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, Courtney Townsend, R. D. Beauchamp

Research output: Contribution to journalArticle

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Abstract

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
JournalSurgery
Volume124
Issue number2
DOIs
StatePublished - 1998
Externally publishedYes

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Adenomatous Polyposis Coli
Aspirin
Catenins
Neoplasms
Intestinal Mucosa
Growth
Germ-Line Mutation
Enterocytes
Essential Genes
Cytoskeleton
Adenoma
Cell Differentiation
Colorectal Neoplasms
Carcinogenesis
Proteins
Anti-Inflammatory Agents
Epithelial Cells
Apoptosis
Mutation
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Surgery

Cite this

Mahmoud, N. N., Dannenberg, A. J., Mestre, J., Bilinski, R. T., Churchill, M. R., Martucci, C., ... Beauchamp, R. D. (1998). Aspirin prevents tumors in a murine model of familial adenomatous polyposis. Surgery, 124(2), 225-231. https://doi.org/10.1016/S0039-6060(98)70124-2

Aspirin prevents tumors in a murine model of familial adenomatous polyposis. / Mahmoud, N. N.; Dannenberg, A. J.; Mestre, J.; Bilinski, R. T.; Churchill, M. R.; Martucci, C.; Newmark, H.; Bertagnolli, M. M.; Townsend, Courtney; Beauchamp, R. D.

In: Surgery, Vol. 124, No. 2, 1998, p. 225-231.

Research output: Contribution to journalArticle

Mahmoud, NN, Dannenberg, AJ, Mestre, J, Bilinski, RT, Churchill, MR, Martucci, C, Newmark, H, Bertagnolli, MM, Townsend, C & Beauchamp, RD 1998, 'Aspirin prevents tumors in a murine model of familial adenomatous polyposis', Surgery, vol. 124, no. 2, pp. 225-231. https://doi.org/10.1016/S0039-6060(98)70124-2
Mahmoud NN, Dannenberg AJ, Mestre J, Bilinski RT, Churchill MR, Martucci C et al. Aspirin prevents tumors in a murine model of familial adenomatous polyposis. Surgery. 1998;124(2):225-231. https://doi.org/10.1016/S0039-6060(98)70124-2
Mahmoud, N. N. ; Dannenberg, A. J. ; Mestre, J. ; Bilinski, R. T. ; Churchill, M. R. ; Martucci, C. ; Newmark, H. ; Bertagnolli, M. M. ; Townsend, Courtney ; Beauchamp, R. D. / Aspirin prevents tumors in a murine model of familial adenomatous polyposis. In: Surgery. 1998 ; Vol. 124, No. 2. pp. 225-231.
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abstract = "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.",
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AU - Mestre, J.

AU - Bilinski, R. T.

AU - Churchill, M. R.

AU - Martucci, C.

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AU - Bertagnolli, M. M.

AU - Townsend, Courtney

AU - Beauchamp, R. D.

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N2 - 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.

AB - 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.

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