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Immunohistochemical analysis of integrin αvβ3 expression on tumor‐associated vessels of human carcinomas
Author(s) -
Max Regina,
Gerritsen Roland R.C.M.,
Nooijen Peet T.G.A.,
Goodman Simon L.,
Sutter Arne,
Keilholz Ulrich,
Ruiter Dirk J.,
De Waal Robert M.W.
Publication year - 1997
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19970502)71:3<320::aid-ijc2>3.0.co;2-#
Subject(s) - pathology , immunohistochemistry , angiogenesis , biology , monoclonal antibody , carcinoma , alpha (finance) , antibody , medicine , cancer research , immunology , construct validity , nursing , patient satisfaction
Expression of the αvβ3 integrin is upregulated on sprouting endothelia. Systemic application of antibody or peptidic inhibitors of αvβ3 function disrupts tumor angiogenesis and reduces growth and invasiveness of human tumors in animal models. We systematically investigated αvβ3 expression on tumor‐associated vessels of 4 different human epithelial tumors and the corresponding normal tissues by means of immunohistochemistry on frozen sections using the αvβ3‐complex specific monoclonal antibody LM609. Variable levels of LM609 staining were found in all carcinoma lesions. A considerable number of tumor tissues (35/50) expressed αvβ3 on more than 50% of their vessels. Inflammatory infiltrates and the possibly hypoxic conditions near necrotic areas of tumors were accompanied by an increased αvβ3 expression. Remarkably, the vasculature in apparently normal tissue also stained for αvβ3. However, the percentages of stained vessels and their staining intensity were lower than in neoplastic tissues. Besides the vascular αvβ3 expression, several extravascular cell types stained positive, in both normal and tumor specimens. Taken together, our findings show a considerable number of colon, pancreas, lung and breast carcinoma lesions with many αvβ3‐expressing vessels that could be targets for anti‐αvβ3‐therapy. Int. J. Cancer 71:320‐324, 1997. © 1997 Wiley‐Liss Inc.