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Gut 1999;45:795-796 doi:10.1136/gut.45.6.795
  • Commentary

Cryptic messages in FAP

  1. A WATSON
  1. Department of Medicine
  2. University of Liverpool
  3. Liverpool, UK
  4. Department of Medicine, GI; MCN C-2104
  5. Vanderbilt University Medical Centre
  6. Nashville, TN 37232–1080, USA
  1. R N DuBOIS
  1. Department of Medicine
  2. University of Liverpool
  3. Liverpool, UK
  4. Department of Medicine, GI; MCN C-2104
  5. Vanderbilt University Medical Centre
  6. Nashville, TN 37232–1080, USA

    See article on page 822

    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 …

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