Abstract
Multiple myeloma (MM) progresses from an avascular to a vascular phase (active MM) accompanied by a significant increase in microvessel density in the bone marrow. This article summarizes the literature concerning the specific role played by vascular endothelial growth factor (VEGF) in this process. Recent applications of antiangiogenic agents that interfere with VEGF signaling and block MM progression are also described.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Angiogenesis Inhibitors / therapeutic use
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Disease Progression
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Endothelial Growth Factors / genetics
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Endothelial Growth Factors / physiology*
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Humans
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Intercellular Signaling Peptides and Proteins / genetics
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Intercellular Signaling Peptides and Proteins / physiology*
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Lymphokines / genetics
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Lymphokines / physiology*
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Multiple Myeloma / blood supply
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Multiple Myeloma / drug therapy
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Multiple Myeloma / physiopathology*
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Neovascularization, Pathologic
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Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors
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Receptors, Vascular Endothelial Growth Factor / genetics
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Receptors, Vascular Endothelial Growth Factor / physiology*
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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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Angiogenesis Inhibitors
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Endothelial Growth Factors
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Intercellular Signaling Peptides and Proteins
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Lymphokines
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Vascular Endothelial Growth Factor A
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Vascular Endothelial Growth Factors
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Receptors, Vascular Endothelial Growth Factor