%0 Journal Article %1 Force.2007 %A Force, T. %A Krause, D. S. %A van Etten, R. A. %D 2007 %J Nat.Rev.Cancer %K & Adaptor Antibodies Benzenesulfonates Biological Delivery Diseases Drug Enzyme Heart Human Humans Indoles Inhibitors Kinase Kinases Models Monoclonal Mutation Neoplasms Protein Protein-Tyrosine Proteins Proto-Oncogene Pyridines Pyrroles Quinazolines Research Signal Systems Transducing Tyrosine adverse antagonists c-abl cells chemically development drug effects growth induced inhibitors physiology protein response therapy toxicity %N 5 %P 332-344 %T Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition %U PM:17457301 %V 7 %X Cancer therapy has progressed remarkably in recent years. In no area has this been more apparent than in the development of "targeted therapies", particularly those using drugs that inhibit the activity of certain tyrosine kinases, activating mutations or amplifications of which are causal, or strongly contributory, to tumorigenesis. However, some of these therapies have been associated with toxicity to the heart. Here we summarize what is known about the cardiotoxicity of cancer drugs that target tyrosine kinases. We focus on basic mechanisms through which interruption of specific signalling pathways leads to cardiomyocyte dysfunction and/or death, and contrast this with therapeutic responses in cancer cells

@article{Force.2007, abstract = {Cancer therapy has progressed remarkably in recent years. In no area has this been more apparent than in the development of "targeted therapies", particularly those using drugs that inhibit the activity of certain tyrosine kinases, activating mutations or amplifications of which are causal, or strongly contributory, to tumorigenesis. However, some of these therapies have been associated with toxicity to the heart. Here we summarize what is known about the cardiotoxicity of cancer drugs that target tyrosine kinases. We focus on basic mechanisms through which interruption of specific signalling pathways leads to cardiomyocyte dysfunction and/or death, and contrast this with therapeutic responses in cancer cells}, added-at = {2010-02-05T11:28:39.000+0100}, author = {Force, T. and Krause, D. S. and van Etten, R. A.}, biburl = {https://www.bibsonomy.org/bibtex/2602435fc1730c5168f565863b795701d/kanefendt}, interhash = {7940d75fc61c61f652ebc5312233fb8d}, intrahash = {602435fc1730c5168f565863b795701d}, journal = {Nat.Rev.Cancer}, keywords = {& Adaptor Antibodies Benzenesulfonates Biological Delivery Diseases Drug Enzyme Heart Human Humans Indoles Inhibitors Kinase Kinases Models Monoclonal Mutation Neoplasms Protein Protein-Tyrosine Proteins Proto-Oncogene Pyridines Pyrroles Quinazolines Research Signal Systems Transducing Tyrosine adverse antagonists c-abl cells chemically development drug effects growth induced inhibitors physiology protein response therapy toxicity}, number = 5, pages = {332-344}, timestamp = {2010-02-05T11:28:55.000+0100}, title = {Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition}, url = {PM:17457301}, volume = 7, year = 2007 }