<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE327nnn/GSE327278/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE327278</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Analysis of transcriptional changes associated with acquired resistance to docetaxel in HR+/HER2- breast cancer cell line MCF-7</name><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.</description><dates><publication>2026/07/14</publication></dates><accession>GSE327278</accession><cross_references><GSM>GSM9652704</GSM><GSM>GSM9652705</GSM><GSM>GSM9652706</GSM><GSM>GSM9652701</GSM><GSM>GSM9652702</GSM><GSM>GSM9652703</GSM><GPL>30173</GPL><GSE>327278</GSE><taxon>Homo sapiens</taxon><PMID>[42729982]</PMID></cross_references></HashMap>