Podcasts about cancer cells

TODAY ON THE ROBERT SCOTT BELL SHOW: Spike Protein Cancer Cells, Lead Water Pipes, EPA Weakens Water Rules, Oreodaphne Californica, States Reform School Meals, Jane Durst-Pulkys, Metabolic Balance, Diet Drink Health Impact, Birds Poop on Certain Cars and MORE! https://robertscottbell.com/spike-protein-cancer-cells-lead-water-pipes-epa-weakens-water-rules-oreodaphne-californica-states-reform-school-meals-jane-durst-pulkys-metabolic-balance-diet-drink-health-impact-birds-poop-on/ https://boxcast.tv/view/spike-protein-cancer-cells-lead-water-pipes-epa-water-rules-jane-durst-pulkys-metabolic-balance---the-rsb-show-10-10-25-hk9cbfvzxxyy7uxe85s2 Purpose and Character The use of copyrighted material on the website is for non-commercial, educational purposes, and is intended to provide benefit to the public through information, critique, teaching, scholarship, or research. Nature of Copyrighted Material Weensure that the copyrighted material used is for supplementary and illustrative purposes and that it contributes significantly to the user's understanding of the content in a non-detrimental way to the commercial value of the original content. Amount and Substantiality Our website uses only the necessary amount of copyrighted material to achieve the intended purpose and does not substitute for the original market of the copyrighted works. Effect on Market Value The use of copyrighted material on our website does not in any way diminish or affect the market value of the original work. We believe that our use constitutes a 'fair use' of any such copyrighted material as provided for in section 107 of the U.S. Copyright Law. If you believe that any content on the website violates your copyright, please contact us providing the necessary information, and we will take appropriate action to address your concern.

Gugs Mhlungu speaks with Dr Nicky Verhoog, senior lecturer of biochemistry at Stellenbosch University and lead researcher, about emerging breast cancer treatment and the potential role of Rooibos in advancing this research. 702 Weekend Breakfast with Gugs Mhlungu is broadcast on 702, a Johannesburg based talk radio station, on Saturdays and Sundays Gugs Mhlungu gets you ready for the weekend each Saturday and Sunday morning on 702. She is your weekend wake-up companion, with all you need to know for your weekend. The topics Gugs covers range from lifestyle, family, health, and fitness to books, motoring, cooking, culture, and what is happening on the weekend in 702land. Thank you for listening to a podcast from 702 Weekend Breakfast with Gugs Mhlungu. Listen live on Primedia+ on Saturdays and Sundays from 06:00 and 10:00 (SA Time) to Weekend Breakfast with Gugs Mhlungu broadcast on 702 https://buff.ly/gk3y0Kj For more from the show go to https://buff.ly/u3Sf7Zy or find all the catch-up podcasts here https://buff.ly/BIXS7AL Subscribe to the 702 daily and weekly newsletters https://buff.ly/v5mfetc Follow us on social media: 702 on Facebook: https://www.facebook.com/TalkRadio702 702 on TikTok: https://www.tiktok.com/@talkradio702 702 on Instagram: https://www.instagram.com/talkradio702/ 702 on X: https://x.com/Radio702 702 on YouTube: https://www.youtube.com/@radio702 See omnystudio.com/listener for privacy information.

