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Detection and analysis of β‐catenin mutations in prostate cancer

E‐cadherin and α‐catenin are components of adherens junctions which mediate calcium‐dependent, cell‐cell adhesion in a homotypic manner. Both these molecules have been defined as useful tumor markers as their altered expression correlates with increased tumor aggressiveness and dedifferentiation. More recently, alterations of a third component of adherens junctions, β‐catenin, have been observed to play a role in several human cancers. Dysregulation of β‐catenin, either by direct mutation or by defects in interacting pathways/regulators, can result in its cytoplasmic accumulation and nuclear translocation. In the nucleus, β‐catenin forms a transcriptional complex capable of upregulating target genes, many of which encode proliferative factors. Given its oncogenic activity and connection to human cancer, we examined the β‐catenin gene and its expression in prostate cancer.