{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE312nnn/GSE312602/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE312602"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Protective effects of metformin against ponatinib-induced toxicity in iPSC-derived cardiomyocytes","description":"Aims: Ponatinib is currently considered the most effective treatment for patients with chronic myeloid leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL), who develop resistance or intolerance to first- and second-line therapy, particularly those with T315I \"gatekeeper\" mutation in BCR-ABL. However, ponatinib is also one of the most cardiotoxic tyrosine kinase inhibitors (TKIs), with toxicity stemming from a combination of contractile dysfunction and inflammatory effects. Our goal was to model and investigate this toxicity in human-induced pluripotent stem-cell derived cardiomyocytes (hiPSC-CMs) and to evaluate whether metformin, a clinically well-tolerated antidiabetic drug with known cardioprotective potential via AMPK pathway activation in various pathologies, can mitigate the damage.","dates":{"publication":"2026/06/02"},"accession":"GSE312602","cross_references":{"GSM":["GSM9349923","GSM9349912","GSM9349913","GSM9349921","GSM9349922","GSM9349916","GSM9349917","GSM9349914","GSM9349915","GSM9349918","GSM9349919","GSM9349920"],"GPL":["24676"],"GSE":["312602"],"taxon":["Homo sapiens"]}}