Turning inflammatory scar cells in the pancreas into helpers to improve treatment response
Official title: Reprogramming inflammatory fibroblasts to overcome therapeutic resistance in pancreatic adenocarcinoma
Funded at Stanford University · NIH-11338560 · Data updated 2026-11-12
This project will try to change inflammatory, scar-forming cells around pancreatic tumors so treatments and the immune system can work better for people with pancreatic ductal adenocarcinoma.
Quick facts
| Grant type | R37 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Stanford University NIH-funded |
| Lab location | 1 site (Stanford, United States) |
| Project start | May 5, 2026 |
| Project end | April 30, 2031 |
| Funding year | 2026 |
| Award (this year) | $357,370 |
| NIH project number | 1R37CA311069-01 |
| Project ID | NIH-11338560 on NIH RePORTER |
Who could benefit from this research
✓Could help
Adults with pancreatic ductal adenocarcinoma—especially those with dense tumor fibrosis or signs of inflammatory CAF activity—who can receive care or participate in research at specialized academic centers.
✕Less likely to help
People with other cancer types, tumors lacking inflammatory fibroblasts, or those unable to access specialized centers are unlikely to benefit directly from this project.
What this research studies
Researchers are focusing on cancer-associated fibroblasts (CAFs), the scar-forming cells that create dense fibrosis around pancreatic tumors and block treatments and immune attacks. Using patient-derived cells and single-cell analysis, they will study how signals like interleukin-1 and the MyD88 pathway drive inflammatory CAFs and make them suppress T cells. The team plans to reprogram or block the harmful signaling in these CAFs in laboratory models to restore T cell function and improve response to therapy. Work is laboratory-based at Stanford using primary human cell models and molecular tools with the goal of informing future clinical approaches.
Why it matters
Potential benefit: If successful, this could make existing therapies and a patient’s own immune system more effective against pancreatic cancer, potentially improving response rates and survival.
How similar studies have gone: Broadly targeting CAFs previously worsened outcomes, but preliminary preclinical work identifying inflammatory CAFs and MyD88-driven suppression provides promising laboratory evidence for this more targeted approach, while clinical benefit remains unproven.
Where this research is happening
-
Stanford University
Stanford, United States Active
Researchers
- Principal investigator: Delitto, Daniel — Stanford University
- Study coordinator: Delitto, Daniel
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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.