Abstract
Considerable evidence is gathering for the involvement of vascular endothelial growth factor (VEGF) in the vascularization and growth of primary tumours as well as in the formation of metastases. The expression of VEGF depends on activated oncogenes and inactivated tumour suppressor genes as well as several other factors (e.g. growth factors, tumour promoters and hypoxia). Substantial expression of the receptors for VEGF is restricted mainly to the tumour blood vessels. The causal involvement of this angiogenic factor in the progression of disease has been successfully evaluated by means of monoclonal antibodies against VEGF, dominant-negative receptor mutants and the use of antisense oligonucleotides against the VEGF mRNA. Thus, the VEGF signalling system seems to be an appropriate target to inhibit tumour angiogenesis and metastases formation.
MeSH terms
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Animals
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Biotechnology
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Endothelial Growth Factors / chemistry
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Endothelial Growth Factors / genetics
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Endothelial Growth Factors / physiology*
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Gene Expression Regulation, Neoplastic
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Genetic Therapy
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Humans
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Lymphokines / chemistry
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Lymphokines / genetics
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Lymphokines / physiology*
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Molecular Structure
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Neoplasms, Experimental / blood supply*
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Neoplasms, Experimental / genetics
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Neoplasms, Experimental / therapy*
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Neovascularization, Pathologic / genetics
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Neovascularization, Pathologic / therapy*
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Oligonucleotides, Antisense / therapeutic use
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Receptor Protein-Tyrosine Kinases / genetics
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Receptor Protein-Tyrosine Kinases / physiology
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Receptors, Growth Factor / genetics
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Receptors, Growth Factor / physiology
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Receptors, Vascular Endothelial Growth Factor
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Signal Transduction
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Vascular Endothelial Growth Factor A
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Vascular Endothelial Growth Factors
Substances
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Endothelial Growth Factors
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Lymphokines
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Oligonucleotides, Antisense
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Receptors, Growth Factor
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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