The findings, published in Nature, show that a small number of pancreatic cancer cells activate genes that stabilize fibrin, a protein that forms a meshwork involved in blood clotting.
The study reveals that cancer cells use this wound-healing system to build a protective environment that prevents cancer-fighting immune cells from reaching pancreatic tumors. In preclinical models, disrupting this protective mechanism slowed tumor growth and improved responses to immunotherapy, pointing to a potential strategy for overcoming pancreatic cancer’s resistance to immune-based treatments.