Podcasts about RNA

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.

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.  

Send us a textDr. Ashwin Gopinath, Ph.D. ( https://ashwingopinath.com/ ) is Co-Founder and CTO of Biostate AI ( https://biostate.ai/ ), a startup building generative AI that predicts the evolution of human disease and drug response based on RNA sequencing data. Its patented wet lab technologies, including BIRT (Barcode-Integrated Reverse Transcription), allow affordable and scalable collection of massive amounts of transcriptomic and genomic data. With sites in Houston, TX, Palo Alto, CA, Bangalore, India, and Shanghai, China, Biostate AI is an international company with collaborations with top hospitals, academic researchers, and biotech/biopharma companies. Dr. Gopinath was an Assistant Professor at MIT, working at the intersection of CMOS nanofabrication, molecular self-assembly, biology, and machine learning.Dr. Gopinath earned his Ph.D. in Electrical Engineering from Boston University, and subsequently worked as a research scientist at Caltech and Google [X].Dr. Gopinath has co-authored over 21 papers in journals including Nature, Science, and the Proceedings of the National Academy of Sciences (PNAS).Dr. Gopinath was awarded the 2017 Robert Dirk Prize in Molecular programming for his contributions to merging DND nanotechnology with conventional semiconductor processing.#AshwinGopinath #BiostateAI #GenerativeAI #RNASequencing #OpticalPhysics #DNANanotechnology #DNAOrigami #MolecularDiagnostics #RNAseq #GenAI #Leukemia #MultipleSclerosis #Reactome #TranscriptomicAgePrediction #ProgressPotentialAndPossibilities #IraPastor #Podcast #Podcaster #ViralPodcast #STEM #Innovation #Technology #Science #ResearchSupport the show

**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

The Flyover Film Festival features a wide of array of flickering images but none is more compelling than the story of Phil Sharp. He was born in a home with a dirt floor to parents who had no high school education. Sharp goes on to earn a Nobel Prize for his work on RNA splicing.CRACKING THE CODE: Phil Sharp and the Biotech RevolutionProducer/director Bill Haney spoke with Terry Meiners about shooting this film and the challenges facing a creator in the editing process. Sharp's story is incredible, and Haney has 900 hours of film that must be whittled down to 90 minutes.This film will be screened Sunday, July 27 at the Speed Cinema.louisvillefilmsociety.org

In this episode of Speaking of Mol Bio, Aistė Serapinaite, an experienced R&D scientist, shares her insights into the world of 1-Step RT-PCR—a method that simplifies RNA analysis by combining reverse transcription and PCR amplification in a single reaction. She explains how traditional RNA workflows once lengthy, multi-step processes were prone to errors and contamination, and how 1-Step RT-PCR has transformed this landscape with speed, efficiency, and fewer handling steps.Listeners learn about the technical workings of 1-Step RT-PCR, including the importance of primer design, RNA quality, and essential controls to ensure reliable results. Aistė highlights the Invitrogen SuperScript IV UniPrime One-Step RT-PCR System, emphasizing features like universal annealing temperatures and high sensitivity, capable of detecting even trace levels of RNA.The episode also explores diverse applications, from gene expression studies and cancer biomarker detection to monitoring viral pathogens such as SARS-CoV-2 and Zika virus. While acknowledging the limitations of 1-Step RT-PCR—like the inability to archive cDNA for future assays—Aistė affirms its role as a fast, robust, and eco-friendly solution for high-throughput molecular biology labs. Whether you're new to molecular workflows or an experienced researcher, this episode offers valuable tips and tools to optimize your RNA experiments.Helpful resource links mentioned in this episode:See how one-step RT-PCR is used for amplicon-based viral genome sequencingView a video on the differences between one-step and two-step RT-PCRAccess the Oligo Perfect Primer Designer toolOrder or check out the brochure for Invitrogen SuperScript IV UniPrime One-Step RT-PCR SystemOrder Invitrogen ezDNase Enzyme Subscribe to get future episodes as they drop and if you like what you're hearing we hope you'll share a review or recommend the series to a colleague.  Visit the Invitrogen School of Molecular Biology to access helpful molecular biology resources and educational content, and please share this resource with anyone you know working in molecular biology. For Research Use Only. Not for use in diagnostic procedures.

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.

This episode continues the discussion regarding the rapid evolution of mRNA technologies since COVID-19. Guests discuss the improvements that have occurred within just a few years, which are making these therapies more reliable, cost-effective and viable for personalized cancer, rare disease chronic disease treatment.Today's episode is sponsored by Eclipsebio. From AI-ready datasets to sequencing validation, they drive RNA success.Explore their solutions at ⁠https://eclipsebio.com/⁠.Host⁠⁠⁠⁠⁠⁠Lori Ellis⁠⁠⁠⁠⁠⁠, Head of Insights, BioSpaceGuests⁠Andy Geall⁠, Co-founder and Chief Development Officer, Replicate Bioscience; Chair of the Board, Alliance for mRNA Medicines⁠Pad Chivukula⁠, Co-founder, CSO & COO, Arcturus TherapeuticsDisclaimer: The views expressed in this discussion by guests are their own and do not represent those of their organizations.

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.

Join The Beyond Terrain Community for free:https://beyond-terrain.circle.so/join?invitation_token=08c95fc3df8ff802b3bd05091df70e5a7bf0f297-2ceb428c-0b15-4d16-be23-81d5a8adb098Links:Part 1: https://www.youtube.com/watch?v=iUr5PW1r1oE&list=PLV0S9i-xQu5WHh2mgQ0aSd0Hm0ecemXm3&ab_channel=BeyondTerrainIn this episode, Dr. Jerneja Tomsic joins us to unravel the myths and misconceptions surrounding the genetic code, RNA, and gene editing.We begin by questioning the very foundation of modern biology—the so-called genetic code—and explore how much of what we believe is built on assumptions, models, and indirect inferences rather than direct observation.The conversation moves into the world of RNA, exposing the exaggerated claims about its role and supposed “superpowers” in diagnostics, vaccines, and cellular control.We then dive into paternity testing, forensic genetics, and heredity, raising serious questions about their reliability, interpretation, and the circular logic often used in these fields.Finally, we tackle the boldest claim of all: gene editing. We discuss GMO foods, to the GMO babies in china, revealing gene editing is more fantasy than science.A powerful and eye-opening episode that invites critical thinking and reclaims clarity in a field clouded by hype and narrative.Keep up with me (socials)https://www.instagram.com/beyond.terrain/https://beyondterrain.com/Our vision at Beyond Terrain is greatly supported by sharing our work!Become a Founding Member in the community!https://beyond-terrain.circle.so/checkout/founding-memberLearn more from and support our esteemed guest, Dr. Tomsichttps://x.com/zianiniSLO

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

This discussion focuses on how mRNA and self-replicating RNA (srRNA) technologies are expanding far beyond COVID vaccines into revolutionary therapeutic applications for cancer and rare diseases. It is clear that mRNA therapeutics offer three major application areas: infectious disease vaccines, therapeutic vaccines for oncology, and protein replacement for monogenic rare diseases.Today's episode is sponsored by Eclipsebio. From AI-ready datasets to sequencing validation, they drive RNA success. Explore their solutions at https://eclipsebio.com/.Host⁠⁠⁠⁠⁠Lori Ellis⁠⁠⁠⁠⁠, Head of Insights, BioSpaceGuestsAndy Geall, Co-founder and Chief Development Officer, Replicate Bioscience; Chair of the Board, Alliance for mRNA MedicinesPad Chivukula, Co-founder, CSO & COO, Arcturus TherapeuticsDisclaimer: The views expressed in this discussion by guests are their own and do not represent those of their organizations.

In this episode of Speaking of Mol Bio, Dr. Beth Webb takes us deep into the world of platelets, often misunderstood components of blood that punch far above their weight in both physiological and pathological processes. As a postdoctoral researcher at the University of Leeds, Dr. Webb explores how endothelial signals influence platelet activity, and how these anucleate cell fragments play roles not only in clotting, but also in immune responses, inflammation, and diseases like cardiovascular disorders and COVID-19.Beth unpacks the technical challenges of isolating and analyzing platelets—particularly in RNA sequencing and qPCR—while stressing the importance of sample purity and the presence of platelet subpopulations. The conversation also touches on the hope of personalized medicine through platelet-based diagnostics and tailored antiplatelet therapies.Beyond the lab, Dr. Webb is an active science communicator, sharing tips on engaging broader audiences through social media, blogs, and video. She emphasizes the importance of resilience, creativity, and starting small when communicating science. Whether you're a cell biologist, a hematology enthusiast, or a fellow communicator, this episode offers something for everyone. Subscribe to get future episodes as they drop and if you like what you're hearing we hope you'll share a review or recommend the series to a colleague.  Visit the Invitrogen School of Molecular Biology to access helpful molecular biology resources and educational content, and please share this resource with anyone you know working in molecular biology. For Research Use Only. Not for use in diagnostic procedures.

