Pancreatic cancer is on track to become the second-leading cause of cancer-related deaths by 2030. Often diagnosed too late for effective treatment, it represents a critical challenge in oncology. But what if we could stop it before it starts?
A breakthrough study led by Professor David Tuveson and Research Investigator Claudia Tonelli at Cold Spring Harbor Laboratory offers exactly that possibility. The researchers discovered that inhibiting the cancer-associated gene FGFR2 significantly slows tumor formation driven by mutant KRAS—which is present in over 95% of pancreatic cancer cases. Even more promising, dual inhibition of FGFR2 and EGFR prevented precancerous cells from turning into full-blown cancer.
“We all have early versions of cancer in many tissues. The goal is to treat them before they become dangerous,” explains Tuveson.
Using genetically engineered mouse models and human-derived organoids, the team demonstrated that blocking FGFR2 curbs KRAS-driven tumor growth. When combined with an EGFR inhibitor, the approach actually reduced the formation of early lesions.
This discovery opens the door to clinical trials using existing FGFR2 and EGFR inhibitors—many of which are already FDA-approved for other cancers—as preventive therapy for high-risk patients, such as those with a family history of pancreatic cancer.
While pancreatic cancer remains a race against time, this research offers a glimpse of a future where interception, not just treatment, becomes a reality.