Trastuzumab-induced cardiotoxicity: is it a personalized risk?

Area of Science:

• Cardiology
• Oncology
• Pharmacology

Background:

• Trastuzumab (TZM) treatment can cause cardiotoxicity, potentially impacting patient compliance and recovery.
• Understanding the molecular mechanisms of TZM-induced cardiotoxicity is essential for risk prediction.
• HER2 signaling in cardiomyocytes, involving neuregulin and HER4, is vital for cardiac function.

Purpose of the Study:

• To review genetic, pharmacological, and clinical data to elucidate mechanisms of TZM-induced cardiotoxicity.
• To identify patient subgroups at higher risk for cardiac adverse events during TZM therapy.

Main Methods:

• Mini-review of existing literature.
• Analysis of genetic, pharmacological, and clinical data related to TZM and cardiotoxicity.
• Focus on HER2 signaling pathways in cardiomyocytes.

Main Results:

• The precise molecular mechanisms of TZM cardiotoxicity remain incompletely understood.
• HER2 genetic polymorphism, specifically the Val655Ile variant, is highlighted as a potential factor in identifying patients at risk.
• HER2 activity is critical for cardiomyocyte function, and its modulation by TZM can lead to cardiac dysfunction.

Conclusions:

• Identifying patients at risk for TZM cardiotoxicity is necessary for treatment adherence and long-term recovery.
• HER2 genetic polymorphism (Val655Ile) may serve as a predictive biomarker for TZM-induced cardiac effects.
• Further research into the molecular mechanisms can improve the safe and effective use of TZM.