LAUSR

Purpose of review Advances in cancer treatments have resulted in significant improvements in survival. Anthracycline chemotherapeutics play a major role in the treatment of hematologic malignancies and solid tumors; however, there is a risk of anthracycline cardiomyopathy in survivors. This focused review will provide a historical context on anthracycline cardiomyopathy and will also review pathophysiologic mechanisms of cardiotoxicity, dosage recommendations, prognosis, and outcomes. Recent findings Anthracycline inhibition of topoisomerase 2&bgr; in cardiomyocytes is believed to be the dominant mechanism of anthracycline-related cardiotoxicity. Emerging data suggest that downregulation of the RNA-binding protein quaking 5 may also be contributing. There is continued lack of agreement regarding what dosage of anthracycline is associated with the highest risk of cardiotoxicity. Summary Ongoing research into the mechanisms of anthracycline cardiotoxicity is warranted to allow for the development of targeted preventive therapies. A consensus definition of anthracycline cardiomyopathy will facilitate analyses of existing data and allow for the conduction of prospective clinical trials in this area.