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The potential breakthrough in RNA vaccine technology has been increasingly discussed on social media. This episode looks at one promising study and its early, early results so far. UF GBM study: https://doi.org/10.1016/j.cell.2024.04.003 RNA Treatment Vaccine Review: https://doi.org/10.1002/ctm2.1384
On today's episode of The Ultimate Assist, John Stockton and Ken Ruettgers sit down with Dr. Brian Hooker, scientist, autism dad, and chief scientific officer at Children's Health Defense, for one of the most explosive interviews yet.Dr. Hooker recounts his son's devastating vaccine injury, his whistleblower role in exposing the CDC's suppression of autism data, and the 16-year nightmare his family endured in vaccine court—only to be denied justice. He unpacks conflicts of interest in vaccine research, the dangers of mercury and aluminum still in shots, and how studies are manipulated to hide the truth. From shedding and genetic susceptibility to Tylenol's hidden role in vaccine injury, Hooker explains what mainstream science refuses to discuss.He also reveals the inside story of testifying alongside Senator Ron Johnson, how Robert F. Kennedy Jr. is shaking up the health establishment, and why new self-amplifying RNA vaccines could be the biggest threat yet.
New Discovery Shakes Life's Origins: Proof of Intelligent Design? This eye-opening conversation uncovers the complexities of life's origin, scrutinizing the RNA world hypothesis against molecular biology's harsh realities. Experts Dr. Brian Miller and Dr. Casey Luskin join Lenny to discuss DNA-protein interdependence, polymerization challenges in water, and why self-organization doesn't explain life's emergence. With probabilistic hurdles in focus, they emphasize the need for a paradigm shift in scientific research to better address these fundamental questions.
Joe Untamed tackles two urgent battles shaping America's future: the rise of radical Islamist influence and the war over truth in public health. Robert Spencer, renowned scholar and director of Jihad Watch, joins us to break down the growing presence of Islamist ideology in U.S. communities—from mass gatherings in Michigan to city councils now dominated by Muslim politicians. What does this mean for American law, culture, and national security? Spencer peels the onion back on the elites enabling this transformation and warns what's at stake if we continue down this path unchecked. Then, Dr. Robert Malone—the original inventor of mRNA vaccine technology—returns to reveal how entrenched bureaucrats and Big Pharma allies are weaponizing science against the American people. With new developments inside HHS and RFK Jr.'s sweeping reforms, Malone exposes the deep state's retaliation, the dangers of indemnifying industries like RNA pesticides, and the long-term health consequences hidden from public view. From vaccine schedules to regulatory corruption, his insights strike at the heart of America's medical and political crises. Together, Spencer and Malone highlight the same underlying truth: powerful elites, whether in religion, government, or corporate boardrooms, are eroding American freedom from within. This is not just about foreign threats or public health—it's about the survival of liberty itself. Tonight's show is a wake-up call, offering clarity, urgency, and solutions for anyone ready to stand against the forces trying to reshape America in their image.
Jordan Sather and Nate Prince return with another hard-hitting episode of MAHA News, diving into the week's biggest health and freedom stories. They kick things off with the Pete and Bobby Challenge, where Pete Hegseth and RFK Jr. put their strength to the test in a push-up and pull-up competition that has everyone talking. From there, the hosts shift into the serious implications of glyphosate spraying in Canada and the broader dangers of genetically engineered crops, highlighting how hidden RNA tinkering in food could impact human genetics and health. The discussion then takes aim at the American Academy of Pediatrics, which is under fire for its push to remove vaccine exemptions and its continued cozy ties with big pharma giants like Pfizer, Merck, and Moderna. RFK Jr.'s sharp rebuke of the AAP sparks debate about liability, childhood vaccine schedules, and health freedom. With side conversations on raw milk legalization, natural detox strategies, and the cultural psyop of green lawns, this episode weaves humor, practicality, and blunt truth into an engaging exploration of health sovereignty.
Matters Microbial #104: Antibiotic “Tolerance” and Biofilms August 21, 2025 Today, Dr. Boo Shan Tseng, Associate Professor at the University of Nevada Las Vegas School of Life Sciences, joins the #QualityQuorum to discuss bacterial biofilms and antibiotic tolerance. Host: Mark O. Martin Guest: Boo Shan Tseng Subscribe: Apple Podcasts, Spotify Become a patron of Matters Microbial! Links for this episode A video overview of biofilms. A comprehensive review article on biofilms. An article describing the impact biofilms have on disease. An article describing the impact of biofilms on implanted medical devices. A link to the Center for Biofilm Engineering at Montana State University that has MANY links of interest. An overview of biofilm development. An overview of confocal laser microscopy. Studying biofilms in flow cells. An article about the role proteins play in biofilm formation, which intersects with the Tseng group's research. The technique of single cell RNA seq. The technique of mRNA-FISH. An article about porins in bacteria, and how that can relate to antibiotic resistance. An article by Dr. Tseng and coworkers on the eDNA and biofilms discussed today. A lovely video of Dr. Tseng talking about the research she and her colleagues carry out in the laboratory. Dr. Tseng's biography from the American Society for Microbiology. Dr. Tseng's laboratory group website with wonderful links and images. Dr. Tseng's faculty website. Intro music is by Reber Clark Send your questions and comments to mattersmicrobial@gmail.com
Hi friends! We're taking a much-needed August pause—we'll have new episodes for you in September. In the meanwhile, enjoy this pick from our archives! _____ [originally aired February 8, 2024] Where do memories live in the brain? If you've ever taken a neuroscience class, you probably learned that they're stored in our synapses, in the connections between our neurons. The basic idea is that, whenever we have an experience, the neurons involved fire together in time, and the synaptic connections between them get stronger. In this way, our memories for those experiences become minutely etched into our brains. This is what might be called the synaptic view of memory—it's the story you'll find in textbooks, and it's often treated as settled fact. But some reject this account entirely. The real storehouses of memory, they argue, lie elsewhere. My guest today is Dr. Sam Gershman. Sam is Professor of Psychology at Harvard University, and the director of the Computational Cognitive Neuroscience Lab there. In a recent paper, he marshals a wide-ranging critique of the synaptic view. He makes a compelling case that synapses can't be the whole story—that we also have to look inside the neurons themselves. Here, Sam and I first discuss the synaptic view and the evidence that seems to support it. We then talk about some of the problems with this classic picture. We consider, for example, cases where memories survive the radical destruction of synapses; and, more provocatively, cases where memories are formed in single-celled organisms that lack synapses altogether. We talk about the dissenting view, long lurking in the margins, that intracellular molecules like RNA could be the real storage sites of memory. Finally, we talk about Sam's new account—a synthesis that posits a role for both synapses and molecules. Along the way we touch on planaria and paramecia; spike-timing dependent plasticity; the patient H.M.; metamorphosis, hibernation, and memory transfer; the pioneering work of Beatrice Gelber; unfairly maligned ideas; and much, much more. Before we get to it, one important announcement: Applications are now open for the 2024 Diverse Intelligences Summer Institute (or DISI)! The event will be held in beautiful, seaside St Andrews, Scotland, from June 30 to July 20. If you like this show—if you like the conversations we have and the questions we ask—it's a safe bet that you'd like DISI. You can find more info at disi.org—that's disi.org. Review of applications will begin on Mar 1, so don't delay. Alright friends, on to my conversation about the biological basis of memory with Dr. Sam Gershman. Enjoy! Notes and links 4:00 - A general audience article on planarian memory transfer experiments and the scientist who conducted them, James V. McConnell. 8:00 - For more on Dr. Gershman's research and general approach, see his recent book and the publications on his lab website. 9:30 - A brief video explaining long-term potentiation. An overview of “Hebbian Learning.” The phrase “neurons that fire together wire together” was, contrary to widespread misattribution, coined by Dr. Carla Shatz here. 12:30 - The webpage of Dr. Jeremy Gunawardena, Associate Professor of Systems Biology at Harvard University. A recent paper from Dr. Gunawardena's lab on the avoidance behaviors exhibited by the single-celled organism Stentor (which vindicates some disputed, century-old findings). 14:00 - A recent paper by C. R. Gallistel describing some of his views on the biological basis of memory. 19:00 - The term “engram” refers to the physical trace of a memory. See recent reviews about the so-called search for the engram here, here, and here. 20:00 - An article on the importance of H.M. in neuroscience. 28:00 - A review about the phenomenon of spike-timing dependent plasticity. 33:00 - An article, co-authored by former guest Dr. Michael Levin, on the evidence for memory persistence despite radical remodeling of brain structures. See our episode with Dr. Levin here. 35:00 - A study reporting the persistence of memories in decapitated planarians. A popular article about these findings. 36:30 - An article reviewing one chapter in the memory transfer history. Another article reviewing evidence for “vertical” memory transfer (between generations). 39:00 - For more recent demonstrations of memory transfer, see here and here. 40:00 - A paper by Dr. Gershman, Dr. Gunawardena, and colleagues reconsidering the evidence for learning in single cells and describing the contributions of Dr. Beatrice Gelber. A general audience article about Gelber following the publication of the paper by Dr. Gershman and colleagues. 45:00 – A recent article arguing for the need to understand computation in single-celled organisms to understand how computation evolved more generally. 46:30 – Another study of classical conditioning in paramecia, led by Dr. Todd Hennessey. 49:00 – For more on plant signaling, see our recent episode with Dr. Paco Calvo and Dr. Natalie Lawrence. 56:00 – A recent article on “serial reversal learning” and its neuroscientific basis. 1:07:00 – A 2010 paper demonstrating a role for methylation in memory. Recommendations The Behavior of the Lower Organisms, by Herbert Spencer Jennings Memory and the Computational Brain, by C. R. Gallistel and Adam Philip King Wetware, by Dennis Bray Many Minds is a project of the Diverse Intelligences Summer Institute, which is made possible by a generous grant from the John Templeton Foundation to Indiana University. The show is hosted and produced by Kensy Cooperrider, with help from Assistant Producer Urte Laukaityte and with creative support from DISI Directors Erica Cartmill and Jacob Foster. Our artwork is by Ben Oldroyd. Our transcripts are created by Sarah Dopierala. Subscribe to Many Minds on Apple, Stitcher, Spotify, Pocket Casts, Google Play, or wherever you listen to podcasts. You can also now subscribe to the Many Minds newsletter here! We welcome your comments, questions, and suggestions. Feel free to email us at: manymindspodcast@gmail.com. For updates about the show, visit our website or follow us on Twitter (@ManyMindsPod) or Bluesky (@manymindspod.bsky.social).
