Pure Monograph

As details emerged last week of the first tailormade cancer vaccine to prove itself in a major treatment trial, researchers began to ask hard questions about what the success truly means. Learn more: scim.ag/4zX2tzM

Working in clinical trial project management? Save the date for the Regulatory Science Symposium at USC’s Aresty Auditorium. @USCMann Jan. 22, 2027 | 9:00 am to 4:30 pm PST Questions? Contact Karen Manrique at [email protected].

Exciting news from the TRIAD cohort! 🎉We’re celebrating another graduate from our clinical trial study! 🐶🎓 Want to help dogs live longer, healthier lives? 🐾 Discover if your doggo is eligible for TRIAD: dogagingproject.org/triad #TRIAD #DogGrad #Dogs

Can probiotics reduce chemotherapy side effects and improve quality of life for cancer patients? @OhioState researchers could provide answers through a clinical trial focused on the gut health of ovarian cancer patients.cancer.osu.edu/news/can-bett…

🖥️ #ASCOAI: Could #AI improve clinical trial recruitment? At #ASCOQLTY26, @ravi_b_parikh & So Hee Ahn, BS, MS, discuss how a neurosymbolic AI model improved prescreening efficiency, inclusivity for a phase III #ProstateCancer trial. 🎥 Watch the video 👉ascoai.org/videos/newsreels/…

For anyone hoping AI will cure all diseases in 5 years, sitting through just ONE advisory board meeting with clinical KOLs is highly recommended. The sheer complexity of running a single clinical trial is humbling. Making it a success? 10x harder. #TechBio #DrugDiscovery #Biotech

Mapping out our body’s zombie cells might finally crack open aging biology. Mayo Clinic researchers published seven studies across Nature journals examining how senescent cells trigger chronic inflammation. The team introduced a gene-profiling tool called SenMayo to identify these nondividing cells across different human tissues and experimental models. Pinpointing cellular culprits so precisely gives drug developers an actual target for healthy longevity. Read more: sciencedaily.com/releases/20… #Biotech #Longevity

There is a remarkable difference between finding evidence that challenges your assumptions and finding evidence that conveniently reassures you that you are the exception. This is an interesting paper by Sniderman and colleagues, examining nearly 294,000 UK Biobank participants and finding that higher HDL cholesterol modifies the association between ApoB and cardiovascular events. The interaction is real, statistically significant, and worthy of further investigation. But the leap from an observational association to suggesting that an individual with an LDL of 574 mg/dL and ApoB above 350 might be immune to atherosclerosis is quite another matter. In fact, the authors specifically caution that the observed interaction should not be taken as firm clinical evidence that ApoB ceases to be atherogenic or doesn't require treatment when HDL is high. That's a rather important sentence to leave out when you're discussing immunity. A statistical model showing attenuation of risk at high HDL is not a clinical trial. Nor does it establish that raising HDL is protective, or that someone with extraordinarily elevated ApoB can safely ignore decades of exposure. We've spent years discovering that increasing HDL cholesterol pharmacologically doesn't reliably reduce cardiovascular events. HDL is an interesting biomarker, but biomarkers and causal mechanisms aren't interchangeable. And then there is the problem of extrapolation. The ordinary distribution of ApoB in UK Biobank is not populated by large numbers of otherwise healthy individuals walking around with an LDL approaching 600. A modeled relationship at the extremes of HDL doesn't validate a personal experiment at the extremes of ApoB. Which brings me to my friend Simon Hill, @theproof, who recently published something I found considerably more rigorous and intellectually open. Simon had coronary CT angiograms suggesting a remarkable 48% reduction in plaque volume over 16.5 months. He could have celebrated, announced that his diet had reversed atherosclerosis, and made an excellent marketing campaign out of it. Instead, he examined the scans using three different analysis platforms. One suggested substantial regression, another progression, and the third essentially no change. Rather than promoting the most flattering result, he openly discussed the uncertainty. That's what scientific curiosity looks like when the evidence doesn't cooperate with your expectations. Simon also has something that makes this discussion more than academic. His father had a myocardial infarction at 41 and his grandfather at 49. Simon is now 40. He has lived with the consequences of cardiovascular disease in his family, and it's understandable that he wants to reduce his risk as much as reasonably possible. He has even started a PCSK9 inhibitor despite having an ApoB around 70–80 without medication. We can debate whether targeting an ApoB below 40 with Repatha offers sufficient additional clinical benefit in someone with his particular risk profile. That's a legitimate discussion. But I applaud his desire to live longer and his willingness to question his own most favorable findings. I understand the emotional component of this better than most. My own coronary calcium score is 90. I take rosuvastatin and ezetimibe, achieved an LDL around 60, and have seen it fall further since starting tirzepatide. I have no particular desire to measure every cubic millimeter of plaque in my coronary arteries. I know there is atherosclerosis, I know what the evidence supports, and I am treating the risk factors I can change. Simon wants more information and more aggressive prevention. I am comfortable treating what I already know. Neither approach requires pretending that uncertainty has disappeared. We physicians spend our lives talking about hazard ratios, plaque volumes, confidence intervals, and relative risk reductions. Yet one disrupted coronary plaque with a superimposed thrombus can turn all those abstractions into a very final event. That's why I care more about preventing myocardial infarctions than winning a competition over whose scan looks better. The remarkable thing about the comparison is that both Simon and Norwitz have favorable personal findings. Simon asks whether his are reliable. Norwitz highlights an observational study that might explain why his own findings are reassuring. There is a lesson there about confirmation bias, and it applies to all of us, physicians included. The Sniderman paper deserves attention. It may teach us something important about HDL biology and cardiovascular risk. But it does not establish immunity from ApoB, and it certainly doesn't overturn the causal evidence supporting LDL lowering. Science progresses when we investigate the observations that don't fit our models, not when we promote the observations that make us feel invulnerable. After all, the goal isn't to prove that your arteries are special. It's to live long enough that they never become the reason you aren't.

