E-cadherin/catenin complex in benign and malignant melanocytic lesions

Citation
R. Silye et al., E-cadherin/catenin complex in benign and malignant melanocytic lesions, J PATHOLOGY, 186(4), 1998, pp. 350-355
Citations number
27
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
JOURNAL OF PATHOLOGY
ISSN journal
00223417 → ACNP
Volume
186
Issue
4
Year of publication
1998
Pages
350 - 355
Database
ISI
SICI code
0022-3417(199812)186:4<350:ECIBAM>2.0.ZU;2-#
Abstract
E-cadherin is a calcium-dependent cell-cell adhesion molecule expressed by melanocytes and responsible for their adhesion to keratinocytes in vitro. I n this study, the expression of E-cadherin and its associated cytoplasmic p roteins alpha, beta-, and gamma-catenin was evaluated in melanocytic lesion s by immunohistochemistry. E-cadherin expression was evaluated in 70 malign ant melanomas and the catenins in 35 of these specimens. Twenty benign mela nocytic naevi were also evaluated for E-cadherin and catenin expression. In normal epidermis, E-cadherin/catenin immunostaining was localized at the i ntercellular borders. In melanomas, a differential loss of E-cadherin expre ssion was observed. Membranous E-cadherin staining was absent in dermal nes ts of melanomas in their radial growth phase and in Clark level II and III lesions, whereas it was present in a high proportion of melanomas in their vertical growth phase, in Clark level IV and V lesions and in metastasizing melanomas. In contrast, superficial compartments of naevi show-ed membrano us E-cadherin immunoreactivity and junctional naevus cell nests displayed h eterogeneous or diffuse cytoplasmic staining. Cytoplasmic alpha- and beta-c atenin, but not gamma-catenin staining were detected in all benign and mali gnant lesions. These findings indicate that qualitative changes in the expr ession and cellular localization of E-cadherin and of alpha-, beta-, and ga mma-catenin occur in melanocytic lesions and mag reflect different stages i n their progression. (C) 1998 John Wiley & Sons, Ltd.