For a long time, scientists have wondered how life has emerged from inanimate chemistry, and whether Earth is the only place where it exists. Charles Darwin speculated about life on Earth beginning in a warm little pond. Some of his contemporaries believed that life existed on Mars. It once seemed inevitable that the truth would be known by now. It is not. For more than a century, the origins and extent of life have remained shrouded in mystery. But, as Mario Livio and Jack Szostak reveal in Is Earth Exceptional?: The Quest for Cosmic Life (Basic Books, 2024), the veil is finally lifting. The authors describe how life's building blocks--from RNA to amino acids and cells--could have emerged from the chaos of Earth's early existence. They then apply the knowledge gathered from cutting-edge research across the sciences to the search for life in the cosmos: both life as we know it and life as we don't. Why and where life exists are two of the biggest unsolved problems in science. Is Earth Exceptional? is the ultimate exploration of the question of whether life is a freak accident or a chemical imperative. Learn more about your ad choices. Visit megaphone.fm/adchoices Support our show by becoming a premium member! https://newbooksnetwork.supportingcast.fm/new-books-network
AI and genetic medicine are converging to transform how we diagnose, treat, and prevent disease. Gene Yeo, Ph.D., unites RNA biology with artificial intelligence to speed the path from genome sequencing to personalized RNA therapeutics. Advances in sequencing have reduced costs dramatically, making interpretation and translation into treatments the real challenge. Using deep learning and large datasets of RNA-binding proteins, Yeo predicts disease vulnerabilities and identifies therapeutic targets, including in neurodegeneration and muscular diseases. Alexis Komor, Ph.D., focuses on DNA, explaining human genetic variation—particularly single-nucleotide variants—and how genome editing technologies like CRISPR can target them. She highlights strategies to correct harmful mutations and explores precise, programmable interventions. Together, their research drives discovery and enables more effective, personalized therapies. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 40459]
AI and genetic medicine are converging to transform how we diagnose, treat, and prevent disease. Gene Yeo, Ph.D., unites RNA biology with artificial intelligence to speed the path from genome sequencing to personalized RNA therapeutics. Advances in sequencing have reduced costs dramatically, making interpretation and translation into treatments the real challenge. Using deep learning and large datasets of RNA-binding proteins, Yeo predicts disease vulnerabilities and identifies therapeutic targets, including in neurodegeneration and muscular diseases. Alexis Komor, Ph.D., focuses on DNA, explaining human genetic variation—particularly single-nucleotide variants—and how genome editing technologies like CRISPR can target them. She highlights strategies to correct harmful mutations and explores precise, programmable interventions. Together, their research drives discovery and enables more effective, personalized therapies. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 40459]
BUFFALO, NY – August 15, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on August 13, 2025, titled “Clinical and analytical validation of MI Cancer Seek®, a companion diagnostic whole exome and whole transcriptome sequencing-based comprehensive molecular profiling assay.” In this study, first authors Valeriy Domenyuk and Kasey Benson, along with corresponding author David Spetzler from Caris Life Sciences in Irving, Texas, introduce MI Cancer Seek, an FDA-approved test designed to deliver comprehensive tumor profiling. MI Cancer Seek demonstrated strong concordance with other FDA-approved companion diagnostics and serves as a powerful tool to guide treatment decisions in both adult and pediatric cancer patients. Cancer remains one of the most complex and diverse diseases to treat. With many targeted therapies currently FDA-approved, selecting the right one for a specific patient requires detailed genetic insights. MI Cancer Seek addresses this need by analyzing both DNA and RNA from a single tumor sample. The tool identifies key biomarkers linked to FDA-approved treatments for several major cancers, including breast, lung, colon, melanoma, and endometrial cancers. One of the most significant strengths of MI Cancer Seek is its ability to deliver accurate and reliable results from minimal tissue input (50 ng). Even when analyzing formalin-fixed paraffin-embedded samples, which are widely used but often degraded, the test maintained high levels of accuracy. It successfully detected important genetic alterations such as PIK3CA, EGFR, BRAF, and KRAS/NRAS mutations and measured tumor mutational burden (TMB) and microsatellite instability (MSI), both of which are key indicators for immunotherapy response. In clinical comparisons, the test achieved over 97% agreement with other FDA-approved diagnostic tools, confirming its reliability in detecting critical biomarkers. Notably, it showed near-perfect accuracy in identifying MSI status in colorectal and endometrial cancers. The researchers also demonstrated that the test maintains precision across different lab conditions and varying DNA input levels, confirming its robustness for routine clinical use. Beyond its role as a companion diagnostic, MI Cancer Seek incorporates additional features developed under its predecessor, MI Tumor Seek Hybrid. These include detection of homologous recombination deficiency, structural variants, and cancer-related viruses. It also includes advanced tools such as the Genomic Probability Score for identifying the tissue of origin in cancers of unknown primary, as well as a gene signature to guide first-line chemotherapy in colorectal cancer. “One limitation to be considered is the low PPA for ERBB2 CNA detection.” By offering deeper genetic insights from a single, small sample, MI Cancer Seek has the potential to streamline diagnostics, reduce testing costs, and connect patients to effective therapies more quickly. As precision medicine continues to expand, this assay stands out as a comprehensive and efficient solution for meeting the evolving needs of modern oncology. DOI - https://doi.org/10.18632/oncotarget.28761 Correspondence to - David Spetzler - dspetzler@carisls.com Video short - https://www.youtube.com/watch?v=D4hd2FxCYY8 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ 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
In the episode, we will explore a common problem with Autism- the Gastrointestinal Tract. The one consistent finding with Autism and GI is a problem exists. However, research on complicated in these complicated and complex areas of human biology despite what appears to be tight controls in the studies. However, one crucial component is missing- Light. In this episode, we will cover how biology structures order from the light input and the chaos from the environment.Major Areas include Enterochromaffin Cells, Serotonin, Aromatic Amino Acids, Vitamin D, Enteric Nervous System, the endocrine systems, and the Hypothalamic-Pitutary-Adrenal Axis.Cause of Autism: https://podcasts.apple.com/us/podcast/from-the-spectrum-finding-superpowers-with-autism/id1737499562?i=1000662271496Su study: https://www.nature.com/articles/s41564-024-01739-1Sunlight and Vitamin D: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3897598/Multi-Axis-Meta-Analysis https://www.nature.com/articles/s41598-022-21327-9Quantum Engineering 33, 54, and 55 https://www.patreon.com/DrJackKruse/postsDaylight Computer Companyuse "autism" for $25 off athttps://buy.daylightcomputer.com/RYAN03139Chroma Iight Devicesuse "autism" for 10% discount athttps://getchroma.co/?ref=autism(0:00) Autism and the GI Tract; inconsistent research; Order versus Chaos- Light and Environment and Health Conditions(3:10) The GI Tract; Gut-Brain Axis; Gut Microbiome and Various Nervous Systems(6:22) POMC; HPA; Stress example(8:19) Common Autism problems in the GI(9:23) Enterochromaffin Cells; Serotonin; Immune and Inflammation(14:09) Melanin/POMC; Clock-Timing; Omentum(16:31) Real-life Acute GI Fix; Bacteria makes Dopamine in the Gut(19:04) Vitamin D Receptors and more Clock-Timing(22:13) Obesity and Autism connection? (uncoupled systems); Biosynthesis of Vit D and specific Wavelength of Light with Shared Biological Processes- DNA, RNA, Aromatic Amino Acids(24:33) Avoiding UV Light implications(26:18) Scientific Literature; Archaea, Bacteria, Fungi, Virus; "confounding" data(30:03) Ubiquinol-7, COQ10, Thiamine Diphosphate; TCA cycles(32:38) Controls (plural) in Research and lack of Control (singular); LIGHT is GREATER than FOOD(38:27) Reviews/Ratings and Contact InfoX: https://x.com/rps47586YT: https://www.youtube.com/channel/UCGxEzLKXkjppo3nqmpXpzuAEmail: info.fromthespectrum@gmail.com
HHS Director Robert F. Kennedy, Jr declared on Friday, August 8, 2024 the CDC and HHS will suspend the use of mRNA vaccines for COVID-19 treatment, and restrict its use in future vaccines due to components that trun RNA into DNA, making the vaccines highly ineffective as well as potentially dangerous.In this short clip. Mr. Kennedy outlines his reasonings and what the Deaprtment and health researchers have discovered thus far since the implementation of mRNAwas introduced four years ago as a therapy for treating coronavirus.
Send us a textIn this episode of the Life Science Success Podcast my guest is John Schmitt, a military veteran, entrepreneur, and Co-Founder & CEO of iXpressGenes who is leveraging innovative RNA biomarker technologies to revolutionize trauma screening in healthcare. With over 20 years of leadership experience in the U.S. Army and a Master's degree in Microbiology and Immunology, John is dedicated to developing data-driven solutions for early detection and prevention of trauma-related diseases.00:00 Introduction and Podcast Overview01:02 Welcoming the Guest: John Schmitt02:00 John Schmitt's Journey to Biotechnology05:58 Military Experience and Leadership Insights13:09 Founding iXpressGenes: The Origin Story17:31 Mission and Objectives of iXpressGenes23:08 Challenges and Innovations in Biomarker Technologies27:42 Personal Leadership and Inspirations35:00 Conclusion and Podcast Wrap-Up
On todays show AI models, quantum computing, mental health, smartphones, cryptocurrency, Tesla, regenerative braking, oil reserves, wind energy, military applications, open source, electric vehicles, hologram technology, parenting, cybersecurity., Energy transition, nuclear power, fusion, hydrocarbons, solar energy, wind energy, material science, AI, tariffs, manufacturing, redistricting, RNA vaccines, youth violence, Trump, China. Have Fun
In this episode of the Epigenetics Podcast, we talked with Erica Korb from the University of Pennsylvania about her work on BRD4 and the histone variant H2BE, which influences synaptic genes and neuronal activity. Dr. Korb discusses the focus of her lab, which centers on epigenetic mechanisms impacting gene regulation in neurons. Her research primarily examines histone biology and its connection to neurodevelopmental disorders, including autism spectrum disorder and intellectual disabilities. Dr. Korb expounds on the collaborative environment at UPenn's Epigenetics Institute, emphasizing how the rich diversity of research topics fosters innovative ideas and projects within the community. Reflecting on her earlier work from her postdoctoral studies, Dr. Korb discusses her first significant findings regarding the protein BRD4. This work demonstrated BRD4's role in mediating transcriptional regulation crucial for learning and memory processes. She explains how disrupting this protein's function in neurons hindered critical gene activations required for memory formation in mice. This foundational understanding opened avenues for exploring the broader implications of chromatin regulation in various neurodevelopmental conditions. Transitioning into her current research endeavors, Dr. Korb reveals how she aims to expand her focus beyond Fragile X syndrome. With her lab now investigating multiple chromatin regulators implicated in various forms of autism spectrum disorders, she describes a recent project where RNA sequencing exposed substantial overlaps in gene expression changes associated with five distinct chromatin modifiers, each contributing uniquely to neuronal function while collectively demonstrating sensitivity to chromatin disruptions. A significant portion of the discussion centers around Dr. Korb's unexpected exploration into how COVID-19 intersects with chromatin biology through a phenomenon known as histone mimicry. Leveraging bioinformatic tools during the pandemic, her lab discovered that certain viral proteins mimic histone sequences, which may lead to altered transcriptional outputs in host cells. This coincidental finding illustrates both the creative adaptability needed in scientific research and the importance of collaborative efforts across disciplines to uncover new insights. The conversation also delves into Dr. Korb's recent work regarding the histone variant H2BE, initiated by one of her graduate students. She explains how prior research only recognized H2BE's expression in the olfactory system, yet her lab has demonstrated its significant role in regulating synaptic genes and memory formation throughout broader neuronal contexts. Notably, they identified a single amino acid change that influences H2BE's function in chromatin accessibility and gene transcription, emphasizing its potential evolutionary conservation across species. In terms of H2BE's role, Dr. Korb elucidates that its activity is integral in response to extracellular stimuli, particularly within the context of neuronal activation. Intriguingly, they found that H2BE expression decreases in reaction to long-term neuronal stimulation, suggesting a complex mechanism of homeostatic plasticity crucial for regulating neuronal activity levels. This research not only advances understanding of chromatin dynamics but also holds implications for neuronal health and disease mechanisms. References Feierman, E. R., Louzon, S., Prescott, N. A., Biaco, T., Gao, Q., Qiu, Q., Choi, K., Palozola, K. C., Voss, A. J., Mehta, S. D., Quaye, C. N., Lynch, K. T., Fuccillo, M. V., Wu, H., David, Y., & Korb, E. (2024). Histone variant H2BE enhances chromatin accessibility in neurons to promote synaptic gene expression and long-term memory. Molecular cell, 84(15), 2822–2837.e11. https://doi.org/10.1016/j.molcel.2024.06.025 Korb, E., Herre, M., Zucker-Scharff, I., Gresack, J., Allis, C. D., & Darnell, R. B. (2017). Excess Translation of Epigenetic Regulators Contributes to Fragile X Syndrome and Is Alleviated by Brd4 Inhibition. Cell, 170(6), 1209–1223.e20. https://doi.org/10.1016/j.cell.2017.07.033 Kee, J., Thudium, S., Renner, D. M., Glastad, K., Palozola, K., Zhang, Z., Li, Y., Lan, Y., Cesare, J., Poleshko, A., Kiseleva, A. A., Truitt, R., Cardenas-Diaz, F. L., Zhang, X., Xie, X., Kotton, D. N., Alysandratos, K. D., Epstein, J. A., Shi, P. Y., Yang, W., … Korb, E. (2022). SARS-CoV-2 disrupts host epigenetic regulation via histone mimicry. Nature, 610(7931), 381–388. https://doi.org/10.1038/s41586-022-05282-z Feierman, E. R., Paranjapye, A., Su, S., Qiu, Q., Wu, H., & Korb, E. (2024). Histone variant H2BE controls activity-dependent gene expression and homeostatic scaling. bioRxiv : the preprint server for biology, 2024.11.01.620920. https://doi.org/10.1101/2024.11.01.620920 Related Episodes Neuroepigenetic Mechanisms and Primate Epigenome Evolution (Boyan Bonev) DNA Methylation Alterations in Neurodegenerative Diseases (Paula Desplats) The Role of Histone Dopaminylation and Serotinylation in Neuronal Plasticity (Ian Maze) 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
What happens when you combine a decade of science, a powerful entrepreneurial story, and two exponential waves—AI and digital biology?You get Geneoscopy.On the latest episode of The Scope Forward Show, I caught up with Dr. Erica Barnell—Co-founder and Chief Science Officer of Geneoscopy. If you don't know Erica yet, you should. She and her team just raised $112 million in a tough VC environment. Their lead assay, ColoSense, is now the first FDA-approved, RNA-based, non-invasive diagnostic test for colorectal cancer and advanced adenomas.But this conversation went far beyond funding and FDA milestones.We talked about:How AI has replaced costly bioinformatics layers and transformed their R&DHow patients are being guided through diagnostics via smart automation (text, email, even Uber Health)What's next in IBD precision diagnostics and biomarker innovationWhy AI is not “artificial” at all—and how to use it without fearWhy GI, like OB/GYN, is primed for disruptionThis wasn't just a company update—it was a glimpse into the future of our entire field.We're in a convergence era. Biology is becoming programmable. Intelligence is being digitized. And GI—if we lean in—has a front-row seat to reinvent itself.
