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Gains and losses of adhesion molecules (CD44, E‐cadherin, and β‐catenin) during oral carcinogenesis and tumour progression
Author(s) -
Bánkfalvi Agnes,
Kraßort Melanie,
Buchwalow Igor B.,
Végh Andras,
Felszeghy Endre,
Piffkó Jozsef
Publication year - 2002
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1204
Subject(s) - cadherin , cd44 , catenin , pathology , carcinogenesis , cell adhesion molecule , biology , metastasis , immunohistochemistry , basal (medicine) , cancer , cancer research , phenotype , medicine , cell , immunology , wnt signaling pathway , gene , endocrinology , genetics , insulin
Abstract The aim of this study was to define whether or not the impaired expression of CD44, E‐cadherin (E‐cad), and β‐catenin (β‐cat) correlates with the clinical evolution and prognosis of oral cancer. Ninety‐three primary oral squamous cell carcinomas (OSCCs) with tumour‐adjacent normal and/or dysplastic mucosa, 30 associated metastases, and 12 recurrences were immunostained for CD44s, ‐v3, ‐v4, ‐v5, ‐v6, ‐v7, ‐v9, E‐cad, and β‐cat. In non‐neoplastic epithelium, all molecules investigated were constitutively expressed in the basal layers. In the majority of dysplasias, immunoreactivity for all adhesion molecules was increased, but there was restricted loss for CD44s, E‐cad, and β‐cat in a few cases. In carcinomas, a striking accumulation of CD44s, v3, v4, v9 and a loss of E‐cad/β‐cat were observed at the invasive tumour front. In metastases and recurrences, besides a loss of CD44s, v4, v7, and E‐cad, a significant increase of v9 was recorded, whereas CD44v5 and v6 remained unchanged. Clinically, reduced expression of CD44v3, E‐cad, and changes of CD44v9 phenotype within the primary tumours correlated significantly with poor prognosis; decreased β‐cat expression was a predictive marker for nodal metastases. These findings indicate that there is some perturbed expression of adhesion molecules during the stepwise course of oral carcinogenesis and tumour progression. Distinct phenotypic alterations project poor prognosis, while others predict metastasis. Some of these restricted molecular changes may serve as potential targets for future antibody‐based tumour therapy. Copyright © 2002 John Wiley & Sons, Ltd.