Alteration of the β-catenin pathway in spiradenoma

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.

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).

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.

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.