Basal cell carcinomas (BCCs) are frequently associated with a peritumo
ral mononuclear infiltrate. Until now, the function of this inflammato
ry infiltrate and its possible role in the control of tumor growth is
unclear. Mechanisms controlling endothelial and target cell adhesivene
ss for leukocytes are important features in the development of a speci
fic local immune response. The expression and distribution of the adhe
sion molecules ICAM-1, VCAM-1 and E-selectin by microvascular endothel
ial cells and tumor cells, together with their leukocyte receptors LFA
-1, VLA-4 and CLA respectively, were studied in 33 BCCs of different h
istological subtypes, in normal skin, ICAM-1 is expressed by resting e
ndothelial cells, whereas VCAM-1 and E-selectin expression correlates
with endothelial activation. The epidermis in normal conditions displa
ys no ICAM-1, VCAM-1, or E-selectin expression. In BCC, endothelial IC
AM-1 expression was only slightly increased compared to normal skin, w
hereas expression of endothelial VCAM-1 and E-selectin was low or abse
nt in all BCCs examined, Peritumoral infiltrates contained mostly LFA-
1-expressing lymphocytes, with minimal VLA-4 and CLA positivity. In no
ne of the cases studied was adhesion molecule expression by BCC tumor
cells identified. The lack of significant expression of adhesion molec
ules on peritumoral vascular endothelial cells and BCC tumor cells doe
s not support the idea of specific, cell-mediated immunity being an im
portant mechanism in limiting BCC tumor spread.