JCO PO author Dr. Asaf Maoz at Dana-Farber Cancer Institute shares insights into article, “Causes of Death Among Individuals with Lynch Syndrome in the Immunotherapy Era.” Host Dr. Rafeh Naqash and Dr. Maoz discuss the causes of death in individuals with LS and the evolving role of immunotherapy. TRANSCRIPT Dr. Rafeh Naqash: Hello, and welcome to JCO Precision Oncology Conversations, where we bring you engaging conversations with authors of clinically relevant and highly significant JCOPO articles. I'm your host, Dr. Rafeh Naqash, podcast editor for JCO Precision Oncology and Associate Professor Medicine, at the OU Health Stephenson Cancer Center. Today, I'm super thrilled to be joined by Dr. Asaf Maoz, Medical Oncologist at Dana-Farber Cancer Institute, Brigham and Women's Hospital, and faculty at the Harvard Medical School, and also lead author on the JCO Precision Oncology article entitled "Causes of Death Among Individuals with Lynch Syndrome in the Immunotherapy Era." This publication will be a concurrent publication with an oral presentation at the annual CGA meeting. At the time of this recording, our guest's disclosures will be linked in the transcript. Asaf, I'm excited to welcome you on this podcast. Thank you for joining us today. Dr. Asaf Maoz: Thank you so much for highlighting our paper. Dr. Rafeh Naqash: Absolutely. And I was just talking to you that we met several years back when you were a trainee, and it looks like you've worked a lot in this field now, and it's very exciting to see that you consider JCOPO as a relevant home for some of your work. And the topic that you have published on is of significant interest to trainees from a precision medicine standpoint, to oncologists in general, covers a lot of aspects of immunotherapy. So, I'm really excited to talk to you about all of this. Dr. Asaf Maoz: Me too, me too. And yeah, I think JCOPO has great content in the area of cancer genetics and has done a lot to disseminate the knowledge in that area. Dr. Rafeh Naqash: Wonderful. So, let's get started and start off, given that we have hosts of different kinds of individuals who listen to this podcast, especially when driving from home to work or back, for the sake of making everything simple, can we start by asking you what is Lynch syndrome? How is it diagnosed? What are some of the main things to consider when you're trying to talk an individual where you suspect Lynch syndrome? Dr. Asaf Maoz: Lynch syndrome is an inherited predisposition to cancer, and it is common. So, we used to think that, or there's a general notion in the medical community that it is a rare condition, but we actually know now from multiple studies, including studies that look at the general population and do genetic testing regardless of any clinical phenotype, that Lynch syndrome is found in about 1 in 300 people in the general population. If you think about it in the United States, that means that there are over a million people living with Lynch syndrome in the United States. Unfortunately, most individuals with Lynch syndrome don't know they have Lynch syndrome at the current time, and that's where a lot of the efforts in the community are being made to help detect more individuals who have Lynch syndrome. Lynch syndrome is caused by pathogenic germline variants in mismatch repair genes, MLH1, MSH2, MSH6, or PMS2, or as a result of pathogenic variants in EPCAM that cause silencing of the MSH2 gene. Dr. Rafeh Naqash: Excellent. Thank you for that explanation. Now, one of the other things I also realized, similar to BRCA germline mutations, where you require a second hit for individuals with Lynch syndrome to have mismatch repair deficient cancers, you also require a second hit to have that second hit result in an MSI-high cancer. Could you help us understand the difference of these two concepts where generally Lynch syndrome is thought of to be cancers that are mismatch repair deficient, but that's not necessarily true for all cases as we see in your paper. Can you tease this out for us a little bit more? Dr. Asaf Maoz: Of course, of course. So, the germline defect is in one of the mismatch repair genes, and these genes are responsible for DNA mismatch repair, as their name implies. Now, in a normal cell, we think that one working copy is generally enough to maintain the mismatch repair machinery intact. What happens in tumors, as you alluded to, is that there is a second hit in the same mismatch repair gene that has the pathogenic germline variant, and that causes the mismatch repair machinery not to work anymore. And so what happens is that there is formation of mutations in the cancer cell that are not present in other cells in the body. And we know that there are specific types of mutations that are associated with defects in mismatch repair mechanisms, and those are associated a lot of times with frameshift mutations. And we have termed them ‘microsatellites'. So there are areas in the genome that have repeats, for example, you know, if you have AAAA or GAGA, and those areas are particularly susceptible to mutations when the mismatch repair machinery is not working. And so we can measure that with DNA microsatellite instability testing. But we can also get a sense of whether the mismatch repair machinery is functioning by looking at protein expression on the surface of cancer cells and by doing immunohistochemistry. More recently, we're also able to infer whether the mismatch repair machinery is working by doing next-generation sequencing and looking at many, many microsatellites and whether they have this DNA instability in the microsatellites. Dr. Rafeh Naqash: Excellent explanation. As a segue to what you just mentioned, and this reminds me of some work that one of my good friends, collaborators, Amin Nassar, whom you also know, I believe, had done a year and a half back, was published in Cancer Cell as a brief report, I believe, where the concept was that when you look at these mismatch repair deficient cancers, there is a difference between NGS testing, IHC testing, and maybe to some extent, PCR testing, where you can have discordances. Have you seen that in your clinical experience? What are some of your thoughts there? And if a trainee were to ask, what would be the gold standard to test individuals where you suspect mismatch repair deficient-related Lynch syndrome cancers? How would you test those individuals? Dr. Asaf Maoz: We do sometimes see discordance, you know, from large series, the concordance rate is very high, and in most series it's over 95%. And so from a practical perspective, if we're thinking about the recommendation to screen all colorectal cancer and all endometrial cancer for mismatch repair deficiency, I think either PCR-based testing or immunohistochemistry is acceptable because the concordance rate is very high. There are rare cases where it is not concordant, doing multiple of the tests makes sense at that time. If you think about the difference between the tests, the immunohistochemistry looks at protein expression, which is a surrogate for whether there is mismatch repair deficiency or not, right? Because ultimately, the mismatch repair deficiency is manifested in the mutations. So if the PCR does not show microsatellite instability and now NGS does not show microsatellite instability, the IHC may be a false positive. At the end of the day, the functional analysis of whether there are actually unstable microsatellites either by PCR or by NGS is what I would consider more informative. But IHC again is an excellent test and concordant with those results in over 95% of cases. Now there is also an issue of sampling. It's possible that there's heterogeneity within the tumor. We published a case in JCOPO about heterogeneity of the mismatch repair status, and that was both by immunohistochemistry, but also by PCR. So there are some caveats and interpreting these tests does require some expertise, and I'm always happy to chat with trainees or whoever has an interesting or challenging case. Dr. Rafeh Naqash: Thanks again for that very easy to understand explanation. Now going to management strategies, could you elaborate a little bit upon the neo-adjuvant data currently, or the metastatic data which I think more people are familiar with for immunotherapy in individuals with MSI-high cancers? Dr. Asaf Maoz: Yeah, that's an excellent question and obviously a very broad topic. Individuals with Lynch syndrome typically develop tumors that are mismatch repair deficient or microsatellite unstable. And we have seen over the last 15 years or so that these tumors, because they have a lot of mutations and because these mutations are very immunogenic, we have seen that they respond very well to immunotherapy. And this has been shown across disease sites and has been shown across disease settings. And for that reason, immunotherapy was approved for MSI-high or mismatch repair deficient cancer regardless of the anatomic site. It was the first tissue-agnostic approval by the FDA in 2017. And so there are exciting studies both in the metastatic setting where we see individuals who respond to immunotherapy for many years, and one could wonder whether their cancer is going to come back or not. And also in the earlier setting, for example, the Cercek et al. study in the New England Journal from Sloan Kettering, where they showed that neoadjuvant immunotherapy can cause durable responses for rectal cancer that is mismatch repair deficient. And in that series, the patients did not require surgery or radiation, which is standard of care for rectal cancer otherwise. And there's also exciting data in the adjuvant space, as was presented in ASCO by Dr. Sinicrope, the ATOMIC study, and many more efforts to bring immunotherapy into the treatment landscape for individuals with MSI-high cancer, including individuals with Lynch syndrome. Dr. Rafeh Naqash: A lot of activity, especially in the neo-adjuvant and adjuvant space over the last two years or so. Now going to the actual reason why we are here is your study. Could you tell us why you looked at this idea of patients who had Lynch syndrome and died, and the reasons for their death? What was the thought that triggered this project? Dr. Asaf Maoz: As we were talking about, we now know that immunotherapy really has changed the treatment landscape for individuals with Lynch syndrome, and that most cancers that individuals with Lynch syndrome do have this mismatch repair deficiency. But we also know that individuals with Lynch syndrome can develop tumors that do not have mismatch repair deficiency, and we call them mismatch repair proficient or microsatellite stable. And there was a series from Memorial Sloan Kettering showing that in colorectal cancer, about 10% of the tumors that individuals with Lynch syndrome developed did not have mismatch repair deficiency. In addition to that, we anecdotally saw that some of our patients with Lynch syndrome died of causes that were not mismatch repair deficient tumors. We wanted to see how that has changed since immunotherapy was approved in a tissue-agnostic manner, meaning that we could look at this regardless of where the cancer started, because we would anticipate that if the tumor was mismatch repair deficient, the patient would be able to access immunotherapy as standard of care. Dr. Rafeh Naqash: Thank you. And then you looked at different aspects of correlations with regards to individuals that had an MSI-high cancer with Lynch syndrome or an MSS cancer with Lynch syndrome. Could you elaborate on some of the important findings that you identified as well as some of the unusual findings that perhaps we did not know about, even though the sample size is limited, but what were some of the unique things that you did identify through this project? Dr. Asaf Maoz: The first question was what cause is leading to death in individuals with Lynch syndrome? And we had 54 patients that we identified that had died since the approval of immunotherapy in 2017, 44 of which died of cancer-related causes. And when we looked at cancer-related causes of death, we wanted to know how many of those were due to mismatch repair deficient tumors versus mismatch repair proficient tumors or MS-stable tumors. And we found, somewhat surprisingly, that 43% of patients in our