Aspirin prevents tumors in a murine model of familial adenomatous polyposis

N. N. Mahmoud, A. J. Dannenberg, J. Mestre, R. T. Bilinski, M. R. Churchill, C. Martucci, H. Newmark, M. M. Bertagnolli, Jr Townsend, R. D. Beauchamp

Research output: Contribution to journalArticlepeer-review

115 Scopus citations


Background. Both human and murine studies suggest that anti- inflammatory drugs prevent intestinal neoplasia. The purpose of this study was to investigate the role of aspirin as a chemopreventive agent for colorectal cancer. Methods. We administered aspirin to the Min/+ mouse, an animal with a germline mutation in Apc, a gene that is essential for normal epithelial cell growth and differentiation. Apc mutation increases cytoplasmic β-catenin, a regulatory protein associated with the cytoskeleton. Min/+ mice develop multiple intestinal adenomas and exhibit altered cell growth in the preneoplastic intestinal epithelium. Results. Aspirin decreased the rate of tumor formation in Min/+ mice by 44%. Aspirin also normalized enterocyte growth by increasing apoptosis and proliferation in the preneoplastic intestinal mucosa. Finally, aspirin produced a decrease in intracellular β-catenin levels, suggesting that modulation of this protein is associated with tumor prevention. Conclusions. These data confirm a role for aspirin in suppression of Apc-associated intestinal carcinogenesis.

Original languageEnglish (US)
Pages (from-to)225-231
Number of pages7
Issue number2
StatePublished - 1998

ASJC Scopus subject areas

  • Surgery


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