Jonathan Cohn and Zeke Emanuel discuss a major pancreatic-cancer breakthrough centered on a new RAS-targeting drug, how it appears to double survival in heavily pre-treated patients, and why the result is being greeted cautiously but enthusiastically. The conversation also turns to the role of federally funded science in enabling the discovery and Emanuel’s warning that current Trump-era NIH policy risks politicizing and weakening the research pipeline.
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Jonathan Cohn frames the segment as a major medical breakthrough, saying the reaction to the pancreatic-cancer trial results has been unusually celebratory. He introduces Zeke Emanuel as an oncologist, former NIH official, University of Pennsylvania vice provost, and author, positioning him to explain both the science and the policy stakes. Emanuel starts with the basic problem: pancreatic cancer is one of the deadliest cancers, affecting roughly 70,000 Americans annually and killing more than 50,000. He emphasizes that it is usually found late, after it has spread, and that existing chemotherapy is often ineffective and brutal. He says this is why pancreatic cancer has long been viewed as unusually hard to treat. The scientific core of the breakthrough, according to Emanuel, is the RAS mutation. …
Tactically, the near-term setup is bullish for the specific pancreatic-cancer program but still headline-sensitive; the big risk is extrapolating a small, early dataset too far before more data land.
Over the next few months, the setup depends on whether frontline studies confirm the survival benefit and preserve tolerability. If they do, this moves from a salvage-therapy story to a broader oncology platform; if not, the current enthusiasm fades quickly.
The structural read is that basic, publicly funded science remains indispensable for turning hard biological problems into therapies. A more politicized grant process would likely reduce the pipeline of future breakthroughs rather than improve it.
Pancreatic cancer is one of the deadliest cancers, with about 70,000 cases and 50,000+ deaths in the U.S. annually.
Emanuel gives an incidence and mortality estimate to underline severity.
The RAS mutation is the key biological driver of pancreatic cancer and was long considered undruggable.
He explains why the disease was so difficult to treat historically.
The new therapy works by combining multiple approaches to deactivate RAS and stop tumor proliferation.
He describes the mechanism as multi-pronged rather than a single direct hit.
Why has pancreatic cancer been so difficult to attack, and what made it this 'impossible' target for research?
Pancreatic cancer is deadly because it's usually found after it has spread, with less than 15% of people surviving 5 years. The key challenge is the RAS mutation — a family of genes that tell cells to divide — which stays permanently 'on' in pancreatic cancer, constantly signaling cells to divide. For a long time researchers called this mutation 'undruggable' because they couldn't find a drug to get in there and turn it off.
What are the side effects of the new pancreatic cancer drug, and is it the same drug Ben Sass is taking?
The side effects include rashes and some diarrhea. Emanuel mentions Ben Sass's rash has looked pretty severe based on pictures he's seen, but notes that Sass has been doing TV and going around, not bedridden from chemotherapy. The drug is notable for having mostly grade 1 or 2 side effects rather than the severe grade 3 or 4 side effects typical of chemotherapy, because it accumulates in the cancer cells rather than affecting normal cells.
What does 'doubled survival' actually mean in practice for this pancreatic cancer drug?
The patients studied had already been pre-treated with standard chemotherapy — their cancer had grown through or recurred after treatment, which is a bad situation. Typically in those situations patients lived an average of 6 months. This drug doubled that to over 13.5 months, with latest reports suggesting patients are going out to 14-16 months. The FDA has authorized moving the drug up into newly diagnosed patients in combination with routine chemotherapy, which is where the real possibility of suppressing or curing the cancer could come.
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