RFK Jr. Halts $500 Million In mRNA Vaccine Funding, Says Technology Prolonged COVID-19 By Encouraging New Mutations
The Making of KOLs: The New Chemist Podcast's Global Journey in Science, Pharma, and Education: Interview with Mohan Uttarwar, CEO & Co-Founder of 1Cell.Ai---In this episode , we sit down with Mohan Uttarwar, CEO & Co-Founder of 1Cell.Ai, to explore how AI-driven single-cell analytics are revolutionizing precision oncology. Discover how the OncoIncytes platform merges ctDNA, live CTCs, single-cell RNA and proteomics for a real-time, multimodal tumor profile—and learn how these insights are sharpening patient selection, accelerating ADC trials, and delivering earlier, more accurate measures of therapeutic response. Mohan also shares his playbook for building a capital-efficient biotech across Silicon Valley and India, the emerging trends set to reshape drug development, and practical advice for chemists, data scientists, and founders looking to break into the field. Tune in this August for a deep dive into the future of cancer research and drug discovery.--Please note: The views of this podcast represent those of my guest(s) and I.Music citation: Open source
Louise Laurent, M.D., Ph.D., presents new insights into placental biology using cutting-edge molecular and imaging technologies. As part of the NIH-funded Human Biomolecular Atlas Program, her research focuses on mapping the structure and function of the placenta across gestation. By combining bulk RNA sequencing, single-cell analysis, spatial transcriptomics, and imaging mass cytometry, Laurent and collaborators identify key differences in cell types and gene expression associated with pregnancy stages and labor. Her team highlights how specific cells like syncytiotrophoblasts and extravillous trophoblasts evolve over time and interact with maternal tissue. This integrated approach offers an unprecedented view of placental development and lays the groundwork for understanding reproductive health and disease. Series: "Motherhood Channel" [Health and Medicine] [Show ID: 40670]
Congressman Ralph Norman, who is now a candidate for governor of South Carolina, shares his motivations for transitioning from Congress to the gubernatorial race and discusses his vision for the state, including infrastructure improvements, term limits, and combating corruption. Congressman Norman also reflects on the successes of Florida under Governor Ron DeSantis and the need for South Carolina to adopt similar strategies. Dr. Peter McCullough, chief scientific officer at The Wellness Company, discusses the potential links between COVID-19 vaccines and the increase in rapid cancer cases. We explore the implications of messenger RNA technology, the influence of pharmaceutical advertising on medical reporting, and the emerging role of Ivermectin in cancer research. Aaron Withe, CEO of the Freedom Foundation, reveals the troubling trends stemming from the significant influence of teachers unions on American culture and politics. Kasim Khan takes a closer look at the dire situation of his father, former Pakistani Prime Minister Imran Khan, who has been imprisoned under disturbing conditions. Khan shares the harrowing details of his father's incarceration, the struggle for human rights, and the international efforts to secure his release. See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.
Good morning from Pharma and Biotech daily: the podcast that gives you only what's important to hear in Pharma e Biotech world.Vinay Prasad's departure from CBER has analysts anticipating a more traditional successor, while GSK streamlines its pipeline and pledges billions in US investments. Susan Monarez is now the confirmed CDC director, and the top biopharma venture capital raises of H1 2025 are summarized. Despite challenges like layoffs and market fluctuations, GSK remains committed to investing in the US despite tariffs. Other headlines include Madrigal's potential $2 billion investment, Biogen and Eisai's Alzheimer's drug update, and Novo Nordisk's new leadership. Trilink Biotechnologies is offering self-amplifying RNA constructs for potential therapeutic advancements.AI biotech companies have secured substantial funding in the first half of 2025, with continued investment pouring into startups within the industry. The top five biopharma venture capital raises of this period are highlighted. There is confusion surrounding Ira's definition of 'drug,' potentially hindering companies from pursuing approval for new formulations and indications. Vinay Prasad's departure from the FDA's Center for Biologics Evaluation and Research, following controversies related to Sarepta, has raised concerns among developers. Despite challenges, four biotech companies are successfully launching their products independently.Over 260 million people are impacted by rare diseases, emphasizing the need for faster evidence generation through global real-world data. GSK's commitment to investing in the US, Merck's cost-cutting measures to support its launch schedule, and Novo Nordisk's new leadership are also highlighted. The FDA has updated regulations regarding Sarepta's DMD gene therapy, making it available for ambulatory patients. Adaptimmune anticipates significant staff reductions following a cell therapy asset sale. Stay tuned for more updates on the latest developments in the biopharma industry.
The HPS Podcast - Conversations from History, Philosophy and Social Studies of Science
Today on The HPS Podcast, we're joined by Hans-Jörg Rheinberger, distinguished historian and philosopher of science and Director Emeritus at the Max Planck Institute for the History of Science in Berlin. Trained first in philosophy and then in molecular biology, Rheinberger is well-recognised for his work on the history and epistemology of experimentation. His influential work, including concepts like “experimental systems” and “epistemic things,” has helped shape how we understand the material, conceptual, and historical dimensions of scientific research. In this episode, Rheinberger:Describes his path from philosophy to molecular biologist, and how time at the lab bench informed his understanding scienceExplains what “experimental systems” are—carefully arranged environments where scientists interact with both the unknown and the tools that make inquiry possibleDefines “epistemic things,” the phenomena that underpin scientific curiosity, and “technical objects,” the stable tools and methods that emerge from research over timeIllustrates these ideas with vivid case examples, from solving the genetic code with synthetic RNA to the invention and evolution of the electron microscopeReflects on the impact of new technologies, automation, and digital visualisation, and what persists — and changes — about experimentation in the contemporary labRelevant LinksHans-Jörg Rheinberger profile – Max Planck Institute for the History of ScienceSplit and Splice: A Phenomenology of Experimentation ( University of Chicago Press), 2023Epistemology of the Concrete: On Historicizing Epistemology (Duke University Press), 2010Toward a History of Epistemic Things (Harvard University Press), 1997Transcript coming soonThanks for listening to The HPS Podcast. You can find more about us on our website, Bluesky, Instagram and Facebook feeds. This podcast would not be possible without the support of School of Historical and Philosophical Studies at the University of Melbourne and the Hansen Little Public Humanities Grant scheme. Music by ComaStudio. Website HPS Podcast | hpsunimelb.org
01:00:36 – Danish Study Reversal: Autism Link ConfirmedA Danish vaccine safety study is quietly corrected to reveal a correlation between aluminum and autism—but the researchers refuse media interviews, triggering accusations of deception. 01:13:42 – Gulf Jab Syndrome and COVID InjuriesThe show draws chilling comparisons between unexplained Gulf War illnesses and post-COVID vaccine injuries—calling both the results of reckless, untraceable experimentation. 01:19:36 – Religious Exemptions Under AttackPediatric elites urge the removal of all non-medical vaccine exemptions. The host argues that this represents a merging of medicine and state tyranny. 01:21:08 – The Blasphemy of “Redeemed” Fetal CellsReligious leaders are condemned for claiming vaccines developed with aborted fetal cells are morally acceptable. The host calls this a spiritual betrayal. 01:26:20 – RNA-Sprayed Food: Next Bioengineering ThreatA Moderna spin-off develops RNA pesticides that replicate in crops. The host warns this could embed genetic manipulation directly into the food supply. 02:27:34 – Cops Blame Social Media, Not AttackersThe Cincinnati police chief says social media made the mob beating "look worse than it was." The show mocks this excuse and blasts bystanders for doing nothing while a man was brutally attacked. 02:37:21 – Diversity Doesn't Stop TyrannyCincinnati's first female police chief faces lawsuits for discriminating against white men. The host mocks DEI hires as superficial fixes that don't change the abusive nature of policing. 02:44:26 – UK Internet Crackdown Triggers VPN SurgeBritish citizens scramble for VPNs as the government rolls out harsh age-verification laws. The segment warns that it's less about child safety and more about censorship and digital control. 02:50:10 – Online Safety Act Instantly Used for CensorshipJust hours after going live, the UK law is used to suppress anti-immigration protests. The host says this proves the law was never about safety—just silencing dissent. 02:54:51 – Eric Peters Returns“My first guest as I come back… is Eric Peters… somebody I really respect, who really gets it.” 03:03:02 – Destroy Trust in Institutions“I'm here to destroy trust in institutions. That's my life mission…”Peters declares that blind faith in government institutions must be dismantled—not restored. 03:20:08 – Masculinity, Compliance & Modern MenDiscussion on emasculation, symbolic submission, and how modern clothing and behavior reflect cultural decline. Jordan Peterson is referenced. 03:47:28 – Hidden Worldview in Media“Very subtle philosophy… if you just accept it without looking critically…”Hollywood and media messaging are described as covert tools of cultural transformation. Follow the show on Kick and watch live every weekday 9:00am EST – 12:00pm EST https://kick.com/davidknightshow Money should have intrinsic value AND transactional privacy: Go to https://davidknight.gold/ for great deals on physical gold/silverFor 10% off Gerald Celente's prescient Trends Journal, go to https://trendsjournal.com/ and enter the code KNIGHTFind out more about the show and where you can watch it at TheDavidKnightShow.com If you would like to support the show and our family please consider subscribing monthly here: SubscribeStar https://www.subscribestar.com/the-david-knight-showOr you can send a donation throughMail: David Knight POB 994 Kodak, TN 37764Zelle: @DavidKnightShow@protonmail.comCash App at: $davidknightshowBTC to: bc1qkuec29hkuye4xse9unh7nptvu3y9qmv24vanh7Become a supporter of this podcast: https://www.spreaker.com/podcast/the-david-knight-show--2653468/support.
01:00:36 – Danish Study Reversal: Autism Link ConfirmedA Danish vaccine safety study is quietly corrected to reveal a correlation between aluminum and autism—but the researchers refuse media interviews, triggering accusations of deception. 01:13:42 – Gulf Jab Syndrome and COVID InjuriesThe show draws chilling comparisons between unexplained Gulf War illnesses and post-COVID vaccine injuries—calling both the results of reckless, untraceable experimentation. 01:19:36 – Religious Exemptions Under AttackPediatric elites urge the removal of all non-medical vaccine exemptions. The host argues that this represents a merging of medicine and state tyranny. 01:21:08 – The Blasphemy of “Redeemed” Fetal CellsReligious leaders are condemned for claiming vaccines developed with aborted fetal cells are morally acceptable. The host calls this a spiritual betrayal. 01:26:20 – RNA-Sprayed Food: Next Bioengineering ThreatA Moderna spin-off develops RNA pesticides that replicate in crops. The host warns this could embed genetic manipulation directly into the food supply. 02:27:34 – Cops Blame Social Media, Not AttackersThe Cincinnati police chief says social media made the mob beating "look worse than it was." The show mocks this excuse and blasts bystanders for doing nothing while a man was brutally attacked. 02:37:21 – Diversity Doesn't Stop TyrannyCincinnati's first female police chief faces lawsuits for discriminating against white men. The host mocks DEI hires as superficial fixes that don't change the abusive nature of policing. 02:44:26 – UK Internet Crackdown Triggers VPN SurgeBritish citizens scramble for VPNs as the government rolls out harsh age-verification laws. The segment warns that it's less about child safety and more about censorship and digital control. 02:50:10 – Online Safety Act Instantly Used for CensorshipJust hours after going live, the UK law is used to suppress anti-immigration protests. The host says this proves the law was never about safety—just silencing dissent. 02:54:51 – Eric Peters Returns“My first guest as I come back… is Eric Peters… somebody I really respect, who really gets it.” 03:03:02 – Destroy Trust in Institutions“I'm here to destroy trust in institutions. That's my life mission…”Peters declares that blind faith in government institutions must be dismantled—not restored. 03:20:08 – Masculinity, Compliance & Modern MenDiscussion on emasculation, symbolic submission, and how modern clothing and behavior reflect cultural decline. Jordan Peterson is referenced. 03:47:28 – Hidden Worldview in Media“Very subtle philosophy… if you just accept it without looking critically…”Hollywood and media messaging are described as covert tools of cultural transformation. Follow the show on Kick and watch live every weekday 9:00am EST – 12:00pm EST https://kick.com/davidknightshow Money should have intrinsic value AND transactional privacy: Go to https://davidknight.gold/ for great deals on physical gold/silverFor 10% off Gerald Celente's prescient Trends Journal, go to https://trendsjournal.com/ and enter the code KNIGHTFind out more about the show and where you can watch it at TheDavidKnightShow.com If you would like to support the show and our family please consider subscribing monthly here: SubscribeStar https://www.subscribestar.com/the-david-knight-showOr you can send a donation throughMail: David Knight POB 994 Kodak, TN 37764Zelle: @DavidKnightShow@protonmail.comCash App at: $davidknightshowBTC to: bc1qkuec29hkuye4xse9unh7nptvu3y9qmv24vanh7Become a supporter of this podcast: https://www.spreaker.com/podcast/the-real-david-knight-show--5282736/support.
