Abstract
Targeted antiangiogenic cancer therapies have revolutionized the treatment of highly vascularized cancers such as metastatic renal cell carcinoma and gastrointestinal stromal tumors. Such agents act by inhibiting the actions of proangiogenic growth factors and their receptor tyrosine kinases, which are known to be overexpressed in cancer. However, these factors also play an important role in normal cardiovascular physiology. This article summarizes the incidences of cardiovascular toxicities (namely hypertension and heart failure) associated with the most commonly used antiangiogenic therapies, and then presents data from preclinical and clinical studies to provide some insight into the underlying molecular mechanisms.
Copyright © 2011 Elsevier Inc. All rights reserved.
MeSH terms
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Angiogenesis Inducing Agents / metabolism
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Angiogenesis Inhibitors / administration & dosage
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Angiogenesis Inhibitors / adverse effects*
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Angiogenesis Inhibitors / metabolism
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Carcinoma, Renal Cell / complications*
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Carcinoma, Renal Cell / drug therapy
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Carcinoma, Renal Cell / metabolism
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Cardiotoxins
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Clinical Trials as Topic
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Drug Evaluation, Preclinical
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Gastrointestinal Stromal Tumors / complications*
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Gastrointestinal Stromal Tumors / drug therapy
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Gastrointestinal Stromal Tumors / metabolism
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Heart Failure* / chemically induced
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Heart Failure* / epidemiology
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Heart Failure* / metabolism
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Heart Failure* / prevention & control
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Humans
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Hypertension* / chemically induced
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Hypertension* / epidemiology
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Hypertension* / metabolism
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Hypertension* / prevention & control
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Incidence
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Molecular Targeted Therapy
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Neovascularization, Pathologic* / drug therapy
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Neovascularization, Pathologic* / etiology
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Neovascularization, Pathologic* / metabolism
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Organs at Risk
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Receptor Protein-Tyrosine Kinases / metabolism
Substances
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Angiogenesis Inducing Agents
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Angiogenesis Inhibitors
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Cardiotoxins
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Receptor Protein-Tyrosine Kinases