Nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, appear to
have clinically significant anticarcinogenic effects in the gastrointestin
al tract. Epidemiological data indicate that use of these drugs is inversel
y associated with the risk of sporadic colorectal cancer, and clinical tria
ls among patients with familial polyposis coli show that NSAIDs can lead to
the regression of large bowel adenomas. Animal studies have reported a sim
ilar efficacy of NSAIDs against experimental carcinogenesis. A consistent p
attern in this research is that continued long-term use of NSAIDs is requir
ed for an anticancer effect-up to 15 or 20 years before a reduced risk of c
olorectal cancer appears. Epidemiological data also suggest possible protec
tive effects in the stomach and esophagus. The mechanisms underlying any ch
emopreventive effect of NSAIDs are not clear. Inhibition of cyclooxygenase
is one possibility, but pathways independent of cyclooxygenase and prostagl
andins are also possible.