Will People Out of This Conversation?   03:14 What Key Diseases Correlate to Diet?   04:35 Where Is Our Society at with Health and Food?   08:06 How Cancer Works in Our Body   14:50 How to Lower Your Risk of Cancer   16:09 Foods That Fuel Cancer   17:56 Debunking “Superfoods”   18:39 Risks of Electrolytes   19:46 Lowering the Body's Defenses: Risk of Consuming Added Sugars   21:26 Alcohol   22:08 Risks of Drinking Alcohol   22:43 How Does Stress Impact Immunity?   24:50 The Relationship Between Stress, Sleep, and Sickness   26:30 Why Lack of Sleep Contributes to Stress: The Glymphatic System   28:00 Deep Sleep Clears Your Mind and Burns Fat!   30:01 Why Are Cancer Cases in Young People Increasing?   32:54 Microplastics in Our Bodies   37:15 How Can I Lower My Exposure to Microplastics?   37:53 Benefits of Green Tea—but the Danger of Teabags!   40:17 Which Tea Has the Best Health Benefits?   41:32 Is Matcha Good for Me?   42:32 The Link Between Cured Meats and Cancer   46:10 My Personal Story with Cancer   58:50 Groundbreaking New Studies with AI   1:02:38 Successful Cancer Treatment Linked to Specific Gut Bacteria   1:09:01 What's the Best Food Diet?   1:13:04 Why Is Japan Considered One of the Healthiest Countries?   1:16:29 The Different Body Fat Types and How They Affect You   1:22:23 Visceral Fat: Dangerous for Cancer   1:33:43 The Link Between Fat and Coffee   1:40:55 Is Fasting Good for Fat Loss?   1:43:08 Brain Diseases   1:46:26 Food Is Medicine   1:52:39 Should We Use Food Supplements?   1:54:15 The Superfoods Helping Our Body  

On today's podcast, Stephanie and Tara talk about Biden's prostate cancer announcement, Trump's visit to Qatar and the UAE, Newsom's new plan for California's budget, Korean research showing cancer cells can be reverted back to normal, China's alleged ability to possibly control the U.S. solar power grid with a kill switch, and CERN has figured out how to turn lead into gold, which makes us question what else can they do? Become a beta tester for our new Unapologetically Outspoken GPT! Use the link here or head over to our website: https://www.thelawofattractiontribe.com/a/2148108179/MpCJCAPZ Want to join the conversation? Connect with Tara and Stephanie on TikTok, X, Rumble, YouTube, Truth Social, Facebook, and IG.https://msha.ke/unapologeticallyoutspoken/ Sign up to get on the waitlist for Stephanie's next Quantum Catalyst program here: https://www.thelawofattractiontribe.com/a/2148109722/MpCJCAPZ  

Prof. Thomas Seyfried is a professor of biology at Boston College and a leading researcher in cancer metabolism. He is best known for his book Cancer as a Metabolic Disease, where he argues that cancer is primarily caused by mitochondrial dysfunction rather than genetic mutations. Seyfried holds a Ph.D. in Genetics and Biochemistry and completed postdoctoral training in neurology at Yale University. His research focuses on metabolic therapies, including ketogenic diets, as potential treatments for cancer and neurological disorders. He has published over 150 scientific papers and is a prominent advocate for rethinking conventional cancer treatment approaches.In our conversation we discuss:(00:00) – Why cancer rates are doubling(06:54) – The real root cause of cancer and evolving treatments(13:07) – Why we believed cancer was mostly genetic(20:52) – The role of mitochondria in preventing cancer(25:54) – Did our ancestors get cancer? Lifespan vs. risk(28:46) – Lessons from the Inuit diet(31:42) – What's the optimal diet for cancer prevention?(42:05) – Understanding and measuring your GKI(46:12) – Intermittent fasting vs. prolonged fasting(55:32) – Cancer treatments and key supplements to know(58:26) – The role of NAD precursors in recoveryLearn more about Prof. SeyfriedUniversity profile - https://www.bc.edu/bc-web/schools/morrissey/departments/biology/people/faculty-directory/thomas-seyfried.htmlBook - https://www.amazon.com/Cancer-Metabolic-Disease-Management-Prevention-ebook/dp/B00852YXZS?ref_=ast_author_mpbWatch full episodes on: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://www.youtube.com/@seankim⁠⁠⁠⁠⁠⁠⁠⁠Connect on IG: ⁠⁠⁠⁠⁠⁠⁠https://instagram.com/heyseankim

