We have previously shown that aspirin’s influence on CRC is mediated at least in part through inhibition of prostaglandin-endoperoxide synthase-2 (PTGS-2; or cyclooxygenase (COX)-2), [9, 10] which catalyzes production of prostaglandin E2 (PGE2), leading to induction of proliferation, migration and invasiveness, promotion of angiogenesis, resistance to apoptosis and modulation of cellular and humoral immunity within the tumor. Here, PTGS2 is linked to neoplasm.