As many of our followers can attest that we're a huge fan of getting to the root of your health issues. With Million Marker's Detect & Detox Kit, you can receive tools necessary to help you reduce your toxic chemical exposures. This information is extremely important for improving your fertility as well as your health. Another new and cutting edge at home testing company or become a huge fan of is the ImYoo. ImYoo couples at home blood collection and single single cell RNA sequencing to be used in immunology studies. This initiative can be very, very beneficial for collecting life changing and life saving data. And today, we're really glad to be joined by my friend and also ImYoo CEO and founder, Tatiana Dobreva, to tell us a little more about this really innovative technology and what ImYoo is doing. Learn more about ImYoo's services: https://www.imyoo.health/Get tested for BPA, phthalates, parabens, and other hormone-disrupting chemicals with Million Marker's Detect & Detox Test Kit: https://www.millionmarker.com/
This week on Careers in Discovery, we're joined by Erica Barnell, Chief Medical Officer and Co-founder of Geneoscopy. Erica shares how Geneoscopy is transforming gastrointestinal health with a platform that uses RNA biomarkers from stool samples to diagnose, monitor, and help prevent colorectal cancer and other GI diseases. She talks about the inspiration behind the company, building a patient-friendly alternative to colonoscopy, and why early detection is key to changing outcomes in colorectal cancer. We also dive into Erica's journey from MD-PhD student to entrepreneur, the challenges of shifting from product development to commercialization, and how she navigates the balance of leadership, family, and growth in a dynamic start-up environment.
**Discussion begins at 5:30**Octopi are some of the most mysterious creatures on earth with their extraordinary intelligence, complex behaviors, and mind boggling abilities. What if these enigmatic beings are not just bizarre animals but some far more extraordinary? Alien life forms, perhaps? The theory that ectopic could be extraterrestrial in origin has gained traction amongst some scientists and researchers due to the strikingly unusual features of these animals - with their highly advanced cognitive abilities, ability to alter their physical appearance, and genetic make up that seems at odds with typical earth organisms. Could octopi be a product of another world, sent to earth by cosmic forces, or arriving here via ancient forgotten means? In this exploration we'll dive deep into these compelling reasons why octopi might not just be Earth's oddities but maybe candidates for alien life.Send us a textSupport the showTheme song by INDA
BUFFALO, NY - July 29, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on July 25, 2025, titled “Comprehensive genomic profiling of over 10,000 advanced solid tumors.” In this study, led by Jean-Paul De La O from Exact Sciences Corporation, researchers analyzed data from over 10,000 solid tumor samples from patients with advanced cancer and found that more than 90 percent contained genetic changes that could guide treatment. This work demonstrates the growing impact of large-scale tumor DNA and RNA testing on patient care. The researchers retrospectively analyzed OncoExTra assay information for 31 types of cancer, including breast, colorectal, prostate, lung, and ovarian cancers. Their analysis revealed that nearly a third of patients had alterations associated with approved drugs for their specific cancer, while another third had changes linked to therapies approved for other cancers. These results show that detailed genetic profiling could expand treatment choices. “Biomarkers associated with on- or off-label FDA-approved therapies were detected in 29.2% and 28.0% of samples, respectively.” Another relevant discovery was that many important mutations occurred at very low levels, which are often missed by simpler tests. By using a broad and highly sensitive approach, the scientists were able to identify these rare mutations. They also reported that 7.5 percent of samples carried gene fusions, unusual genetic events that can drive cancer growth. Such findings can be critical in selecting therapies that specifically target these abnormalities. The study also highlighted the value of RNA sequencing in detecting fusion events that traditional DNA tests might miss. Prostate cancer and certain sarcomas showed particularly high rates of these fusion alterations. This type of information can refine cancer diagnosis and improve therapy planning. In addition, the researchers identified changes in several major cancer-related pathways, including those that control cell growth, DNA repair, and immune system response. Alterations in these pathways can point to newer treatment options, such as immunotherapy or drugs designed to block specific cell signals. Overall, this study shows that comprehensive genomic profiling can guide more personalized cancer care by identifying mutations, gene fusions, and other molecular patterns. Advanced testing methods like the OncoExTra assay reveal treatment opportunities even in advanced cancers, ensuring that subtle but important genetic changes are detected. DOI - https://doi.org/10.18632/oncotarget.28757 Correspondence to - Jean-Paul De La O - jdelao@exactsciences.com Video short - https://www.youtube.com/watch?v=awiRhDfiMTE Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28757 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, solid tumors, comprehensive genomic profiling, matched therapy, gene fusions, limit of detection To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
Dr. George Sledge, Executive VP and Chief Medical Officer of Caris Life Sciences, is using advanced molecular testing, including DNA, RNA, and protein analysis, to identify specific mutations and characteristics of a patient's tumor, allowing for more personalized and targeted treatment. The company is developing liquid biopsies to detect cancer early, identify minimal residual disease, and assess the potential for future cancer development. Caris has a database of over half a million patients whose tumors have undergone next-generation sequencing, allowing them to draw increasingly accurate conclusions. The future of precision oncology is expected to involve broader and earlier use of next-generation sequencing as the cost of the test continues to decrease significantly. George explains, "Caris Life Sciences is a molecular diagnostics company. Patients and their physicians send us tumor samples that can be obtained either from the primary tissue or from a distant recurrent site. When they come to us, we do several things. We look at DNA, what's called whole exome. We look at RNA, what's called whole transcriptome. We also frequently look at the protein level at immunohistochemistry, looking at slides that have been stained to look for particular molecular lesions that may be important from a treatment standpoint. Based on all of these, we're able to provide patients with information about which drugs represent the most appropriate treatment for their disease. This, of course, allows you to go to a drug that hopefully will be less toxic and more effective for your particular disease." "When we look at the very specific mutations that manifest themselves at the level of either DNA or RNA, this requires fairly high technology, what's called next-generation sequencing, which allows us to pick up all these individual mutations that make up a particular patient's cancer. And every patient's cancer is different. Every patient's cancer involves different combinations of mutations that result in different responses to different treatments." #CarisLifeSciences #CancerResearch #PrecisionMedicine #RealWorldData #AccestoCare #HealthEquity #NextGenerationSequencing #NGS #LiquidBiopsy #ClinicoGenomic #Biomarkers #PanCancer carislifesciences.com Listen to the podcast here
Dr. George Sledge, Executive VP and Chief Medical Officer of Caris Life Sciences, is using advanced molecular testing, including DNA, RNA, and protein analysis, to identify specific mutations and characteristics of a patient's tumor, allowing for more personalized and targeted treatment. The company is developing liquid biopsies to detect cancer early, identify minimal residual disease, and assess the potential for future cancer development. Caris has a database of over half a million patients whose tumors have undergone next-generation sequencing, allowing them to draw increasingly accurate conclusions. The future of precision oncology is expected to involve broader and earlier use of next-generation sequencing as the cost of the test continues to decrease significantly. George explains, "Caris Life Sciences is a molecular diagnostics company. Patients and their physicians send us tumor samples that can be obtained either from the primary tissue or from a distant recurrent site. When they come to us, we do several things. We look at DNA, what's called whole exome. We look at RNA, what's called whole transcriptome. We also frequently look at the protein level at immunohistochemistry, looking at slides that have been stained to look for particular molecular lesions that may be important from a treatment standpoint. Based on all of these, we're able to provide patients with information about which drugs represent the most appropriate treatment for their disease. This, of course, allows you to go to a drug that hopefully will be less toxic and more effective for your particular disease." "When we look at the very specific mutations that manifest themselves at the level of either DNA or RNA, this requires fairly high technology, what's called next-generation sequencing, which allows us to pick up all these individual mutations that make up a particular patient's cancer. And every patient's cancer is different. Every patient's cancer involves different combinations of mutations that result in different responses to different treatments." #CarisLifeSciences #CancerResearch #PrecisionMedicine #RealWorldData #AccestoCare #HealthEquity #NextGenerationSequencing #NGS #LiquidBiopsy #ClinicoGenomic #Biomarkers #PanCancer carislifesciences.com Download the transcript here
In this JCO Article Insights episode, Michael Hughes summarizes “International Myeloma Society and International Myeloma Working Group Consensus Recommendations on the Definition of High-Risk Multiple Myeloma" by Avet-Loiseau et al. published on June 09, 2025 along with an interview with author Dr Nikhil C. Munshi, MD. TRANSCRIPT Michael Hughes: Welcome to this episode of JCO Article Insights. This is Michael Hughes, JCO's editorial fellow. Today I am interviewing Dr. Nikhil Munshi on the “International Myeloma Society and International Myeloma Working Group Consensus Recommendations on the Definition of High-Risk Multiple Myeloma” by Avet-Loiseau et al. At the time of this recording, our guest has disclosures that will be linked in the transcript. While some patients with multiple myeloma live for decades after treatment, others exhibit refractory or rapidly relapsing disease irrespective of treatment administered. We term this “high-risk myeloma.” Multiple risk stratification systems have been created, starting with the Durie-Salmon system in 1975 and evolving with the advent of novel therapeutics and novel treatment approaches. In 2015, the Revised International Staging System (R-ISS) was introduced, which incorporated novel clinical and cytogenetic markers and remained, until recently, a mainstay of risk stratification in newly diagnosed disease. Myeloma as a field has, just in the past few years, though, undergone explosive changes. In particular, we have seen groundbreaking advances not only in treatments - the introduction of anti-CD38 agents and the advent of cellular and bispecific therapies - but also in diagnostic technology and our understanding of the genetic lesions in myeloma. This has led to the proliferation of numerous trials employing different definitions of high-risk myeloma, a burgeoning problem for patients and providers alike, and has prompted attempts to consolidate definitions and terminology. Regarding cytogenetic lesions, at least, Kaiser et al's federated meta-analysis of 24 therapeutic trials, published here in the JCO in February of 2025 and recently podcasted in an interview with associate editor Dr. Suzanne Lentzsch, posited a new cytogenetic classification system to realize a shared platform upon which we might contextualize those trial results. This article we have here by Dr. Avet-Loiseau, Dr. Munshi, and colleagues, published online in early June of this year and hot off the presses, is the definitive joint statement from the International Myeloma Society (IMS) and the International Myeloma Working Group (IMWG). What is high-risk multiple myeloma for the modern era? The IMS and IMWG Genomics Workshop was held in July 2023 and was attended by international myeloma experts, collaborating to reach consensus based on large volumes of data presented and shared. The datasets included cohorts from the Intergroupe Francophone du Myélome (IFM); the HARMONY project, comprised of multiple European academic trials; the FORTE study, findings from which solidified KRd as a viable induction regimen; the Grupo Español de Mieloma Múltiple (GEM) and the PETHEMA Foundation; the German-Speaking Myeloma Multicenter Group (GMMG); the UK-based Myeloma XI, findings from which confirmed the concept of lenalidomide maintenance; Emory 1000, a large, real-world dataset from Emory University in Atlanta; the Multiple Myeloma Research Foundation Clinical Outcomes in Multiple Myeloma to Personal Assessment of Genetic Profile (CoMMpass) dataset; and some newly diagnosed myeloma cohorts from the Mayo Clinic. Data were not pooled for analyses and were assessed individually - that is to say, with clear a priori understanding of whence the data had been gathered and for what original purposes. Consensus on topics was developed based on the preponderance of data across studies and cohorts. In terms of results, substantial revisions were made to the genomic staging of high-risk multiple myeloma, and these can be sorted into three major categories: A) alterations to the tumor suppressor gene TP53; B) translocations involving chromosome 14: t(14;16) (c-MAF overexpression), t(14;20) (MAFB overexpression), and t(4;14) (NSD2 overexpression); and C) chromosome 1 abnormalities: deletions of 1p or additional copies of 1q. In terms of category A, TP53 alterations: Deletion of 17p is present in up to 10% of patients at diagnosis and is enriched in relapsed or refractory disease. This is well-documented as a high-risk feature, but the proportion of the myeloma cells with deletion 17p actually impacts prognosis. GEM and HARMONY data analyses confirmed the use of 20% clonal cell fraction as the optimal threshold value for high-risk disease. That is to say, there must be the deletion of 17p in at least 20% of the myeloma cells on a FISH-analysis of a CD138-enriched bone marrow sample to qualify as high-risk disease. TP53 mutations can also occur. Inactivating mutations appear to have deleterious effects similar to chromosomal losses, and the biallelic loss of TP53, however it occurs, portends particularly poor prognosis. This effect is seen across Myeloma XI, CoMMpass, and IFM cohorts. Biallelic loss is rare, it appears to occur in only about 5% of patients, but next-generation sequencing is nevertheless recommended in all myeloma patients. Category B, chromosome 14 translocations: Translocation t(14;16) occurs in about 2% to 3% of patients with newly diagnosed disease. In the available data, primarily real-world IFM data, t(14;16) almost always occurs with chromosome 1 abnormalities. Translocation t(4;14) occurs in about 10% to 12% of newly diagnosed disease, but only patients with specific NSD2 alterations are, in fact, at risk of worse prognosis, which clinically appears to be about one in every three of those patients. And so together, the CoMMpass and Myeloma XI data suggest that translocation t(4;14) only in combination with deletion 1p or gain or amplification of 1q correlates with worse prognosis. Translocation t(14;20) occurs in only 2% of newly diagnosed disease. Similar to translocation t(4;14), it doesn't appear to have an effect on prognosis, except if the translocation co-occurs with chromosome 1 lesions, in which case patients do fare worse. Overall, these three translocations - t(14;16), t(4;14), and t(14;20) - should be considered high-risk only if chromosome 1 aberrations are also present. In terms of those