Prostaglandins are arachidonate metabolites produced in virtually all mammalian tissues and possess diverse biologic capabilities, including vasoconstriction, vasodilatation, stimulation or inhibition of platelet aggregation, and immunomodulation, primarily immunosupression (1–4). They are implicated in the promotion of development and growth of malignant tumors (4–7). They are also involved in the response of tumor and normal tissues to cytotoxic agents such as ionizing radiation (8). Prostaglandin production is mediated by two cyclooxygenase enzymes: cyclooxygenase-1 and cyclooxygenase-2. Cyclooxygenase-1 is constitutively expressed and is ubiquitous, and cyclooxygenase-2 is induced by diverse inflammatory stimuli (7, 9).

Nonsteroidal anti-inflammatory drugs (NSAIDs) or agents inhibit cyclooxygenase enzymes and consequently can prevent, inhibit, or abolish the effects of prostaglandins. Increasing evidence shows that NSAIDs can inhibit the development of cancer in both experimental animals and in humans (7), can reduce the size of established tumors (6–8), and can increase the efficacy of cytotoxic anticancer agents (8). Our own investigations have demonstrated that the NSAID indomethacin prolongs tumor growth delay and increases the tumor cure rate in mice after