Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Anthracyclines/trastuzumab: new aspects of cardiotoxicity and molecular mechanisms.

Authors: Rochette, L  Guenancia, C  Gudjoncik, A  Hachet, O  Zeller, M  Cottin, Y  Vergely, C 
Citation: Rochette L, etal., Trends Pharmacol Sci. 2015 Jun;36(6):326-48. doi: 10.1016/ Epub 2015 Apr 17.
Pubmed: (View Article at PubMed) PMID:25895646
DOI: Full-text: DOI:10.1016/

Anticancer drugs continue to cause significant reductions in left ventricular ejection fraction resulting in congestive heart failure. The best-known cardiotoxic agents are anthracyclines (ANTHs) such as doxorubicin (DOX). For several decades cardiotoxicity was almost exclusively associated with ANTHs, for which cumulative dose-related cardiac damage was the use-limiting step. Human epidermal growth factor (EGF) receptor 2 (HER2; ErbB2) has been identified as an important target for breast cancer. Trastuzumab (TRZ), a humanized anti-HER2 monoclonal antibody, is currently recommended as first-line treatment for patients with metastatic HER2(+) tumors. The use of TRZ may be limited by the development of drug intolerance, such as cardiac dysfunction. Cardiotoxicity has been attributed to free-iron-based, radical-induced oxidative stress. Many approaches have been promoted to minimize these serious side effects, but they are still clinically problematic. A new approach to personalized medicine for cancer that involves molecular screening for clinically relevant genomic alterations and genotype-targeted treatments is emerging.


Molecular Pathway Annotations
Objects Annotated

Additional Information

RGD Object Information
RGD ID: 10395260
Created: 2015-08-27
Species: All species
Last Modified: 2015-08-27
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.