Why the study?
EGFR-TKIs carry a reported risk of cardiac dysfunction, but their cardiotoxicity is not fully understood.
Do EGFR-TKIs cause cardiotoxicity as measured by decreased contractility in human iPS cell-derived cardiomyocytes and real-world pharmacovigilance data?
Do EGFR-TKIs cause cardiotoxicity as measured by decreased contractility in human iPS cell-derived cardiomyocytes and real-world pharmacovigilance data?
Contractile analysis using human iPS cell-derived cardiomyocytes is a useful in vitro model to assess and predict TKI-induced cardiac dysfunction in humans.
EGFR-TKI cardiotoxicity risk in NSCLC remains incompletely defined; leaves open need for prospective monitoring studies.
【Introduction】Tyrosine kinase inhibitors (TKIs) have improved the survival of patients with various types of cancer. Growing evidence suggest that cancer therapy-related cardiotoxicity has become important as the serious adverse event associated with many TKIs. Epidermal growth factor receptor-TKI (EGFR-TKI), which has demonstrated efficacy in patients with non-small-cell lung cancer, has been reported to have a risk of cardiac dysfunction. However, cardiotoxicity of EGFR-TKIs has not been fully understood. Here we evaluated the effects of EGFR-TKIs on contractility using human iPS cell-derived cardiomyocytes (hiPSC-CMs).
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Yanagida et al. (2022) studied this question.
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