A survival–stratification model of human colorectal carcinomas with β‐catenin and p27kip1

The stabilization and nuclear translocation of β‐catenin are early events in the majority of sporadic colorectal carcinomas (CRC). β‐catenin up‐regulates c‐Myc and cyclin D1, which antagonize the association of the cyclin‐dependent kinase (Cdk) inhibitor, p27kip1, with Cdk2, thus allowing cell cycle progression through G1 to S‐phase. Lack of p27 is a significant predictor of poor survival in a series of 136 CRC specimens. A combination of molecules in the same pathway may be a better prognostic factor.

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