Can Pancreatic Cancer Be Stopped in Its Tracks? A Radical Tactic Raises Hopes

Posted on 4 October, 2026 by Mehrdad Fathi

With prospects for new treatments at an all-time high, researchers are looking for ways to boost survival by treating the disease early.

Armed with new tools and fresh optimism, researchers seeking to subdue pancreatic cancer — one of the world’s deadliest — are chasing a radical strategy: cancer interception.

In this approach, tissues that are growing abnormally are treated to keep them from turning cancerous and spreading. Interception is already being trialled for breast and skin cancers, among others. But now the success of a new drug that quashes pancreatic tumours is raising scientists’ hopes that interception could succeed even for this recalcitrant cancer.

Cancer interception was one of the main themes at September’s American Association for Cancer Research Conference (AACR) on Pancreatic Cancer in San Diego, California — the first such meeting since the US Food and Drug Administration approved the landmark pancreatic-cancer drug daraxonrasib (Rasonque) in August. Its success has renewed optimism that researchers can combine it or other emerging therapies with early-detection methods to revolutionize how pancreatic tumours are treated.

A combination of early-detection techniques and interception is “going to be the breakthrough strategy that really changes survival,” says Diane Simeone, director of the Moores Cancer Center at University of California San Diego Health. At the AACR meeting, Simeone argued that such an approach could more than triple the proportion of people who survive for five years after being diagnosed with pancreatic cancer — from 13.7% to 50%.

It’s a lofty aspiration, but other researchers are also eyeing interception. “We’re so excited that we are at this juncture now to even be considering this,” says Anirban Maitra, director of the Perlmutter Cancer Center at New York University Langone Health. “This wasn’t possible even a few years ago.”

Precautionary Principle

Pancreatic tumours are notoriously wily: they are often highly invasive, impervious to most treatments, and can wrap themselves around major arteries and veins, making the growths difficult to remove.

Even so, five-year survival rates can top 80% when such tumours are caught early, Simeone says. But the symptoms of pancreatic cancer are vague, and people often do not seek medical attention right away. More than half of pancreatic cancers are not diagnosed until after the disease has spread to other organs — a statistic that has remained mostly unchanged since Simeone first opened her cancer research laboratory 30 years ago.

To improve early detection, she and her colleagues have launched a clinical study called PRECEDE, which aims to enrol 20,000 people who have a family history of pancreatic cancer, certain abnormal growths on their pancreas, or a genetic profile that elevates their risk of the disease. The goal is to see whether — and by how much — frequent monitoring for pancreatic cancer will improve survival. So far, the team has enrolled a little more than 12,000 people, Simeone said at the conference. More than 50 participants have been diagnosed with pancreatic cancer — many of them at the earliest stages of the disease.

The PRECEDE team plans to use samples from the study to evaluate experimental blood tests for early cancer detection, and to explore artificial-intelligence methods to detect abnormalities on the participants’ scans before they become visible to the naked eye.

In addition, Simeone says the PRECEDE consortium might test whether therapies such as daraxonrasib can boost survival rates when given immediately after surgery to remove pre-cancerous growths or early-stage tumours. Currently, daraxonrasib is only approved for advanced cancers.

Testing Tolerance

Researchers at the AACR meeting heard about studies in mice that suggest the approach could work. Ben Stanger, a cancer researcher at the University of Pennsylvania in Philadelphia, and his team studied mice bearing mutations in a gene called Kras; these mutations produce proteins that can cause cancer. When the mice developed tiny, precancerous pancreatic growths, the researchers administered a drug that, like daraxonrasib, disarms KRAS and related cancer-promoting proteins. The treatment improved the animals’ survival. “It is super exciting,” Stanger says, but adds that it could take years to determine how best to deploy the technique in people.

One key first step is determining whether people will be willing to take powerful cancer drugs when they are otherwise healthy, says Maitra, who is also planning a clinical trial of a drug that inhibits KRAS proteins for pancreatic cancer interception.

Daraxonrasib is known to cause severe rashes as well as other adverse reactions. “It’s not like popping an aspirin or a vitamin,” says Maitra. Researchers might first need to work out whether small doses of the drug would be effective, he says, or wait for second-generation drugs with fewer side effects to be developed.

Cancer Vaccine

Others are exploring new approaches for interception. Earlier this year, researchers reported that in 90% of participants in a clinical trial, a cancer vaccine — a therapy that trains the immune system to destroy cancer cells — induced production of immune cells that target mutated KRAS proteins that promote pancreatic cancer. It is too soon to know whether the vaccine can prevent cancer, but the hope is that it could be given to people at high risk of the disease, including those who have had pre-cancerous growths removed.

At the AACR meeting, Sahar Nissim, a gastroenterologist and cancer researcher at the Dana-Farber Cancer Institute in Boston, Massachusetts, described his work with pancreatic acinar cells, which secrete digestive enzymes. When acinar cells acquire certain mutations in the KRAS gene, it can set them on a path toward becoming cancerous. Along the way, they begin to lose their normal cellular identity.

Nissim and his colleagues have developed drugs that force the cells to retain their acinar identity, and are testing whether this can prevent tumours in mice with Kras gene mutations.

Nissim compares this kind of interception with giving cholesterol medicine to people who are at high risk of cardiovascular disease. “We don’t wait for them to have a heart attack,” he says. “But we haven’t really had that same paradigm in cancer.”

Source: Nature (2026). doi: https://doi.org/10.1038/d41586-026-03119-7

References:

1. Wadlow, R. et al. Cancer Res. 86, PR002 (2026).

2. Than, M. T. et al. Science 391, 1161–1166 (2026).

3. Haldar, S. D. et al. Cancer Discov. https://doi.org/10.1158/2159-8290.CD-25-2245 (2026).