Abstract

The initial genetic alteration in colorectal carcinoma is mutation of the APC gene. As a result, the expected rate of apoptosis in colorectal cells is attenuated leading to the expansion of the progeny of the APC mutant cells and hence tumor formation1. The up-regulation of cyclooxygenase-2 (Cox-2) occurs at this early stage of colorectal carcinoma and high expression is observed in multiple intestinal neoplasm (Min) mice, the model of familiar adenomatous polyposis2,3, and in 85% of human colorectal carcinomas4. The over-expression of Cox-2 inhibits apoptosis in rat intestinal cells5 and non-steroidal anti-inflammatory drugs (NSAIDs), such as sulindac sulfide, indomethacin and aspirin promote apoptosis in colorectal carcinoma cells. NSAIDs serve in chemoprevention of colorectal cancer in experimental animal models indicating Cox as a target for preventing colorectal tumors in man6,7. However, the functional role of the mutated APC, the overexpression Cox-2 and the inhibition of apoptosis is not clearly understood.

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