RGD Reference Report - Anthracyclines/trastuzumab: new aspects of cardiotoxicity and molecular mechanisms. - Rat Genome Database

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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/j.tips.2015.03.005. Epub 2015 Apr 17.
RGD ID: 10395260
Pubmed: PMID:25895646   (View Abstract at PubMed)
DOI: DOI:10.1016/j.tips.2015.03.005   (Journal Full-text)

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.



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Objects Annotated

Genes (Rattus norvegicus)
Top2a  (DNA topoisomerase II alpha)
Top2b  (DNA topoisomerase II beta)

Genes (Mus musculus)
Top2a  (topoisomerase (DNA) II alpha)
Top2b  (topoisomerase (DNA) II beta)

Genes (Homo sapiens)
TOP2A  (DNA topoisomerase II alpha)
TOP2B  (DNA topoisomerase II beta)


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