This episode is brought to you by ⁠⁠The Primal Tallow Balm.⁠⁠ PREVENT Cancer (Free Guide): http://www.theprimal.com/lab/eat-high-fat-the-fastest-way-to-kill-cancer-cellsProf Seyfried's Book 'Cancer As A Metabolic Disease': https://amzn.to/4c7PHUaProfessor Seyfried will discuss a new way to treat cancer using metabolic therapy, which is a combination of glucose and glutamine targeted therapies, along with a high-fat ketogenic diet. Professor Seyfried will explain why cancer is not a genetic disease and how the standard of care destroys all cells in the body, leaving patients sick and frail after therapy. Professor Seyfried will also share real success stories, including Pablo Kelly, who was diagnosed with a glioblastoma, given 9 months to live, and survived almost 8 years with metabolic therapy. This episode is important for understanding how to actively treat cancer with nutrition, metabolic therapy, and mitochondria science, and how to prevent cancer through lifestyle changes. Free Carnivore Calculator ⁠https://carnivore-diet.netlify.app/⁠Free Meal Planner https://carnivore-guide.vercel.app/

In this episode, Sarah Hall and Beth Wilmes continue the discussion of topics around reducing recurrence/disease progression by introduce the topic of CTDNA testing, also known as liquid biopsy. They explain how this test measures small fragments of cancer DNA in the blood and its potential benefits and limitations. The conversation includes insights from Dr. Cynthia Ax, an integrative breast surgical oncologist, who shares her perspectives on why doctors and patients opt for CTDNA testing, the emotional impacts of receiving test results, and the importance of a holistic approach to cancer care. The episode also touches on issues like the challenge of making lifestyle changes post-diagnosis, the collaborative potential between medical practitioners, and the critical role of mental health in the healing process. Dr. Cythia Aks: https://www.linkedin.com/in/cynthia-aks-865bb423/ Guest Profile: https://www.bestieswithbreastiespodcast.com/guests/cynthia-aks/ 00:00 Welcome to Besties with Breasty 00:58 Introduction to CT DNA Testing 02:38 Guest Introduction: Dr. Cynthia Ax 02:56 Sponsor Message: Faith Through Fire Survivorship Bootcamp 04:11 In-Depth Discussion with Dr. Ax 10:04 Challenges in Patient Lifestyle Changes 14:43 The Role of Primary Care in Survivorship 20:36 Boobs in the News: Peeled Bananas Mystery 21:11 The Mysterious Banana Plates 21:54 Community Reactions and Theories 23:31 Personal Anecdotes and Banana Dislike 25:06 Cancer Cells and Immune System 25:56 Empowering Patients with Knowledge 27:35 The Importance of Mental Health 32:05 Final Thoughts and Sponsor Message