cohort actually died of tumors that were microsatellite stable or mismatch repair proficient, meaning of tumors that are not typically associated with Lynch syndrome. This is not entirely surprising as a cause of death because we know that immunotherapy does not typically work for tumors that are microsatellite stable. And so in the metastatic setting, there are much less cases of durable remissions with treatment. But it was helpful to have that figure as an important benchmark. There are previous studies about causes of death in Lynch syndrome, and particularly from the Prospective Lynch Syndrome Database in Europe. Those have provided really important information about cause of death by cancer site, but they typically don't have mismatch repair status and are more difficult to interpret in that regard. They also don't include a large number of individuals who have PMS2 Lynch syndrome, which is the most common, but least penetrant form of Lynch syndrome. Dr. Rafeh Naqash: As far as the subtype of pathogenic germline variants is concerned, did you notice anything unusual? And I've always had this question, and you may know more about this data, is: In the bigger context of immunotherapy, does the type of the pathogenic germline variant for Lynch syndrome associated MSI-high cancers, does that impact or have an association with the kind of outcomes, how soon a cancer progresses or how many exceptional responders perhaps with MSI-high cancers actually have a certain specific pathogenic germline variant? Dr. Asaf Maoz: That's an excellent question, and certainly we need more data in that space. We know that the type of germline mutation, or the gene in which there is a germline pathogenic variant, determines to a large degree the cancer risk, right? So we know that individuals who have germline pathogenic variants in MLH1 or MSH2 have a much higher colorectal cancer risk than, for example, PMS2. We know that for PMS2, the risks are more limited to colorectal and endometrial, and may be lower risk of other cancers. We also know that, you know, the spectrum of disease may change based on the pathogenic germline variants. For example, individuals who have MSH2 associated Lynch syndrome have more risk of additional cancers in other organs like the urinary tract and other less common Lynch-associated tumors. The question about response to therapy is one where we have much less information. There are studies that are trying to assess this, but I don't think the answer is there yet. Some of the non-clinical data looks at how many mutations there are based on the pathogenic variant and what the nature of those mutations are, whether they're more frameshift or others. But I think we still need more clinical data to understand whether the response to immunotherapy differs. It's also complicated by the fact that the immunotherapy landscape is changing, especially in the metastatic setting, now with the approval of combination ipilimumab and nivolumab for first-line treatment of colorectal cancer that is microsatellite unstable. But in our study, we did find that, as you would expect, there is an enrichment in MS-stable cancers among those with PMS2 Lynch syndrome. Again, our denominator is those who died, right? So this is not the best way to look at the question whether this is overall true, that is more addressed by the study that Sloan Kettering published. But we do see, as we would anticipate, that there are more microsatellite stable cancers among those with PMS2 Lynch syndrome that died. Dr. Rafeh Naqash: A lot to uncover there for sure. This study and perhaps some of the other work that you're doing is slowly advancing our understanding of some of these concepts. So I'd like to shift gears to a couple of provocative questions that I generally like to ask. The first is, in your opinion, and you may or may not have data to back this up, which is okay, and that's why we're having a conversation about it. In your opinion, do you think the type or the quality of the neoantigen is different based on the pathogenic germline variant and a Lynch syndrome associated MSI-high cancer? Dr. Asaf Maoz: I think there are some data out there that, you know, I can't cite off the top of my mind, but there are some data out there that suggest that that may be the case. I think the key question is the quality, right? I think that whether these differences that are found on a molecular level also translate to a clinical difference in response is something that is unknown at this moment. Some people hypothesize that if the tumor has less neoantigens, there's less of a response to immunotherapy. But I think we really need to be careful before making those assertions on a clinical level. I do think it's a really important question that needs to be answered, among others because, you know, in the colorectal space, for example, where we have both the option of doing ipilimumab with nivolumab and the option of doing pembrolizumab, we don't really know which patients need the CTLA-4 blockade versus which patients can receive PD-1 blockade alone and avoid the potential excess toxicity of the CTLA-4 blockade. There are a lot of interesting questions there that still need to be answered. And of course, individuals with Lynch syndrome are just a fraction of those individuals who have MSI-high cancer. So there's also the question about whether non-Lynch syndrome associated MSI-high cancer responds differently to immunotherapy than Lynch syndrome associated MSI-high cancer. A lot of very interesting questions in the field for sure. Dr. Rafeh Naqash: Absolutely. My second question is more about trying to understand the role of ctDNA, MRD monitoring in individuals with Lynch syndrome. If somebody has a germline, you know, Lynch syndrome MSI-high cancer, when you do a tumor-informed ctDNA assessment, what do you capture generally there? Because, and this question stems from a discussion I've had with somebody regarding EGFR lung cancer, since I treat individuals with lung cancer, and the concept generally is that even if the tissue showed EGFR, but for MRD monitoring, when you do a barcoded sequence of different tumor specific mutations, it's not actually the EGFR that they track in the blood when they do ctDNA assessment. But from a Lynch syndrome standpoint, if you have a germline, right, which is the first hit, and then you have the somatic in the tumor, which is the second hit, are you aware or have you tried to look into this where what is exactly being followed if one had to follow MRD in a Lynch syndrome MSI-high colorectal cancer? Dr. Asaf Maoz: I think a lot of the MRD assays are proprietary, and so we don't receive information about what the mutations that are being tracked are. In general, the idea is to track mutations that we would not expect to disappear as part of resistant mechanisms. We want these to be truncal mutations. We want these to be mutations in which resistance is not expected to result in reversion mutations. But what specifically is being tracked is something that I don't know because these assays, the tumor-informed ones, are proprietary, and we don't get the results regarding specific mutations. When it's circulating tumor DNA that is not necessarily tumor-informed, we do get those results, but that is less so about the specific selection of mutations. Dr. Rafeh Naqash: Thank you for clarifying that question to some extent, of course, as you said, we don't know a lot, and we don't know what we don't know. That's the most important thing that I've learned in the process of understanding precision medicine and genomics, and it's a very fast-paced evolving field. Last question related to your project, what is the next step? Are you planning any next steps as a bigger multicenter study or validation of some sort? Dr. Asaf Maoz: There are two big questions that this study raises. One, is this true across multiple other sites, right? Because this is a single center study, and we really need additional centers to look at their data and validate whether they are also seeing that a substantial portion of deaths in individuals with Lynch syndrome are attributable to mismatch repair proficient cancer. The other question is whether we can look at specifically MSI-high cancer versus MS-stable cancer and understand what the mortality rate for each of those are. From a clinical perspective, it's important to counsel individuals with Lynch syndrome about general cancer screening outside of mismatch repair deficient tumors and to understand that there is also a risk of mismatch repair proficient tumors and that treatment for those tumors would be different. There's a lot of work to be done in the future. Another major area of need is to see whether tumors that are microsatellite stable can be sensitized to immunotherapy, and that is beyond the Lynch syndrome field, but that is something that certainly would benefit these individuals with Lynch syndrome who develop mismatch repair proficient cancer. Dr. Rafeh Naqash: That's very interesting to hear, and we'll look forward to seeing some of those developments shape in the next few years. Now, I'd like to spend a minute, minute and a half on you specifically as a researcher, clinician, scientist. Could you briefly highlight - because I remember meeting you several years back as a trainee, with your interest in genomics, computational research - could you briefly tell us what led you to hereditary cancer syndromes based on your research and work? What are some of the things that you learned along the way that other early career investigators can perhaps take lessons from? Dr. Asaf Maoz: Big questions there, thanks for asking. I got interested in the field of hereditary cancer syndromes when I came to the United States and started doing lab research in Stephen Gruber's lab at the time at USC. He's now at City of Hope. And my interest was originally looking at immunotherapy and immunology, but I went to the case conferences where we were learning about individuals with hereditary cancer, and those were kind of earlier days where we were still trying to figure out how to test and what the implications for these individuals would be. And through fellowship, I was also very interested in that, and I did my senior fellowship years with Dr. Yurgelun here at Dana-Farber, who is the director of the Lynch Syndrome Center. And I I think it's the combination between being able to treat individuals based on precision medicine and what the germline mutation is, but also the ability to prevent cancer and to develop strategies to intercept cancer early that is really appealing to me in this field. It's also a great field to be in because it's a small field. If you come to the CGA-IGC meeting, you'll be able to interact with everyone. Everyone is super collaborative, super nice, and I really recommend it to trainees. The CGA-IGC annual meeting is really a great opportunity to learn more and experience some of the advancement specifically in the GI hereditary space. Lessons for trainees. I think there are a lot of lessons that I could think about, but I think finding strong and supportive mentors is one of the things that has helped me most. I think that just having close relationship with your mentor, having frequent discussions and honest discussions about what is feasible, what is going to make a difference for your patients and your research and what you want to focus on is really important. And so I think if I had to choose one thing, I would say choose a mentor that you trust, that you feel you have a good relationship with, and that has the availability to support you. Dr. Rafeh Naqash: Thank you so much for those insightful comments, and thank you for sharing with us your journey, your project, and some of your interesting thoughts on this concept of hereditary cancers. Hopefully, we'll see more of this work being published in JCOPO through your lab or work from others. Dr. Asaf Maoz: Thank you so much. I appreciate the opportunity to be here. Dr. Rafeh Naqash: Thank you for listening to JCO Precision Oncology Conversations. Don't forget to give us a rating or review and be sure to subscribe so you never miss an episode. You can find all ASCO shows at ASCO.org/podcasts. The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.

