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01.09.2009 | Original Article | Ausgabe 3/2009

Virchows Archiv 3/2009

Adhesion molecules and p16 expression in endocervical adenocarcinoma

Zeitschrift:
Virchows Archiv > Ausgabe 3/2009
Autoren:
Elisabetta Carico, Franco Fulciniti, Maria Rosaria Giovagnoli, Nunzia Simona Losito, Gerardo Botti, Giulio Benincasa, Maria Giuseppina Farnetano, Aldo Vecchione

Abstract

An immunohistochemical (IHC) study has been conducted on 34 cases of untreated endocervical adenocarcinomas collected among three institutions (Ospedale S. Andrea, Rome; Istituto Nazionale Tumori “Fondazione G. Pascale”, Naples; and Clinica Malzoni, Avellino). The E-cadherin and α- and β-catenin complex status has been investigated along with p16INK4a in all studied cases with the aim to study whether the pattern of expression of the cadherin–catenin complex could be causally related to the expression of P16INK4a protein. Results were evaluated for statistical significance by a non-parametric test (Kruskal–Wallis). Endocervical adenocarcinomas as a group were uniformly expressing p16INK4a except for two cases, and all lesions displayed downregulation of the cadherin–catenin complex, without demonstrating statistically significant differences among the different histotypes. The lack of nuclear accumulation of β-catenin found in this group of lesions probably implies that no alteration of the β-catenin/Wnt metabolic pathway is present in endocervical adenocarcinoma, as opposed to what is found in the literature for squamous carcinoma of the cervix. The diffuse expression of p16INK4a protein in this group of neoplasms stresses the important role of high-risk human papillomavirus infection in neoplastic causation possibly via the viral E7-mediated inactivation of pRB tumor-suppressor protein and also underlines the useful role of p16INK4a immunostaining in the diagnostic algorithm of endocervical adenocarcinomas. In consideration of these findings, investigation of downstream β-catenin genes c-myc and cyclin D1 is sought as possibly contributive in the molecular pathogenesis of endocervical adenocarcinoma.

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