Enhanced intestinal adenomatous polyp formation in Pms2(-/-);Min mice

Sean M. Baker, Allie C. Harris, Jen Lan Tsao, Tom J. Flath, C. Eric Bronner, Melissa Gordon, Darryl Shibata, R. Michael Liskay

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Analysis of two human familial cancer syndromes, hereditary nonpolyposis colorectal cancer and familial adenomatous polyposis, indicates that mutations in either one of four DNA mismatch repair gene homologues or the adenomatous polyposis coli (APC) gene, respectively, are important for the development of colorectal cancer. To further investigate the role of DNA mismatch repair in intestinal tumorigenesis, we generated mice with mutations in both Apc and the DNA mismatch repair gene, Pms2. Whereas Pms2-deficient mice do not develop intestinal tumors, mice deficient in Pms2 and heterozygous for Min, an allele of Apc, develop approximately three times the number of small intestinal adenomas and four times the number of colon adenomas relative to Min and Pms2(+/-); Min mice. Although Pms2 deficiency dearly increases adenoma formation in the Min background, histological analysis indicated no clear evidence for progression to carcinoma.

Original languageEnglish (US)
Pages (from-to)1087-1089
Number of pages3
JournalCancer Research
Issue number6
StatePublished - Mar 15 1998


ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Baker, S. M., Harris, A. C., Tsao, J. L., Flath, T. J., Bronner, C. E., Gordon, M., Shibata, D., & Liskay, R. M. (1998). Enhanced intestinal adenomatous polyp formation in Pms2(-/-);Min mice. Cancer Research, 58(6), 1087-1089.