Up to 41% of hepatocellular carcinomas (HCCs) result from activating mutations in the gene encoding β-catenin. HCC-associated mutations stabilize the β-catenin protein, leading to nuclear and/or cytoplasmic localization of β-catenin and downstream activation of Wnt target genes. In patient HCC samples, β-catenin nuclear and cytoplasmic localization are typically patchy, even among HCC with highly active mutations.
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