Immunohistochemical expression of β‐catenin, E‐cadherin, cyclin D1 and c‐myc in benign trichogenic tumors

BACKGROUND: beta-catenin gene mutations have been reported in vast majority of pilomatrixomas (PMXs). beta-catenin, a component of the adhesion molecules of the cytoskeleton, is degraded at the cytoplasm. Excess cytoplasmic beta-catenin enters into the nucleus and activates the transcription of several genes encoding c-myc, cyclin D1 and others. Sublocation of beta-catenin has been demonstrated by immunohistochemistry. The aim of this study was to determine the role of beta-catenin-related proteins in various benign trichogenic tumors. METHODS: We investigated the expression of beta-catenin, E-cadherin, c-myc and cyclin D1 immunohistochemically, and the expression of these molecules were compared between two groups consisting of 12 PMXs and 12 other benign trichogenic tumors (OBTTs). RESULTS: In PMX group, nuclear and/or cytoplasmic expression of beta-catenin was associated with a loss of membranous expression of E-cadherin (p = 0.002). In OBTT group, a membranous expression of E-cadherin and beta-catenin was observed, and there was a stronger nuclear immunoreactivity of cyclin D1 compared with PMX group (p = 0.006). CONCLUSIONS: In PMX, nuclear and/or cytoplasmic beta-catenin expression of tumoral cells is not related with beta-catenin-related gene expressions (c-myc or cyclin D1). The molecular behaviour of OBTTs is clearly different from that of PMXs in terms of to E-cadherin and beta-catenin expression.