Join me as I sit down with Dr. Limor Goren — cancer researcher, molecular biologist, and founder of Kyoord — to explore olive oil's powerful health benefits. Dr. Goren, renowned for her work on oleocanthal, a potent polyphenol in high-phenolic olive oil, has shown how it selectively punctures cancer cell lysosomes, triggering cell death while sparing healthy cells. In this episode, we discuss what polyphenols are, their healing properties, and how high-oleocanthal olive oils are made — plus tips for choosing the best one for your kitchen. From groundbreaking research to sourcing award-winning oils in Corfu, Greece, Dr. Goren's journey offers a science-backed look at how one simple ingredient can transform your health.Suggested Resources:Kyoord olive oil (code wellnstrong10 for a discount)Oleocanthal, an Antioxidant Phenolic Compound in Extra Virgin Olive Oil (EVOO): A Comprehensive Systematic Review of Its Potential in Inflammation and CancerOleocanthal rapidly and selectively induces cancer cell death via lysosomal membrane permeabilizationLysosomal membrane permeabilization in cell deathThis episode is proudly sponsored by: KyoordKyoord makes small-batch Greek olive oils that are exceptionally rich in polyphenols—powerful compounds shown to fight inflammation, support brain health, and protect against chronic disease. It's the brand I personally use and trust daily, and you can try it yourself at kyoord.com with code WELLNSTRONG for 10% off your first order.Send me a text!Kyoord makes small-batch Greek olive oils that are exceptionally rich in polyphenols—powerful compounds shown to fight inflammation, support brain health, and protect against chronic disease. It's the brand I personally use and trust daily, and you can try it yourself at kyoord.com with code WELLNSTRONG for 10% off your first order. This episode is proudly sponsored by: SizzlefishLet's talk about fueling your body with the best nature has to offer. If you're looking for premium, sustainable seafood delivered straight to your door, you need to check out Sizzlefish! Head to sizzlefish.com and use my code “wellnstrong” at checkout for an exclusive discount on your first order. Trust me, you're going to taste the difference with Sizzlefish!Join the WellnStrong mailing list for exclusive content here!Want more of The How To Be WellnStrong Podcast? Subscribe to the YouTube channel. Follow Jacqueline: Instagram Pinterest TikTok Youtube To access notes from the show & full transcripts, head over to WellnStrong's Podcast Page