Eric Topol (00:05):Hello, it's Eric Topol from Ground Truths, and I've got some really exciting stuff to talk to you about today. And it's about the announcement for a new Center for pediatric CRISPR Cures. And I'm delight to introduce doctors Jennifer Doudna and Priscilla Chan. And so, first let me say this is amazing to see this thing going forward. It's an outgrowth of a New England Journal paper and monumental report on CRISPR in May. [See the below post for more context]Let me introduce first, Dr. Doudna. Jennifer is the Li Ka Shing Chancellor's Chair and a Professor in the departments of chemistry and of molecular and cell biology at the University of California Berkeley. She's also the subject of this book, one of my favorite books of all time, the Code Breaker. And as you know, the 2020 Nobel Prize laureate for her work in CRISPR-Cas9 genome editing, and she founded the Innovative Genomics Institute (IGI) back 10 years ago. So Jennifer, welcome.Jennifer Doudna (01:08):Thank you, Eric. Great to be here.Eric Topol (01:10):And now Dr. Priscilla Chan, who is the co-founder of the Chan Zuckerberg Initiative (CZI) that also was started back in 2015. So here we are, a decade later, these two leaders. She is a pediatrician having trained at UCSF and is committed to the initiative which has as its mission statement, “to make it possible to cure, prevent, and manage all diseases in this century.” So today we're going to talk about a step closer to that. Welcome, Priscilla.Priscilla Chan (01:44):Thank you. Thanks for having me.Eric Topol (01:46):Alright, so I thought we'd start off by, how did you two get together? Have you known each other for over this past decade since you both got all your things going?Jennifer Doudna (01:56):Yes, we have. We've known each other for a while. And of course, I've admired the progress at the CZI on fundamental science. I was an advisor very early on and I think actually that's how we got to know each other. Right, Priscilla?Priscilla Chan (02:11):Yeah, that's right. We got to know each other then. And we've been crisscrossing paths. And I personally remember the day you won the Nobel Prize. It was in the heart of the pandemic and a lot of celebrations were happening over Zoom. And I grabbed my then 5-year-old and got onto the UCSF celebration and I was like, look, this is happening. And it was really cool for me and for my daughter.Eric Topol (02:46):Well, it's pretty remarkable convergence leading up to today's announcement, but I know Priscilla, that you've been active in this rare disease space, you've had at CZI a Rare As One Project. Maybe you could tell us a bit about that.Priscilla Chan (03:01):Yeah, so at CZI, we work on basic science research, and I think that often surprises people because they know that I'm a pediatrician. And so, they often think, oh, you must work in healthcare or healthcare delivery. And we've actually chosen very intentionally to work in basic science research. In part because my training as a pediatrician at UCSF. As you both know, UCSF is a tertiary coronary care center where we see very unusual and rare cases of pediatric presentations. And it was there where I learned how little we knew about rare diseases and diseases in general and how powerful patients were. And that research was the pipeline for hope and for new discoveries for these families that often otherwise don't have very much access to treatments or cures. They have a PDF that maybe describes what their child has. And so, I decided to invest in basic science through CZI, but always saw the power of bringing rare disease patient cohorts. One, because if you've ever met a parent of a child with rare disease, they are a force to be reckoned with. Two, they can make research so much better due to their insights as patients and patient advocates. And I think they close the distance between basic science and impact in patients. And so, we've been working on that since 2019 and has been a passion of ours.Eric Topol (04:40):Wow, that's great. Now Jennifer, this IGI that you founded a decade ago, it's doing all kinds of things that are even well beyond rare diseases. We recently spoke, I know on Ground Truths about things as diverse as editing the gut microbiome in asthma and potentially someday Alzheimer's. But here you were very much involved at IGI with the baby KJ Muldoon. Maybe you could take us through this because this is such an extraordinary advance in the whole CRISPR Cures story.Jennifer Doudna (05:18):Yes, Eric. It's a very exciting story and we're very, very proud of the teamwork that went into making it possible to cure baby KJ of his very rare disease. And in brief, the story began back in August of last year when he was born with a metabolic disorder that prevented him from digesting protein, it's called a urea cycle disorder and rare, but extremely severe. And to the point where he was in the ICU and facing a very, very difficult prognosis. And so, fortunately his clinical team at Children's Hospital of Philadelphia (CHOP) reached out to Fyodor Urnov, who is the Director of Translational Medicine at the IGI here in the Bay Area. They teamed up and realized that they could quickly diagnose that child because we had an IRB approved here at the IGI that allowed us to collect patient samples and do diagnosis. So that was done.Jennifer Doudna (06:26):We created an off-the-shelf CRISPR therapy that would be targeted to the exact mutation that caused that young boy's disease. And then we worked with the FDA in Washington to make sure that we could very safely proceed with testing of that therapy initially in the lab and then ultimately in two different animal models. And then we opened a clinical trial that allowed that boy to be enrolled with, of course his parents' approval and for him to be dosed and the result was spectacular. And in fact, he was released from the hospital recently as a happy, healthy child, gaining lots of weight and looking very chunky. So it's really exciting.Eric Topol (07:16):It's so amazing. I don't think people necessarily grasp this. This timeline [see above] that we'll post with this is just mind boggling how you could, as you said Jennifer, in about six months to go from the birth and sequencing through cell specific cultures with the genome mutations through multiple experimental models with non-human primates even, looking at off-target effects, through the multiple FDA reviews and then dosing, cumulatively three dosing to save this baby's life. It really just amazing. Now that is a template. And before we go to this new Center, I just wanted to also mention not just the timeline of compression, which is unimaginable and the partnership that you've had at IGI with I guess Danaher to help manufacture, which is just another part of the story. But also the fact that you're not just even with CRISPR 1.0 as being used in approvals previously for sickle cell and β-thalassemia, but now we're talking about base editing in vivo in the body using mRNA delivery. So maybe you could comment on that, Jennifer.Jennifer Doudna (08:38):Yeah, very good point. So yeah, we used a version of CRISPR that was created by David Liu at the Broad Institute and published and available. And so, it was possible to create that, again, targeted to the exact mutation that caused baby KJ's disease. And fortunately, there was also an off-the-shelf way to deliver it because we had access to lipid nanoparticles that were developed for other purposes including vaccinations. And the type of disease that KJ suffered from is one that is treatable by editing cells in the liver, which is where the lipid nanoparticle naturally goes. So there were definitely some serendipity here, but it was amazing how all of these pieces were available. We just had to pull them together to create this therapy.Eric Topol (09:30):Yeah, no, it is amazing. So that I think is a great substrate for starting a new Center. And so, maybe back to you Priscilla, as to what your vision was when working with Jennifer and IGI to go through with this.Priscilla Chan (09:45):I think the thing that's incredibly exciting, you mentioned that at CZI our mission is to cure, prevent, and manage all disease. And when we talked about this 10 years ago, it felt like this far off idea, but every day it seems closer and closer. And I think the part that's super exciting about this is the direct connection between the basic science that's happening in CRISPR and the molecular and down to the nucleotide understanding of these mutations and the ability to correct them. And I think many of us, our imaginations have included this possibility, but it's very exciting that it has happened with baby KJ and CHOP. And we need to be able to do the work to understand how we can treat more patients this way, how to understand the obstacles, unblock them, streamline the process, bring down the cost, so that we better understand this pathway for treatment, as well as to increasingly democratize access to this type of platform. And so, our hope is to be able to do that. Take the work and inspiration that IGI and the team at CHOP have done and continue to push forward and to look at more cases, look at more organ systems. We're going to be looking in addition to the liver, at the bone marrow and the immune system.Priscilla Chan (11:17):And to be able to really work through more of the steps so that we can bring this to more families and patients.Eric Topol (11:30):Yeah, well it's pretty remarkable because here you have incurable ultra-rare diseases. If you can help these babies, just think of what this could do in a much broader context. I mean there a lot of common diseases have their roots with some of these very rare ones. So how do you see going forward, Jennifer, as to where you UC Berkeley, Gladstone, UCSF. I'm envious of you all up there in Northern California I have to say, will pull this off. How will you get the first similar case to KJ Muldoon going forward?Jennifer Doudna (12:13):Right. Well, IGI is a joint institute, as you probably know, Eric. So we were founded 10 years ago as a joint institute between UC Berkeley and UCSF. And now we have a third campus partner, UC Davis and we have the Gladstone Institute. So we've got an extraordinary group of clinicians and researchers that are coming together for this project and the Center to make it a success. We are building a clinical team at UCSF. We have several extraordinary leaders including Jennifer Puck and Chris Dvorak, and they are both going to be involved in identifying patients that could be enrolled in this program based on their diagnosis. And we will have a clinical advisory group that will help with that as well. So we'll be vetting patients probably right after we announce this, we're going to be looking to start enrolling people who might need this type of help.Eric Topol (13:18):Do you think it's possible to go any faster right now than the six months that it took for KJ?Jennifer Doudna (13:26):I think it could be. And here's the reason. There's a very interesting possibility that because of the type of technology that we're talking about with CRISPR, which fundamentally, and you and I have talked about this previously on your other podcast. But we've talked about the fact that it's a programmable technology and that means that we can change one aspect of it, one piece of it, which is a piece of a molecule called RNA that's able to direct CRISPR to the right sequence where we want to do editing and not change anything else about it. The protein, the CRISPR protein stays the same, the delivery vehicle stays the same, everything else stays the same. And so, we're working right now with FDA to get a platform designation for CRISPR that might allow streamlining of the testing process in some cases. So it'll obviously come down to the details of the disease, but we're hopeful that in the end it will be possible. And Priscilla and I have talked about this too, that as AI continues to advance and we get more and more information about rare diseases, we'll be able to predict accurately the effects of editing. And so, in some cases in the future it may be possible to streamline the testing process even further safely.Eric Topol (14:51):And I also would note, as you both know, well this administration is really keen on genome editing and they've had a joint announcement regarding their support. And in my discussions with the FDA commissioner, this is something they are very excited about. So the timing of the new Center for pediatric CRISPR Cures is aligned with the current administration, which is good to see. It's not always the case. Now going back, Priscilla, to your point that not just for the liver because delivery has been an issue of course, and we're going to try to get after a lot of these really rare diseases, it's going to go beyond there. So this is also an exciting new dimension of the Center, as you said, to go after the bone marrow for hematopoietic cells, perhaps other organs as well.Priscilla Chan (15:42):I mean what the expertise and feasibility, the immune system is going to be the next target. Jennifer Puck has been a pioneer in this work. She's the one who designed the newborn screen that will be the tool that picks up these patients as they are born. And I think the thing that's tremendous is the immune system, first of all is active in many, many diseases, not just these cases of children born with partial or absence of immune systems. And the course right now that these babies are left with is complete isolation and then a very long and arduous course of a bone marrow transplant with high morbidity and mortality. And even if after the transplant you have complications like graft versus host and immunosuppression. And so, the idea of being able to very specifically and with less the conditioning and morbidity and mortality of the treatment, being able to address this is incredible. And the implications for other diseases like blood cancers or other hematopoietic diseases, that's incredible. And that actually has an incredibly broad base of patients that can benefit from the learnings from these babies with severe combined immunodeficiencies.Eric Topol (17:10):Yeah, I think that goes back to a point earlier maybe to amplify in that previous CRISPR generation, it required outside the body work and it was extremely laborious and time consuming and obviously added much more to the expense because of hospitalization time. This is different. This is basically doing this inside the affected patient's body. And that is one of the biggest reasons why this is a big step forward and why we're so fortunate that your Center is moving forward. Maybe before we wrap up, you might want to comment, Jennifer on how you were able to bring in to build this platform, the manufacturing arm of it, because that seems to be yet another dimension that's helpful.Jennifer Doudna (18:01):Indeed, yes. And we were again fortunate with timing because you mentioned briefly that the IGI had set up a program with the Danaher Corporation back in January of last year. We call it our Beacon project. And it's focused on rare disease. And it's a really interesting kind of a unique partnership because Danaher is a manufacturing conglomerate. So they have companies that make molecules, they make proteins, they make RNA molecules, they make delivery molecules. And so, they were excited to be involved with us because they want to be a provider of these types of therapies in the future. And they can see the future of CRISPR is very exciting. It's expanding, growing area. And so, that agreement was in place already when the baby KJ case came to our attention. And so, what we're hoping to do with Danaher is again, work with them and their scientists to continue to ask, how can we reduce the cost of these therapies by reducing the cost of the molecules that are necessary, how to make them efficiently. We already, it's very interesting, Fyodor Urnov has toured their plant in North Dakota recently, and he found in talking to their engineers, there are a number of things that we can already see will be possible to do that are going to make the process of manufacturing these molecules faster and cheaper by a lot.Eric Topol (19:28):Wow.Jennifer Doudna (19:28):So it's a win-win for everybody. And so, we're really excited to do that in the context of this new Center.Eric Topol (19:36):Oh, that's phenomenal because some of these disorders you don't have that much time to work with before they could be brain or organ or vital tissue damage. So that's great to hear that. What you built here is the significance of it can't be under emphasized, I'll say because we have this May report of baby KJ, which could have been a one-off and it could have been years before we saw another cure of an ultra-rare disorder. And what you're doing here is insurance against that. You're going to have many more cracks at this. And I think this is the excitement about having a new dedicated Center. So just in closing, maybe some remarks from you Priscilla.Priscilla Chan (20:24):I just want to emphasize one point that's really exciting as we talk about these ultra-rare cases that they're often like one in a million. All these learnings actually help maximize the impact of lots of research across the sector that impacts actually everyone's health. And so, our learnings here from these patients that have very significant presentations that really can stand to benefit from any treatment is hopefully paving the way for many, many more of us to be able to live healthier, higher quality lives through basic science.Eric Topol (21:13):And over to you, Jennifer.Jennifer Doudna (21:15):Couldn't agree more. It's a really interesting moment. I think what we hope we are, is we're at sort of an inflection point where, as I mentioned earlier, all the pieces are in place to do this kind of therapeutic and we just need a team that will focus on doing it and pulling it together. And also learning from that process so that as Priscilla just said, we are ultimately able to use the same strategy for other diseases and potentially for diseases that affect lots of people. So it's exciting.Eric Topol (21:46):For sure. Now, if I could just sum up, this is now a decade past the origination of your work of CRISPR and how already at the first decade culminated in sickle cell disease treatment and β-thalassemia. Now we're into the second decade of CRISPR. And look what we've seen, something that was unimaginable until it actually happened and was reported just a little over a month ago. Now going back to Priscilla's point, we're talking about thousands of different rare Mendelian genomic disorders, thousands of them. And if you add them all up of rare diseases, we're talking about hundreds of millions of people affected around the world. So this is a foray into something much bigger, no less the fact that some of these rare mutations are shared by common diseases and approaches. So this really big stuff, congratulations to both of you and your organizations, the Innovative Genomics Institute and the Chan Zuckerberg Initiative for taking this on. We'll be following it with very deep interest, thank you.****************************************************Thanks for listening, reading and subscribing to Ground Truths.If you found this interesting PLEASE share it!That makes the work involved in putting these together especially worthwhile.Thanks to Scripps Research, and my producer, Jessica Nguyen, and Sinjun Balabanoff for video/audio support.All content on Ground Truths—its newsletters, analyses, and podcasts, are free, open-access.Paid subscriptions are voluntary and all proceeds from them go to support Scripps Research. They do allow for posting comments and questions, which I do my best to respond to. Please don't hesitate to post comments and give me feedback. Let me know topics that you would like to see covered.Many thanks to those who have contributed—they have greatly helped fund our summer internship programs for the past two years. Get full access to Ground Truths at erictopol.substack.com/subscribe