chromosome 1 aberrations, category C, first deletions of 1p: Occurring in about 13% to 15% of newly diagnosed disease, deletion 1p eliminates critical cell checkpoints and normal apoptotic signaling. In the IFM and CoMMpass dataset analyses, biallelic deletion of 1p and monoallelic deletion of 1p co-occurring with additional copies of 1q denote high-risk. In terms of the other aberration in chromosome 1 possible in myeloma, gain or amplification of 1q: This occurs in up to 35% to 37% of newly diagnosed disease. It upregulates CKS1B, which is a cyclin-dependent kinase, and ANP32E, a histone acetyltransferase inhibitor. GEM and IFM data suggest that gain or amplification of 1q - there was no clear survival detriment to amplification - is best considered as a high-risk feature only in combination with the other risk factors as above. Now, in terms of any other criteria for high-risk disease, there remains one other item, and that has to do with tumor burden. There has been a consensus shift, really, in both the IMS and IMWG to attempt to develop a definition of high-risk disease which is based on biologic features rather than empirically observed and potentially temporally dynamic features, such as lactate dehydrogenase. Beta-2 microglobulin remains an independent high-risk indicator, but care must be taken when measuring it, as renal dysfunction can artificially inflate peripheral titers. The consensus conclusion was that a beta-2 microglobulin of at least 5.5 without renal failure should be considered high-risk but should not preclude detailed genomic profiling. So, in conclusion, the novel 2025 IMS-IMWG risk stratification system for myeloma is binary. It's either high-risk disease or standard-risk disease. It's got four criteria. Number one, deletion 17p and/or a TP53 mutation. Clonal cell fraction cut-off, remember, is 20%. Or number two, an IGH translocation - t(4;14), t(14;16), t(14;20) - with 1q gain and/or deletion of 1p. Or a monoallelic deletion of 1p with 1q additional copies or a biallelic deletion of 1p. Or a beta-2 microglobulin of at least 5.5 only when the creatinine is normal. This is a field-defining work that draws on analyses from across the world to put forward a dominant definition of high-risk disease and introduces a new era of biologically informed risk assessment in myeloma. Now, how does this change our clinical approach? FISH must be performed on CD138-enriched samples and should be performed for all patients. Next-generation sequencing should also be performed on all patients. Trials will hopefully now begin to include this novel definition of high-risk multiple myeloma. It does remain to be seen how data from novel therapeutic trials, if stratified according to this novel definition, will be interpreted. Will we find that therapies being evaluated at present have differential effects on myelomas with different genetic lesions? Other unanswered questions also exist. How do we go about integrating this into academic and then community clinical practice? How do we devise public health interventions for low-resource settings? To discuss this piece further, we welcome the esteemed Dr. Nikhil Munshi to the podcast. Dr. Munshi is a world-renowned leader in multiple myeloma and the corresponding author on this paper. As Professor of Medicine at Harvard Medical School, Director of the Multiple Myeloma Effector Cell Therapy Unit, and Director of Basic and Correlative Science at the Jerome Lipper Multiple Myeloma Center of the Dana-Farber Cancer Institute, he has presided over critical discoveries in the field. Thank you for joining us, Dr. Munshi. Dr. Nikhil Munshi: Oh, it's my pleasure being here, Michael, to discuss this interesting and important publication. Michael Hughes: I had a few questions for you. So number one, this is a comprehensive, shall we say, monumental and wide-ranging definition for high-risk myeloma. How do you hope this will influence or impact the ways we discuss myeloma with patients in the exam room? And how do we make some of these components recommended, in particular next-generation sequencing, feasible in lower-resource settings? Dr. Nikhil Munshi: So those are two very important questions. Let's start with the first: How do we utilize this in our day-to-day patient care setting? So, as you know well, we have always tried to identify those patients who do not do so well with the current existing treatment. And for the last 30 years, what constitutes a myeloma of higher risk has continued to change with improvement in our treatment. The current definition basically centers around a quarter of the patients whose PFS is less than 2 to 3 years. And those would require some more involved therapeutic management. So that was a starting point of defining patients and the features. As we developed this consensus amongst ourselves - and it's titled as “International Myeloma Society, International Myeloma Working Group Consensus Recommendation” - this IMS-IMWG type of recommendation we have done for many years, improvising in various areas of myeloma care. Now, here, we looked at the data that was existing all across the globe, utilizing newer treatment and trying to identify that with these four-drug regimens, with transplant and some of the immunotherapy, which group of patients do not do as well. And this is where this current algorithm comes up. So before I answer your question straight, “How do we use it?” I might like to just suggest, “What are those features that we have identified?” There are four features which constitute high-risk disease in the newer definition. Those with deletion 17p with 20% clonality and/or TP53 mutation. Number two, patients with one of the translocations - t(4;14), t(14;16), or t(14;20) - co-occurring with 1q amplification or deletion 1p32. And that's a change. Previously, just the translocation was considered high-risk. Now we need a co-occurrence for it to be called high-risk. The third group is patients having biallelic deletion 1p32 or monoallelic deletion 1p32 along with 1q amplification. And finally, patients with high beta-2 microglobulin, more than or equal to 5.5 mg/dL, with normal creatinine less than 1.2 mg/dL. And the question, “How do we use this?” There are multiple areas where we incorporate high-risk features in our treatment algorithm. One of the first areas is where we would consider the induction regimen. If a patient has a high-risk disease, we would definitely consider a four-drug regimen rather than a three-drug regimen, although we are beginning to incorporate four-drug for all groups. That's one important thing. Number two, those are the patients where we do consider consolidation with transplant or maybe in the new world, considering some of the immunotherapeutic consolidation more early or more aggressively. Number three, these are the patients who get a little bit more maintenance therapy. So normally, lenalidomide might end up being our standard maintenance regimen. In patients who have high-risk disease, we incorporate either addition of daratumumab or the anti-CD38 targeting antibody and/or addition of proteasome inhibitor, either bortezomib or carfilzomib. So you would have multi-drug maintenance therapy in these patients. And in high-risk patients, we follow them with maintenance longer periods of time. One very critically important point to keep in mind is that to get the better outcome in high-risk disease, we must try to get them into MRD negativity because there is clear data that patients who do achieve MRD negativity, despite having high-risk disease, have a much superior outcome. They become near to standard-risk disease. And so, in high-risk patients, I would try to do whatever various options I have to try and get them into MRD-negative status. And when these patients relapse, we do not wait for the classic progression criteria to be met before we intervene. We would propose and suggest that we intervene earlier before the disease really blasts off. And so there are a number of areas in our setting where this high-risk definition will help us intervene appropriately and also with appropriate aggressiveness to achieve better outcome, to make this similar to standard-risk disease. Michael Hughes: Thank you, Dr. Munshi. And thoughts on how to really integrate this not only into academic centers but also lower-resource settings? Dr. Nikhil Munshi: So that's a very important question, Michael. And when we were developing this consensus, we were very cognizant of that fact. So wherever available, I think we are recommending that over a period of next 2, 3, 5 years, we should begin to switch over to sequencing-based methods because two components of this definition, one is TP53 mutation, which we cannot do without sequencing, and also reliably detecting deletion 1p requires sequencing-based method. So in the low-resource countries - and there are many in this world, and also even in our own country, patients may not be able to afford it - the older method with FISH or similar such technology, which is more affordable, is also acceptable for current time. They may miss a very small number of patients, maybe 2% to 3%, where these finer changes are not picked up, but a majority of this would be captured by them. So the current practice might still be applicable with some limitation in those patient populations, and that's what we would recommend. What is happening, fortunately, is that actually sequencing-based method is becoming cheaper. And in many centers, it is cheaper to do the sequencing rather than to do the FISH analysis. And so my hope is that even in low-resource centers, sequencing might be more economical in the end. It's, I think, the access to technology, which is a little bit limited currently, but it's hopefully becoming available soon. Michael Hughes: Thank you, Dr. Munshi. And staying for a minute and looking at the multiple myeloma subsets which might be missed by this really still very broad-ranging high-risk definition, at least by prior risk stratification systems, right, there is this group of patients who have standard-risk cytogenetics by R-ISS or R2-ISS, but they have primary refractory disease or they relapse early. We call these, as you are well aware, functionally high-risk disease. What proportion of previously FHR, functionally high-risk, myeloma patients do you expect to be captured by this novel definition? Dr. Nikhil Munshi: So I think the newer definition - and we can look at it both ways, but the newer definition should capture most of the functionally high-risk definition. To put it differently, Michael, there are patients who we know are, as you mentioned, functionally high-risk. Those are the patients who might have plasma cell leukemia, those who might have extramedullary disease, those who might not respond to our four-drug induction. If you don't respond to the four-drug induction, almost by definition, they are high-risk. However, a majority of them have one of the abnormalities that we are describing here. There would be a very small proportion which may not have. And if they do not have, we know one of the important components of this definition here is also that the genome, we know, keeps on evolving. So there may be a very small clone with the high-risk feature which was not obvious in the beginning. Following treatments or following relapse, that clone predominates, and now the patient's disease becomes high-risk. So the definition would incorporate or would capture these functional high-risk patients, but as you said, in countries where resources are not available, using this functional high-risk would also be helpful and advantageous. Sometimes LDH ends up being a high-risk. In our studies, LDH has not come out to be high-risk anymore because the features we are describing captures most of those patients, but those alternatives, older, can still be considered if other newer techniques are not available. Michael Hughes: Got you. And in terms of these older definitions, yes, that incorporate tumor burden, these empirical observations about how myeloma presents, do you foresee any additional tumor burden indicators being added to future definitions of high-risk disease? Or do you instead see this particular definition as a major waypoint on the journey towards a fully biologically grounded definition of high-risk disease? Dr. Nikhil Munshi: I think your second part is what is going to happen. I think the tumor burden-related definition is being now replaced by the biological or genomic-based definition. And I think at some point, it will be quite fully replaced. One component not here, and it is because one thing, we don't have enough data; number two, we don't know how it will pan out, is also the influence of the microenvironment on the risk definition. For example, the immune system, the immune function, etc. But not enough data exists to suggest how it would change the current definition. So in future, would a definition be totally genomic or it could be more integrative? And my personal guess is that it would be more integrative and that some immune features might come into the picture, especially now that we are using immune-based therapy as a very important component of treatment - CAR T-cells, bispecific, and antibody-based treatments. What role the immune system plays in either supporting tumor or what role suppression of the anti-tumor immunity plays? They all will be important how patient outcomes end up being, and which in turn could translate into how patient's risk stratification might happen. So I think the older tumor burden-related definitions probably will become things of the past. What we have currently proposed and consensus developed is the new path forward, and over time, some microenvironmental influences, if defined and found to be important, may get some more incorporation if it compares favorably with the genomic features. Michael Hughes: Thank you, Dr. Munshi for that enlightening response. To conclude the podcast, I'd like to look to the future and to the immediate future, what are the next steps for high-risk disease definition between now and discussing an integrated genomic-microenvironment-based definition? Will we see attempts to refine? Will we see a multi-level system, things like this? Dr. Nikhil Munshi: Yeah, so I think the current definition will be here to stay for the next 10 years or so. I think this has been developed using a large amount of data, so we do believe that this will remain fine. It has been validated now within the last six months by a few of the other studies. So there won't be a quick change. But we will try to, all of us will try to innovate. And as you very rightly bring up, the areas of research would include looking at the expression or transcriptomic component. Does that matter? And we do believe a small number of patients will have transcriptomic changes, not looked at the DNA changes, and may play a role. There are newer components, so long non-coding RNA, for example, is going to be an important component to look at, how it impacts the disease outcome, etc. There are also some of the proteomic-related changes which may become important in our studies. And then as we discussed, microenvironment and immunological changes. So these are the future areas of ongoing research where we all should collect data, and then in the next 5 to 10 years, we'll have another group meeting to see has anything changed or any of the features have become more important. Most of the time, some of the older features are lost because they are not as critically high-risk, and the newer features come in. And so the historical background for just one second, there was a time when chromosome 13 was considered a high-risk disease. We now don't even mention it because it's not high-risk. The newer treatments have improved the outcome. t(4;14) used to be a high-risk disease. Now by itself today, in this definition by itself is not; it needs to be with something else. And so I think this is a great sign of progress. As we improve the treatment and outcomes, some of the features will become less important, new features will come up, and we'll need to keep on evolving with time and with technology and make it better for patients. Michael Hughes: Thank you so much, Dr. Munshi, for your wisdom, for your sagacity, for your historical perspective as well. Thank you for listening to JCO Article Insights. Please come back for more interviews and article summaries. And be sure to leave us a rating and review so others can find our show. For more podcasts and episodes from ASCO, please visit 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.