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Get your FREE copy of the Breast Cancer Checklist here: https://dramycancer.com/checklist What if the food on your plate could actually target breast cancer cells—and stop them in their tracks? Inside this video, I'm breaking down 9 powerful foods that research shows can weaken, starve, and even kill breast cancer cells. These aren't obscure superfoods that are impossible to find—they're everyday ingredients you can add to your meals starting today. You'll discover how simple nutrition shifts can lower inflammation, boost your immune system, and put you back in control of your health after cancer. So let me show you how it's done. Join the Cancer Freedom Program Apply HERE: https://dramycancer.com/checklist #cancerfighter #cancersurvivor #breastcancer #breastcancersurvivors #cancerrecovery #cancernutrition #mastectomy #tamoxifen #anastrozole #letrozole #exemestane PS - Whenever you're ready, here are the 2 best ways I can help you… “Breast Cancer Checklist” FREE Click HERE: https://dramycancer.com/checklist Join the Cancer Freedom Program Apply HERE: https://www.cancerfreedomprogram.com/?utm_source=podcast&utm_content=cancer_freedom_podcast Let's Connect: Website: https://www.cancerfreedomprogram.com/?utm_source=podcast&utm_content=cancer_freedom_podcast Instagram: https://www.instagram.com/dramymorris/  

