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
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.