BUFFALO, NY - April 2, 2025 – A new #research paper was #published in Oncotarget, Volume 16, on March 21, 2025, titled “NSD2-epigenomic reprogramming and maintenance of plasma cell phenotype in t(4;14) myeloma." Researchers Andrea Gunnell, Scott T. Kimber, Richard Houlston, and Martin Kaiser from The Institute of Cancer Research, London, studied how a gene called NSD2 affects the behavior of multiple myeloma (MM) cells. Their findings reveal that NSD2 plays a key role in helping cancer cells retain their identity as plasma cells—white blood cells that normally help the immune system fight infections. This discovery could shape future treatment strategies for patients with a high-risk form of MM known as t(4;14) myeloma. Multiple myeloma is a type of blood cancer that begins in plasma cells found in the bone marrow. About 20% of patients have a genetic change called t(4;14), which makes the NSD2 gene highly active. The research team compared two types of myeloma cells: one with high NSD2 activity and one where NSD2 was turned off. They found that when NSD2 is active, it changes how DNA is folded and how genes are switched on or off, especially genes that help the cells act like plasma cells. When NSD2 was turned off, important markers like CD38 were reduced, and other genes normally silent in plasma cells were activated. The study indicated that NSD2 does not directly affect the main genes responsible for plasma cell creation. Instead, it influences many other genes that help maintain the cancer cell's identity, which contributes to cancer growth and survival. The researchers also observed physical changes in the cancer cells. Cells with active NSD2 looked and behaved more like typical plasma cells, while cells without NSD2 appeared more immature and lost important surface markers. These changes were linked to differences in how the DNA was organized inside the cells. These findings are especially important as new drugs are being developed to block NSD2. The study suggests that turning off NSD2 could change how MM cells respond to existing treatments. For example, if NSD2 is blocked and CD38 levels drop, the change might affect therapies that target CD38. However, the rise of other immune-related genes might make certain immunotherapies more effective. “Identifying the biological consequences of NSD2 over-expression in MM is not only relevant to informing new therapeutic interventions through indirect targeting of downstream effectors, but also to anticipate possible consequences of targeting NSD2 directly.” In summary, this study shows how NSD2 helps myeloma cells keep their cancerous identity by reorganizing the DNA and influencing gene activity. Understanding this role could help researchers design better treatment approaches and possibly overcome resistance to current therapies in t(4;14) myeloma. DOI - https://doi.org/10.18632/oncotarget.28706 Correspondence to - Andrea Gunnell - andrea.gunnell@icr.ac.uk Video short - https://www.youtube.com/watch?v=hibkjUpRq7I Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

Dr. Elizabeth Comen, MD, is a distinguished board-certified oncologist,researcher and author. She is an award-winning researcher and has beenpublished in prestigious scientific journals, including Nature, Cancer Cell and The Journal of Clinical Oncology. Her book “All In Her Head” empowers women to take charge of their health and to learn about the misconceptions of women's health. Her work has been featured on The Today Show, Good Morning America and Oprah. She joins us on The Vault to discuss ways that we can prevent cancer, how to address anxiety around cancer and how to advocate for your health as a woman in today's healthcare system. She addresses myths around hormone replacement therapy and cancer. We also discuss how to live a more purpose driven life as a physician and healthcare professional. What are the myths around HRT and cancer? How can I advocate for better healthcare as a woman in today's healthcare system? Ways to address cancer anxiety? How to prevent cancer and poor health outcomes? How to support loved ones who have been diagnosed with cancer? What are ways to encourage loved ones to get cancer screenings? How to Cope with High Functioning Depression.Follow Dr. Elizabeth Comen: Dr. Elizabeth Comen Instagram https://www.instagram.com/drelizabethcomen/ Dr. Elizabeth Comen Book https://www.amazon.com/All-Her-Head-Medicine-Matters/dp/0063293013 Dr. Elizabeth Comen Website https://www.drelizabethcomen.com/Follow Dr. Judith:Instagram: https://instagram.com/drjudithjoseph TikTok: https://www.tiktok.com/@drjudithjoseph Facebook: https://www.facebook.com/drjudithjoseph Website: https://www.drjudithjoseph.com/Sign up for my newsletter here: https://www.drjudithjoseph.com/newsletter-sign-upDisclaimer: You may want to consider your individual mental health needs with a licensed medical professional. This page is not medical advice.

