¹Laboratory of Histopathology, Istituto Dermopatico dell'Immacolata-Istituto di Ricovero e Cura a Carattere Scientifico (IDI-IRCCS), Rome, Italy

Correspondence: Dr B Bellei, PhD, Laboratory of Histopathology, Istituto Dermopatico dell'Immacolata, Via Monti di Creta 104, 00167 Rome, Italy. E-mail: b.bellei@libero.it

Received 23 February 2004; Revised 7 April 2004; Accepted 7 April 2004; Published online 11 June 2004.

Abstract

-Catenin is a ubiquitously cytoplasmic protein that has a critical role in embryonic development and mature tissue homeostasis through its effects on E-cadherin-mediated cell adhesion and Wnt-dependent signal transduction. Mutations that alter specific -catenin residues important for GSK-3 phosphorylation, or increase the half-life of the protein, were identified in human cancer. However, the role of the Wnt pathway in B- and T-cell oncogenesis has not been extensively investigated. To assess the role of -catenin defects in primary cutaneous lymphomas, we examined the expression pattern and the genetic alteration of -catenin on 79 samples from 74 patients with primary cutaneous lymphomas from B- and T-cell origin. Immunohistochemical analysis revealed -catenin deregulation in five primary cutaneous B-cell lymphomas (21%) and in 21 primary cutaneous T-cell lymphomas (42%) without nuclear accumulation suggesting that activation and accumulation of -catenin may play an important role in the development of skin lymphomas. Mutation analysis of -catenin exon 3, which included the responsible element for Wnt signaling, was therefore done in 19 samples. However, genetic alterations of -catenin exon 3 were not detected in any of these cases suggesting that other regulatory mechanisms may be relevant in activating -catenin signaling in cutaneous lymphomas.