Michelle C. Ward

The paper profiles gene expression in DOX-treated cardiomyocytes over time, identifying a chronic gene signature enriched for p53 target genes and DNA damage response genes.

The paper identifies RNA-protein modules linked to anthracycline-induced cardiotoxicity and atrial fibrillation risk through multi-omics integration.

This study compares the cardiotoxicity of CX-5461 and Doxorubicin in iPSC-derived cardiomyocytes, finding CX is less cytotoxic and induces fewer gene expression changes.

This study shows anthracyclines alter chromatin accessibility in cardiomyocytes, overlapping with cardiovascular disease risk loci.

The paper identifies DNA damage-associated protein co-expression modules in cardiomyocytes and shows their relationship to genetic variation tolerance and CVD risk.

The paper investigates the shared gene expression response to TOP2-inhibiting breast cancer drugs in cardiomyocytes and identifies genetic factors associated with inter-individual variation in cardiotoxicity.

The paper identifies gene-environment interactions in gene regulation across cell types and treatments, revealing many genes missed by GTEx.

The paper identifies dynamic eQTLs in cardiomyocytes under hypoxic stress, showing how genetic variation affects gene expression differently across conditions.

The paper investigates how non-genetic variability in iPSC lines affects their response to WNT inhibition and cardiac differentiation, identifying 91 signature genes and X chromosome dosage differences as key factors.

The paper compares hypoxia responses in human and chimpanzee iPSC-derived cardiomyocytes, finding conserved transcriptional responses and species-specific regulatory differences.

The paper examines H3K9me3 marking of transposable elements in human and chimpanzee induced pluripotent stem cells, finding limited species-specificity and no strong link to gene expression divergence.

The paper examines regulatory variation in iPSCs and differentiated cells, finding lower individual variation in iPSCs and identifying shared chromatin regions for some cell type-specific QTLs.