Cell adhesion molecules' altered profile in benign and malignant salivary gland tumors. The paradigm of beta4-integrin, desmoglein-2, ICAM-1 and CD44s.

Abstract

Background: Alterations in intercellular and cell-extracellular matrix connections contribute to tumour development. This study investigates the expression of specific cell adhesion molecules (CAMs) in salivary gland tumors (SGTs).

Methods: Formalin-fixed, paraffin- embedded tissue specimens of different types of 34 benign and 31 malignant SGTs and normal salivary glands were studied using Envision/HRP immunohistochemical technique for Desmoglein-2 (Dsg-2), beta4-integrin, CD44s and ICAM-1. Intensity of staining was evaluated in a semi-quantitative manner. Results were analyzed using Kendall's τ and Spearman's ρ as correlation criteria.

Results: Dsg-2 in intercellular space, beta4-integrin in cell-basal membrane, and CD44s in both types of contacts were strongly expressed in normal acinar and ductal cells, whereas ICAM-1 was expressed only at the endothelium and sparse stromal cells and monocytes. Strong correlation was found between Dsg-2 expression in adenomas and controls and between adenocarcinomas and controls. In adenomas, a distinct cytoplasmic presence of Dsg-2 was observed in addition to the usual membranous expression, with decreased expression in comparison with normal tissue. In malignant SGTs, Dsg-2 expression was absent. In most SGTs, beta4-integrin was expressed also with a distinct pattern, involving the cytoplasm and the unpolarised membrane, while CD44 was found only on the membrane. Strong correlation between beta4-integrin expression in adenomas and controls was noted, while CD44 expression was found to be correlated significantly between adenocarcinomas and controls (p < 0.001). Regarding ICAM-1, its expression was found increased in adenomas, with non-specific distribution in malignant SGTs and strong correlation between the histological subtypes and controls (p < 0.001).

Conclusion: The different expression profile of CAMs in SGTs could possibly suggest a role on their pathogenesis, representing a model of how neoplastic cells can take advantage of normal tissue architecture and cell-extracellular matrix interactions.