<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/GSE292nnn/GSE292716/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Genomics</omics_type><species>Homo sapiens</species><gds_type>Genome binding/occupancy profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE292716</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Super-enhancers-driven SOX4/SMAD3 enhances AXL signaling via membrane phospholipid remodeling to accelerate leukemia progression [ChIP-seq]</name><description>Cancer often involves aberrant epigenetic activation. In CML-BP, super - enhancer - driven SOX4 and SMAD3 form an auto - regulatory axis. They co - regulate epigenome, activate AXL - related pathways, and mediate membrane phospholipid remodeling. Bemcentinib, an AXL inhibitor, can inhibit CML - BP progression. SOX4/SMAD3 are key factors and Bemcentinib a potential therapy.</description><dates><publication>2026/05/15</publication></dates><accession>GSE292716</accession><cross_references><GSM>GSM8864096</GSM><GSM>GSM8864085</GSM><GSM>GSM8864097</GSM><GSM>GSM8864086</GSM><GSM>GSM8864094</GSM><GSM>GSM8864095</GSM><GSM>GSM8864092</GSM><GSM>GSM8864093</GSM><GSM>GSM8864090</GSM><GSM>GSM8864091</GSM><GSM>GSM8864104</GSM><GSM>GSM8864102</GSM><GSM>GSM8864103</GSM><GSM>GSM8864100</GSM><GSM>GSM8864089</GSM><GSM>GSM8864101</GSM><GSM>GSM8864087</GSM><GSM>GSM8864098</GSM><GSM>GSM8864099</GSM><GSM>GSM8864088</GSM><GPL>30209</GPL><GSE>292716</GSE><taxon>Homo sapiens</taxon><PMID>[41721601]</PMID></cross_references></HashMap>