The Cancer Research Machine Trump Is Gutting Just Delivered a Big Breakthrough
There’s new hope for one of the deadliest cancers. But Trump’s war on research puts future discoveries at risk.
IT IS NOT EASY TO OVERWHELM CANCER SCIENTISTS, a world-weary bunch who are constantly dealing with setbacks in their experiments—and, all too frequently, deaths among their patients. But it happened on Sunday morning, inside a darkened Chicago convention hall, when Harvard-based researcher Brian Wolpin announced the results of clinical trials for a drug called daraxonrasib.
Wolpin spoke in a monotone, addressing fellow oncologists from around the world. Above him and around the room, on a set of projection screens, a seemingly simple line graph revealed something extraordinary: Daraxonrasib had nearly doubled survival time for pancreatic cancer patients who’d already been through a preliminary round of chemotherapy.
As Wolpin read off the numbers, a few members of the audience clapped, then a few more, and then they started standing until eventually most of the room was on its feet. “It was sustained,” Adam Feuerstein, the veteran biotech correspondent from STAT, tweeted about the reaction. “I’ve never seen anything like it in the middle of a talk.”
The news made headlines across the country, and it’s easy to see why. Pancreatic cancer took more than 50,000 American lives last year, according to estimates, making it the nation’s third-deadliest cancer. Until now, it has stubbornly resisted the kinds of treatment advances that have allowed patients with several other cancers to live a lot longer, and in some cases “beat” their cancers altogether.
That’s still a long way off for pancreatic cancer, because this new drug is not a cure. That near-doubling of survival time means that the patients already past the first phase of treatment survived for another 13.2 months on average when they got daraxonrasib, as opposed to 6.7 months if they went on the secondary chemo drugs typically administered at that point. And those who do benefit from the new drug will have to live with side effects, including intense rashes and serious gastrointestinal problems—a subject that former Nebraska Senator Ben Sasse, who is now on daraxonrasib, has discussed frequently during interviews about his battle with the disease.
But overall the side effects are less severe than they are for the existing alternative of more chemotherapy. It is among the reasons Sasse has called daraxonrasib a “miracle drug.” More importantly, the findings by Wolpin and other scientists show it’s possible to treat a cancer once considered “undruggable.” Researchers in the future may be able to stretch pancreatic cancer survival rates even more—by, among other things, deploying daraxonrasib as an initial treatment rather than a follow-up to chemo.
“That’s where, if this really has the possibility of either totally suppressing or—you know, God willing—even curing this, that would be a huge, huge breakthrough,” Ezekiel Emanuel, the oncologist who is now vice provost for global initiatives at the University of Pennsylvania, told me in an interview.
The “if” from Emanuel’s interview—which you can watch above—is an important caveat. Plenty of similarly promising cancer breakthroughs have, with further study and development, proved disappointing.
But plenty have panned out, too. In fact, one of the more oddly underappreciated stories of modern history is the steady, very real progress against cancer: The five-year survival rate for all cancers combined reached 70 percent for the first time last year, up from about 50 percent in the 1970s, according to the American Cancer Society.
Behind these advances are decades of scientific research, which brings us to a bittersweet asterisk to the pancreatic cancer announcement: The news comes right as the foundation for that progress—consistent research funding from the federal government—is being undermined by the Trump administration.
IN THE LAST SIXTEEN MONTHS, Trump and his lieutenants have repeatedly ordered agencies to hold back promised funding for scientific research, alter the grantmaking process behind that research, and at times freeze out whole research institutions. Many of those institutions, like Harvard, are among the most widely respected, most productive universities in the world, accounting for a wildly disproportionate share of global medical innovation.
And there may be more trouble coming.
The administration last month formally proposed to change the way the government scrutinizes funding applications. Under the new system, a grant that had passed through the scientific peer-review process that agencies have long used would then have to get approval from political appointees, who would ensure funding decisions “align” with administration priorities. Critics fear that could mean anything from nixing studies that focus on gender or racial differentials (as Elon Musk’s DOGE did to many government grants that they claimed sounded like DEI) to favoring studies carried out in red states or those likely to boost drug-development efforts from biotech companies friendly to Trump.
