Alteration of the β-catenin pathway in spiradenoma.

BACKGROUND: Although skin carcinogenesis has been widely investigated, only limited information is available for epidermal tumors, while even less is known about other skin structures. Alterations in the β-catenin pathway have been reported in several epidermal tumors, while little is known about in adnexal tumors. This study was performed to assess alterations in the β-catenin pathway associated with adnexal tumors, and to investigate the mechanisms underlying these alterations.

METHODS: β-Catenin expression in 48 adnexal tumors (trichoepithelioma, trichofolliculoma, pilomatricoma, syringoma, eccrine poroma, spiradenoma, sebaceous hyperplasia and nevus sebaceus) was assessed using immunohistochemistry. The tumors showing intense nuclear reactivity for β-catenin were further evaluated by immunohistochemistry for β-catenin degradation complex such as adenomatosis polyposis coli (APC), Axin and glycogen synthase kinase 3β (GSK-3β).

RESULTS: Intense nuclear immunoreactivity for β-catenin was observed in pilomatricoma and spiradenoma. Among 12 eccrine spiradenomas, APC was downregulated in 2 (16.7%) cases, and Axin and GSK-3β were downregulated in 11 (91.7%) and 10 (83.3%) cases, respectively.

CONCLUSIONS: This is the first reported analysis of the role of alterations in the β-catenin pathway in spiradenoma. We suggest that downregulation of Axin and GSK-3β in the β-catenin pathway may be an important signaling alteration in the development of spiradenoma.