{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE327nnn/GSE327278/"]},"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=GSE327278"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Analysis of transcriptional changes associated with acquired resistance to docetaxel in HR+/HER2- breast cancer cell line MCF-7","description":"Resistance to neoadjuvant chemotherapy in HR+/HER2- breast cancers is increasingly recognized as a consequence of tumor cell plasticity rather than fixed genetic alterations. Large-scale genomic analyses comparing tumors before and after chemotherapy have failed to identify recurrent mutations that consistently account for treatment failure. Instead, resistance is thought to arise predominantly through non-genetic, adaptive mechanisms, including the acquisition of gene expression changes that allow cancer cells to survive chemotherapy-induced stress and later re-enter proliferative programs.To uncover transcriptional adaptations to docetaxel, a chemotherapeutic agent used in the NAC clinical setting, we performed bulk RNA-sequencing on parental and docetaxel-resistant MCF-7 cells.","dates":{"publication":"2026/07/14"},"accession":"GSE327278","cross_references":{"GSM":["GSM9652704","GSM9652705","GSM9652706","GSM9652701","GSM9652702","GSM9652703"],"GPL":["30173"],"GSE":["327278"],"taxon":["Homo sapiens"],"PMID":["[42729982]"]}}