Abstract
Despite aggressive surgery, radiotherapy and chemotherapy, malignant gliomas remain uniformly fatal. To progress, these tumours stimulate the formation of new blood vessels through processes driven primarily by vascular endothelial growth factor (VEGF). However, the resulting vessels are structurally and functionally abnormal, and contribute to a hostile microenvironment (low oxygen tension and high interstitial fluid pressure) that selects for a more malignant phenotype with increased morbidity and mortality. Emerging preclinical and clinical data indicate that anti-VEGF therapies are potentially effective in glioblastoma--the most frequent primary brain tumour--and can transiently normalize tumour vessels. This creates a window of opportunity for optimally combining chemotherapeutics and radiation.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Antineoplastic Agents / pharmacology*
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Blood Vessels / drug effects
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Blood Vessels / pathology
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Blood Vessels / physiopathology
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Brain Edema / pathology
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Brain Edema / physiopathology
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Brain Edema / prevention & control
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Brain Neoplasms / blood supply*
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Brain Neoplasms / drug therapy
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Brain Neoplasms / physiopathology*
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Glioblastoma / blood supply
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Glioblastoma / drug therapy
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Glioblastoma / physiopathology
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Humans
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Neovascularization, Pathologic / drug therapy
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Neovascularization, Pathologic / metabolism*
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Neovascularization, Pathologic / physiopathology*
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Vascular Endothelial Growth Factor A / antagonists & inhibitors*
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Vascular Endothelial Growth Factor A / metabolism
Substances
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Antineoplastic Agents
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Vascular Endothelial Growth Factor A