| Why do kinase inhibitors cause cardiotoxicity and what can be done about it? | |
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MedLine Citation:
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PMID: 20728698 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Cancer growth and metastasis are often driven by activating mutations in, or gene amplications of, specific tyrosine or serine/threonine kinases. Kinase inhibitors (KIs) promised to provide targeted therapy-specifically inhibiting the causal or contributory kinases driving tumor progression while leaving function of other kinases intact. These inhibitors are of 2 general classes: (1) monoclonal antibodies that are typically directed against receptor tyrosine kinases or their ligands and (2) small molecules targeting specific kinases. The latter will be the focus of this review. This class of therapeutics has had some remarkable successes, including revolutionizing the treatment of some malignancies (eg, imatinib [Gleevec] in the management of chronic myeloid leukemia) and adding significantly to the management of other difficult to treat cancers (eg, sunitinib [Sutent] and sorafenib [Nexavar] in the management of renal cell carcinoma). But in some instances, cardiotoxicity, often manifest as left ventricular dysfunction and/or heart failure, has ensued after the use of KIs in patients. Herein we will explore the mechanisms underlying the cardiotoxicity of small-molecule KIs, hoping to explain how and why this happens, and will further examine strategies to deal with the problem. |
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Authors:
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Hui Cheng; Thomas Force |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Progress in cardiovascular diseases Volume: 53 ISSN: 1873-1740 ISO Abbreviation: Prog Cardiovasc Dis Publication Date: 2010 Sep-Oct |
Date Detail:
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Created Date: 2010-08-23 Completed Date: 2010-09-27 Revised Date: 2013-05-02 |
Medline Journal Info:
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Nlm Unique ID: 0376442 Medline TA: Prog Cardiovasc Dis Country: United States |
Other Details:
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Languages: eng Pagination: 114-20 Citation Subset: AIM; IM |
Copyright Information:
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Copyright 2010 Elsevier Inc. All rights reserved. |
Affiliation:
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Center for Translational Medicine and Cardiology Division, Thomas Jefferson University, Philadelphia, PA 19107, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antineoplastic Agents / adverse effects*, chemistry Drug Design Heart Failure / chemically induced*, pathology, prevention & control Humans Myocytes, Cardiac / drug effects*, pathology Neoplasms / drug therapy*, enzymology Protein Kinase Inhibitors / adverse effects*, chemistry Risk Assessment Structure-Activity Relationship Ventricular Dysfunction, Left / chemically induced*, pathology, prevention & control |
| Chemical | |
Reg. No./Substance:
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0/Antineoplastic Agents; 0/Protein Kinase Inhibitors |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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