Aspirin and Pancreatic Ductal Adenocarcinoma: A Comprehensive Narrative Review of Chemoprevention and Clinical Outcomes

Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers, with a consistently low five-year survival rate. The increase in cases and resistance to standard treatments makes it important to explore ways to prevent this disease. Aspirin, a non-steroidal anti-inflammatory drug, has gained attention for its possible cancer-fighting properties. This review summarizes current evidence on how aspirin use relates to PDAC risk and outcomes. Recent studies show mixed results. Some studies indicate a significant risk reduction, especially in diabetics, while others show no connection. Proposed biological mechanisms include COX-dependent and independent pathways. These pathways involve blocking cyclooxygenase-2, altering insulin signaling, and reducing oncogenic KRAS activity. There is also evidence that aspirin may affect how cancer spreads. Long-term use appears to be linked to lower rates of metastatic disease at diagnosis and higher rates of surgical resectability. The role of aspirin in PDAC is complicated and seems affected by dosage, length of use, and individual factors like diabetes status. Future research should prioritize personalized strategies. This includes using molecular subtyping and well-planned combination therapies to effectively utilize aspirin in managing PDAC.