A Kyoto University research group has developed a new type of protein that marks out cancer cells for easier removal.

Access the FREE Water Fasting Masterclass Now: https://www.katiedeming.com/the-healing-power-of-fasting/What lifestyle choices can reduce your risk before cancer develops? (Video ReRelease)Dr. Katie Deming sat down with Dr. Thomas Seyfried, professor of biology at Boston College and author of Cancer as a Metabolic Disease. Together, they explore how cancer cells depend on sugar and glutamine for fuel, why the mitochondria, not DNA mutations, may be at the heart of the disease, and what this understanding means for prevention and treatment.Key Highlights:Can dietary changes, fasting, and exercise support treatment once cancer is diagnosed? Why should patients and doctors pay attention to the Glucose Ketone Index (GKI) to measure how the body is fueling itself?What can you do today to reduce your risk of chronic illness?Dr. Seyfried explains the Warburg Effect, the role of dysfunctional mitochondria in cancer growth, and why standard treatments may sometimes work against us by feeding cancer's energy needs.Listen, learn the surprising story of how weight loss, not a new drug, led to dramatic tumor reduction in lab studies. Dr. Thomas Seyfried: https://www.bc.edu/bc-web/schools/morrissey/departments/biology/people/faculty-directory/thomas-seyfried.htmlAccess the FREE Water Fasting Masterclass Now: https://www.katiedeming.com/the-healing-power-of-fasting/ Transform your hydration with the system that delivers filtered, mineralized, and structured water all in one. Spring Aqua System: https://springaqua.info/drkatieMORE FROM KATIE DEMING M.D. Save your spot for the next LIVE fasting call here: https://www.katiedeming.com/the-healing-power-of-fasting/ Work with Dr. Katie: www.katiedeming.comEmail: INFO@KATIEDEMING.COM 6 Pillars of Healing Cancer Workshop Series - Click Here to Enroll Follow Dr. Katie Deming on Instagram: https://www.instagram.com/katiedemingmd/ Please Support the Show Share this episode with a friend or family member Give a Review on Spotify Give a Review on Apple Podcast DISCLAIMER: The Born to Heal Podcast is intended for informational purposes only and is not a substitute for seeking professional medical advice, diagnosis, or treatment. Individual medical histories are unique; therefore, this episode should not be used to diagnose, treat, cure, or prevent any disease without consulting your healthcare provider.

