Science does not often advance in sudden epiphanies that yield "Eureka" moments. More typical are years of failed experiments, dogged hypothesis-testing, and incremental discoveries that are, at best, inconclusive. And then, sometimes, eventually, the accumulated knowledge results in a breakthrough. Two recent examples are stunning advances in cancer medicine—one for pancreatic cancer, the other for melanoma—that are rewriting what doctors can promise their patients. But to understand why these achievements matter so profoundly, it is instructive to appreciate how long they took.
A Pill That Doubled Survival for the Disease That Kills Almost Everyone
Pancreatic cancer is the third-leading cause of cancer deaths in the United States, claiming nearly 53,000 lives every year. It is typically diagnosed late, treated poorly, and survived by almost no one. When doctors tell a Stage 4 pancreatic cancer patient their prognosis, they are often speaking in terms of weeks and months, not years. For decades, this grim arithmetic barely changed—not because researchers weren't trying, but because the cancer seemed almost engineered to resist them.
The biological culprit was known. A gene called KRAS, first identified in 1982, is mutated in roughly ninety percent of pancreatic-cancer cases. When it is functioning normally, the KRAS gene produces a protein that controls cell growth, turning it on when needed and off when not. When mutated, that protein gets stuck in the "on" position, driving relentless, unchecked cell proliferation. Researchers understood this as early as the 1980s. They simply could not do anything about it.
The reason was structural. KRAS, unlike many cancer targets, presents almost no surface for a drug to grab on to. Its protein is nearly smooth—"like a golf ball with very shallow ridges," as one researcher described it. The molecule's fierce affinity for GTP, the cellular fuel it binds, meant that early drug candidates were simply out-competed. Despite extensive academic and industry efforts spanning four decades, KRAS resisted every therapeutic approach, earning the grim designation that haunts oncologists: "undruggable."
The turnaround began slowly—almost invisibly—in laboratories most patients will never hear of. In 2012, two independent research groups conducting fragment-based screening found hints that KRAS was not entirely impenetrable. A small pocket had been identified near one of KRAS's structural features, the so-called Switch II region. It was a crack in the armour. For drug developers, it was huge.
Over the following decade, chemists and biologists laboured to widen that crack into something a drug could exploit. One pioneering platform, built on complex chemistry and pursued through years of largely unglamorous bench science, eventually gave rise to a molecule at Revolution Medicines designated RMC-6236. It is now known by its clinical name, daraxonrasib.
The clinical-trial results, when they came, were startling enough to draw a standing ovation at a cancer conference from an audience of normally reserved cancer researchers. At the 2026 American Society of Clinical Oncology annual meeting in Chicago on 31 May, Dr. Brian Wolpin presented the results of an international phase 3 clinical trial involving 500 patients with metastatic pancreatic cancer who had already undergone chemotherapy. Those who received daraxonrasib lived a median of 13.2 months, compared to just 6.7 months for those receiving standard chemotherapy. Progression-free survival also doubled, from 3.6 months to 7.2 months.
"In the patient population that was being evaluated, six months is huge. It is a definite win," said Matthew Katz, a surgical oncologist at MD Anderson Cancer Center. "The possibility is unlike, really, anything we've seen in pancreatic cancer in many years," added Chris Chen of Stanford University School of Medicine.
What makes daraxonrasib particularly remarkable is its breadth of application. KRAS mutations come in multiple variants—G12D, G12V, G12R, Q61X, and others—and daraxonrasib appears to act against nearly all of them. This is enormously important. Rather than helping only patients who carry the "right" mutation, the drug may be applicable to the overwhelming majority of pancreatic cancer cases. The US Food and Drug Administration, recognising this potential, granted Breakthrough Therapy designation in June 2025 and has been actively accelerating its review.
