The oncogenic activation of β-catenin

Abstract The activation of β-catenin to an oncogenic state can result from the inactivation of the tumor suppressor adenomatous polyposis coli (APC), by direct mutation in the β-catenin gene, or by the activation of wnt receptors. Once activated, β-catenin most likely promotes tumor progression through its persistent interaction with one or more of its numerous downstream targets.

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