Abstract
We report the suppressed vascular CD34 expression in renal cell carcinoma. This was found by quantitatively analyzing CD34 expression on normal and tumor derived EC by flow cytometry. In vitro studies revealed that culture of umbilical cord or dermis derived microvascular EC with angiogenic factors such as basic fibroblast growth factor (bFGF) and vascular endothelial cell growth factor induced downregulation of CD34. This angiogenesis-induced downregulated expression of CD34 adhesion molecule may contribute to the tumor mediated escape mechanism from immune surveillance. It is concluded that there are quantitative differences in expression of endothelial CD34 in different compartments of the vasculature, that angiogenic factors affect this expression and that subpopulations of EC exist with differences in EAM expression.
MeSH terms
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Antibodies / metabolism
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Antigens, CD34 / metabolism*
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Bromodeoxyuridine / analysis
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Carcinoma, Renal Cell / metabolism*
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Cell Division / drug effects
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E-Selectin / metabolism
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Endothelial Growth Factors / pharmacology
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Endothelium, Vascular / chemistry
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Endothelium, Vascular / drug effects
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Endothelium, Vascular / metabolism*
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Fibroblast Growth Factor 2 / pharmacology
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Flow Cytometry
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Humans
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Hyaluronan Receptors / metabolism
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Intercellular Adhesion Molecule-1 / immunology
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Kidney / metabolism
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Kidney Neoplasms / metabolism*
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Lymphokines / pharmacology
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Platelet Endothelial Cell Adhesion Molecule-1 / immunology
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Tumor Necrosis Factor-alpha / pharmacology
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Vascular Endothelial Growth Factor A
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Vascular Endothelial Growth Factors
Substances
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Antibodies
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Antigens, CD34
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E-Selectin
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Endothelial Growth Factors
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Hyaluronan Receptors
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Lymphokines
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Platelet Endothelial Cell Adhesion Molecule-1
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Tumor Necrosis Factor-alpha
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Vascular Endothelial Growth Factor A
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Vascular Endothelial Growth Factors
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Fibroblast Growth Factor 2
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Intercellular Adhesion Molecule-1
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Bromodeoxyuridine