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Constitutive β-catenin/Tcf activity, the primary transforming events in colorectal carcinoma, occurs through induction of the Wnt pathway orAPC gene mutations that cause familial adenomatous polyposis. Mice carryingApc mutations in their germ line (ApcMin ) develop intestinal adenomas. Here, the crossing ofApcMin withcyclin D1−/− mice reduced the intestinal tumor number in animals genetically heterozygous or nullizygous forcyclin D1 . Decreased tumor number in the duodenum, intestines, and colons ofApcMin /cyclin D1+/− mice correlated with reduced cellular proliferation and increased differentiation. Cyclin D1 deficiency reduced DNA synthesis and induced differentiation of colonic epithelial cells harboring mutant APC but not wild-type APC cells in vivo. In previous studies, the complete loss of cyclin D1 through homozygous genetic deletion conveyed breast tumor resistance. The protection of mice, genetically predisposed to intestinal tumorigenesis, through cyclin D1 heterozygosity suggests that modalities that reduce cyclin D1 abundance could provide chemoprotection.

Cyclin D1 Genetic Heterozygosity Regulates Colonic Epithelial Cell Differentiation and Tumor Number in ApcMin Mice

Cyclin D1 Genetic Heterozygosity Regulates Colonic Epithelial Cell Differentiation and Tumor Number in Apc^Min Mice