Journal of cutaneous pathology · 2011
Alteration of the β-catenin pathway in spiradenoma.
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Im Myung, Kim Dae H, Park Joon S, Chung Hyun, Lee Young, Kim Chang D, Seo Young J, Lee Jeung H
Аннотация
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.
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.