Chemoprevention of gastrointestinal malignancies with nonsteroidal antiinflammatory drugs

Cancer. 2002 Feb 15;94(4):950-63.


In multiple studies, the chronic use of nonsteroidal antiinflammatory drugs (NSAIDs) has been associated with a decreased incidence of several types of gastrointestinal (GI) neoplasia. This effect may be mediated by one of several intracellular mechanisms, some of which involve the inhibition of the cyclooxygenase-2 (COX-2) isoenzyme. In multiple studies of colorectal carcinoma, chronic NSAID use has shown a protective effect, with the majority of studies demonstrating a 30-70% risk reduction associated with NSAID use. The effect of NSAIDs on other types of GI neoplasia is less clear, but evidence suggests that chronic NSAID use may diminish the risk of esophageal and gastric carcinomas. Data assessing the effects of NSAIDs on the incidence of pancreatic and hepatic malignancies currently are too sparse and inconsistent to draw any conclusions. The newer COX-2 specific agents may provide a less GI-toxic alternative to nonselective NSAIDs as chemoprotective agents.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Chemoprevention*
  • Cyclooxygenase 2
  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors / pharmacology
  • Cyclooxygenase Inhibitors / therapeutic use
  • Disease Models, Animal
  • Gastrointestinal Neoplasms / prevention & control*
  • Humans
  • Isoenzymes / antagonists & inhibitors
  • Isoenzymes / metabolism
  • Membrane Proteins
  • Prostaglandin-Endoperoxide Synthases / metabolism


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