We have tested the hypothesis that enteric bacteria are necessary for formation of intestinal adenomas in C57BL/6-ApcMin/+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-ApcMin/+ mice mutated at the beige locus, which controls natural killer activity, are also unaltered in adenoma multiplicity.

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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.

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