Scientists at Oregon State University and Oregon Health and Science University have teamed up to find new ways to treat endometriosis, ovarian cancer and other health conditions using nanoparticles and magnetic fields. Joining us to tell us more about this fascinating research are OPB science reporter Jes Burns, who is also the host and producer behind the “All Science. No Fiction.” video series, and OPB cinematographer and editor Brooke Herbert. This episode was recorded with a live audience at the Tomorrow Theater in Portland.   You can see the video about the medical applications of magnetic nanoparticles here.   For more Evergreen episodes and to share your voice with us, visit our showpage. Follow OPB on Instagram, host Jenn Chávez and Oregon Field Guide. You can sign up for OPB’s newsletters to get what you need in your inbox regularly.   Don’t forget to check out our many podcasts, which can be found on any of your favorite podcast apps: Hush Timber Wars Season 2: Salmon Wars Politics Now Think Out Loud And many more! Check out our full show list here.

On today's episode, our solar system is being invaded by particles from another star system and combating cancer by switching tumor cells back into healthy cells. Plus, on This Day in History, the first electric burglar alarm is installed. Scientists Think Visitors From Another Star System May Have Infiltrated Our Galactic Neighborhood | Popular Mechanics 'Cosmic Highway' Discovered: How Alpha Centauri's Debris May Link Our Solar System to Faraway Stars | Daily Galaxy [2502.03224] A Case Study of Interstellar Material Delivery: α Centauri Fighting Cancer Without Fighting: Scientists Switch Tumor Cells Back to Healthy Ones at 'Critical' Moment | Good News Network ​Almanac: The burglar alarm - CBS News Our Father's Beginning | Wayback Machine Who Was Augustus Russell Pope | Wayback Machine Contact the show - coolstuffcommute@gmail.com Learn more about your ad choices. Visit megaphone.fm/adchoices

Episode 2608: In this episode, Vinnie Tortorich and Chris Shaffer discuss how ketones fight cancer cells, another claim made by a GLP-1 med, and more. https://vinnietortorich.com/2025/02/ketones-fight-cancer-cells-episode-2608 PLEASE SUPPORT OUR SPONSORS YOU CAN WATCH ALL THE PODCAST EPISODES ON YOUTUBE - Ketones Fight Cancer Cells Chris Stapleton and trends in country music. (2:00) UPenn study references that the Keto diet can fight off cancer in early stages, and if undergoing chemo, can help with recovery. (20:00) Dr. Thomas Seyfried has been on the show discussing this. (22:00) Vinnie is an N=1 experiment of this. He believes that keeping himself in ketosis helped to stave off a remission in his cancer. He was told his cancer would return in 5 years; however, it didn't return for almost 17 years. His experience this time around was a bit different, but still better than his first battle with cancer. (24:00) He shares all the random advice he was given as “remedies” for his cancer while living in Hollywood. Hims/Hers and GLP-1s. The FDA should look at how this product is advertised without disclaimers. (38:00) Chris reviews a study suggesting that Wegovy lessens alcohol use. (42:00) They discuss why they have their doubts about this. It appears to be just another angle to try to advocate the use of the drug as alcohol use disorders are very complicated. Pure Vitamin Club and NSNG Foods are up and running and back to full speed! More News If you are interested in the NSNG® VIP group, closed for registration, but you can get on the wait list - Don't forget to check out Serena Scott Thomas on Days Of Our Lives on the Peacock channel.  “Dirty Keto” is available on Amazon! You can purchase or rent it . Make sure you watch, rate, and review it! Eat Happy Italian, Anna's next cookbook is available!  You can go to You can order it from . Anna's recipes are in her cookbooks, website, and Substack–they will spice up your day! Don't forget you can invest in Anna's Eat Happy Kitchen through StartEngine.  Details are at Eat Happy Kitchen. There's a new NSNG® Foods promo code you can use! The promo code ONLY works on the NSNG® Foods website, NOT on Amazon. https://nsngfoods.com/ [the_ad id="20253"] PURCHASE  DIRTY KETO (2024) The documentary launched in August 2024! Order it TODAY! This is Vinnie's fourth documentary in just over five years. Visit my new Documentaries HQ to find my films everywhere: Then, please share my fact-based, health-focused documentary series with your friends and family. Additionally, the more views, the better it ranks, so please watch it again with a new friend! REVIEWS: Please submit your REVIEW after you watch my films. Your positive REVIEW does matter! PURCHASE BEYOND IMPOSSIBLE (2022) Visit my new Documentaries HQ to find my films everywhere: REVIEWS: Please submit your REVIEW after you watch my films. Your positive REVIEW does matter! FAT: A DOCUMENTARY 2 (2021) Visit my new Documentaries HQ to find my films everywhere: FAT: A DOCUMENTARY (2019) Visit my new Documentaries HQ to find my films everywhere:

