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.

Author affiliations

1. Center for Translational Medicine and Cardiology Division, Department of Medicine, Thomas Jefferson University, 1025 Walnut Street, Philadelphia, Pennsylvania 19107, USA.
2. Department of Pathology, Massachusetts General Hospital, 55 Fruit Street, Boston, Massachusetts 02114, USA.
3. Molecular Oncology Research Institute and Division of Hematology/Oncology, Tufts-New England Medical Center, 750 Washington Street, Boston, Massachusetts 02111, USA.

Correspondence to: Thomas Force¹ Email: thomas.force@jefferson.edu

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