title: Prevention of anthracycline-induced cardiotoxicity: challenges and opportunities.
abstract: Anthracycline compounds are major culprits in chemotherapy-induced cardiotoxicity, which is the chief limiting factor in delivering optimal chemotherapy to cancer patients. Although extensive efforts have been devoted to identifying strategies to prevent anthracycline-induced cardiotoxicity, there is little consensus regarding the best approach. Recent advances in basic mechanisms of anthracycline-induced cardiotoxicity provided a unified theory to explain the old reactive-oxygen species hypothesis and identified topoisomerase 2β as the primary molecular target for cardioprotection. This review outlines current strategies for primary and secondary prevention of anthracycline-induced cardiotoxicity resulting from newly recognized molecular mechanisms and identifies knowledge gaps requiring further investigation.
authors.affiliation: The University of Texas MD Anderson Cancer Center, Houston, Texas.
authors.forename: Pimprapa
authors.initials: P
authors.lastname: Vejpongsa
authors.affiliation: The University of Texas MD Anderson Cancer Center, Houston, Texas; Texas Heart Institute, Houston, Texas. Electronic address: etyeh@mdanderson.org.
authors.forename: Edward T H
authors.initials: ET
authors.lastname: Yeh
mesh_terms: D018943:Anthracyclines / Q000009:adverse effects*; D000903:Antibiotics, Antineoplastic / Q000009:adverse effects*; D002986:Clinical Trials as Topic; D004317:Doxorubicin / Q000627:therapeutic use; D006331:Heart Diseases / Q000139:chemically induced* / Q000517:prevention & control*; D006333:Heart Failure / Q000150:complications; D006801:Humans; D009369:Neoplasms / Q000150:complications / Q000188:drug therapy*; D017382:Reactive Oxygen Species
chemical_list: D018943:Anthracyclines; D000903:Antibiotics, Antineoplastic; D017382:Reactive Oxygen Species; D004317:Doxorubicin
keywords: cancer; cardiomyopathy; cardioprotection; chemotherapy; doxorubicin; heart failure