The role of the cyclooxygenase-2 - prostaglandin E2 cascade in pancreatic cancer associated angiogenesis

Abstract

Medical therapy has failed to make any significant impact on survival in pancreatic cancer. Non Steroidal Anti-inflammatory Drugs (NSAIDs) have shown promise in several gastrointestinal (Gl) cancers. Evidence has suggested a similar effect in pancreatic cancer. Cyclooxygenase-2 (COX-2), a major target of NSAIDs, is upregulated in pancreatic cancer and is associated with worse prognosis. COX-2 upregulation has been shown to correlate with angiogenesis and production of pro- angiogenic growth factors, especially Vascular Endothelial Growth Factor (VEGF), in several Gl cancers. Although this relationship between COX-2 and angiogenesis in pancreatic cancer would seem a viable target, clinical trials of COX-2 or VEGF inhibitors have demonstrated no survival benefit.