Will the country be safe this July 4 season?  Is there any reason we should pray before we go anyplace?  Why are 4 titans in the AI-digital world now Lieutenant Colonels in the Army?  What new changes to vaxxine safety studies will "address unmet public health needs" of the American public?  Please join me as the world swerves into a breathtaking descent into the most warned-of days in scripture.   ON OR ABOUT JULY 4? Barricades going up in DC: https://halturnerradioshow.com/index.php/news-selections/national-news/barricades-going-up-around-dc-white-house-and-us-treasury Dr. Martin, watch out for July 4: https://rumble.com/v6t6zzz-dr-david-martin.html Dr. Martin re July 4 (dissemination of contagion): https://rumble.com/v6t6zzz-dr-david-martin.html Dr. Martin on July 4: https://substack.com/profile/94300893-amy-lynn-rdn/note/c-128625909?utm_source=notes-share-action&r=12g59e Download National Blueprint for Biodefense: https://biodefensecommission.org/reports/the-national-blueprint-for-biodefense/ DC being boarded up: https://t.me/GodsRoadmap/2469 DC being boarded up: https://halturnerradioshow.com/index.php/news-selections/national-news/barricades-going-up-around-dc-white-house-and-us-treasury Journalist Jon Fleetwood re next plandemic/July 4: https://www.vigilantfox.com/p/exclusive-darpas-shocking-bioterror?r=12g59e&utm_campaign=post&utm_medium=web&showWelcomeOnShare=false   VAXX / NEXT PANDEMIC Attorney does study that CDC won't – vaxxed v. unvaxxed: https://substack.com/@tlionel/note/c-118695784?utm_source=notes-share-action&r=12g59e 500 new vaxxes by 2030: https://strangesounds.org/2023/02/the-who-plans-to-introduce-over-500-new-vaccines-by-2030-covid-19-vaccines-are-just-the-first-of-many-coming-soon.html What does name AstraZeneca mean its Greek origins?: https://greeknewsondemand.com/2024/05/19/what-the-name-astrazeneca-really-mean-does-it-have-to-do-with-culling-the-population/ Gates to Al Jazeera – how to prepare: https://winepressnews.com/2023/01/07/bill-gates-tells-al-jazeera-how-to-prepare-for-the-next-pandemic-and-to-moderate-some-of-the-insanity-online/ DARPA's bioterror plot?: https://www.vigilantfox.com/p/exclusive-darpas-shocking-bioterror?r=12g59e&utm_campaign=post&utm_medium=web&showWelcomeOnShare=false CDC official admits they covered up MMR injuries:  https://substack.com/@fallofthecabalofficial/note/c-130399890?utm_source=notes-share-action&r=12g59e Study out of Sweden - messenger RNA does change your DNA:  https://substack.com/@fallofthecabalofficial/note/c-130113610?utm_source=notes-share-action&r=12g59e Slovak official claims DNA in vaxxes turns people into GMO's: https://www.aussie17.com/p/breaking-news-slovak-government-official?r=12g59e&utm_campaign=post&utm_medium=web&showWelcomeOnShare=false Embalmers still finding blood clots in deceased: https://substack.com/@sageofquay/note/p-167037411?utm_source=notes-share-action&r=12g59e Air in masks is deadly: https://substack.com/@justindeschamps/note/c-129536683?utm_source=notes-share-action&r=12g59e Uh-oh, Ozempic linked to cancers: https://substack.com/@phrygiofphrygia/note/c-128524547?utm_source=notes-share-action&r=12g59e 1995 film outlining the contamination of human blood by forced vaxxination: https://substack.com/@collective143/note/c-127924696?utm_source=notes-share-action&r=12g59e Drug review period reduced to matter of weeks: https://open.substack.com/pub/thewinepress/p/fda-cuts-drug-review-time-to-weeks?r=12g59e&utm_campaign=post&utm_medium=web&showWelcomeOnShare=false   ENVIRONMENTAL MODIFICATION Let's steal carbon and land from plants: https://thewinepress.substack.com/p/trumps-one-big-beautiful-bill-contains?utm_source=substack&publication_id=832192&post_id=164186427&utm_medium=email&utm_content=share&utm_campaign=email-share&triggerShare=true&isFreemail=true&r=12g59e&triedRedirect=true Chemtrail patents, etc: https://youtu.be/rf78rEAJvhY?

