How different KRAS mutations drive pancreatic cancer and point to new treatment targets
Official title: Defining the oncogenic potential and therapeutic dependencies of PDAC-associated KRAS variants
Funded at Weill Medical Coll of Cornell Univ · NIH-11237619 · Data updated 2026-11-12
This project studies how specific changes in the KRAS gene cause pancreatic ductal adenocarcinoma and aims to reveal weaknesses that could become new treatment targets for people with this cancer.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Weill Medical Coll of Cornell Univ NIH-funded |
| Lab location | 1 site (New York, United States) |
| Project start | November 25, 2024 |
| Project end | November 30, 2029 |
| Funding year | 2026 |
| Award (this year) | $636,046 |
| NIH project number | 5R01CA290616-02 |
| Project ID | NIH-11237619 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with pancreatic ductal adenocarcinoma whose tumors are known or suspected to carry KRAS mutations (especially G12D, G12V, or G12R) would be most relevant to this work.
✕Less likely to help
Patients without KRAS-mutant PDAC or with other non-PDAC pancreatic conditions are unlikely to gain direct benefit from this specific project.
What this research studies
This work compares common and less-common KRAS mutations (like G12D, G12V, and G12R) using advanced mouse models and lab-grown pancreatic organoids to see how tumors start and grow. The team will examine how other genetic changes, such as loss of p53, interact with each KRAS variant to promote aggressive cancer. By mapping the cellular behaviors and dependencies tied to each mutation, researchers hope to find molecular vulnerabilities that drugs could target. Findings are intended to guide more precise therapies for people whose tumors carry these specific KRAS changes.
Why it matters
Potential benefit: If successful, the research could identify mutation-specific targets that lead to new, more effective treatments tailored to different KRAS-mutant pancreatic cancers.
How similar studies have gone: Previous mouse and organoid studies established that KRASG12D drives PDAC, but exploring less-common variants like KRASG12R is newer and less-tested, making parts of this work novel.
Where this research is happening
-
Weill Medical Coll of Cornell Univ
New York, United States Active
Researchers
- Principal investigator: Chandwani, Rohit — Weill Medical Coll of Cornell Univ
- Study coordinator: Chandwani, Rohit
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About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.