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January 18, 2017Clinical and Translational MedicineOpen Access

The antineoplastic drug, trastuzumab, dysregulates metabolism in iPSC‐derived cardiomyocytes

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Population

Human iPSC-derived cardiomyocytes and ERBB2-overexpressing breast cancer cell lines

Comparison

Trastuzumab or lapatinib for 48 hours vs Untreated cells

Design

Preclinical

Follow-up

up to 96 hours

Authors

BNBrian M. NecelaNemours Children’s ClinicBABianca C. AxenfeldMayo Clinic in FloridaDSDaniel SerieFederal Reserve Bank of San Francisco

Discussion

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Implication

May identify trastuzumab cardiotoxicity pathways in iPSC-CMs; leaves open clinical translation.

Structured PICO

P
Population
Human iPSC-derived cardiomyocytes (iCell) and ERBB2-overexpressing breast cancer cell lines (SKBR3, BT474, HCC1954, MDA-MB-453, HCC1569, and HCC1419)
I
Intervention
Trastuzumab (100 µg/mL) or lapatinib (2 µM) for 48 hours (up to 96 hours for metabolic assays)
C
Comparator
Untreated cells
O
Outcome
Differential gene expression (via transcriptome sequencing) and metabolic changes (glucose uptake and lactate production)surrogate

Trastuzumab induces early dysregulation of cardiac gene expression and metabolism, specifically decreasing glucose uptake, which may represent an early mechanism and potential biomarker of cardiotoxicity.

Cite This Study

Necela et al. (2017) studied this question.

synapsesocial.com/papers/6a73e3580375516f85f161cchttps://doi.org/10.1186/s40169-016-0133-2
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