BUFFALO, NY - August 13, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on July 29, 2025, titled “PCAIs stimulate MAPK, PI3K/AKT pathways and ROS-Mediated apoptosis in aromatase inhibitor-resistant breast cancer cells while disrupting actin filaments and focal adhesion.” In this study, led by first author Jassy Mary S. Lazarte and corresponding author Nazarius S. Lamango from Florida A&M University College of Pharmacy and Pharmaceutical Sciences, researchers investigated a new class of compounds called polyisoprenylated cysteinyl amide inhibitors (PCAIs) as a potential treatment for aromatase inhibitor (AI) therapy resistant breast cancer. Aromatase inhibitors are a common treatment for estrogen receptor-positive (ER+) breast cancer, but many patients eventually develop resistance, leaving fewer therapeutic options. The study focused on a PCAI compound called NSL-YHJ-2-27, which was tested in long-term letrozole-treated breast cancer cells (LTLT-Ca), an experimental model of AI therapy resistance. NSL-YHJ-2-27 activated two major signaling pathways, MAPK and PI3K/AKT. Although these pathways typically support cancer cell survival, their overstimulation by PCAIs led to increased oxidative stress, damaging the cells and inducing cell death by apoptosis. The compound also reduced levels of RAC1 and CDC42, proteins involved in maintaining cell shape and movement. These alterations resulted in cytoskeletal disruption and reduced structural integrity, making the cancer cells more vulnerable and less capable of spreading. Importantly, the effects of NSL-YHJ-2-27 persisted after the compound was removed, suggesting long-term control over AI resistant cancer cells may be possible. “PCAIs inhibited cell proliferation and colony formation by 95% and 74%, respectively, increased active caspase 7 and BAX 1.5-fold and 56%, respectively. NSL-YHJ-2-27 (10 μM) induced LTLT-Ca spheroid degeneration by 61%.” As a new class of targeted molecules, PCAIs represent an innovative approach distinct from traditional endocrine therapies. Their ability to affect multiple cellular mechanisms simultaneously makes them promising candidates for future drug development. Overall, this study presents a promising new approach for treating AI therapy-resistant breast cancer. By targeting cellular pathways that support survival and mobility, PCAIs like NSL-YHJ-2-27 could provide a novel strategy to manage advanced or resistant forms of the disease. Further research, including in vivo studies and clinical trials, will be essential to confirm these findings and evaluate their therapeutic potential. DOI - https://doi.org/10.18632/oncotarget.28759 Correspondence to - Nazarius S. Lamango - nazarius.lamango@famu.edu Video short - https://www.youtube.com/watch?v=8xQEilloO9Q Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28759 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, PCAIs, ROS, MAPK, PI3K/AKT, LTLT-Ca cells 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

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.