The drug is not a cure. But for a disease that reduces hope to days and weeks, giving patients an average of six additional months—months they might spend hiking, attending a grandchild's graduation, or simply experiencing normalcy—is a profound human achievement. And it is an achievement that was purchased over four decades with the currency of publicly funded basic science that often seemed to be disconnected from any clinical success.
The Immune Cells That Were Always There
If the pancreatic cancer story is about engineering a drug to do something the body cannot, the melanoma story is the inverse: harnessing something the body already knows how to do.
Melanoma, an aggressive cancer arising from the pigment cells of the skin, has long been one of oncology's most sobering diagnoses when discovered late. Almost two-thirds of patients with metastatic melanoma were destined to die within five years. Even as immunotherapy drugs like pembrolizumab (Keytruda) and nivolumab (Opdivo) transformed earlier-stage melanoma treatment, patients whose cancer progressed through those treatments faced extremely limited options.
On 16 February 2024, the FDA granted accelerated approval to lifileucel (brand name Amtagvi). It is manufactured from a patient's own tumour: surgeons extract a piece of the melanoma, isolate the immune cells—called tumour-infiltrating lymphocytes, or TILs—that have migrated into it, expand those cells into the billions in a laboratory, and infuse them back into the patient. The idea is that these particular immune cells are already "trained" to recognise and kill the cancer. The lab process simply gives them the numbers to win the fight.
Lifileucel is the first cellular therapy to be approved for any solid tumour—a milestone whose importance cannot be overstated. In the Phase 2 clinical trial that formed the basis for approval, among 73 patients who received the approved dose, nearly a third saw meaningful reductions in tumour size, including complete responses in several participants. Among those who responded, roughly forty percent remained free of cancer progression a year after treatment.
The approval was the culmination of more than thirty years of research, largely driven by Dr. Steven Rosenberg, chief of the surgery branch at the National Cancer Institute—who received the 2024 American Society of Clinical Oncology Award for Lifetime Achievement in Cancer Research for his contributions. Rosenberg began exploring the idea that immune cells could be extracted, amplified, and used to fight solid tumours in the late 1980s, at a time when most of his peers regarded such an ambition with deep scepticism.
The foundational work required establishing not just that TILs existed inside tumours, but that they could be reliably cultivated outside the body, that they retained their tumour-recognition capabilities after expansion, and that a patient's immune system could be appropriately primed to receive them. None of these questions had obvious answers, and resolving each one took years of painstaking laboratory and early clinical work.
Early commercial data in 2026 from Iovance Biotherapeutics showed response rates in real-world patients even higher than those seen in the clinical trial—evidence that the therapy, now deployed across diverse populations, is delivering on its promise. Meanwhile, researchers are not resting. A next-generation oncolytic virus—a genetically engineered herpes simplex virus—has shown the ability to shrink not only injected tumours in advanced melanoma but, remarkably, uninjected tumours as well, suggesting the virus can convert a patient's immune system into a kind of self-propagating weapon against cancer. Its Biologics License Application is currently under review by the FDA.
What Basic Research Actually Means
There is a political economy of science that rarely makes the news. Grant committees want "translational" research—work with immediate clinical relevance. Drug companies usually invest in molecules within striking distance of approval. Government agencies are pressured to fund science that solves problems now. This pressure is understandable, and even rational, in isolation. But it is also, over long horizons, self-defeating.
The road to daraxonrasib ran through four decades of structural biology, medicinal chemistry, and molecular pharmacology, much of which had no clear, near-term commercial application. This was the kind of research I did as an undergraduate, graduate student, and NIH Research Fellow. The road to lifileucel ran through thirty-plus years of immunology, cell biology, and clinical trial failures that would have discouraged any investor. As one detailed account of daraxonrasib's origins concludes, "this was not a single breakthrough moment. It was a progression across the full research ecosystem, each building on the last."
