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Enhanced Intestinal Adenomatous Polyp Formation in Pms2^-/-;Min Mice¹

Departments of Molecular and Medical Genetics [R. M. L., A. C. H., T. J. F., C. E. B.] and Pathology [M. G.], Oregon Health Sciences University, Portland, Oregon 97201; Department of Nutritional Sciences, University of California, Berkeley, California 94720-3104 [S. M. B.]; and Department of Pathology, University of Southern California School of Medicine, Los Angeles, California 90033 [J-L. T., D. S.]

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 clearly increases adenoma formation in the Min background, histological analysis indicated no clear evidence for progression to carcinoma.

¹ Work performed in the laboratory of R. M. L. was supported by NIH Grants GM45413 and GM32741. Work performed in the laboratory of D. S. was supported by NIH Grants CA58704 and CA70858.

² To whom requests for reprints should be addressed, at Department of Molecular and Medical Genetics, Oregon Health Sciences University, 3181 SW Sam Jackson Park Road, Portland, Oregon 97201. Phone: (503) 494-3475; Fax: (503) 494-6886; E-mail: liskaym@ohsu.edu.

Received 12/ 8/97. Accepted 1/29/98.

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