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Intestinal Neoplasia in the Apc^Min Mouse: Independence from the Microbial and Natural Killer (beige Locus) Status¹

McArdle Laboratory for Cancer Research [L. C., A. R. M.] and Laboratory of Genetics [W. F. D., K. A. G., C. L.]. University of Wisconsin, Madison, Wisconsin 53706; Department of Medicine, Division of Gastroenterology [D. J. M., R. F. J.] and Department of Biostatistics, Comprehensive Cancer Center [M. A. N.], University of Wisconsin, Madison, Wisconsin 53792

We have tested the hypothesis that enteric bacteria are necessary for formation of intestinal adenomas in C57BL/6-Apc^Min/+mouse. Germ-free mice developed 2-fold fewer adenomas than conventional controls in the medial small intestine (7.3 versus 14.9; P < 0.003), but there were no significant differences in the rest of the intestinal tract. We conclude that microbial status does not strongly alter the adenoma phenotype in this mouse model of familial adenomatous polyposis. In parallel, we have found that C57BL/6-Apc^Min/+ mice mutated at the beige locus, which controls natural killer activity, are also unaltered in adenoma multiplicity.

¹ This research has been supported by the National Cancer Institute through Contract CN-35550, R01 CA50585, and Core Grant CA07075. K. A. G. and C. L. were supported in part by Training Grants T32-CA09135 and T32-GM07133.

² To whom requests for reprints should be addressed, at 1400 University Avenue, Madison, WI 53706. Phone: (608) 262-4977; Fax: (608) 262-2824; E-mail: dove@oncology.wisc.edu.

³ Present address: Department of Pharmacology, University of Wisconsin Medical School, Madison, WI 53706.

⁴ Present address: Bock Laboratories, University of Wisconsin, Madison, WI 53706.

⁵ Present address: Department of Human Oncology, University of Wisconsin Comprehensive Cancer Center, Madison, WI 53792.

Received 11/ 4/96. Accepted 1/17/97.

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