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Transcriptomic analysis of the effect of trastuzumab in human iPSC-CMs

ABSTRACT: Transcriptomic analysis of the effect of trastuzumab in human iPSC-CMs

PROVIDER: PRJNA477344 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7407800_1.fastq.gz	Fastqsanger.gz
	SRR7407800_2.fastq.gz	Fastqsanger.gz
	SRR7407801_1.fastq.gz	Fastqsanger.gz
	SRR7407801_2.fastq.gz	Fastqsanger.gz
	SRR7407802_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of the effect of trastuzumab in human iPSC-CMs

Project description:We used human iPSC-CMs generated from healthy individuals and performed RNA-sequencing after 7 days of trastuzumab treatment to examine the mechanism associated with contraction dysfunction in iPSC-CMs after trastuzumab treatment. Transcriptome analysis revealed the key role of an altered energy metabolism pathway for cardiomyocytes in the disease pathogenesis.

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Transcriptomic analysis of the effect of iron overload in human iPSC-CMs

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Rhesus iPSC-CMs response to anoxia, comparing with human iPSC-CMs

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Project description:Trastuzumab is a monoclonal targeted therapy widely used to treat human epidermal growth factor receptor 2 (HER2+) over expressed breast cancer which confers an aggressive cancer type and comprises ~25% of breast cancer. Trastuzumab yields improved breast cancer related outcomes, but survival benefits are in part offset by cardiotoxicity - as evidenced by 10-15% of patients develop cardiomyopathy and 2-4% develop congestive heart failure. Approximately 20-30% of patients have either temporary or permanent discontinuation of trastuzumab therapy due to its cardiotoxicity, raising concern for inadequate cancer treatment and recurrence. Current screening strategies for trastuzumab-induced cardiotoxicity rely on non-invasive imaging such as echocardiography, but conventional imaging techniques provide limited a priori risk stratification for cardiotoxicity. We have utilized patient-specific iPSC-CMs derived from HER2+ breast cancer patients with and without evidence of TIC as a model to better elucidate the mechanisms of Trastuzumab-indued cardiotoxicity.

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

Project description:Background: The targeted ERBB2 therapy, trastuzumab, has had a tremendous impact on management of patients with HER2+ breast cancer, leading to development and increased use of further HER2 targeted therapies. The major clinical side effect is cardiotoxicity but the mechanism is largely unknown. On the basis that gene expression is known to be altered in multiple models of heart failure, we examined differential gene expression of iPSC derived cardiomyocytes treated at day 11 with the ERBB2 targeted monoclonal antibody, trastuzumab for 48 hours and the small molecule tyrosine kinase inhibitor of EGFR and ERBB2. Methods: Transcriptome sequencing was performed on four replicates from each group (48 hours untreated, 48 hours trastuzumab and 48 hours lapatinib) and differential gene expression analyses were performed on each treatment group relative to untreated cardiomyocytes. Results: 517 and 1,358 genes were differentially expressed, p<0.05, respectively in cardiomyocytes treated with trastuzumab and lapatinib. Gene ontology analyses revealed in cardiomyocytes treated with trastuzumab, significant down-regulation of genes involved in small molecule metabolism (p=3.22x10-9) and cholesterol (p=0.01) and sterol (p=0.03) processing. Conclusions: Our study suggests dysregulation of cardiac gene expression and metabolism as key elements of ERBB2 signaling that could potentially be early biomarkers of cardiotoxicity.

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