{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE318nnn/GSE318882/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE318882"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"A complex mutational signature generated by cytarabine resistance","description":"T cell acute lymphoblastic leukemia (T-ALL) patients generally respond well to chemotherapy, but T-ALL cells at relapse are typically resistant to chemotherapy. The specific mechanisms leading to chemoresistance are incompletely understood. Here we use Mcm2 hypomorph (Mcm2hypo) T-ALL cell lines, which are prone to copy number variant mutations, to identify acquired mutations that underlie chemoresistance. We successfully generated 11 chemotherapy-resistant T-ALL cell lines, identifying excellent candidate genes responsible for resistance due to acquired mutations, including CNV, SNV, and small indels.These candidates included amplification of Abcb1a/b associated with vincristine resistance, amplification of Dhfr associated with methotrexate resistance, loss of Nr3c1 associated with prednisone resistance and loss of Dck associated with cytarabine resistance.","dates":{"publication":"2026/04/01"},"accession":"GSE318882","cross_references":{"GSM":["GSM9505455","GSM9505456","GSM9505453","GSM9505454","GSM9505459","GSM9505448","GSM9505449","GSM9505457","GSM9505447","GSM9505458","GSM9505462","GSM9505451","GSM9505452","GSM9505460","GSM9505461","GSM9505450"],"GPL":["30172"],"GSE":["318882"],"taxon":["Mus musculus"]}}