ADHESION MOLECULE EXPRESSION IN BASAL-CELL-CARCINOMA

Citation
M. Verhaegh et al., ADHESION MOLECULE EXPRESSION IN BASAL-CELL-CARCINOMA, EJD. European journal of dermatology, 8(4), 1998, pp. 252-255
Citations number
23
Categorie Soggetti
Dermatology & Venereal Diseases
ISSN journal
11671122
Volume
8
Issue
4
Year of publication
1998
Pages
252 - 255
Database
ISI
SICI code
1167-1122(1998)8:4<252:AMEIB>2.0.ZU;2-G
Abstract
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.