Abstract
Recent studies on angiogenesis in human solid tumors have underlined its importance as therapeutic target. In particular, of interest is to suppress the function of several positive regulators including vascular endothelial growth factors (VEGF), basic fibroblast growth factor and thymidine phosphorylase, because they are evident to be responsible for the promotion of neovascularization in a variety of tumor types. In this review, we picked up VEGF, probably one of most promising target, and discuss about the therapeutic tools for controlling VEGF function in human tumors.
MeSH terms
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Antibiotics, Antineoplastic / pharmacology
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Antibiotics, Antineoplastic / therapeutic use*
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Cyclohexanes
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Endothelial Growth Factors / antagonists & inhibitors*
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Endothelial Growth Factors / metabolism
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Humans
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Lymphokines / antagonists & inhibitors*
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Lymphokines / metabolism
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Neoplasms / blood supply*
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Neoplasms / drug therapy
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Neoplasms / metabolism
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Neovascularization, Pathologic / drug therapy*
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O-(Chloroacetylcarbamoyl)fumagillol
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Receptor Protein-Tyrosine Kinases / antagonists & inhibitors
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Receptor Protein-Tyrosine Kinases / metabolism
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Receptors, Growth Factor / antagonists & inhibitors
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Receptors, Growth Factor / metabolism
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Receptors, Vascular Endothelial Growth Factor
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Sesquiterpenes / pharmacology
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Sesquiterpenes / therapeutic use*
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Vascular Endothelial Growth Factor A
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Vascular Endothelial Growth Factors
Substances
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Antibiotics, Antineoplastic
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Cyclohexanes
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Endothelial Growth Factors
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Lymphokines
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Receptors, Growth Factor
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Sesquiterpenes
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Vascular Endothelial Growth Factor A
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Vascular Endothelial Growth Factors
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Receptor Protein-Tyrosine Kinases
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Receptors, Vascular Endothelial Growth Factor
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O-(Chloroacetylcarbamoyl)fumagillol