Tatiana Antonelli-Abella sits down with the winners of the 2024-25 cohort of the MENAT Regenerative Agriculture Initiative. Now in its second year, the Venture Programme received 660 registration and 190 innovation solutions, each focused on soil regeneration, climate and water-resilient agricultural practices, and addressing food security. This years's winners are: Omaima Marhane from Actinobacteria, developing solutions to tackle water stress in arid soils. Dr. Budour A. Alghamdi, Eng. Wafa A. Alrasheed, and Dr. Adil E. Abdelnour from Farm to 2Fs, turning animal waste into bioenergy and fertilizer. ⁠Teodoro Garcia-Millan, Fran Robson, and Veronica Greco from RedDot, revolutionizing pest control with RNA-based technology. You can find out more about the Venture Programme, the winners, and the Top 20 solutions here. You can also listen to the winners of the first cohort here. We also want to thank our partners, HSBC and ⁠Saudi Awal Bank, who worked with us to both upskill and empower innovative solutions like these through funding and mentorship, helping them progress towards becoming viable commercial possibilities.

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

Broadcast from KSQD, Santa Cruz on 6-26-2025: Dr. Dawn opens with groundbreaking results from Vertex Pharmaceuticals' stem cell treatment for severe type 1 diabetes. The experimental therapy, Zimislecel, converts stem cells into pancreatic islet cells and infuses them into patients. In a 12-person study, 10 patients no longer need insulin after one year. The cells migrated to the liver and began producing insulin in response to glucose levels. Patients with hypoglycemic unawareness saw complete elimination of dangerous episodes after three months. However, patients must take lifelong immunosuppressive drugs to prevent rejection. The research represents 25 years of work by Harvard's Doug Melton. A caller asks about Keytruda treatment for melanoma. Dr. Dawn explains it's an immunotherapy drug targeting programmed death receptors that cancer cells hijack to evade immune response. The drug can cause serious immune overreactions but is standard for metastatic melanoma. Treatment protocols depend on cancer staging. For young patients with decades to lose, aggressive treatment is often justified despite risks. An email about morning arthritis pain leads to chronotherapy research discussion. Macrophages have energy levels that peak in the morning when inflammasome activation is quicker and more robust, explaining why arthritis pain is worst after overnight rest. Treatment timing could optimize anti-inflammatory medications by taking them at bedtime. Another email about eye irritation prompts diagnostic discussion. Dr. Dawn recommends examining for bacterial blepharitis before assuming food allergies and testing antihistamine drops. For elimination diets, common allergens include wheat, dairy, corn, soy, and peanuts. However, without other symptoms, food allergies are unlikely causes of isolated eye problems. Dr. Dawn explores advancing CAR-T cell therapy using RNA technology. Traditional therapy costs up to $500,000 per patient requiring lab reprogramming. New RNA-containing nanoparticles temporarily create antigen receptors for about one week. Mouse studies eliminated detectable tumors at highest doses. While effects are temporary, this could dramatically reduce costs and complexity. She discusses DNA forensics evolution from O.J. trial era to current technologies. New paleogenomics technology can analyze fragmented DNA from hair, previously considered unusable. Mitochondrial DNA analysis can definitively exonerate suspects. This led to Charles Fane's release after 17 years on death row when hair evidence proved innocence and identified the actual perpetrator. Dr. Dawn introduces Barrett's esophagus screening replacing invasive endoscopy. Patients swallow a capsule containing a compressed sponge that expands in the stomach and is pulled out via string, collecting esophageal cells. The test identifies abnormalities with 100-fold increased cancer risk when positive and 98% accuracy when negative, allowing targeted endoscopy only for high-risk patients. She concludes discussing body composition analysis superiority over BMI. Studies found overweight BMI showed 3.6 times higher heart disease risk, while large waist circumference showed four times higher risk. However, BMI had no significant relationship with overall mortality. Dr. Dawn advocates for bioimpedance analysis devices to measure body fat percentage and track muscle loss.

