Changing pancreatic cancer's scar-like tissue to make treatments work better
Official title: Reprogramming PDAC Stroma by Targeting Coagulation in the Tumor Microenvironment
Funded at University of Illinois at Urbana-Champaign · NIH-11181324 · Data updated 2026-11-12
This project tests therapies that block blood-clotting signals in pancreatic cancer to help chemotherapy and immunotherapy work better for people with pancreatic ductal adenocarcinoma.
Quick facts
| Grant type | U01 cooperative agreement |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Illinois at Urbana-Champaign NIH-funded |
| Lab location | 1 site (Champaign, United States) |
| Project start | September 1, 2022 |
| Project end | August 31, 2027 |
| Funding year | 2025 |
| Award (this year) | $932,376 |
| NIH project number | 5U01CA274304-05 |
| Project ID | NIH-11181324 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with pancreatic ductal adenocarcinoma, particularly those with dense, treatment-resistant tumors or those willing to donate tumor or blood samples for research, would be the most relevant candidates.
✕Less likely to help
People without PDAC, those whose tumors lack dense stromal features, or patients who cannot undergo experimental procedures are unlikely to benefit from this specific approach.
What this research studies
I will explain what the team plans to do and why it matters for patients like you. Researchers aim to soften and reprogram the dense, scar-like stroma around pancreatic tumors by targeting coagulation signals such as thrombin, PAR1, and fibrin. They will use laboratory models, animal studies, and patient-derived samples to see whether these interventions improve drug delivery and allow immune cells to reach the tumor. The goal is to change the tumor environment in ways that make standard treatments like chemo and immunotherapy more effective without removing stroma that helps restrain the cancer.
Why it matters
Potential benefit: If successful, this approach could make chemotherapy and immunotherapy more effective for people with pancreatic cancer and slow tumor progression.
How similar studies have gone: Previous laboratory and animal studies show that modifying stromal components can improve drug delivery but that complete stromal removal can worsen outcomes, and targeting the coagulation/thrombin-PAR1 axis is an emerging preclinical strategy with promising but not yet clinical-proven results.
Where this research is happening
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University of Illinois at Urbana-Champaign
Champaign, United States Active
Researchers
- Principal investigator: Han, Bumsoo — University of Illinois at Urbana-Champaign
- Study coordinator: Han, Bumsoo
Related research
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Targeting autophagy to treat KRAS-mutant pancreatic cancer
This grant explores using approved drugs to block autophagy in KRAS-mutant pancreatic cancer to improve treatment outcomes.
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Reprogramming PDAC stroma by targeting blood clotting in the tumor environment
A cancer research grant aimed at turning the tough, fibrous pancreatic cancer environment into one that helps treatments work better and supports the body’s immune response.
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Understanding paracrine signals in pancreatic cancer to improve drug delivery
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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.