title: Alteration of the β-catenin pathway in spiradenoma.
abstract: 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.
authors.affiliation: Department of Dermatology, School of Medicine, Chungnam National University, Daejeon, Korea. im1177@hanmail.net
authors.forename: Myung
authors.initials: M
authors.lastname: Im
authors.forename: Dae H
authors.initials: DH
authors.lastname: Kim
authors.forename: Joon S
authors.initials: JS
authors.lastname: Park
authors.forename: Hyun
authors.initials: H
authors.lastname: Chung
authors.forename: Young
authors.initials: Y
authors.lastname: Lee
authors.forename: Chang D
authors.initials: CD
authors.lastname: Kim
authors.forename: Young J
authors.initials: YJ
authors.lastname: Seo
authors.forename: Jeung H
authors.initials: JH
authors.lastname: Lee
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000378:metabolism; D006607:Adenoma, Sweat Gland / Q000378:metabolism* / Q000473:pathology; D025601:Adenomatous Polyposis Coli Protein / Q000378:metabolism; D060466:Axin Protein; D014408:Biomarkers, Tumor / Q000378:metabolism; D002467:Cell Nucleus / Q000378:metabolism / Q000473:pathology; D015536:Down-Regulation; D038362:Glycogen Synthase Kinase 3 / Q000378:metabolism; D000071679:Glycogen Synthase Kinase 3 beta; D006801:Humans; D012097:Repressor Proteins / Q000378:metabolism; D015398:Signal Transduction; D013544:Sweat Gland Neoplasms / Q000378:metabolism* / Q000473:pathology; D051176:beta Catenin / Q000378:metabolism*
chemical_list: C555337:APC protein, human; D048868:Adaptor Proteins, Signal Transducing; D025601:Adenomatous Polyposis Coli Protein; D060466:Axin Protein; D014408:Biomarkers, Tumor; C495270:CTNNB1 protein, human; D012097:Repressor Proteins; D051176:beta Catenin; C000605506:GSK3B protein, human; D000071679:Glycogen Synthase Kinase 3 beta; D038362:Glycogen Synthase Kinase 3