Broadcast from KSQD, Santa Cruz on 6-26-2025: Dr. Dawn opens with groundbreaking results from Vertex Pharmaceuticals' stem cell treatment for severe type 1 diabetes. The experimental therapy, Zimislecel, converts stem cells into pancreatic islet cells and infuses them into patients. In a 12-person study, 10 patients no longer need insulin after one year. The cells migrated to the liver and began producing insulin in response to glucose levels. Patients with hypoglycemic unawareness saw complete elimination of dangerous episodes after three months. However, patients must take lifelong immunosuppressive drugs to prevent rejection. The research represents 25 years of work by Harvard's Doug Melton. A caller asks about Keytruda treatment for melanoma. Dr. Dawn explains it's an immunotherapy drug targeting programmed death receptors that cancer cells hijack to evade immune response. The drug can cause serious immune overreactions but is standard for metastatic melanoma. Treatment protocols depend on cancer staging. For young patients with decades to lose, aggressive treatment is often justified despite risks. An email about morning arthritis pain leads to chronotherapy research discussion. Macrophages have energy levels that peak in the morning when inflammasome activation is quicker and more robust, explaining why arthritis pain is worst after overnight rest. Treatment timing could optimize anti-inflammatory medications by taking them at bedtime. Another email about eye irritation prompts diagnostic discussion. Dr. Dawn recommends examining for bacterial blepharitis before assuming food allergies and testing antihistamine drops. For elimination diets, common allergens include wheat, dairy, corn, soy, and peanuts. However, without other symptoms, food allergies are unlikely causes of isolated eye problems. Dr. Dawn explores advancing CAR-T cell therapy using RNA technology. Traditional therapy costs up to $500,000 per patient requiring lab reprogramming. New RNA-containing nanoparticles temporarily create antigen receptors for about one week. Mouse studies eliminated detectable tumors at highest doses. While effects are temporary, this could dramatically reduce costs and complexity. She discusses DNA forensics evolution from O.J. trial era to current technologies. New paleogenomics technology can analyze fragmented DNA from hair, previously considered unusable. Mitochondrial DNA analysis can definitively exonerate suspects. This led to Charles Fane's release after 17 years on death row when hair evidence proved innocence and identified the actual perpetrator. Dr. Dawn introduces Barrett's esophagus screening replacing invasive endoscopy. Patients swallow a capsule containing a compressed sponge that expands in the stomach and is pulled out via string, collecting esophageal cells. The test identifies abnormalities with 100-fold increased cancer risk when positive and 98% accuracy when negative, allowing targeted endoscopy only for high-risk patients. She concludes discussing body composition analysis superiority over BMI. Studies found overweight BMI showed 3.6 times higher heart disease risk, while large waist circumference showed four times higher risk. However, BMI had no significant relationship with overall mortality. Dr. Dawn advocates for bioimpedance analysis devices to measure body fat percentage and track muscle loss.

A surgeon in burns reconstruction, Matt Klein swapped the operating room for the equally high-pressure environment of drug development. In this episode of Pathfinders in Biopharma, he sets out the vision for the company he now leads, PTC Therapeutics – a pioneer in the field of RNA therapies, now powering towards profitability with treatment candidates for a host of rare diseases.

Bobby Kennedy pimping for Big Tech while ignoring the crimes of Big PHARMA was not on my bingo card. But the backlash has been glorious as Americans responded with a resounding ‘oh hell no'!Yesterday, RFK testified before the House Energy and Commerce Health Subcommittee, stating his vision that "every American is wearing a wearable within four years" as part of his "Make America Healthy Again" (MAHA) agenda. He announced the launch of "one of the biggest advertising campaigns in HHS history" to promote wearable health devices, such as smartwatches, fitness trackers, and continuous glucose monitors, which track metrics like heart rate, blood pressure, and glucose levels.Yes it's bad and reeks of technocracy and cronyism with his connection to the Means siblings who own companies which would profit from free government ad campaign and taxpayer funded incentives.Even worse?His agency is still injecting babies with COVID shots.His agency is still ignoring the millions suffering with COVID shot related injuries & the families of those who were killed.His agency is now poised to approve 500+ new mRNA technologies including self-amplifying RNA.He still refuses to end the HHS COVID emergency declaration which would end SO much of the suffering and prevent them from locking us down again.So what is going on here?Big show with Doc Malik to discuss this and more!!Staying healthy means staying OUT of the hospital and as far away from the medical industrial complex as possible. The secret is daily, consistent nutrient support with collagen to combat inflammation which is the mother of most adverse health issues.I ONLY use Native Path Collagen and they are ramping up another huge stock up sale on collagen for the Joy audience! Get 45% off your entire order today!!! Go to https://www.getnativepathcollagen.com/joyWe discuss this and MORE today on the SJ Show!Join the Rumble LIVE chat and follow my Rumble Page HERE so you never miss an episode: https://rumble.com/c/TheShannonJoyShowShannon's Top Headlines June 25, 2025:RFK ‘Leans In' To Wearables: https://www.beckershospitalreview.com/healthcare-information-technology/digital-health/rfk-jr-leans-into-wearables/Open AI Scores 200 Million Dollar Contract From US Military: https://www.technocracy.news/openai-scores-200-million-military-contract/What The Tech Bros Will Do In The Army: https://www.wired.com/story/what-lt-col-boz-and-big-techs-enlisted-execs-will-do-in-the-army/Trump's EOs bring technocratic dictatorship closer to reality: https://www.stridentconservative.com/trumps-eos-brings-technocratic-dictatorship-closer-to-reality250 Million Acre Bonanza: Technocrats' Big Beautiful Land Grab: https://www.technocracy.news/250-million-acre-bonanza-technocrats-big-beautiful-land-grab/Bank Of International Settlements is quietly building the beast system as we 'wage war' ... https://www.bis.org/publ/arpdf/ar2025e3.htmSJ Show Notes:Please support Shannon's independent network with your donation HERE: https://www.paypal.com/donate/?hosted_button_id=MHSMPXEBSLVTSupport Our Sponsors:Wars and rumors of wars wreak havoc on markets and economic development and can even lead to complete financial collapse and a currency RESET which benefits only the 1%. Regular Americans can benefit with foresight and protect their wealth with physical gold and silver.It's NOT too late! Call Colonial Metals today and you may qualify for up to $7,500 in FREE silver! Check out my landing page here: https://colonialmetalsgroup.com/joyWith lockdowns looming, threats of bio-terror and cyber attacks, the chaos is everywhere. You NEED to be prepared and your one stop shop is The Satellite Phone Store. They have EVERYTHING you need when the POWER goes OUT. Use the promo code JOY for 10% off your entire order TODAY! www.SAT123.com/JoyPlease consider Dom Pullano of PCM & Associates! He has been Shannon's advisor for over a decade and would love to help you grow! Call his toll free number today: 1-800-536-1368 Or visit his website at https://www.pcmpullano.comSee Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Welcome back to America's #1 Daily Podcast,  featuring America's #1 Real Estate Coaches and Top EXP Realty Sponsors in the World, Tim and Julie Harris. Ready to become an EXP Realty Agent and join Tim and Julie Harris?  Visit: https://whylibertas.com/harris or text Tim directly at 512-758-0206. ******************* 2025's Real Estate Rollercoaster: Dodge the Career-Killers with THIS Mastermind!

Dzięki sztucznej inteligencji i na podstawie danych RNA można przewidzieć chorobę lub powiedzieć coś o stanie zaawansowania dolegliwości - mówi w studiu TOK FM prof. Ewa Bartnik. Ekspertka jest biolożką i genetyczką z Instytutu Genetyki i Biotechnologii Uniwersytetu Warszawskiego, członkinią Komitetu Genetyki Człowieka i Patologii Molekularnej Polskiej Akademii Nauk.

Episode: 2934 Reading the Molecules of Life.  Today, we read the molecules of life.

John Rinn, professor at the University of Colorado and co-founder of Lincswitch Therapeutics, on exploring long non-coding RNA.

Alberto Vazquez-Salazar, PhD, is a NASA postdoctoral fellow working at UCLA in the lab of Professor Irene Chen. He studies how life may have started on Earth by focusing on a molecule called RNA, or ribonucleic acid, which is a critical molecule that exists in all living things. His work is a part of astrobiology that explores how life began on Earth and how we might find signs of life elsewhere in the universe. In this episode of Further Together, Vazquez-Salazar talks to host Michael Holtz about how science has always seemed to be part of his life. Growing up in Mexico City, his mom, a botanist, kept books and plant specimens everywhere. “Science was just part of everyday life,” he says. “It was as normal as finding cereal in the pantry.” Listen to learn more about Vazquez-Salazar's journey to NASA. To learn more about the NASA Postdoctoral Program and when applications open, visit https://npp.orau.org/index.html

