The prevention of colorectal cancer by aspirin use

Biomed Pharmacother. 1999 Aug;53(7):303-8. doi: 10.1016/S0753-3322(00)88500-5.


Epidemiologic studies indicate strongly that aspirin use reduces the risk of colorectal cancer and adenoma by approximately 40 to 50%. Perhaps up to ten years of use may be required before a benefit is apparent in colorectal cancer. The chemo-preventive actions of aspirin and other non-steroidal anti-inflammatory agents (NSAIDs) in colorectal carcinogenesis are also supported by animal studies, and by intervention studies that demonstrate that the anti-inflammatory agent sulindac causes regression of adenomas in familial adenomatous polyposis. Despite this evidence, the clinical implications are not clear because of increased gastro-intestinal irritation and bleeding episodes related to chronic aspirin use. Emerging evidence suggests that the anti-tumor properties of NSAIDs may be related primarily to the inhibition of cyclooxygenase-2 (COX-2), one of the two isoenzymes of the COX enzyme family. If confirmed, a new generation of selective COX-2 inhibitors may retain some of the chemo-preventive properties of NSAIDs with fewer side-effects. Firm recommendations regarding the use of aspirin or other NSAIDs to prevent colorectal cancer must await further research. For now, the decision must lie with the patient, in consultation with his or her healthcare provider, after a careful weighing of all potential risks and benefits.

Publication types

  • Review

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • Aspirin / pharmacology
  • Aspirin / therapeutic use*
  • Clinical Trials as Topic
  • Colorectal Neoplasms / prevention & control*
  • Cyclooxygenase 1
  • Cyclooxygenase 2
  • Enzyme Inhibitors / therapeutic use*
  • Humans
  • Isoenzymes / metabolism*
  • Membrane Proteins
  • Prostaglandin-Endoperoxide Synthases / metabolism*


  • Anti-Inflammatory Agents, Non-Steroidal
  • Enzyme Inhibitors
  • Isoenzymes
  • Membrane Proteins
  • Cyclooxygenase 1
  • Cyclooxygenase 2
  • PTGS1 protein, human
  • PTGS2 protein, human
  • Prostaglandin-Endoperoxide Synthases
  • Aspirin