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Expression of adhesion molecules and extracellular matrix proteins in glioblastomas: relation to angiogenesis and spread
Author(s) -
VITOLO D.,
PARADISO P.,
UCCINI S.,
RUCO L.P.,
BARONI C.D.
Publication year - 1996
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1046/j.1365-2559.1996.d01-471.x
Subject(s) - extracellular matrix , angiogenesis , cell adhesion molecule , beta (programming language) , cd31 , alpha (finance) , pathology , integrin , biology , tenascin c , immunohistochemistry , tenascin , cancer research , microbiology and biotechnology , immunology , fibronectin , medicine , cell , biochemistry , construct validity , nursing , patient satisfaction , computer science , programming language
We studied the immunohistochemical expression of inducible adhesion molecules, integrins and extracellular matrix proteins in 10 cases of glioblastoma multiforme in order to investigate their angiogenesis, local 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 macrophage markers (CD68, PAM‐1). Immunohistologically, they were subtyped into: 1 solid‐glomeruloid ICAM‐1, α 2 β 1 , α 3 β 1 , α 5 β 1 negative; 2 channelled‐branching ICAM‐1 negative and α 2 β 1 , α 3 β 1 , α 5 β 1 positive; 3 channelled‐telangiectatic ICAM‐1, α 2 β 1 , α 3 β 1 , α 5 β 1 positive. In channelled proliferations, the expression and distribution of tenascin and merosin in the basal membrane was similar to that of normal brain vessels. The expression of all these molecules might indicate different steps of maturation of endothelial proliferations. The majority of endothelial proliferations may be immunohistologically considered as incomplete vascular structures; this might account for the low metastasizing tendency and low recruitment of leukocytes by these tumours. Neoplastic astrocytes were GFAP‐1, ICAM‐1, VCAM‐1, α 2 β 1 , α 3 β 1 and α 5 β 1 immunoreactive and α 6 β 4 negative; this allows them to interact with extracellular matrix proteins and might, in part, explain the tendency of glioblastomas to infiltrate locally.