Dr. Nathan Pennell and Dr. Cheryl Czerlanis discuss challenges in lung cancer screening and potential solutions to increase screening rates, including the use of AI to enhance risk prediction and screening processes. Transcript Dr. Nate Pennell: Hello, and welcome to By the Book, a monthly podcast series for ASCO Education that features engaging discussions between editors and authors from the ASCO Educational Book. I'm Dr. Nate Pennell, the co-director of the Cleveland Clinic Lung Cancer Program and vice chair of clinical research for the Taussig Cancer Center. I'm also the editor-in-chief for the ASCO Educational Book.  Lung cancer is one of the leading causes of cancer-related mortality worldwide, and most cases are diagnosed at advanced stages where curative treatment options are limited. On the opposite end, early-stage lung cancers are very curable. If only we could find more patients at that early stage, an approach that has revolutionized survival for other cancer types such as colorectal and breast cancer.  On today's episode, I'm delighted to be joined by Dr. Cheryl Czerlanis, a professor of medicine and thoracic medical oncologist at the University of Wisconsin Carbone Cancer Center, to discuss her article titled, "Broadening the Net: Overcoming Challenges and Embracing Novel Technologies in Lung Cancer Screening." The article was recently published in the ASCO Educational Book and featured in an Education Session at the 2025 ASCO Annual Meeting. Our full disclosures are available in the transcript of this episode.  Cheryl, it's great to have you on the podcast today. Thanks for being here. Dr. Cheryl Czerlanis: Thanks, Nate. It's great to be here with you. Dr. Nate Pennell: So, I'd like to just start by asking you a little bit about the importance of lung cancer screening and what evidence is there that lung cancer screening is beneficial. Dr. Cheryl Czerlanis: Thank you. Lung cancer screening is extremely important because we know that lung cancer survival is closely tied to stage at diagnosis. We have made significant progress in the treatment of lung cancer, especially over the past decade, with the introduction of immunotherapies and targeted therapies based on personalized evaluation of genomic alterations. But the reality is that outside of a lung screening program, most patients with lung cancer present with symptoms related to advanced cancer, where our ability to cure the disease is more limited.  While lung cancer screening has been studied for years, the National Lung Screening Trial, or the NLST, first reported in 2011 a significant reduction in lung cancer deaths through screening. Annual low-dose CT scans were performed in a high-risk population for lung cancer in comparison to chest X-ray. The study population was comprised of asymptomatic persons aged 55 to 74 with a 30-pack-year history of smoking who were either active smokers or had quit within 15 years. The low-dose CT screening was associated with a 20% relative risk reduction in lung cancer-related mortality. A similar magnitude of benefit was also reported in the NELSON trial, which was a large European randomized trial comparing low-dose CT with a control group receiving no screening. Dr. Nate Pennell: So, this led, of course, to approval from CMS (Centers for Medicare and Medicaid Services) for lung cancer screening in the Medicare population, probably about 10 years ago now, I think. And there are now two major trials showing an unequivocal reduction in lung cancer-related mortality and even evidence that it reduces overall mortality with lung cancer screening. But despite this, lung cancer screening rates are very low in the United States. So, first of all, what's going on? Why are we not seeing the kinds of screening rates that we see with mammography and colonoscopy? And what are the barriers to that here? Dr. Cheryl Czerlanis: That's a great question. Thank you, Nate. In the United States, recruitment for lung cancer screening programs has faced numerous challenges, including those related to socioeconomic, cultural, logistical, and even racial disparities. Our current lung cancer screening guidelines are somewhat imprecise and often fail to address differences that we know exist in sex, smoking history, socioeconomic status, and ethnicity. We also see underrepresentation in certain groups, including African Americans and other minorities, and special populations, including individuals with HIV. And even where lung cancer screening is readily available and we have evidence of its efficacy, uptake can be low due to both provider and patient factors. On the provider side, barriers include having insufficient time in a clinic visit for shared decision-making, fear of missed test results, lack of awareness about current guidelines, concerns about cost, potential harms, and evaluating both true and false-positive test results.  And then on the patient side, barriers include concerns about cost, fear of getting a cancer diagnosis, stigma associated with tobacco smoking, and misconceptions about the treatability of lung cancer. Dr. Nate Pennell: I think those last two are really what make lung cancer unique compared to, say, for example, breast cancer, where there really is a public acceptance of the value of mammography and that breast cancer is no one's fault and that it really is embraced as an active way you can take care of yourself by getting your breast cancer screening. Whereas in lung cancer, between the stigma of smoking and the concern that, you know, it's a death sentence, I think we really have some work to be made up, which we'll talk about in a minute about what we can do to help improve this.  Now, that's in the U.S. I think things are probably, I would imagine, even worse when we leave the U.S. and look outside, especially at low- and middle-income countries. Dr. Cheryl Czerlanis: Yes, globally, this issue is even more complex than it is in the United States. Widespread implementation of low-dose CT imaging for lung cancer screening is limited by manpower, infrastructure, and economic constraints. Many low- and middle-income countries even lack sufficient CT machines, trained personnel, and specialized facilities for accurate and timely screenings. Even in urban centers with advanced diagnostic facilities, the high screening and follow-up care costs can limit access. Rural populations face additional barriers, such as geographic inaccessibility of urban centers, transportation costs, language barriers, and mistrust of healthcare systems. In addition, healthcare systems in these regions often prioritize infectious diseases and maternal health, leaving limited room for investments in noncommunicable disease prevention like lung cancer screening. Policymakers often struggle to justify allocating resources to lung cancer screening when immediate healthcare needs remain unmet. Urban-rural disparities exacerbate these challenges, with rural regions frequently lacking the infrastructure and resources to sustain screening programs. Dr. Nate Pennell: Well, it's certainly an intimidating problem to try to reduce these disparities, especially between the U.S. and low- and middle-income countries. So, what are some of the potential solutions, both here in the U.S. and internationally, that we can do to try to increase the rates of lung cancer screening? Dr. Cheryl Czerlanis: The good news is that we can take steps to address these challenges, but a multifaceted approach is needed. Public awareness campaigns focused on the benefits of early detection and dispelling myths about lung cancer screening are essential to improving participation rates. Using risk-prediction models to identify high-risk individuals can increase the efficiency of lung cancer screening programs. Automated follow-up reminders and screening navigators can also ensure timely referrals and reduce delays in diagnosis and treatment. Reducing or subsidizing the cost of low-dose CT scans, especially in low- or middle-income countries, can improve accessibility. Deploying mobile CT scanners can expand access to rural and underserved areas.  On a global scale, integrating lung cancer screening with existing healthcare programs, such as TB or noncommunicable disease initiatives, can enhance resource utilization and program scalability. Implementing lung cancer screening in resource-limited settings requires strategic investment, capacity building, and policy interventions that prioritize equity. Addressing financial constraints, infrastructure gaps, and sociocultural barriers can help overcome existing challenges. By focusing on cost-effective strategies, public awareness, and risk-based eligibility criteria, global efforts can promote equitable access to lung cancer screening and improve outcomes.  Lastly, as part of the medical community, we play an important role in a patient's decision to pursue lung cancer screening. Being up to date with current lung cancer screening recommendations, identifying eligible patients, and encouraging a patient to undergo screening often is the difference-maker. Electronic medical record (EMR) systems and reminders are helpful in this regard, but relationship building and a recommendation from a trusted provider are really essential here. Dr. Nate Pennell: I think that makes a lot of sense. I mean, there are technology improvements. For example, our lung cancer screening program at The Cleveland Clinic, a few years back, we finally started an automated best practice alert in our EMR for patients who met the age and smoking requirements, and it led to a six-fold increase in people referred for screening. But at the same time, there's a difference between just getting this alert and putting in an order for lung cancer screening and actually getting those patients to go and actually do the screening and then follow up on it. And that, of course, requires having that relationship and discussion with the patient so that they trust that you have their best interests. Dr. Cheryl Czerlanis: Exactly. I think that's important. You know, certainly, while technology can aid in bringing patients in, there really is no substitute for trust-building and a personal relationship with a provider. Dr. Nate Pennell: I know that there are probably multiple examples within the U.S. where health systems or programs have put together, I would say, quality improvement projects to try to increase lung cancer screening and working with their community. There's one in particular that you discuss in your paper called the "End Lung Cancer Now" initiative. I wonder if you could take us through that. Dr. Cheryl Czerlanis: Absolutely. "End Lung Cancer Now" is an initiative at the Indiana University Simon Comprehensive Cancer Center that has the vision to end suffering and death from lung cancer in Indiana through education and community empowerment. We discuss this as a paradigm for how community engagement is important in building and scaling a lung cancer screening program.  In 2023, the "End Lung Cancer Now" team decided to focus its efforts on scaling and transforming lung cancer screening rates in Indiana. They developed a task force with 26 experts in various fields, including radiology, pulmonary medicine, thoracic surgery, public health, and advocacy groups. The result of this work is an 85-page blueprint with key recommendations that any system and community can use to scale lung cancer screening efforts. After building strong infrastructure for lung cancer screening at Indiana University, they sought to understand what the priorities, resources, and challenges in their communities were. To do this, they forged strong partnerships with both local and national organizations, including the American Lung Association, American Cancer Society, and others. In the first year, they actually tripled the number of screening low-dose CTs performed in their academic center and saw a 40% increase system-wide. One thing that I think is the most striking is that through their community outreach, they learned that most people prefer to get medical care close to home within their own communities. Establishing a way to support the local infrastructure to provide care became far more important than recruiting patients to their larger system.  