It’s impossible to be definitive about what impact this broad attack on research is having or will have. Scientific discovery is a process that plays out over many years and sometimes decades, and the damage is likely to show up as an absence of innovation. That’s awfully hard to measure.
But it’s possible to get some sense of what’s at stake by looking at recent breakthroughs, to see what role federal funding played in making them possible. Daraxonrasib turns out to be a pretty good case study.
BRIAN WOLPIN KNOWS as well as anybody how helpless clinicians have felt when trying to treat pancreatic cancer. He remembers seeing cases in the mid-2000s, when he was fresh out of his oncology residency and in his first years at the Dana-Farber Cancer Institute, one of the world-class academic hospitals clustered down the street from Fenway Park in Boston.
“I think I saw several patients that first year of fellowship who had pancreatic cancer, and they all died in like three months,” Wolpin told me in an interview via Zoom. “I just couldn’t believe it. You come to Boston, Harvard, Dana-Farber—it’s like a mecca of medicine. It’s not supposed to happen here, right? You’re supposed to have figured this out.”
But scientists weren’t anywhere close. The five-year survival rate for pancreatic cancer back then was around 7 percent, by far the lowest among more common cancers. A big reason for that is pancreatic cancer is typically a stealth killer, growing inside the organ and then spreading before it finally causes symptoms that trigger testing and diagnosis. It was only in relatively rare cases—such as when physicians diagnosed the cancer early, sometimes by accident— that traditional treatments including chemotherapy offered hope of long-term survival.
But chemotherapy is not the only way doctors can treat tumors. One of the big advances of the past quarter-century has been the development of what’s known as targeted therapies. These treatments seek out the mutations that cause cancerous cells, typically binding with them in ways that interfere with or simply halt the process that causes these cells to grow uncontrollably. Targeted therapies have dramatically improved both symptoms and survival for some people with breast, lung, and blood cancers.
An essential element in any targeted therapy is knowing the right target to hit. And scientists knew about a likely pancreatic cancer target long before Wolpin started his research.
Back in the 1980s, scientists discovered a mutation in something called the KRAS gene that accounts for the vast majority of pancreatic cancer cases. The gene has what is basically an on/off switch for cell growth. Sometimes, a mistake in the code has a “catastrophic” effect, as science writer Ruxandra Teslo explained recently in the “Works in Progress” Substack: The mutation locks KRAS “permanently in the ‘on’ position. Cells receive a continuous, unrelenting instruction to proliferate.”
But the KRAS mutation turned out to have a “slippery” surface: Scientists couldn’t find the biochemical crevices or protrusions that in other kinds of cancers allow targeted therapies to bind. “To get the drug to stick, there has to be some divot for it to stick into, and this was just a fully round ball and everything bounced off of it,” Wolpin said.
Soon private capital that had poured into the field dried up, as the whole enterprise acquired an air of futility—not just for investors, but for potential investigators as well.
“Most people told me not to do pancreatic cancer, because it was too hard—and if that was your career, you had a high likelihood of failure,” Wolpin said. In a particularly cruel twist, the cancer’s speedy lethality made it tough to learn from human subjects. They weren’t living long enough to generate research findings.
“We didn’t know that much, honestly, and there weren’t that many people working on it,” Wolpin said.
TWO SETS OF DISCOVERIES over the last two decades changed that. One was the development of mouse models, by researchers at MIT and Dana-Farber, that allowed scientists to study the tumors more thoroughly. Another was the discovery of one small pocket on the KRAS surface, from researchers at Vanderbilt and the University of California-San Francisco—and in particular, UCSF professor Kevan Shokat—that proved it was possible to bind chemicals to KRAS after all.
“He found things that would stick to it,” Wolpin said of Shokat. “Even though the class of drugs that came out of that initially were not very relevant to pancreatic cancer per se, the concept that you could do that was definitely a turning point.”