BUFFALO, NY — July 28, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 6, on June 13, 2025, titled “Development of a novel transcriptomic measure of aging: Transcriptomic Mortality-risk Age (TraMA).” In this study, led by Eric T. Klopack from the University of Southern California, researchers created a new RNA-based aging measure that predicts health risks and mortality. This measure, called Transcriptomic Mortality-risk Age (TraMA), uses gene expression data to estimate a person's biological aging. This finding offers a new and potentially more accurate way to track aging and understand health risks, especially for older adults. Aging is a complex biological process that affects multiple systems in the body and increases the risk of disease and death. Scientists have long looked for reliable ways to measure biological aging. While DNA methylation and blood biomarkers are commonly used, this study focused on RNA—a molecule that reflects gene activity. By analyzing RNA sequencing data from nearly 4,000 U.S. adults aged 50 and older, the team developed TraMA to predict the probability of dying within four years. TraMA proved to be a strong and independent predictor of early death, multiple chronic diseases, poor cognitive function, and difficulties with daily activities. It was also tested in another large group of long-lived families and in several smaller datasets from patients with conditions like diabetes, sepsis, and cancer. The results confirmed the tool's usefulness across different populations and health conditions. “TraMA was also externally validated in the Long Life Family Study and several publicly available datasets.” Unlike earlier RNA-based aging measures, which were often built using small or non-representative samples, TraMA was developed using modern RNA sequencing technology results and a nationally representative dataset. This increases its reliability and potential for broad public health applications. The tool also demonstrated unique advantages over popular biological aging measures like GrimAge and PhenoAge, capturing distinct aspects of aging and health decline. Importantly, TraMA tracks biological processes related to inflammation, immune function, and kidney and brain health, systems that play key roles in aging. It was also sensitive to behavioral and socioeconomic factors. For instance, smoking, obesity, and low physical activity were associated with older TraMA scores. TraMA was also sensitive to changes in biological aging. In one study, researchers measured TraMA at two different time points and found that the more recent scores were better at predicting who would die. This suggests that TraMA can track changes in a person's aging as their health evolves. It also performed well in both large-scale surveys and small clinical samples, making it a useful tool in many types of research. By offering a new, accurate, and flexible method for measuring biological aging, TraMA may help researchers better understand how genes, lifestyle, and environment influence aging. This tool opens the door to more precise research on improving health and extending lifespan. DOI - https://doi.org/10.18632/aging.206272 Corresponding author - Eric T. Klopack - klopack@usc.edu Video short - https://www.youtube.com/watch?v=Tl0CApUz8cU Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts To learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Program notes:0:40 Human Phenotype project1:43 Metabolomics2:42 25 year follow up3:43 Two control groups4:00 CBT via telehealth or online5:00 2000 people with chronic pain6:00 Completion rate for videos lower6:50 RNA analysis in cancer molecular diagnostics7:50 4.8% failure rate8:50 CNS or blood cancers primarily9:25 Middle age exposure to air pollution and later cognition10:25 Poorer processing speed earlier in life11:58 End
HELP SUPPORT US AS WE DOCUMENT HISTORY HERE: https://gogetfunding.com/help-keep-wam-alive/# GET NON-MRNA FREEZE DRIED MEAT HERE: https://wambeef.com/ Use code WAMBEEF to save 20%! GET HEIRLOOM SEEDS & NON GMO SURVIVAL FOOD HERE: https://heavensharvest.com/ USE Code WAM to save 5% plus free shipping! Get local, healthy, pasture raised meat delivered to your door here: https://wildpastures.com/promos/save-20-for-life/bonus15?oid=6&affid=321 USE THE LINK & get 20% off for life and $15 off your first box! Josh Sigurdson reports on the plot by the architects of Moderna's mRNA vaccines to spray RNA on crops which would biologically change the plants and potentially make them more poisonous for human consumption. This plot comes from Flagship Pioneering, Moderna's parent company which plans to use AI-generated RNA libraries mirroring the same mRNA platforms used in Moderna's covid injections to target plants that we eat. This mimics EcoHealth Alliance's plans to aerosoliE biological agents over human populations and interestingly as we've reported before, Yale had come up with nasal spray mRNA "vaccines" years ago which we've theorized has already been used on the population. Then there's the PREP Act which grants the US government the authority to spray experimental drugs or inject people under the guise of "emergency." The University of California wrote many years ago about the goal to create mRNA lettuce among other fruits and vegetables. As has the University of Mexico City. Recent updated articles from April this year in Nature Magazine talk about covertly giving people mRNA or modRNA through lettuce. Then there's the already established idea of injecting animals with mRNA, modRNA or saRNA which there has already been found traces of in meat at grocery stores. Now, with massive shortages of meat as well as the Bird Flu fearmongering, we could see serious consequences. They want to force this on us one way or another. Without us knowing or via emergency orders and technocratic ration based systems. We are facing true evil. Stay tuned for more from WAM! DITCH YOUR DOCTOR! https://www.livelongerformula.com/wam Get a natural health practitioner and work with Christian Yordanov! Mention WAM and get a FREE masterclass! You will ALSO get a FREE metabolic function assessment! GET YOUR APRICOT SEEDS at the life-saving Richardson Nutritional Center HERE: https://rncstore.com/r?id=bg8qc1 Use code JOSH to save money! BUY GOLD HERE: https://firstnationalbullion.com/schedule-consult/ Avoid CBDCs! SIGN UP FOR HOMESTEADING COURSES NOW: https://freedomfarmers.com/link/17150/ Get Prepared & Start The Move Towards Real Independence With Curtis Stone's Courses! GET YOUR WAV WATCH HERE: https://buy.wavwatch.com/WAM Use Code WAM to save $100 and purchase amazing healing frequency technology! GET ORGANIC CHAGA MUSHROOMS HERE: https://alaskachaga.com/wam Use code WAM to save money! See shop for a wide range of products! GET AMAZING MEAT STICKS HERE: https://4db671-1e.myshopify.com/discount/WAM?rfsn=8425577.918561&utm_source=refersion&utm_medium=affiliate&utm_campaign=8425577.918561 USE CODE WAM TO SAVE MONEY! GET YOUR FREEDOM KELLY KETTLE KIT HERE: https://patriotprepared.com/shop/freedom-kettle/ Use Code WAM and enjoy many solutions for the outdoors in the face of the impending reset! PayPal: ancientwonderstelevision@gmail.com FIND OUR CoinTree page here: https://cointr.ee/joshsigurdson PURCHASE MERECHANDISE HERE: https://world-alternative-media.creator-spring.com/ JOIN US on SubscribeStar here: https://www.subscribestar.com/world-alternative-media For subscriber only content! Pledge here! Just a dollar a month can help us alive! https://www.patreon.com/user?u=2652072&ty=h&u=2652072 BITCOIN ADDRESS: 18d1WEnYYhBRgZVbeyLr6UfiJhrQygcgNU World Alternative Media 2025
In this episode of the Epigenetics Podcast, we talked with Dr. Joseph Ecker from the Salk Institute about his work on high-resolution genome-wide mapping technologies, specifically how the regulation of gene expression is influenced by DNA methylation, chromatin accessibility, and non-coding RNAs across various cell types and developmental stages. During our conversation, we delve into Dr. Ecker's contributions to the characterization of the genome of Arabidopsis thaliana, a project pivotal in the plant genomics field, where he collaborated on the early sequencing efforts that dramatically outpaced expectations. He highlights the technological advancements that enabled such efficient sequencing and how this foundational work opened new avenues for exploring transcriptional activity. We also discuss Dr. Ecker's pivotal work on the comprehensive DNA methylation map of Arabidopsis, which he developed in collaboration with other researchers. This groundbreaking study established the links between methylation patterns and gene expression, paving the way for further research into how these epigenetic marks influence over gene regulation. He elaborates on the significance of transitioning from traditional methods to more sophisticated techniques, such as RNA-seq, and the lessons learned from sequencing projects that have since been applied to human biology. Dr. Ecker's transition to studying human cells is further explored as he discusses the profiling of DNA methylation in induced pluripotent stem cells (iPSCs), revealing how epigenetic memory can influence cellular differentiation and development. He underscores the importance of understanding these methylation patterns, particularly as they relate to conditions like Alzheimer's disease and stem cell biology, where he examines potential applications of his findings in medical research. As our conversation progresses, we touch upon Dr. Ecker's ongoing projects that utilize advanced multi-omic techniques to investigate the epigenomes of the human brain, focusing on how DNA methylation and gene expression change with age and in the context of neurodegenerative diseases. He details the collaboration efforts with various consortia aimed at cataloging gene regulatory networks and understanding the complex interactions that take place within the brain throughout different life stages. References Mozo T, Dewar K, Dunn P, Ecker JR, Fischer S, Kloska S, Lehrach H, Marra M, Martienssen R, Meier-Ewert S, Altmann T. A complete BAC-based physical map of the Arabidopsis thaliana genome. Nat Genet. 1999 Jul;22(3):271-5. doi: 10.1038/10334. PMID: 10391215. Zhang X, Yazaki J, Sundaresan A, Cokus S, Chan SW, Chen H, Henderson IR, Shinn P, Pellegrini M, Jacobsen SE, Ecker JR. Genome-wide high-resolution mapping and functional analysis of DNA methylation in arabidopsis. Cell. 2006 Sep 22;126(6):1189-201. doi: 10.1016/j.cell.2006.08.003. Epub 2006 Aug 31. PMID: 16949657. Lister R, O'Malley RC, Tonti-Filippini J, Gregory BD, Berry CC, Millar AH, Ecker JR. Highly integrated single-base resolution maps of the epigenome in Arabidopsis. Cell. 2008 May 2;133(3):523-36. doi: 10.1016/j.cell.2008.03.029. PMID: 18423832; PMCID: PMC2723732. Lister R, Pelizzola M, Dowen RH, Hawkins RD, Hon G, Tonti-Filippini J, Nery JR, Lee L, Ye Z, Ngo QM, Edsall L, Antosiewicz-Bourget J, Stewart R, Ruotti V, Millar AH, Thomson JA, Ren B, Ecker JR. Human DNA methylomes at base resolution show widespread epigenomic differences. Nature. 2009 Nov 19;462(7271):315-22. doi: 10.1038/nature08514. Epub 2009 Oct 14. PMID: 19829295; PMCID: PMC2857523. Lister R, Pelizzola M, Kida YS, Hawkins RD, Nery JR, Hon G, Antosiewicz-Bourget J, O'Malley R, Castanon R, Klugman S, Downes M, Yu R, Stewart R, Ren B, Thomson JA, Evans RM, Ecker JR. Hotspots of aberrant epigenomic reprogramming in human induced pluripotent stem cells. Nature. 2011 Mar 3;471(7336):68-73. doi: 10.1038/nature09798. Epub 2011 Feb 2. Erratum in: Nature. 2014 Oct 2;514(7520):126. PMID: 21289626; PMCID: PMC3100360. Related Episodes Epigenetic Reprogramming During Mammalian Development (Wolf Reik) Single Cell Epigenomics in Neuronal Development (Tim Petros) 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
Sheng Zhong, Ph.D. pioneers technologies that advance women's reproductive health. Zhong develops a minimally invasive method to analyze extracellular RNA secreted by embryos during IVF. By sequencing tiny samples of spent culture media, they generate comprehensive RNA profiles and use machine learning to identify biomarkers that predict embryo quality with accuracy comparable to traditional imaging. This breakthrough offers a gentler, data-driven alternative for assessing embryo viability, with the potential to improve live birth rates and support families navigating infertility. Zhong's research highlights the power of molecular innovation to transform fertility care and address critical challenges in women's health. Series: "Motherhood Channel" [Health and Medicine] [Show ID: 40676]
Sheng Zhong, Ph.D. pioneers technologies that advance women's reproductive health. Zhong develops a minimally invasive method to analyze extracellular RNA secreted by embryos during IVF. By sequencing tiny samples of spent culture media, they generate comprehensive RNA profiles and use machine learning to identify biomarkers that predict embryo quality with accuracy comparable to traditional imaging. This breakthrough offers a gentler, data-driven alternative for assessing embryo viability, with the potential to improve live birth rates and support families navigating infertility. Zhong's research highlights the power of molecular innovation to transform fertility care and address critical challenges in women's health. Series: "Motherhood Channel" [Health and Medicine] [Show ID: 40676]
Sheng Zhong, Ph.D. pioneers technologies that advance women's reproductive health. Zhong develops a minimally invasive method to analyze extracellular RNA secreted by embryos during IVF. By sequencing tiny samples of spent culture media, they generate comprehensive RNA profiles and use machine learning to identify biomarkers that predict embryo quality with accuracy comparable to traditional imaging. This breakthrough offers a gentler, data-driven alternative for assessing embryo viability, with the potential to improve live birth rates and support families navigating infertility. Zhong's research highlights the power of molecular innovation to transform fertility care and address critical challenges in women's health. Series: "Motherhood Channel" [Health and Medicine] [Show ID: 40676]
Foundation models are machine learning models trained on large datasets and applicable for a wide range of use cases. Chief Editor Barbara Cheifet speaks with Drs. Brian Hie and Marie Lopez about how these models are being used for analysis of the function and structure of DNA, RNA, and proteins, and how they are being developed for clinical use. Hosted on Acast. See acast.com/privacy for more information.
