{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE337nnn/GSE337023/"]},"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=GSE337023"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Genomic and transcriptomic profiling of whole-genome-doubled triple-negative breast cancer cell populations","description":"To investigate whether the mechanism of whole-genome doubling (WGD) results in distinct genomic and transcriptomic phenotypes, we compared three routes to WGD against their respective parental aneuploid controls across two triple-negative breast cancer (TNBC) cell lines (HCC1806 and MDA-MB-231). WGD mechanisms included naturally occurring cell-cell fusion and two drug-induced cell-cycle error mechanisms: mitotic slippage (MS) and cytokinesis failure (CF). All populations were profiled in biological triplicate by TagSeq (3' tag-based RNA-seq) for transcriptomic analysis and low-pass whole-genome sequencing (WGS) for copy-number profiling.","dates":{"publication":"2026/07/05"},"accession":"GSE337023","cross_references":{"GSM":["GSM9846896","GSM9846898","GSM9846897","GSM9846911","GSM9846900","GSM9846899","GSM9846910","GSM9846913","GSM9846902","GSM9846901","GSM9846912","GSM9846904","GSM9846915","GSM9846914","GSM9846903","GSM9846906","GSM9846917","GSM9846916","GSM9846905","GSM9846919","GSM9846908","GSM9846907","GSM9846918","GSM9846909"],"GPL":["30173"],"GSE":["337023"],"taxon":["Homo sapiens"]}}