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pubmed:abstractText |
Breast cancer, a leading cause of increased morbidity and mortality among women, overexpresses the human epidermal growth factor receptor 2 in approximately 20% to 30% of cases. Trastuzumab (Trz), a monoclonal antibody against the human epidermal growth factor receptor 2, improves survival in breast cancer patients in both the adjuvant and metastatic settings. Despite the therapeutic benefits of Trz, there is an increased incidence of cardiotoxicity, particularly when administered following anthracycline-based chemotherapy. The pathogenesis underlying Trz-mediated cardiotoxicity remains poorly understood. The present review focuses on the current understanding of Trz-mediated cardiotoxicity from both the basic and clinical science perspectives.
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