Intestinal Tumor Load in the Min/+ Mouse Model is not Correlated with Eicosanoid Biosynthesis

  • Jay Whelan
  • Chun-Hung Chiu
  • Michael F. McEntee
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 469)

Abstract

Several lines of evidence demonstrate an inverse relationship between the use of nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin and aspirin-like drugs, and intestinal cancer. NSAIDs have been shown to reduce the risk of intestinal cancer in humans by 50%.1–4 It is well known that the anti-inflammatory properties of NSAIDs are related to their ability to inhibit prostaglandin biosynthesis. Cyclooxygenase (COX) catalyzes the committed step in prostaglandin formation. Two isoforms of cyclooxygenase exist, COX-1 and COX-2. NSAIDs can inhibit both. COX-1 is the constitutively expressed isoform, and COX-2 is the inducible form of the enzyme involved in inflammation.5–7

Keywords

Arachidonic Acid Familial Adenomatous Polyposis Adenomatous Polyposis Coli Tumor Number Tumor Load 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1999

Authors and Affiliations

  • Jay Whelan
    • 1
  • Chun-Hung Chiu
    • 1
  • Michael F. McEntee
    • 2
  1. 1.Department of NutritionUniversity of TennesseeKnoxvilleUSA
  2. 2.Department of PathologyUniversity of TennesseeKnoxvilleUSA

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