Although the selective COX-2inhibitor stimulated VEGF production by pancreatic cancer cells through a PPAR-γ mediated mechanism also in COX-2 expressingpancreatic cancers, the potential proangiogenic and tumor-promoting effect inCOX-2 positive cancers was masked by a significant reduction of COX-2 generatedproangiogenic and protumorigenic prostanoids [42]. This evidence concerns the gene VEGFA and neoplasm.