In exciting news, "End Lung Cancer Now" has partnered with the IU Simon Comprehensive Cancer Center and IU Health to launch Indiana's first and only mobile lung screening program in March of 2025. This mobile program travels around the state to counties where the highest incidence of lung cancer exists and there is limited access to screening. The mobile unit parks at trusted sites within communities and works in partnership, not competition, with local health clinics and facilities to screen high-risk populations. Dr. Nate Pennell: I think that sounds like a great idea. Screening is such an important thing that it doesn't necessarily have to be owned by any one particular health system for their patients. I think. And I love the idea of bringing the screening to patients where they are. I can speak to working in a regional healthcare system with a main campus in the downtown that patients absolutely hate having to come here from even 30 or 40 minutes away, and they'd much rather get their care locally. So that makes perfect sense.  So, under the current guidelines, there are certainly things that we can do to try to improve capturing the people that meet those. But are those guidelines actually capturing enough patients with lung cancer to make a difference? There certainly are proposals within patient advocacy communities and even other countries where there's a large percentage of non-smokers who perhaps get lung cancer. Can we expand beyond just older, current and heavy smokers to identify at-risk populations who could benefit from screening? Dr. Cheryl Czerlanis: Yes, I think we can, and it's certainly an active area of research interest. We know that tobacco is the leading cause of lung cancer worldwide. However, other risk factors include secondhand smoke, family history, exposure to environmental carcinogens, and pulmonary diseases like COPD and interstitial lung disease. Despite these known associations, the benefit of lung cancer screening is less well elucidated in never-smokers and those at risk of developing lung cancer because of family history or other risk factors. We know that the eligibility criteria associated with our current screening guidelines focus on age and smoking history and may miss more than 50% of lung cancers. Globally, 10% to 25% of lung cancer cases occur in never-smokers. And in certain parts of the world, like you mentioned, Nate, such as East Asia, many lung cancers are diagnosed in never-smokers, especially in women. Risk-prediction models use specific risk factors for lung cancer to enhance individual selection for screening, although they have historically focused on current or former smokers.  We know that individuals with family members affected by lung cancer have an increased risk of developing the disease. To this end, several large-scale, single-arm prospective studies in Asia have evaluated broadening screening criteria to never-smokers, with or without additional risk factors. One such study, the Taiwan Lung Cancer Screening in Never-Smoker Trial, was a multicenter prospective cohort study at 17 medical centers in Taiwan. The primary outcome of the TALENT trial was lung cancer detection rate. Eligible patients aged 55 to 75 had either never smoked or had a light and remote smoking history. In addition, inclusion required one or more of the following risk factors: family history of lung cancer, passive smoke exposure, history of TB or COPD, a high cooking index, which is a metric that quantifies exposure to cooking fumes, or a history of cooking without ventilation. Participants underwent low-dose CT screening at baseline, then annually for 2 years, and then every 2 years for up to 6 years. The lung cancer detection rate was 2.6%, which was higher than that reported in the NLST and NELSON trials, and most were stage 0 or I cancers. Subsequently, this led to the Taiwan Early Detection Program for Lung Cancer, a national screening program that was launched in 2022, targeting 2 screening populations: individuals with a heavy history of smoking and individuals with a family history of lung cancer.  We really need randomized controlled trials to determine the true rates of overdiagnosis or finding cancers that would not lead to morbidity or mortality in persons who are diagnosed, and to establish whether the high lung detection rates are associated with a decrease in lung cancer-related mortality in these populations. However, the implementation of randomized controlled low-dose CT screening trials in never-smokers has been limited by the need for large sample sizes, lengthy follow-up, and cost.  In another group potentially at higher risk for developing lung cancer, the role of lung cancer screening in individuals who harbor germline pathogenic variants associated with lung cancer also needs to be explored further. Dr. Nate Pennell: We had this discussion when the first criteria came out because there have always been risk-based calculators for lung cancer that certainly incorporate smoking but other factors as well and have discussion about whether we should be screening people based on their risk and not just based on discrete criteria such as smoking. But of course, the insurance coverage for screening, you have to fit the actual criteria, which is very constrained by age and smoking history. Do you think in the U.S. there's hope for broadening our screening beyond NLST and NELSON criteria? Dr. Cheryl Czerlanis: I do think at some point there is hope for broadening the criteria beyond smoking history and age, beyond the criteria that we have typically used and that is covered by insurance. I do think it will take some work to perhaps make the prediction models more precise or to really understand who can benefit. We certainly know that there are many patients who develop lung cancer without a history of smoking or without family history, and it would be great if we could diagnose more patients with lung cancer at an earlier stage. I think this will really count on there being some work towards trying to figure out what would be the best population for screening, what risk factors to look for, perhaps using some new technologies that may help us to predict who is at risk for developing lung cancer, and trying to increase the group that we study to try and find these early-stage lung cancers that can be cured. Dr. Nate Pennell: Part of the reason we, of course, try to enrich our population is screening works better when you have a higher pretest probability of actually having cancer. And part of that also is that our technology is not that great. You know, even in high-risk patients who have CT scans that are positive for a screen, we know that the vast majority of those patients with lung nodules actually don't have lung cancer. And so you have to follow them, you have to use various models to see, you know, what the risk, even in the setting of a positive screen, is of having lung cancer.  So, why don't we talk about some newer tools that we might use to help improve lung cancer screening? And one of the things that everyone is super excited about, of course, is artificial intelligence. Are there AI technologies that are helping out in early detection in lung cancer screening? Dr. Cheryl Czerlanis: Yes, that's a great question. We know that predicting who's at risk for lung cancer is challenging for the reasons that we talked about, knowing that there are many risk factors beyond smoking and age that are hard to quantify. Artificial intelligence is a tool that can help refine screening criteria and really expand screening access. Machine learning is a form of AI technology that is adept at recognizing patterns in large datasets and then applying the learning to new datasets. Several machine learning models have been developed for risk stratification and early detection of lung cancer on imaging, both with and without blood-based biomarkers. This type of technology is very promising and can serve as a tool that helps to select individuals for screening by predicting who is likely to develop lung cancer in the future.  A group at Massachusetts General Hospital, represented in our group for this paper by my co-authors, Drs. Fintelmann and Chang, developed Sybil, which is an open-access 3D convolutional neural network that predicts an individual's future risk of lung cancer based on the analysis of a single low-dose CT without the need for human annotation or other clinical inputs. Sybil and other machine learning models have tremendous potential for precision lung cancer screening, even, and perhaps especially, in settings where expert image interpretation is unavailable. They could support risk-adapted screening schedules, such as varying the frequency and interval of low-dose CT scans according to individual risk and potentially expand lung cancer screening eligibility beyond age and smoking history. Their group predicts that AI tools like Sybil will play a major role in decoding the complex landscape of lung cancer risk factors, enabling us to extend life-saving lung cancer screening to all who are at risk. Dr. Nate Pennell: I think that that would certainly be welcome. And as AI is working its way into pretty much every aspect of life, including medical care, I think it's certainly promising that it can improve on our existing technology.  We don't have to spend a lot of time on this because I know it's a little out of scope for what you covered in your paper, but I'm sure our listeners are curious about your thoughts on the use of other types of testing beyond CT screening for detecting lung cancer. I know that there are a number of investigational and even commercially available blood tests, for example, for detection of lung cancer, or even the so-called multi-cancer detection blood tests that are now being offered, although not necessarily being covered by insurance, for multiple types of cancer, but lung cancer being a common cancer is included in that. So, what do you think? Dr. Cheryl Czerlanis: Yes, like you mentioned, there are novel bioassays such as blood-based biomarker testing that evaluate for DNA, RNA, and circulating tumor cells that are both promising and under active investigation for lung cancer and multi-cancer detection. We know that such biomarker assays may be useful in both identifying lung cancers but also in identifying patients with a high-risk result who should undergo lung cancer screening by conventional methods. Dr. Nate Pennell: Anything that will improve on our rate of screening, I think, will be welcome. I think probably in the future, it will be some combination of better risk prediction and better interpretation of screening results, whether those be imaging or some combination of imaging and biomarkers, breath-based, blood-based. There's so much going on that it is pretty exciting, but we're still going to have to overcome the stigma and lack of public support for lung cancer screening if we're going to move the needle. Dr. Cheryl Czerlanis: Yes, I think moving the needle is so important because we know lung cancer is still a very morbid disease, and our ability to cure patients is not where we would like it to be. But I do believe there's hope. There are a lot of motivated individuals and groups who are passionate about lung cancer screening, like myself and my co-authors, and we're just happy to be able to share some ways that we can overcome the challenges and really try and make an impact in the lives of our patients. Dr. Nate Pennell: Well, thank you, Dr. Czerlanis, for joining me on the By the Book Podcast today and for all of your work to advance care for patients with lung cancer. Dr. Cheryl Czerlanis: Thank you, Dr. Pennell. It's such a pleasure to be with you today. Thank you. Dr. Nate Pennell: And thank you to our listeners for joining us today. You'll find a link to Dr. Czerlanis' article in the transcript of this episode.  Please join us again next month for By the Book's next episode and more insightful views on topics you'll be hearing at the education sessions from ASCO meetings throughout the year, and our deep dives on approaches that are shaping modern oncology. Disclaimer: 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. Follow today's speakers:     Dr. Nathan Pennell    @n8pennell   @n8pennell.bsky.social Dr. Cheryl Czerlanis Follow ASCO on social media:     @ASCO on X (formerly Twitter)     ASCO on Bluesky    ASCO on Facebook     ASCO on LinkedIn     Disclosures:    Dr. Nate Pennell:        Consulting or Advisory Role: AstraZeneca, Lilly, Cota Healthcare, Merck, Bristol-Myers Squibb, Genentech, Amgen, G1 Therapeutics, Pfizer, Boehringer Ingelheim, Viosera, Xencor, Mirati Therapeutics, Janssen Oncology, Sanofi/Regeneron       Research Funding (Institution): Genentech, AstraZeneca, Merck, Loxo, Altor BioScience, Spectrum Pharmaceuticals, Bristol-Myers Squibb, Jounce Therapeutics, Mirati Therapeutics, Heat Biologics, WindMIL, Sanofi    Dr. Cheryl Czerlanis: Research Funding (Institution): LungLife AI, AstraZeneca, Summit Therapeutics

