The distribution of cellular adhesion molecules in pigmented skin lesions

Open Access
Publisher Website
Google Scholar
Abstract
Background. The process of multistep tumor development has been studied thoroughly in the development of malignant melanomas. The authors investigated the expression of cellular adhesion molecules in nevomelanocytic lesions to explore a postulated role of adhesion molecules in cell-cell and cell-matrix interactions during tumor development. Methods. Sections of 20 nevocellular nevi, 35 dysplastic nevi, 6 melanomas in situ, and 20 malignant melanomas were investigated with respect to their expression of intercellular adhesion molecule-1 (ICAM-1), inducible cell adhesion molecule-110 (INCAM-110)/vascular cell adhesion molecule-1 (VCAM-1), E-selectin, lymphocyte function-associated antigen-1 (LFA-1), and the integrins for very late antigen-(VLA) alpha-(α) 2 and VLA-α6; for these studies, monoclonal antibodies were used and indirect immunoperoxidase and immunofluorescence staining methods were performed. Results. In the transformation from benign to malignant neoplasms, the expression of ICAM-1 was upregulated strongly. The expression of VLA-α2 on tumor cells increased whereas that of VLA-α6 decreased; these alterations corresponded to changes previously observed in their ligands within the extracellular matrix. These results were statistically significant. In addition, ICAM-1, INCAM-110/VCAM-1, and E-selectin were detected in activated endothelial cells, probably as a result of cytokine activation. The ligand for ICAM-1, LFA-1, was confined to mononuclear cells. Conclusions. The increase in ICAM-1 and VLA-α2 expression and the decrease of VLA-α6 expression may, in combination with specific matrix alterations, lead to a change in cell-cell and cell-matrix interaction, thereby contributing to the invasive property of melanocytic tumor cells. The neoexpression of INCAM-110/VCAM-1 and E-selectin in pigmented skin lesions may play a role in both infiltrative growth and the generation of a host reaction toward these tumors.