An early analysis of 662,424 men and women enrolled in the U.S. Cancer Prevention Study (CPS) II cohort showed that aspirin use at least 16 times per month was associated with a 40% reduced risk of colon cancer mortality over a 6-year period.
Aspirin’s most well-characterized pharmacologic activity is the permanent modification of the prostaglandin-endoperoxide synthetase (PTGS) or COX enzymes. These enzymes are rate limiting for the conversion of arachidonic acid to prostaglandins and related eicosanoids. COX-1 isoenzyme is constitutively expressed in most tissues, whereas growth factors, oncogenes, tumour promoters, and inflammatory cytokines induce the COX-2 isoenzyme. It is reasonably well-established that aspirin’s vascular benefits are largely due to acetylation of platelet-activated PTGS-1 or COX-1 that occurs even with low doses (
I agree with Shalayel's elaborate explanation. However, a redaction of his lengthy (not to mention very technical) explanation highlights only a single issue - whether aspirin should be used as an anti-inflammatory, in the protection against cancers. I guess this answers the question of why aspirin is used to prevent cancers (in your case, colorectal cancer).
I suggest you read this very fascinating article published in the Lancet Oncology journal
http://www.ncbi.nlm.nih.gov/pubmed/19410194
Hope this helps.
Rabin
Several epidemiologic studies suggest that aspirin or other NSAIDs have a protective effect. This is consistent with studies showing that some NSAIDs cause polyp regression in patients with FAP in whom the rectum was left in place after colectomy. It is suspected that this effect is mediated by inhibition of the enzyme cyclooxygenase-2 (COX-2), which is highly expressed in 90% of colorectal carcinomas and 40% to 90% of adenomas and is known to promote epithelial proliferation, particularly in response to injury.
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