Dr. Michael Klaper presents the scientific evidence behind disease reversal through plant-based nutrition. Discover how dietary changes can lead to significant health improvements and disease prevention. #PlantBasedNutrition #DiseaseReversal #HealthScience

Romain Banchereau joins the show to discuss and debate this Cancer Cell paper on molecular subtypes in urothelial cancer and implications for checkpoint blockade.

Professor Thomas Seyfried joins the conversation to challenge the conventional view of cancer as a genetic disease, presenting it instead as a metabolic disorder influenced by lifestyle factors. With over 30 years of research, Seyfried argues that current cancer treatments may exacerbate the disease. He discusses the role of glucose and glutamine in cancer metabolism and emphasizes the potential of metabolic therapy, including ketogenic diets, for prevention and management. Explore the compelling intersection of biochemistry, lifestyle, and cancer with Seyfried's groundbreaking insights.Sponsors:ZocDoc: https://www.zocdoc.com/neuroHone Health Hormone Testing: https://honehealth.com/Momentous - Use code NEURO to get 20% off your order - https://www.livemomentous.com/neuro Timestamp 0:00 Challenging Cancer's Genetic Theory with Metabolic Insights4:54 Cancer as a Metabolic Disorder Not a Genetic Disease13:05 Challenging the Genetic Theory of Cancer Amidst Confirmation Bias15:27 Booking Doctor Appointments Easily with ZocDoc16:27 Mitochondria's Role in Cancer Cell Proliferation and Fermentation21:08 Mitochondrial Dysfunction and Its Role in Cancer Development31:23 Cancer Cells' Fermentation and Mitochondrial Dysfunction37:33 Metabolic Therapy as a Non-Toxic Cancer Treatment Alternative46:39 Exploring Diets and Metabolic Pressure on Cancer Cells49:36 Exercise and Diet in Cancer Treatment Targeting Glutamine50:50 Ketogenic Lifestyle's Impact on Cancer and Chronic Diseases52:40 Targeting Glucose and Glutamine to Combat Pancreatic Cancer54:36 Impact of Modern Lifestyle on Health and Chronic Diseases58:26 Metabolic Therapy as a Disruptive Cancer Prevention and TreatmentThe Neuro Athletics Newsletter Instagram: @louisanicola_Twitter : @louisanicola_YouTube: @Louisa NicolaThe Neuro Experience Podcast is proud to have hosted: Dr Andrew Huberman, Dr Gabrielle Lyon, Dr Layne Norton, Thomas DeLauer, Shawn Stevenson, Dr. Rocio Salas-Whalen, Saad Alam, Uma Naidoo, Dr. Lanna Cheuck, Angela Lee Pucci, Jillian Turecki, Dr. Jordan Feigenbaum, Dr. Darren Candow, Dr. Sue Varma, Evy Poumpouras, Dr Casey Means, Renee Deehan, Dr Chris Palmer, Dr Charles Brenner, Dr Joe Zundell, Dr Ray Dorsy, Dr Dale Bredeson, Dr. Ben Bikman

This week Zorba and Karl discuss standing work desks, and they examine new research that found certain foods disrupt your body's fight against cancer cells. Plus, they share a delicious recipe for Marinated winter squash with sage.