Aron Knickerbocker, President and CEO of Aulos Bioscience,  is on a mission to extend the lives of cancer patients through safer and more effective immunotherapy using AI and machine learning to accelerate drug discovery and optimization. The company's lead drug candidate is an antibody that was designed using AI to harness the power of interleukin-2 to activate the immune system against tumors.  The advantages of AU-007 over previous IL-2 therapies include the ability to selectively activate tumor-fighting immune cells while avoiding toxicity due to vascular leakage. Current trials are underway in advanced melanoma and non-small cell lung cancer, which are showing the potential for durable responses and immune memory. Aron explains, "So Aulos has really been founded to carry out a mission to extend the lives of patients with innovative, safe, and ultimately effective cancer immunotherapy. And you mentioned IL-2, which is the naturally occurring protein that we're seeking to harness and redirect in productive ways to help the patients. And this has really been kind of a driver for me over the years, wanting to improve on cancer patient care. This is a company with an important mission and a great team, and our program is really interesting. It's harnessing IL-2 in such a way that it sends it to the cells that are capable of attacking the tumor and killing the tumor cells, and keeps it away from the cells that suppress the immune response. It's really kind of using a double-edged sword in a productive way to help patients with cancer." "So this is the first antibody to go into human clinical trials. It was designed in part by leveraging an AI platform, as you noted. And that platform was created by our collaborators at Biologic Design. They're the company that created this molecule. And what biologic design does is essentially using an AI system that has machine learning algorithms that drive it. It mimics what the immune system does normally. So when we get sick and we need to make antibodies to something, our immune system says, Do I already have something that will kind of bind to the target or the virus or whatever it's trying to hit? And then it will optimize that. It will go through a process of rapid change. And what the AI system and the machine learning algorithms that have been trained on millions of antibodies in the targets to which they bind do is recognize patterns much like an AI chatbot might recognize language patterns." #AulosBio #Antibodies #MedAi #AI #IL2 #Onocology #Cancer #NSCLC #AdvancedCutaneousMelanoma #DrugDiscovery #BiologicDesign #Tregs aulosbio.com Listen to the podcast here

Aron Knickerbocker, President and CEO of Aulos Bioscience,  is on a mission to extend the lives of cancer patients through safer and more effective immunotherapy using AI and machine learning to accelerate drug discovery and optimization. The company's lead drug candidate is an antibody that was designed using AI to harness the power of interleukin-2 to activate the immune system against tumors.  The advantages of AU-007 over previous IL-2 therapies include the ability to selectively activate tumor-fighting immune cells while avoiding toxicity due to vascular leakage. Current trials are underway in advanced melanoma and non-small cell lung cancer, which are showing the potential for durable responses and immune memory. Aron explains, "So Aulos has really been founded to carry out a mission to extend the lives of patients with innovative, safe, and ultimately effective cancer immunotherapy. And you mentioned IL-2, which is the naturally occurring protein that we're seeking to harness and redirect in productive ways to help the patients. And this has really been kind of a driver for me over the years, wanting to improve on cancer patient care. This is a company with an important mission and a great team, and our program is really interesting. It's harnessing IL-2 in such a way that it sends it to the cells that are capable of attacking the tumor and killing the tumor cells, and keeps it away from the cells that suppress the immune response. It's really kind of using a double-edged sword in a productive way to help patients with cancer." "So this is the first antibody to go into human clinical trials. It was designed in part by leveraging an AI platform, as you noted. And that platform was created by our collaborators at Biologic Design. They're the company that created this molecule. And what biologic design does is essentially using an AI system that has machine learning algorithms that drive it. It mimics what the immune system does normally. So when we get sick and we need to make antibodies to something, our immune system says, Do I already have something that will kind of bind to the target or the virus or whatever it's trying to hit? And then it will optimize that. It will go through a process of rapid change. And what the AI system and the machine learning algorithms that have been trained on millions of antibodies in the targets to which they bind do is recognize patterns much like an AI chatbot might recognize language patterns." #AulosBio #Antibodies #MedAi #AI #IL2 #Onocology #Cancer #NSCLC #AdvancedCutaneousMelanoma #DrugDiscovery #BiologicDesign #Tregs aulosbio.com Download the transcript here

New research shows that respiratory viruses, like the flu and COVID-19, could “wake up” dormant cancer cells. We speak with with James DeGregori, the senior author of the study and deputy director of the Colorado Cancer Center. Then, Theodore "Bubbles" Anderson was the only Colorado native to play in the Negro Baseball League. A century later, he's been inducted into the Colorado Sports Hall of Fame, thanks to the efforts of sports journalist Justin Adams. 

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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

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.

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!  

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]

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

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

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:

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