In a recent newspaper article, MIT President Dr. Sally Kornbluth offered a personal reminiscence that will be familiar to many laboratory scientists:
Most successful scientists are optimists. They have to be, since the vast majority of experiments fail. In graduate school, I remember sitting in the lab at Rockefeller University in New York at 3 a.m., surrounded by stacks of culture dishes for growing cancer cells, none quite showing me what I hoped to find. But glimmers of interesting changes in the cells promised future success and made me feel the experiments wanted to work. That optimism drove me to keep trying. One day, they did work and I uncovered a new insight about a process in those cancer cells that no one had described before.
This is the paradox that cancer researchers understand viscerally but that policymakers and the public often struggle to internalise: The most commercially valuable discoveries in medicine often emerge from research that was not designed to be commercially valuable. The curiosity-driven, hypothesis-led, "what-if" investigations at the bottom of funding priority lists are precisely the work that makes the dramatic breakthroughs possible.
The patients who are now, in 2026, watching their pancreatic tumours shrink by 76 percent—who are, against all odds, hiking mountains and attending family events, and speaking to journalists about "miracle drugs"—are the downstream beneficiaries of decades of upstream science that is invisible to them. They are living proof that basic research is not a luxury. It is the architecture upon which cures are eventually built.
What Comes Next?
Neither daraxonrasib nor lifileucel is yet a complete victory. Daraxonrasib is not yet approved; it is available through expanded access in the US and it is undergoing larger trials. Lifileucel carries significant logistical and tolerability challenges and its label contains prominent FDA warnings regarding treatment-related risks. The treatments are expensive, access is limited, and the oncology community is urgently working to identify which patients benefit most.
But the directions of these breakthroughs are unmistakable. Researchers are now combining daraxonrasib with narrower KRAS inhibitors that target specific mutations, hoping the combination will foreclose the cancer's escape routes. They are also exploring KRAS "degraders"—related compounds that don't just block the mutant protein but instruct the body to discard it entirely. For TIL therapy, researchers are extending the approach to other solid tumours, asking whether the logic that worked in melanoma might generalise.
These next steps will likely take years. They will require more basic science, more failed experiments, more rejected hypotheses, and more grant applications. They will require, in other words, more patience than any patient can afford and more faith than any investor likes to offer. They will require, once again, the long game—the one that basic research plays, and that these two breakthroughs have just demonstrated, again, is a game worth playing.
But US science policy is moving away from keeping US scientists in the game. Last month, Steve Usdin, the Washington editor of Biocentury, described the impacts of a new rule from the Office of Management and Budget on federal research grants that "would require senior political appointees to review and approve every discretionary federal grant before it is awarded, explicitly barring them from deferring to peer reviewers, and would mandate that all grant programs align with the president's policy priorities, rather than scientific need or expert consensus." He continued:
It seeks to introduce ideological tests on applicants and institutions that receive grants, bar most international scientific collaboration, and allow political appointees to cancel grants at any time without providing an explanation. The proposal also would allow agencies to make grants that haven't been publicly announced, opening the process to corruption and favoritism.
If implemented, the proposal would represent the most serious assault on U.S. science since World War II. Even those who agree with the Trump administration's views on social and political issues should be alarmed. Future administrations with very different views may not abandon the temptation to wield control over scientific funding to advance ideological agendas.
MIT President Kornbluth deserves the last word on the lasting impacts of the new policies:
Without basic scientific research, supported by the kind of farsighted public investment that allows large-scale, undirected, curiosity-driven inquiry, the scientific pipeline will run dry.
In daily life, people may not feel the effects right away, or even in ten years. But we will feel it. And when someone we love needs therapies that could have emerged but didn't, or when other countries now investing in science can launch new science-based industries or run their societies on vast resources of fusion energy or reap the benefits of quantum computing power or advanced medical breakthroughs, America will wish it [had] sustained its leadership in scientific research here and now.
Henry I. Miller, a physician and molecular biologist, is the Glenn Swogger Distinguished Scholar at the Science Literacy Project. He was the founding director of the FDA's Office of Biotechnology.