Read&Learn @ReadLearn10

GLP-1 drugs in people with obesity (no diabetes) and the link to reduction of cancer Among nearly 230,000 individuals, there was >40% overall reduction in 13 cancers associated with obesity with just 2 years of follow-up. Not proof of cause and effect, but consistent with many recent reports on the link between GLP-1 drugs with less cancer annalsofoncology.org/article/S0923-…

#ASCO26 This one is special. This is the hottest paper of 2026 and potentially in the history of pancreatic cancer. Let’s dive in. RASolute 302: Daraxonrasib vs investigator’s choice chemotherapy in previously treated metastatic pancreatic cancer Abstract LBA5 (soon!) Presentation: May 31, 2026, 3:21-3:33 PM CDT For decades, pancreatic cancer has been where good ideas go to die. We have optimized chemotherapy. We have sequenced chemotherapy. We have celebrated modest gains. But the central driver of PDAC has always been sitting there in plain sight: RAS. More than 90% of pancreatic cancers have oncogenic RAS mutations, and until recently, we had essentially nothing direct to do about it. Daraxonrasib is an oral RAS(ON) multiselective inhibitor targeting the active GTP-bound state of mutant and wild-type RAS. And in RASolute 302, it delivered. Quick hits: 📌 Phase 3 international randomized trial 500 patients with previously treated mPDAC Daraxonrasib vs investigator’s choice chemotherapy 🧬 RAS G12 population 91.8% of patients had RAS G12 mutations 📈 OS in RAS G12 population 13.2 vs 6.6 months HR 0.40 P<0.001 📈 OS in overall population 13.2 vs 6.7 months HR 0.40 P<0.001 📊 PFS in RAS G12 population 7.3 vs 3.5 months HR 0.45 P<0.001 📊 PFS in overall population 7.2 vs 3.6 months HR 0.49 P<0.001 🔥 12-month OS Overall population: 53.2% vs 17.3% ⚠️ Toxicity matters, but this was not just more efficacy for more toxicity Grade ≥3 AEs: 61.8% vs 69.6% TRAEs leading to discontinuation: 1.2% vs 11.2% This is the kind of survival curve we almost never get to see in pancreatic cancer. This validates RAS(ON) inhibition in the most RAS-addicted major cancer. It takes a target we have talked about for decades and turns it into a clinically meaningful survival benefit in a randomized phase 3 trial. The next questions come fast: 1L combinations, maintenance, perioperative disease, sequencing, resistance, toxicity management, and whether this becomes a new backbone. RAS is here, and it couldn’t have come sooner. nejm.org/doi/full/10.10… @TheGutonclab @UGrewalMD @TimothyJBrownMD @OncoAlert @Onco_Nexus @ASCO @NazliDizman @LauraAlderMD @DVAraujoMD @DrBarbiOnc @LauraEsfeller @FunchainMD @YGaritaonaindia @DrSAHaddad @jgong15 @iandresmeraz @SakditadMD @RamilaShilpakar @RohitBanwar @lungoncdoc

Cheryl cheerleads the removal of a pair of Black Racers from Dr Oz's patio.

When scientists first tested GLP-1, it did nothing. The molecule behind Ozempic, Wegovy and Mounjaro looked completely useless—until a chemist guessed the body was cutting it down first. The real origin of GLP-1 🧵

Advanced therapies for Crohn’s disease can yield different results according primary location. Interestingly, JAK inhibitors may be better for colonic vs ileal disease. 📸: pmc.ncbi.nlm.nih.gov/articles/PMC12…

New England Journal of Medicine (NEJM) is a top medican journal with a an impact factor of 78.5 And a paper with an AI-generated image (notice the nonsensical ruler) was able to get past NEJM editors and peer reviewers. I've been saying this for the last three years that people forget to use their common sense when it comes to AI.

New @Nature study: >50% of lung cancer metastases are seeded by other metastases, not the primary tumor. This "seeding from seeding" reveals a complex evolutionary cascade that allows cancer to colonize the body. nature.com/articles/s4158…

Eye-opening to see how experts use AI - this is a masterclass on how to design a prompt 📌

🚨She thought she was just kissing in front of the camera, but within 10 seconds came the surprise…

Turning tic-tac-toe into an epic football trick shot battle

Richard Feynman's Lectures on Physics are timeless: their main strength is in demonstrating how to reason about physics. You may not know that all the lectures are completely online: Vol 1: feynmanlectures.caltech.edu/I_toc.html Vol 2: feynmanlectures.caltech.edu/II_toc.html Vol 3: feynmanlectures.caltech.edu/III_toc.html

Spring Break in Florida in the '80s

This guy 😅😂

Invented in 1905 by German physicist Heinrich Rubens, the Rubens Tube makes sound visible using fire

Available as a PDF on ResearchGate 🆓 🔗: researchgate.net/profile/Arumug…

A 5★ new review of the GLP-1 drugs, what they have achieved, and where the field is headed with so many new molecules and combinations @TheLancet thelancet.com/journals/lance…

The Paclitaxel + Carboplatin "CarboTaxol" doublet is the bread and butter of oncology for a reason. 🍞🧈 But why does this specific combo work so well? It’s all about the "Freeze and Snap" synergy. ❄️💥 1️⃣ The Freezer (Paclitaxel): Paclitaxel stabilizes microtubules, preventing depolymerization. It freezes the cell’s skeleton in the M-phase (Mitosis). The cell tries to divide but gets stuck. 🛑  2️⃣ The Snap (Carboplatin): While the cell is arrested and stressed, Carboplatin slides in. It acts as an alkylating agent, forming reactive platinum complexes that bind to DNA (cross-linking). 🧬🔗  🤝 The Synergy (Why 1+1 = 3): The magic lies in the timing. Paclitaxel arrests cells in the G2/M phase. Cells in this phase are less efficient at repairing the DNA damage caused by Carboplatin. The "Freeze" prevents the "Repair," leading to accumulation of DNA damage ➡️ Apoptosis (Cell Death). ☠️  💡 Clinical Pearl (The Sequence Matters): This is why we often administer Taxane before Platinum. Giving Paclitaxel first avoids the antagonistic effect where Carboplatin might inhibit the uptake or cytotoxicity of the taxane. It also reduces thrombocytopenia! 📉🩸 #Oncology #MedTwitter #OncTwitter @OncoAlert @myesmo @esmo_open @asco

Cost of giving birth in the US 🇺🇸🤯

Normal vs Abnormal Heartbeat

This is amazing!