Abstract
Cardiotoxicity remains an important adverse reaction of chemotherapy used in the treatment of breast cancer, leading to increased morbidity and mortality. Anthracyclines, taxanes, and trastuzumab are the most commonly used cytotoxic drugs for the treatment of breast cancer. Cardiotoxicity may vary from asymptomatic forms to irreducible heart failure and death. Susceptibility for the occurrence of chemotherapy-induced cardiotoxicity and treatment resistance is multifactorial, with interindividual variability, determined by the interaction between genetic and phenotypic factors. Implementation of pharmacogenomic findings into clinical practice might be useful, to predict cardiotoxicity and to allow appropriate therapeutic measures. This review will summarize the cellular mechanisms of chemotherapy-induced cardiotoxicity in breast cancer patients and will discuss the role of the genetic susceptibility for cardiac dysfunction.
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