EXPRESSION OF ADHESION MOLECULES AND EXTRACELLULAR-MATRIX PROTEINS INGLIOBLASTOMAS - RELATION TO ANGIOGENESIS AND SPREAD

Citation
D. Vitolo et al., EXPRESSION OF ADHESION MOLECULES AND EXTRACELLULAR-MATRIX PROTEINS INGLIOBLASTOMAS - RELATION TO ANGIOGENESIS AND SPREAD, Histopathology, 28(6), 1996, pp. 521-528
Citations number
43
Categorie Soggetti
Cell Biology",Pathology
Journal title
ISSN journal
03090167
Volume
28
Issue
6
Year of publication
1996
Pages
521 - 528
Database
ISI
SICI code
0309-0167(1996)28:6<521:EOAMAE>2.0.ZU;2-Z
Abstract
We studied the immunohistochemical expression of inducible adhesion mo lecules, integrins and extracellular matrix proteins in 10 cases of gl ioblastoma multiforme in order to investigate their angiogenesis, loca l invasiveness, poor metastasizing properties and their lack of tumour infiltrating leukocytes. In glioblastomas endothelial proliferations represent. the majority of vascular structures; they were positive for endothelial markers (vWF, CD31, VE-cadherin) and negative for macroph age markers (CD68, PAM-1), Immunohistologically, they were subtyped in to: 1 solid-glomeruloid ICAM-1, alpha(2) beta(1), alpha(3) beta 1, alp ha(5) beta(1) negative; 2 channelled-branching ICAM-1 negative and alp ha(2) beta(1), alpha(3) beta(1), alpha(5) beta(1) positive; 3 channell ed-telangiectatic ICAM-1, alpha(2) beta(1), alpha(3) beta(1), alpha(5) beta(1) positive, In channelled proliferations, the expression and di stribution of tenascin and merosin in the basal membrane was similar t o that of normal brain vessels, The expression of all these molecules might indicate different steps of maturation of endothelial proliferat ions, The majority of endothelial proliferations may be immunohistolog ically considered as incomplete vascular structures; this might accoun t for the low metastasizing tendency and low recruitment of leukocytes by these tumours, Neoplastic astrocytes were GFAP-1, ICAM-1, VCAM-1, alpha(2) beta(1), alpha(3) beta(1) and alpha(5) beta(1) immunoreactive and alpha(6) beta(4) negative; this allows them to interact with extr acellular matrix proteins and might, in part, explain the tendency of glioblastomas to infiltrate locally.