Commentary
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A series of remarkable clinical, epidemiological, and laboratory studies has shown that aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) such as sulindac, can prevent the development of colorectal cancer and cause regression of pre-existing adenomas.1 Aspirin is one of the most potent chemopreventive agents against colorectal cancer. However, its mechanism for causing a reduction in colorectal cancer risk and mortality is unknown.2 The anti-inflammatory properties of NSAIDs are thought to reside in their ability to inhibit prostaglandin production at sites of inflammation.
Cyclooxygenase (COX) is a key enzyme in the production of
prostaglandins, and aspirin can inhibit its activity directly.
Initially, COX was thought to be a single enzyme, but in 1991 a second
COX isoform was discovered (COX-2) which is induced by cytokines, growth factors, and tumour promoters.3 COX-1 is expressed
constitutively in many tissues and is inhibited by aspirin and other
commonly used NSAIDs. Contrastingly, COX-2 can be induced
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