In this bite-sized H-Files episode, I unpack 5 hard-won lessons from my conversation with Nigel Theobald, CEO of N4 Pharma.After a decade of building a biotech platform for RNA delivery, Nigel knows exactly how brutal, and how rewarding this space can be.You'll walk away with:The one sentence every founder must write downWhy you can't bootstrap biotechHow to pivot with purposeThe truth about investor trustAnd why execution matters more than competitionHit play and take notes. Your future self will thank you.

What does it really take to bring a biotech product to market?Nigel Theobald, founder and CEO of N4 Pharma, joins me to share the real highs and lows of turning science into a scalable business.We dive into:The challenges of RNA drug deliveryHow to stay resilient when plans changeBuilding a virtual, world-class teamThe path from platform to productThis is a must-listen for anyone in biotech, medtech, or startup life.

Broadcast from KSQD, Santa Cruz on 5-22-2025: Dr. Dawn explores groundbreaking cancer research using high-throughput "digital twin" analysis to reverse colon cancer cells back to normal states, identifying three master molecular switches that can induce normal cell differentiation without killing the cancer cells, thus avoiding traditional chemotherapy side effects. She discusses remarkable results from Memorial Sloan Kettering showing 80% of patients with mismatch repair deficient tumors, including all 49 rectal cancer patients, saw complete tumor disappearance after six months of dostarlimab immunotherapy, with no recurrence at five years and minimal side effects. The program covers innovative CRISPR applications, including targeting previously "undruggable" cancer mutations like KRAS and BRAF by selectively degrading mutant RNA messages while preserving healthy genes, offering unprecedented precision in cancer treatment. Dr. Dawn explains a clever immunotherapy approach that disguises tumors as pig organs using Newcastle disease virus carrying alpha-gal enzyme, tricking the immune system into mounting fierce attacks against cancer cells, showing promising results in both monkey and human trials. She describes fascinating research using cryoshocked tumor cells as Trojan horses, where liquid nitrogen-treated cancer cells carrying CRISPR gene editing tools directly seek out tumors, offering superior targeting compared to injecting CRISPR. The show reveals how cancers create protective acid walls around themselves to repel immune cells, with individual cancer cells pumping lactic acid away from the tumor center to form pH 5.3 barriers that kill attacking CD8 T cells within hours. Dr. Dawn discusses breakthrough mRNA cancer vaccines for glioblastoma using patients' own tumor cells, showing rapid immune system activation within 48 hours and extending survival in both dogs and humans with this aggressive brain cancer. She explores the "flower code" mechanism where cancer cells gaslight healthy cells through epigenetic manipulation, expressing dominant "flower win" codes to overpower normal cells expressing "flower lose" codes in biological turf wars. The program addresses systemic problems in cancer classification, explaining how organ-based categorization delays access to effective treatments, with patients waiting years for drugs that could help based on molecular profiles rather than tumor location. Dr. Dawn concludes by highlighting medical discrimination against people with Duffy null phenotype, primarily affecting African Americans, whose naturally lower neutrophil counts lead to reduced chemotherapy doses and excluded clinical trial participation despite no increased infection risk.

Broadcast from KSQD, Santa Cruz on 5-22-2025: Dr. Dawn explores groundbreaking cancer research using high-throughput "digital twin" analysis to reverse colon cancer cells back to normal states, identifying three master molecular switches that can induce normal cell differentiation without killing the cancer cells, thus avoiding traditional chemotherapy side effects. She discusses remarkable results from Memorial Sloan Kettering showing 80% of patients with mismatch repair deficient tumors, including all 49 rectal cancer patients, saw complete tumor disappearance after six months of dostarlimab immunotherapy, with no recurrence at five years and minimal side effects. The program covers innovative CRISPR applications, including targeting previously "undruggable" cancer mutations like KRAS and BRAF by selectively degrading mutant RNA messages while preserving healthy genes, offering unprecedented precision in cancer treatment. Dr. Dawn explains a clever immunotherapy approach that disguises tumors as pig organs using Newcastle disease virus carrying alpha-gal enzyme, tricking the immune system into mounting fierce attacks against cancer cells, showing promising results in both monkey and human trials. She describes fascinating research using cryoshocked tumor cells as Trojan horses, where liquid nitrogen-treated cancer cells carrying CRISPR gene editing tools directly seek out tumors, offering superior targeting compared to injecting CRISPR. The show reveals how cancers create protective acid walls around themselves to repel immune cells, with individual cancer cells pumping lactic acid away from the tumor center to form pH 5.3 barriers that kill attacking CD8 T cells within hours. Dr. Dawn discusses breakthrough mRNA cancer vaccines for glioblastoma using patients' own tumor cells, showing rapid immune system activation within 48 hours and extending survival in both dogs and humans with this aggressive brain cancer. She explores the "flower code" mechanism where cancer cells gaslight healthy cells through epigenetic manipulation, expressing dominant "flower win" codes to overpower normal cells expressing "flower lose" codes in biological turf wars. The program addresses systemic problems in cancer classification, explaining how organ-based categorization delays access to effective treatments, with patients waiting years for drugs that could help based on molecular profiles rather than tumor location. Dr. Dawn concludes by highlighting medical discrimination against people with Duffy null phenotype, primarily affecting African Americans, whose naturally lower neutrophil counts lead to reduced chemotherapy doses and excluded clinical trial participation despite no increased infection risk.

올뉴 삼테성즈! 2025년 5월호. 스페인 정전과 재생에너지 그리고 중국의 미사일 기술-오프닝 PPL노벨상 수상자가 직접 쓴 RNA의 모든 것, 'RNA의 역사'!- 오로라 여행 매진! 대기 예약 링크는 아래에.https://www.sciencepeople.co.kr/39684-2/- 이용의 디벼보기스페인 정전 사태로 짚어 본 우리나라 재생에너지 발전의 허와 실- K2 박사인도 공군의 라팔을 격추한 파키스탄 공군의 중국제 미사일, 그 기술을 알아보다- 전체 자료https://www.slideshare.net/slideshow/2025-5-pdf/279475466- 과학과사람들 회원 '사람들' 가입 링크https://www.sciencepeople.co.kr/membership/about-membership/과학과 사람들 제공