曲妥单抗诱导的心脏毒性：它是否是一个个体化的风险因素？

Title:Trastuzumab-Induced Cardiotoxicity: Is it a Personalized Risk?

Volume: 15 Issue: 13

Author(s): Gerard A. Milano, Emilie Serres, Jean-Marc Ferrero and Joseph Ciccolini

Affiliation:

关键词: 心脏毒性，遗传多态性，人类表皮生长因子受体2，个体化治疗，曲妥单抗

摘要: Optimal identification of the risk of developing cardiotoxicity upon trastuzumab (TZM) treatment appears necessary as this risk may impair treatment compliance and compromise long-term recovery. To better understand and predict cardiac toxicity, the molecular mechanisms underlying this phenomenon need to be known. HER2 is present at the cell surface of cardiomyocytes. Neuregulin is produced by cardiac endothelial cells and binds to HER4, thus leading to dimerization with HER2 and subsequent cell signaling necessary for normal cardiac function. Decreasing HER2 activity has a major impact on cardiomyocyte function. However, the precise molecular mechanisms responsible for TZM-induced cardiac dysfunction are still unclear. This mini-review aims to summarize genetic, pharmacological and medical data helping to identify mechanisms that could explain cardiotoxicity. Of potential interest, these mechanisms highlight the importance of HER2 genetic polymorphism (Val655Ile) in the identification of patients at risk of developing TZMinduced cardiac effects.

Cite this article as:

Gerard A. Milano, Emilie Serres, Jean-Marc Ferrero and Ciccolini Joseph, Trastuzumab-Induced Cardiotoxicity: Is it a Personalized Risk?, Current Drug Targets 2014; 15 (13) . https://dx.doi.org/10.2174/1389450115666141114151911