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Suppression of intestinal polyposis in Apc delta716 knockout mice by inhibition of cyclooxygenase 2 (COX-2).

Two cyclooxygenase isozymes catalyze conversion of arachidonic acid to prostaglandin H2: constitutive COX-1 and inducible COX-2. To assess the role of COX-2 in colorectal tumorigenisis, we determined the effects of COX-2 gene (Ptgs2) knockouts and a novel COX-2 inhibitor on Apc delta716 knockout mice, a model of human familial adenomatous polyposis. A Ptgs2 null mutation reduced the number and size of the intestinal polyps dramatically. Furthermore, treating Apc delta716 mice with a novel COX-2 inhibitor reduced the polyp number more significantly than with sulindac, which inhibits both isoenzymes. These results provide direct genetic evidence that COX-2 plays a key role in tumorigenesis and indicate that COX-2-selective inhibitors can be a novel class of therapeutic agents for colorectal polyposis and cancer.

Pubmed ID: 8945508


  • Oshima M
  • Dinchuk JE
  • Kargman SL
  • Oshima H
  • Hancock B
  • Kwong E
  • Trzaskos JM
  • Evans JF
  • Taketo MM



Publication Data

November 29, 1996

Associated Grants


Mesh Terms

  • Adenomatous Polyposis Coli
  • Adenomatous Polyposis Coli Protein
  • Animals
  • Cyclooxygenase 2
  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors
  • Cytoskeletal Proteins
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Enzyme Inhibitors
  • Extracellular Space
  • Female
  • Furans
  • Gene Dosage
  • Gene Expression Regulation, Enzymologic
  • Gene Expression Regulation, Neoplastic
  • Genes, APC
  • Intestinal Mucosa
  • Isoenzymes
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mutagenesis
  • Prostaglandin-Endoperoxide Synthases
  • Sulindac
  • Time Factors