Background. The process of multistep tumor development has been studie
d thoroughly in the development of malignant melanomas. The authors in
vestigated the expression of cellular adhesion molecules in nevomelano
cytic lesions to explore a postulated role of adhesion molecules in ce
ll-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 th
eir expression of intercellular adhesion molecule-1 (ICAM-1), inducibl
e cell adhesion molecule-110 (INCAM-110)/vascular cell adhesion molecu
le-1 (VCAM-1), E-selectin, lymphocyte function-associated antigen-1 (L
FA-1), and the integrins for very late antigen-(VLA) alpha-(alpha) 2 a
nd VLA-alpha 6; for these studies, monoclonal antibodies were used and
indirect immunoperoxidase and immunofluorescence staining methods wer
e performed. Results. In the transformation from benign to malignant n
eoplasms, the expression of ICAM-1 was upregulated strongly. The expre
ssion of VLA-alpha 2 on tumor cells increased whereas that of VLA-alph
a 6 decreased; these alterations corresponded to changes previously ob
served in their ligands within the extracellular matrix. These results
were statistically significant. In addition, ICAM-1, INCAM-11O/VCAM-1
, and E-selectin were detected in activated endothelial cells, probabl
y as a result of cytokine activation. The ligand for ICAM-1, LFA-1, wa
s confined to mononuclear cells. Conclusions. The increase in ICAM-1 a
nd VLA-alpha 2 expression and the decrease of VLA-alpha 6 expression m
ay, 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 INC
AM-11O/VCAM-1 and E-selectin in pigmented skin lesions may play a role
in both infiltrative growth and the generation of a host reaction tow
ard these tumors.