Overview

• The STRESS signature comprises 10 STAT3-induced genes, including Integrin β3, that forecast PDAC onset and tumor aggressiveness more accurately than existing gene markers.
• In mouse and human pancreatic cells under inflammatory and hypoxic stress, STAT3 activation drives ITGB3 expression, promoting both tumor initiation and accelerated progression.
• Blocking the STAT3–ITGB3 inflammatory pathway in preclinical PDAC models significantly delayed tumor formation, demonstrating proof of concept for targeted intervention.
• Chemotherapy-induced inflammation and cellular stress were found to activate the same STAT3–ITGB3 axis, highlighting potential effects on treatment resistance and patient response.
• Research teams are now translating these findings into clinical applications by developing early detection assays for PDAC and exploring molecules to inhibit inflammation-driven ITGB3 activation across epithelial cancers.