One of the scientists who took notice was Nobel Prize-winning physician and researcher Harold Varmus, then head of the National Cancer Institute, who saw the possibility of a breakthrough but realized that private investors spooked by past failures wouldn’t invest. He launched something called the RAS initiative, a research project based out of the Frederick National Laboratory that funded studies all across the world.1
“The RAS initiative helped push people to think, ‘We’ve got to go back, we’ve got to do this, we can’t just throw up our hands,’” Wolpin said. And it was in the flurry of research that followed that he and counterparts at other institutions—like Eileen O’Reilly at Memorial Sloan Kettering, and Zev Wainberg at UCLA—conducted new studies, eventually partnering with Revolution Medicines, the biotech company that developed and is now producing daraxonrasib.2
Money for the RAS Initiative came out of the budget of the National Cancer Institute, which is a federal agency. The Frederick National Laboratory is a federal facility. The labs at Dana-Farber, MIT, Memorial Sloan Kettering, UCLA, Vanderbilt—all benefited from sustained, generous federal funding, as did labs at countless other institutions that have been contributing research ever since the initial identification of KRAS back in the 1980s.
“All of the biology that was understood about RAS, that RAS is important, that RAS causes cancer when it’s mutated, how RAS works, the fact that RAS is present in so many pancreatic cancers—all that comes from the academic research that went before it,” Wolpin said. “Much of that is federally funded.”
It would be a serious mistake to say that federal funding was singularly responsible for the development of daraxonrasib. Revolution Medicines did the essential work that pharmaceutical companies always do—namely, taking the insights from scientific research and turning them into safe, effective drugs. That required (among other things) running extensive and expensive trials, a point made to me not just by Wolpin but also by Catharine Young, a senior fellow at the Harvard School of Public Health.
“They did it with private capital, and they deserve that credit,” Young, who served as assistant director for policy for the Biden administration’s Cancer Moonshot project, told me in an interview.
“But,” she added, “we simply wouldn’t be here today if not for that very defined and impactful federal funding. It was critical, absolutely critical.”
THE TRUMP ADMINISTRATION’S ATTEMPTS to cut or interfere with that kind of federal funding have not been entirely successful.
They’ve run into opposition from Congress, where support for research remains bipartisan and where appropriators refused to approve the kind of big cuts Trump proposed in his budget last year. They’ve also run into opposition from the courts, which have ruled that some of the actions the administration has taken to limit or cut off funding violates the laws chartering agencies like the National Institutes of Health, of which the National Cancer Institute is part.
But other Trump administration actions that reduced funding have survived legal scrutiny. And now the administration is pushing this new proposal that would leave funding decisions in the hands of political appointees who quite possibly have no scientific backgrounds. That’s alarming even to scientists like Emanuel who have called for reforming federal grant-making, in order to (for example) shift money over to younger researchers who may think up newer approaches to old questions.
“Politicization of science and research is not the reform [of government funding mechanisms] needed,” Emanuel said.
And while it’s always possible policies will change, because the administration proposing those policies has a change of heart or—eventually—another administration takes over, real damage has already been done.
“I think we are going to start missing key pieces of research, because of the withdrawal of support for scientific research and the ecosystem,” Young said. “That will be invisible to us for many, many years, but it will be the patients ultimately that are affected by it, because they are the ones that will not have these—in some cases—amazing breakthroughs twenty or thirty years from now.”
Wolpin told me patients are also the ones on his mind. And while he declined to comment on the ongoing political debate specifically, he mentioned to me that at the end of his plenary session—the one where he spoke in a monotone in front of those basic, but amazing, lines on a graph—the moderator asked him to make a closing statement.
“I hadn’t expected that, so I just said I felt like this was all a call to science,” Wolpin told me. “This shows you that [the breakthrough on pancreatic cancer] didn’t come out of the blue. It’s decades of investment that got us here. Decades of investment in science.”
Just to clarify, “RAS” refers to a class of genes related to cell growth. “KRAS” refers to one particular type, though it’s an important one because mutations in it are frequently linked to cancer. People frequently use the two interchangeably in conversation.
A smaller company called Warp Drive Bio, started by a Harvard scientist named Greg Verdine, did much of the initial work. Revolution then acquired it. This is frequently how drug development works nowadays.
Trump works for people with lots of money who don't want to share the money they reaped from others' efforts. They try to frame disease as the result of "sinful living" and "co-morbidities" as if that somehow justifies unnecessary death. Of course, they will be the first in line for these treatments when their time comes. Their time will come.
Outstanding science writing Jonathan. I follow you closely. This moment is critical. Thank you.