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U.S. Cancer Research Just Made a Massive Breakthrough. Why Is Trump Cutting It? (w/ Zeke Emanuel)

Channel: The Bulwark Published: 2026-06-03 07:00
The Bulwark

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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Detailed summary

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. …

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Main takeaways

  1. Pancreatic cancer has long been considered one of oncology’s hardest problems because it is usually detected late and standard chemotherapy is weak.
  2. The breakthrough discussed is a RAS-targeting approach, led by daraxonrasib, that appears to materially extend survival in pre-treated patients.
  3. Emanuel is enthusiastic but careful: the data are early, the patient count is still limited, and the result should not be framed as a cure yet.
  4. The drug’s tolerability is notable; rash and diarrhea are mentioned, but severe toxicity appears less common than with conventional chemotherapy.
  5. Emanuel credits decades of federally funded basic science for making the discovery possible.
  6. He strongly warns that politicizing NIH grants would damage scientific quality and slow future breakthroughs.
  7. The transcript is as much a policy argument as a medical one: the research system matters as much as the drug result.

Market read by horizon

Short term

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.

  • The immediate catalyst is the positive pancreatic-cancer trial readout and the FDA’s willingness to let the drug move earlier in treatment.
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  • Near-term attention will focus on whether the drug can be used in newly diagnosed patients and whether the benefit holds up in larger samples.
  • Watch for further safety data, especially on rash and other tolerability issues, since the conversation repeatedly stresses caution.
Mid term

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.

  • Over the next several weeks to months, the key question is whether the apparent survival improvement persists as the drug is tested in frontline pancreatic cancer.
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  • Validation would come from larger cohorts showing consistent efficacy, manageable side effects, and a meaningful extension of life versus standard therapy.
  • If results hold, the narrative could shift from ‘promising salvage therapy’ to a potential new backbone of treatment for this disease.
Long term

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.

  • Structurally, the transcript argues that long-duration public funding is essential to turning once-‘undruggable’ biology into real therapies.
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  • If the RAS breakthrough generalizes, it would reinforce the idea that deep molecular biology can unlock cancers previously thought resistant to drug development.
  • The broader regime implication is that science policy is not a side issue: political interference in NIH funding could slow the next wave of breakthroughs.
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Key claims (8)

BEARISH healthcare innovation pancreatic cancer

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.

MIXED healthcare innovation RAS mutation

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.

BULLISH oncology drug development daraxonrasib

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.

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Assets discussed (6)

pancreatic cancer
BULLISH other

The discussion centers on a major treatment breakthrough that could materially improve outcomes in a deadly cancer.

RAS mutation
BULLISH other

Emanuel says the new therapy works by targeting the RAS mutation that drives the disease.

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Speakers

HOST Jonathan Cohn GUEST Zeke Emanuel

Interview (5 Q&A)

pancreatic cancer difficulty

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.

side effects

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.

survival data

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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Where this transcript pushes against consensus

  • The claim that the drug could meaningfully transform pancreatic-cancer treatment is still premature because the evidence base is early and limited.
  • Emanuel’s policy critique is forceful, but some of the comparison to Soviet-style research control is rhetorical rather than empirical.
  • The transcript implies strong causality between federal funding and the breakthrough, but the exact contribution of each funding source is not quantified.
  • The discussion of Ben Sasse’s experience is anecdotal and does not establish typical tolerability across broader patient populations.

Topics

pancreatic cancerRAS mutationdaraxonrasibrevolution medicineschemotherapy side effectsNIH fundingfederal researchscientific politicizationcancer drug developmentbasic science

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