In this special live recording from our Lexington AI Meetup, we sit down with Steve Crossan, a founding member of Google DeepMind's AlphaFold team and former Google product leader. Steve helped launch groundbreaking AI research as part of the team that built AlphaFold, the model that cracked one of biology's grand challenges.AlphaFold can predict a protein's 3D structure using only its amino acid sequence - a task that once took scientists months or years now completed in minutes. With the release of AlphaFold 3, the model now maps not just proteins, but how they interact with DNA, RNA, drugs, and antibodies - a huge leap for drug discovery and synthetic biology.Steve breaks down the origin story of AlphaFold, the future of AI-powered science, and what's next for healthcare, drug development, and beyond. A special thank you to Brent Seales and Randall Stevens for helping us coordinate Steve's talk during his visit in Lexington!If you'd like to stay up to date about upcoming Middle Tech events, subscribe to our newsletter at middletech.beehiiv.com.
In this week's podcast, Andreas Munk Holm is joined by Jean Schmitt at Jolt Capital and Rob Blackie at Crampton Blackie to explore one of the most consequential deep tech opportunities Europe faces: RNA. With roots in foundational biology and applications from cancer therapy to precision agriculture, RNA is both a symbol and a stress test of Europe's capacity to scale science into sovereignty.The conversation is based on their Landmark 2025 Report on the State of RNA in Europe, a data-rich, in-depth analysis of patents, funding flows, regulatory bottlenecks, and startup activity across the continent.Here's what's covered:03:05 The State of RNA in Europe05:59 Challenges in Commercialization and Investment09:09 The Landscape of RNA Companies in Europe15:02 Regulatory Challenges in RNA Development17:58 The Future of RNA in Europe26:54 Navigating Regulatory Challenges in Biocontrol Products30:46 The Impact of European Policies on Innovation32:41 Learning from Global Regulatory Practices40:34 The Exodus of Talent and Innovation from Europe45:59 Funding Challenges for RNA Companies in Europe
BUFFALO, NY - July 18, 2025 – A new #editorial was #published in Volume 16 of Oncotarget on July 16, 2025, titled “microRNAs in soft tissue sarcoma: State of the art and barriers to translation.” In this article, Elizaveta K. Titerina, Alessandro La Ferlita, and Joal D. Beane from Ohio State University discuss the role of microRNAs in soft tissue sarcomas (STS), a rare and diverse group of cancers that begin in connective tissues, like bone or fat. The authors explain how these small molecules regulate cancer-related processes and highlight their potential as non-invasive biomarkers for diagnosis and monitoring. They also outline the main challenges that need to be addressed before microRNA-based strategies can be used in clinical settings. Soft tissue sarcomas include over 50 subtypes, making precise diagnosis and effective treatment difficult. The editorial describes how microRNAs influence cancer growth, spread, and response to therapies. Because microRNAs are stable in body fluids like blood and saliva, they could be used for early detection and to help guide treatment decisions. Such as, certain groups of microRNAs are linked to how patients respond to specific drugs, showing their potential as tools for precision medicine. “For example, miR-17-92 and miR-106b-25 clusters have been associated with sensitivity or resistance to eribulin in STS.” The authors also explain that microRNAs could help distinguish between tumor types that are often difficult to differentiate, such as benign lipomas and malignant liposarcomas. Recognizing these differences is crucial for guiding treatment decisions. Specific patterns of microRNA expression in blood samples may enable clinicians to make quicker and more reliable diagnoses without the need for invasive procedures. Beyond their diagnostic role, microRNAs are also being explored as therapeutic tools, but applying microRNA-based therapies to patients remains challenging. These molecules can act as either cancer promoters or suppressors, depending on the environment, which complicates the development of safe and targeted treatments. However, new delivery methods such as lipid nanoparticles show promise in improving precision and safety. Overall, microRNAs are emerging as an important focus in STS research, offering new possibilities for advancing diagnosis, prognosis, and treatment. As researchers continue to address the current challenges, these small molecules could become valuable tools in improving cancer care. DOI - https://doi.org/10.18632/oncotarget.28754 Correspondence to - Joal D. Beane, joal.beane@osumc.edu Video short - https://www.youtube.com/watch?v=MlLGA8BObPQ Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28754 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, soft tissue sarcoma, liposarcoma, microRNA, small non-coding RNA, cancer biomarkers To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
Dr. Joshua Reuss joints that podcast to discuss the latest changes to the living guideline on stage IV NSCLC with driver alterations. He discusses the new evidence for NSCLC with EGFR mutations and NRG1 fusions and how this impacts the latest recommendations from the panel. He shares ongoing research that the panel will review in the future for further updates to this living guideline, and puts the updated recommendations into context for clinicians treating patients with stage IV NSCLC. Read the full living guideline update “Therapy for Stage IV Non-Small Cell Lung Cancer With Driver Alterations: ASCO Living Guideline, Version 2025.1” at www.asco.org/thoracic-cancer-guidelines TRANSCRIPT This guideline, clinical tools, and resources are available at www.asco.org/thoracic-cancer-guidelines. Read the full text of the guideline and review authors' disclosures of potential conflicts of interest in the Journal of Clinical Oncology, https://ascopubs.org/doi/10.1200/JCO-25-01061 Brittany Harvey: Hello and welcome to the ASCO Guidelines Podcast, one of ASCO's podcasts delivering timely information to keep you up to date on the latest changes, challenges, and advances in oncology. You can find all the shows, including this one, at asco.org/podcasts. My name is Brittany Harvey, and today I'm interviewing Dr. Joshua Reuss from Georgetown University, co-chair on "Therapy for Stage IV Non–Small Cell Lung Cancer With Driver Alterations: ASCO Living Guideline, Version 2025.1." It's great to have you here today, Dr. Reuss. Dr. Joshua Reuss: Thank you. Happy to be here. Brittany Harvey: And then before we discuss this guideline, I'd like to note that ASCO takes great care in the development of its guidelines and ensuring that the ASCO conflict of interest policy is followed for each guideline. The disclosures of potential conflicts of interest for the guideline panel, including Dr. Reuss, who has joined us here today, are available online with the publication of the guideline in the Journal of Clinical Oncology, which is linked in the show notes. So to dive into what we're here today to talk about, Dr. Reuss, this living clinical practice guideline for systemic therapy for patients with stage IV non–small cell lung cancer with driver alterations is updated on an ongoing basis. So what prompted this latest update to the recommendations? Dr. Joshua Reuss: Yes, thank you. It's very important that we have living guidelines that are continuously updated. We obviously don't live in a static environment where things are non-changing, and we really need to apply the most up-to-date and current evidence to treat our patients with the most effective strategies, the most groundbreaking strategies. And so to have guidelines that can be disseminated, particularly these ASCO guidelines, to treating providers is incredibly important. So, with any of these updates, we review ongoing studies, published work, for the quality of evidence to see if it's something that warrants making adjustments to our guidelines or at least incorporating the information so that providers can review it and incorporate this into their own personal decision-making. So in this particular update, we reviewed evidence particularly pertaining to EGFR-mutated non–small cell lung cancer and non–small cell lung cancer harboring an NRG1 fusion. Brittany Harvey: Yes, certainly there's a lot of new evidence in the advanced non–small cell lung cancer field, and so we appreciate the panel's continuous review of this evidence. So then you just mentioned two separate areas where the panel reviewed new evidence. So starting with that first one, what updated evidence did the panel review on first-line treatment options for patients with EGFR alterations, and how did this impact the recommendations? Dr. Joshua Reuss: Yes, so advanced EGFR-mutated non–small cell lung cancer, at least with classical activating alterations - that is our exon 19 deletions and our exon 21 L858R mutations - is something that's really evolved rapidly in the last few years. You know, for many years, we basically, for the frontline treatment setting, were saying, "Okay, we have a targeted therapy, osimertinib. We're going to give that, and we're going to see what effect we can get out of that," with, you know, a median time of duration of treatment response averaging around 18 months, knowing that there are some that that's a lot longer and some that are a lot shorter. But recently, we've seen a lot of data emerging on combination strategies. The guideline has already been updated to incorporate two of these combinations: osimertinib with chemotherapy based off of the FLAURA2 trial, and then the combination of amivantamab with lazertinib based off of the MARIPOSA trial. And that was data on progression-free survival that was published and led to those particular recommendations. Now, more recently, we've seen data come out in smaller, randomized studies for other combinations. And more recently, we reviewed the RAMOSE study. So this was a phase II, open-label, randomized trial for patients with tyrosine kinase inhibitor–naive and really, treatment-naive advanced EGFR-mutated non–small cell lung cancer harboring one of these two classical EGFR alterations, randomized to either osimertinib alone or osimertinib with the combination of ramucirumab, which is an anti-VEGF agent. There's been a lot of data, preclinical and clinical, for the role of VEGF blockade, particularly in EGFR-mutated non–small cell lung cancer, so exploring the combination of this for synergy in the frontline setting really made a lot of sense. So again, this was a phase II trial that randomized patients prospectively to one of these two regimens. The population here is really what we typically see with EGFR-mutated non–small cell lung cancer, predominantly a younger population - median age on this study was 65 - predominantly female - 71% female - and predominantly nonsmokers. Now, what this study showed was that at a median follow-up of 16.6 months, the progression-free survival favored the combination arm with a median progression-free survival of 24.8 months with the combination of osimertinib plus ramucirumab versus 15.6 months for osimertinib alone, for a hazard ratio of benefit of 0.55. The landmark one- and two-year endpoints for progression-free survival also favored the combination arm, and response rates were relatively comparable between groups, with overall adverse events being more frequent in the combination group, specifically high blood pressure, proteinuria, and epistaxis, which are our common adverse events related to VEGF-blocking agents. So, it's good to see data in this space. Now, of note, though, this was a phase II study, so not a phase III level of evidence. In addition, when looking at the population, this was a randomized, multicenter study, but it was a US-only population. There was also some imbalance in the number of visits between arms, so the combination arm was seen more frequently than the arm that got osimertinib alone. Now, the imaging assessments were no different, but obviously this could lead to potential confounding, at least in timing of awareness of potential side effects and and things being brought to the attention of investigators. So very promising data here, but because, you know, of this being a phase II study, this actually led to no changes in the guideline at this time. Brittany Harvey: Understood. Yes, as you mentioned prior, it's important to understand the full body of evidence and to review the trials even when it doesn't impact the recommendations. Dr. Joshua Reuss: And I will say that, you know, there is an ongoing phase III study looking at a very similar combination. It's the phase III ECOG-ACRIN trial of the combination of osimertinib plus bevacizumab versus osimertinib alone in this specific population. So, you know, I think we will see phase III–level data for a combination of VEGF with osimertinib, but again, promising phase II data that did not lead to a change in the recommendation at this time. Brittany Harvey: Absolutely. We'll look forward to that ongoing trial to learn more about combination in this patient population. So then moving to that second patient population that you mentioned earlier where the panel reviewed evidence, what is the updated evidence and recommendation for patients with NRG1 fusions? Dr. Joshua Reuss: Yeah, so this was an exciting update that we made more recently with this unique iteration of the living guidelines. So, NRG1 fusions, this is perhaps a newer kid on the block in terms of driver alterations that has been known to be identified in non–small cell lung cancer among other solid tumors. It is very rare, occurring in less than 1% of solid tumors, but something that we know is a unique oncogenic pathway that can lead to oncogenesis and cancer development, including in non–small cell lung cancer. So up until now, unfortunately, there have not been targeted therapies that target this unique alteration. It's somewhat different than other driver alterations where there's a top-level signaling change in a protein. This is more of a ligand alteration that then alters, that then enables activation of more classical pathways, but again, through upregulation of a unique ligand. So a slightly different pathway but something that we know should be able to be targeted to promote patient survival for those with NRG1 fusions. So the therapy here is a therapy called zenocutuzumab. It's an IgG1 bispecific antibody against HER2 and HER3. So it prevents the downstream dimerization and signaling