This week Zorba and Karl discuss standing work desks, and they examine new research that found certain foods disrupt your body's fight against cancer cells. Plus, they share a delicious recipe for Marinated winter squash with sage.

In this episode, Dr. Jessica Steier and Dr. Sarah Scheinman discuss the complexities of cancer with Dr. Joe Zundell, a cancer biologist. They explore the definition of cancer, its prevalence, and the hallmarks that characterize cancer cells. The conversation delves into the mechanisms of cancer growth, including sustaining proliferative signaling, evading growth suppression through the P53 gene, and the process of apoptosis. The discussion aims to make these complex topics accessible to a broader audience while highlighting the importance of understanding cancer biology. In this conversation, Dr. Joe Zundell discusses the complexities of cancer biology, focusing on key hallmarks such as immune response, replicative immortality, angiogenesis, and metastasis. He emphasizes the importance of early detection and the challenges of targeting cancer cells without affecting healthy cells. The discussion highlights the need for careful consideration of information regarding cancer treatment and the significance of working with healthcare professionals. All our sources from this episode are available at: https://www.unbiasedscipod.com/episodes/ (00:00) Introduction  (05:28) Understanding Cancer: Definitions and Statistics (10:15) The Hallmarks of Cancer: An Overview (15:14) Sustaining Proliferative Signaling in Cancer (20:07) Evading Growth Suppression: The Role of P53 (25:17) Apoptosis: The Controlled Cell Death Mechanism (30:21) Understanding Cancer: Immune Response and Cell Death (33:31) Replicative Immortality: The Hayflick Limit (38:27) Angiogenesis: Blood Vessel Formation in Tumors (46:32) Invasion and Metastasis: The Spread of Cancer (54:22) Final Thoughts: The Complexity of Cancer Treatment and Early Detection Interested in advertising with us? Please reach out to advertising@airwavemedia.com, with “Unbiased Science” in the subject line. PLEASE NOTE: The discussion and information provided in this podcast are for general educational, scientific, and informational purposes only and are not intended as, and should not be treated as, medical or other professional advice for any particular individual or individuals. Every person and medical issue is different, and diagnosis and treatment requires consideration of specific facts often unique to the individual. As such, the information contained in this podcast should not be used as a substitute for consultation with and/or treatment by a doctor or other medical professional. If you are experiencing any medical issue or have any medical concern, you should consult with a doctor or other medical professional. Further, due to the inherent limitations of a podcast such as this as well as ongoing scientific developments, we do not guarantee the completeness or accuracy of the information or analysis provided in this podcast, although, of course we always endeavor to provide comprehensive information and analysis. In no event may Unbiased Science or any of the participants in this podcast be held liable to the listener or anyone else for any decision allegedly made or action allegedly taken or not taken allegedly in reliance on the discussion or information in this podcast or for any damages allegedly resulting from such reliance. The information provided herein do not represent the views of our employers. Learn more about your ad choices. Visit megaphone.fm/adchoices

The Caterpillar Virus May Slow The Growth Of Cancer Cells bonus 58 Fri, 08 Nov 2024 02:38:27 +0000 1cNhAGvyJnAhlcGnOXcvjd2F6WHoFvLM news,pop culture,comedy,society & culture The Mens Room Daily Podcast news,pop culture,comedy,society & culture The Caterpillar Virus May Slow The Growth Of Cancer Cells From sinners to saints, kings to commoners, rock stars and regular folks. Everyone is here and they're sharing their stories. Sit down and grab a beer with the men of The Mens Room. 2024 © 2021 Audacy, Inc. Society & Culture False https://player.amperwavepodcasting.