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dc.contributor.authorTohma, Y.-
dc.contributor.authorFukaya, K.-
dc.contributor.authorFujisawa, H.-
dc.contributor.authorHayashi, Yoshihiro-
dc.contributor.authorTachibana, Osamu-
dc.contributor.authorKida, S.-
dc.contributor.authorYamashita, J.-
dc.contributor.authorSaito, K.-
dc.description.abstractThe Ca2+-dependent cell adhesion molecule E-cadherin has been known to express in normal and reactive Schwann cells in rodents, and to play an important role in Schwann cell-Schwann cell adhesion and maintenance of peripheral nervous tissue architecture. However, little is known about expression of E-cadherin in schwannomas. The aim of the present study was to investigate the cellular expression and localization of E-cadherin, and its associated protein, alpha E-, alpha N- and beta-catenins in human schwannomas, which are supposed to derive from Schwann cells. We tested the hypothesis that these proteins might show an altered expression/distribution in schwannoma cells which correlates with their neoplastic behavior, including sparse cell-cell contact, as seen those in meningiomas and various carcinomas. In human schwannomas, however, E-cadherin, alpha E-catenin, and beta-catenin were detected by western blotting and i m m u n o h i s t o c h e m i s t r y, whereas alpha N-catenin was not. Immunoprecipitation using anti-E-cadherin antibody resulted in alpha E-catenin forming a complex with Ecadherin. SSCP analysis revealed no mutations in the transmembrane domain or in intracellular cateninbinding site of E-cadherin. These data suggest that the Ecadherin- alpha E-catenin complex is well preserved in human schwannoma cells, which is compatible with its benign behavior, and these molecules might be used as additional cell markers of Schwann cell-derived
dc.publisherMurcia : F. Hernándezes
dc.relation.ispartofHistology and histopathologyes
dc.subjectBrain tumores
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicinaes
dc.titleExpression of E-cadherin-catenin complex in human benign schwannomases
Appears in Collections:Vol.17, nº 1 (2002)

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