that occurs as a result of this NRG1 fusion and upregulation of the NRG1 signal. This was, as you can imagine with a rare alteration, a large phase II registrational study that examined this in advanced solid tumors containing the NRG1 fusion. This is the NRG1 registrational trial. And this study enrolled patients with advanced solid tumors who had progressed on prior therapy. Patients were treated with zenocutuzumab 750 milligrams IV every two weeks. Among 158 response-evaluable solid tumor patients, the response rate was 30%, median duration of response of 11.1 months, and a median progression-free survival of 6.8 months. Now, in those with non–small cell lung cancer, that made up 93 response-evaluable patients, very similar outcomes there: a response rate of 29%, median duration of response of 12.7 months, and a median progression-free survival of 6.8 months. This therapy did appear to be well tolerated. The most common higher-grade emergent side effects - grade 3 or higher - were anemia occurring in 5% and elevated liver numbers occurring in 3%. So this is a subsequent-line study, so this led to the updated recommendation that clinicians may offer zenocutuzumab in the subsequent-line setting for patients with advanced non–small cell lung cancer who harbor NRG1 fusions. So I think this does speak toward the incredible importance of next-generation sequencing and molecular testing for patients, particularly to include testing that looks at the RNA. These large fusions can sometimes be very challenging to detect on DNA sequencing platforms alone, so it's important to, if you have a high level of suspicion for an alteration like this, perhaps some of the mucinous adenocarcinomas where it's been challenging to find a driver alteration, and it's someone who is a never-smoker, really would want to include molecular testing that assesses the RNA level and not just the DNA. Brittany Harvey: Absolutely. It's important to have all the biomarkers available so that clinicians are able to use that to inform their decision-making. So then, given these changes in the guideline, what should clinicians know as they implement this latest living guideline update? And how do these changes impact patients? Dr. Joshua Reuss: Yeah, I think talking in reverse order of what we just discussed here, there is a new guideline update for NRG1 fusions. So I think making sure that that's being evaluated, that clinicians are testing for that and really looking for that result that should be incorporated in in most next-generation large sequencing assays to get that result, but it's very important that that is not overlooked now that we do have a therapy that's available in the subsequent-line setting, though it is important to note that patients with NRG1 fusions, at least the limited data that there is suggests that the efficacy to standard chemoimmunotherapy regimens is overall poor. So physicians unfortunately might be facing this question for second-line therapy in patients with NRG1 fusions sooner rather than later. For the former, for EGFR-altered non–small cell lung cancer and how do we incorporate VEGF-containing regimens into these patients? Our guideline top-level update did not change based off of review of this new study, but it's important for clinicians to know what other combinations may exist. You know, there are phase III studies looking at this combination in the frontline setting. And of course, there is data on other bispecific molecules that incorporate VEGF in the subsequent-line setting, particularly a combination that includes the VEGF/PD-1 bispecific antibody ivonescimab that's being studied in the HARMONi-A trial for patients with EGFR-mutated advanced non–small cell lung cancer, for which we hope to get some more definitive data in the coming months. Brittany Harvey: Definitely. And then you've just mentioned a few ongoing trials where we're looking for evidence to inform future updates. But thinking beyond that, into the future, what is the panel examining for future updates to this living guideline? Dr. Joshua Reuss: It's a very exciting time to be in the world of treating advanced non–small cell lung cancer, particularly patients with driver alterations, because there is so much evolving data that's changing our practice in real time, again highlighting the importance of these living guideline updates. I'd say there's many things that we're excited to see. You know, a lot of the combination regimens in EGFR-mutated non–small cell lung cancer for which there are approvals and current recommendations in our guideline, particularly osimertinib plus chemotherapy and amivantamab plus lazertinib - those are the two approved combination strategies in the front line - we are now seeing the emergence of overall survival data for those combinations. So obviously that is something that's going to be very important for the committee to review and incorporate into guideline updates. There are several new therapies coming down the road for other driver populations. We recently saw an approval for taletrectinib for ROS1 fusion–positive non–small cell lung cancer, so it's going to be important that the committee reviews the data and the publications regarding that therapy. And then there are other novel therapies that we're looking to see updated data on. There are multiple antibody-drug conjugates, which take the potent power of a chemotherapy molecule and attempt to make that targeted with an antibody targeting to a unique feature on the cancer cell. And there are several antibody-drug conjugates that are in development at various levels of promise in this space, particularly in EGFR-mutated non–small cell lung cancer, and I anticipate seeing some emerging data for that coming up in the near future as well. So really, lots to be excited in the space and lots for our committee to review to give guidance on so that these patients can really receive the top-level care wherever they are being treated in the country and throughout the world. Brittany Harvey: Yes, we'll await this new data to continue to provide optimal options for patients with stage IV non–small cell lung cancer with driver alterations. So, Dr. Reuss, I want to thank you so much for your work to rapidly and continuously update and review the evidence for this guideline and thank you for your time today. Dr. Joshua Reuss: Thank you so much. Brittany Harvey: And finally, thank you to all of our listeners for tuning in to the ASCO Guidelines Podcast. To read the full guideline, go to www.asco.org/thoracic-cancer-guidelines. You can also find many of our guidelines and interactive resources in the free ASCO Guidelines app, which is available on the Apple App Store or the Google Play Store. If you have enjoyed what you've heard today, please rate and review the podcast and be sure to subscribe so you never miss an episode. 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 Meredith Landry, Managing Editor of Citeline's Custom Content, in conversation with Tom Hickey, Director of Therapeutic Strategy at Novotech, a global full-service clinical CRO dedicated to accelerating the development of advanced and novel therapeutics. In this episode, recorded at the annual BIO conference in Boston, Tom offers a sharp and timely look at the state of RNA therapeutics and shares how innovation in delivery technologies, regulatory strategy, and partnership models is shaping the next generation of RNA-based medicines. With Novotech's deep experience in the space, Tom provides actionable insights for biotech leaders looking to position their RNA programs for long-term success.
David Barton, Brian Kemp, and Olve Peersen join TWiV to discuss RNA recombination among enteroviruses and its role in foiling poliovirus eradication. Hosts: Vincent Racaniello, Alan Dove, and Rich Condit Guests: David Barton, Brian Kemp, and Olve Peersen Subscribe (free): Apple Podcasts, RSS, email Become a patron of TWiV! Links for this episode Support science education at MicrobeTV Enterovirus C recombination groups (J Virol) Poliovirus polymerase L420 facilitates RNA recombination (J Virol) Picornavirus RNA recombination counteracts error catastrophe (J Virol) Extended primer grip and picornavirus RNA recombination (J Virol) Timestamps by Jolene Ramsey. Thanks! Intro music is by Ronald Jenkees Send your virology questions and comments to twiv@microbe.tv Content in this podcast should not be construed as medical advice.
In this episode of the Epigenetics Podcast, we talked with Sarah Teichmann from the University of Cambridge about the Human Cell Atlas. In the Interview we explore Sarah Teichmann's impressive career trajectory, covering her current role as Chair of Stem Cell Medicine at the Cambridge Stem Cell Institute and Vice President of Translational Research at GlaxoSmithKline. Professor Teichmann explains her unique dual appointments, a rare arrangement that allows her to bridge academia and industry effectively. As the conversation shifts focus to computational biology, she takes us on a historical journey from her PhD work at the MRC Laboratory of Molecular Biology to the present advancements driven by next-generation sequencing and artificial intelligence methods. Professor Teichmann emphasizes that the landscape of biological research has evolved significantly, particularly in the realm of data-driven methodologies. The conversation then transitions seamlessly into her pivotal role in advancing single-cell genomics, where she discusses the motivation behind using single-cell RNA sequencing methods in her research on T cells. This technique offered unmatched insights compared to bulk sequencing techniques, allowing for a more detailed understanding of cell states and their complex interactions within tissues. A highlight of the episode is Professor Teichmann's insights on the Human Cell Atlas project, which she co-founded in 2017. She elaborates on the ambitious vision to map all human cells, likening the endeavor to the Human Genome Project. Through the atlas, researchers aim to create a detailed reference map that facilitates a deeper understanding of human health and disease. Professor Teichmann shares the collaborative efforts that led to its inception and the importance of international cooperation in scientific research. The discussion culminates with an exploration of the biggest scientific findings thus far from the Human Cell Atlas. Among the revelations, she notes the astounding complexity and diversity of cell types identified, particularly within the immune system, and the unexpected locations of certain cell types during human development. She also highlights significant discoveries related to COVID-19, demonstrating the immediate real-world impact of their work. References https://www.humancellatlas.org The Human Cell Atlas: towards a first draft atlas Kock, K. H., Tan, L. M., Han, K. Y., Ando, Y., Jevapatarakul, D., Chatterjee, A., Lin, Q. X. X., Buyamin, E. V., Sonthalia, R., Rajagopalan, D., Tomofuji, Y., Sankaran, S., Park, M. S., Abe, M., Chantaraamporn, J., Furukawa, S., Ghosh, S., Inoue, G., Kojima, M., Kouno, T., … Prabhakar, S. (2025). Asian diversity in human immune cells. Cell, 188(8), 2288–2306.e24. https://doi.org/10.1016/j.cell.2025.02.017 Related Episodes The Discovery of Genomic Imprinting (Azim Surani) 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
Liberated Life Series | Episode 753 Join Josh Trent, host of the Wellness + Wisdom Podcast, live at the Biohacking Conference in Austin (TX), as he reveals why you aren't broken but bioenergetically burdened, and how playful, spiritual practices can become your path to freedom, dissolving transgenerational stress responses. We ALL have problems. Stop hiding. Start living life liberated. Learn how to set yourself free from self-sabotage, limiting beliefs, thoughts, and behaviors so you will have lifelong confidence and clarity of purpose through a thriving community and practical tools, guiding you to play a new reality game. Join Josh and others in the Liberated Life Tribe to: Discover lifelong confidence, clarity, and a true sense of purpose with practical tools and a supportive community. Learn to rewrite your reality + master a new “reality game.” Unlock your highest potential in your physical, mental, emotional, spiritual + financial SELF beyond your wildest dreams through accessing the power of surrender to trust life + create new results. Join the Tribe Today (It's FREE) Listen To Episode 753 As Josh Trent Uncovers: [00:00] Core Philosophy + Framework of Emotional Epigenetics Why trauma and lineage can be healed through a playful, spiritual approach rather than traditional serious therapy methods. How people are 'bioenergetically burdened' rather than broken, and no one needs to be fixed. Why patterns are written into our biology, but can be rewritten with love. How both fear and luck are passed epigenetically through generations. The role of RNA histone modification and methylation in generational trauma transmission and healing. How stress responses are passed down for up to five generations in mice when exposed to trauma. Why emotions only last 90 seconds. [08:55] Personal Journey + Transformation Josh's personal story of childhood trauma with father's demons and mother's manic bipolar disorder leading to bioenergetic burdens. The progression through addictive behaviors, including food, pornography, and body image issues, despite achieving six-pack abs. How the pivotal moment occurred when credit card debt reached $80k, his mother was institutionalized, leading to spiritual surrender and the podcast launch. [11:35] Healing Methodology How to practice the circular breathing technique, connecting with the ancestral presence and body awareness. Why the capacitor represents mental, emotional, spiritual, financial, and physical harmony. How David Hawkins' emotional scale demonstrates the growth path from survival emotions to courage and pride. [14:25] Practical Application of Emotional Epigenetics How the neural system prioritizes safety over time and reality. Why triggers activate regardless of the current context. How the L.I.F.E. Method activation program, with 88 different practices, offers a comprehensive healing approach. Why playfulness serves as spiritual warfare against heavy programming and media negativity. The greatest freedom is achieved when biology no longer argues with reality, eliminating the need for masks or excessive effort. Why the current generation is blessed with resources that previous generations lacked. Leave Wellness + Wisdom a Review on Apple Podcasts
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