Immunohistochemical expression of beta-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.