Abstract

This Introduction is the first article in a new thematic series on Cardiovascular Toxicities/Effects of Anticancer Therapeutics , which includes the following articles: Introduction to Cardiotoxicity Review Series Molecular Mechanisms of Cardiovascular Toxicity of Targeted Cancer Therapeutics The Vulnerability of the Heart as a Pluricellular System: Lessons From Unexpected Triggers of Heart Failure in Targeted Cancer Therapy Cardiovascular Disease: Hidden Killer in Adult Survivors of Childhood Cancer Emerging Anticancer Strategies: Is There Cause for Concern? Yes! Thomas Force Guest Editor Nowhere have greater strides been made in the treatment of lethal diseases than in oncology. Part of this stems from the fact that in the majority of cancers, tissue is available to clinicians and researchers. This has allowed the identification of specific mutations and/or gene amplifications that drive cell transformation and cancer progression. Not surprisingly, these proteins have become central targets for anticancer drug therapy. Many of these mutations or amplifications are in tyrosine kinases1 or, to a lesser extent, serine-threonine kinases, and identification of these has created an explosion in the development of “targeted therapeutics,” drugs aimed specifically at the causal or contributory molecule(s) driving the cancer. Targeted therapeutics directed at specific kinases are either small molecule inhibitors or monoclonal antibodies. This field has had some notable clinical successes, including the monoclonal antibody trastuzumab (Herceptin) that targets the human epidermal growth factor …

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