Show notes
We're dropping this bonus episode because something genuinely historic happened in oncology and we couldn't wait until our regular schedule to talk about it. Dr. Mark Lewis, GI medical oncologist, pancreatic cancer survivor, and one of our absolute favorite guests. He just got back from ASCO, the Super Bowl of oncology, where a new drug called daraxonrasib received one of only about six standing ovations in the conference's history, including applause that broke out mid-sentence when researchers showed the survival data on-screen. The drug targets a mutation that drives the vast majority of pancreatic cancer and has been considered "undruggable" for decades and it works not by attacking the mutation directly, but by cutting off the downstream signals it sends, like snipping the wire instead of fighting with the switch.
The results are remarkable. In patients who had already received standard chemotherapy, daraxonrasib roughly doubled survival time and delivered it in pill form rather than an IV every two weeks, a meaningful quality-of-life difference for people who are already facing the hardest year of their lives. Mark walks us through the science, the side effects (rash, because RAS proteins live in skin too), the path to FDA approval, and what this means beyond pancreatic cancer, the same KRAS mutations show up in about 30% of lung cancers and 40% of colon cancers.
Takeaways:
Pancreatic cancer has been devastatingly hard to treat, 85% of patients are incurable at diagnosis because it spreads silently and there's no good screening, leaving most patients with a median survival of about a year on IV chemotherapy.
KRAS, the mutation driving nearly all pancreatic cancer, was long considered "undruggable", the protein was so smooth and spherical that no drug could bind to it, and researchers were actively discouraged from pursuing it as a target.
Daraxonrasib works by cutting the power rather than fighting the switch, instead of binding to the KRAS protein itself, it uses molecular glue to interrupt the downstream growth signals the mutation sends, an approach that took decades to develop and wasn't taken seriously until now.
The trial results roughly doubled survival and the treatment is a daily pill, not an IV, patients who had already been treated with chemotherapy gained approximately an additional year of life with improved quality of life, which represents one of the most significant advances in pancreatic cancer treatment in decades.
This breakthrough has implications far beyond the pancreas, KRAS mutations drive about 30% of lung cancers and 40% of colon cancers too, and proving the target is druggable opens the door to a new generation of treatments across multiple cancer types.
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