JAMA today: Should prediction markets allow bets on clinical trial outcomes? jamanetwork.com/journals/jam…

📣 Request for Information: Strategies to Advance RAPIDs and Real-World Evidence for Serious Mental Illnesses and Related Brain Disorders NIH’s National Institute of Mental Health (NIMH) seeks input on strategies to build a coordinated evidence base that can guide the clinical practice and implementation of rapid-acting psychotropic interventional drugs (RAPIDs) for treating serious mental illnesses and related brain disorders. 📆 Comments are Due November 9, 2026 🔗 Learn more and submit a response: bit.ly/4sQ9oIN

Next week, our CMO and COO head to Chicago for @American_Heart's #AHA26 Scientific Sessions. We look forward to connecting with the #cardiovascular community & engaging in conversations about the importance of identifying CVD risk earlier to prevent disease & extend healthspan.

I believe we are going to solve aging like a problem. Longevity escape velocity asks us to imagine a future in which each medical advance gives us more time to reach the next. Imagine gaining 3 years of lifespan each year? That is a future worth building. We can pursue it by turning discoveries into treatments that preserve health, restore function and keep more possibilities open. I believe we will solve aging like a problem. Each healthy year gained gives us another chance to add more than 1-year, reaching longevity escape velocity like a rocket leaving Planet Death forever.

Dr. @annachodos.bsky.social, discusses longevity and factors that can support healthy aging in a new article for Your Local Epidemiologist, “Forget living to 150: What actually helps you age well.” Read more: yourlocalepidemiologist.subs…

🧠 New in #GeroScience | Open Access What molecular patterns do Alzheimer’s disease and dementia with Lewy bodies share? In “A pattern to rule them all: tracing a human brain map of molecular aspects shared by Alzheimer’s disease and dementia with Lewy bodies,” Riccardo Rocco Ferrari and colleagues explore shared molecular features of these two major neurodegenerative diseases. 🔬 Understanding these common molecular patterns may help advance our knowledge of disease mechanisms and identify new directions for research into neurodegeneration and brain aging. 📖 Read the open-access article: rdcu.be/ZDnpU3mdYYza #AlzheimersDisease #DementiaWithLewyBodies #Neurodegeneration #BrainHealth #AgingResearch #Geroscience

Cate Lockhart, PharmD, PhD, Chief Science Officer, AMCP & Executive Director, BBCIC and AMCP Research Institute (ARI) spoke with Pharmaceutical Commerce about how payers and health technology assessment bodies weigh real-world evidence (RWE). "In a survey conducted through the Academy of Managed Care Pharmacy's (AMCP) Research Institute, 80% of payers that were surveyed reported wanting to use real-world evidence (RWE) in their formulary and coverage decision-making, despite just 18% regularly using it in their processes. AMCP has since published payer-focused RWE standards, including a checklist manufacturers can use as a template when sharing RWE with payer decision-makers." Read more: pharmaceuticalcommerce.com/v… Learn more about AMCP Research Institute: amcp.org/research-Institute #RWE #healthcare #managedcarepharmacy #evidence #AMCPResearch #AMCPNexus

Th distinct features of colon cancer in the young at single-nucleus resolution, both unfavorable and potentially helpful for understanding why this is on the rise @NatureMedicine nature.com/articles/s41591-0…