<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/GSE291nnn/GSE291144/</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=GSE291144</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Transcriptomic profiling of cells treated with a novel CDK12/13 inhibitor, CTX-439</name><description>We developed a novel clinical-grade CDK12/13 inhibitor, CTX-439, and analyzed transcriptomic changes upon CTX-439 treatment. CTX-439 downregulated a large number of genes including DDR genes. By analyzing rRNA-depleted nuclear RNA, CTX-439 caused a defect in 3' end processing, showing an increased readthrough transcription. This caused rapid MCL1 downregulation, which can be combined with BCL-xL inhibition to induce apoptosis.</description><dates><publication>2026/09/14</publication></dates><accession>GSE291144</accession><cross_references><GSM>GSM8829723</GSM><GSM>GSM8829712</GSM><GSM>GSM8829724</GSM><GSM>GSM8829713</GSM><GSM>GSM8829725</GSM><GSM>GSM8829714</GSM><GSM>GSM8829726</GSM><GSM>GSM8829715</GSM><GSM>GSM8829716</GSM><GSM>GSM8829706</GSM><GSM>GSM8829717</GSM><GSM>GSM8829718</GSM><GSM>GSM8829707</GSM><GSM>GSM8829719</GSM><GSM>GSM8829708</GSM><GSM>GSM8829709</GSM><GSM>GSM8829720</GSM><GSM>GSM8829721</GSM><GSM>GSM8829710</GSM><GSM>GSM8829722</GSM><GSM>GSM8829711</GSM><GPL>28038</GPL><GSE>291144</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>