<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/GSE290nnn/GSE290257/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></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=GSE290257</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Transcriptional rewiring by enhancer methylation in CBFA2T3-GLIS2–driven pediatric acute megakaryoblastic leukemia</name><description>Chemotherapy resistance and relapse remain major challenges in pediatric acute myeloid leukemia (pAML), particularly in acute megakaryoblastic leukemia (AMKL) driven by the CBFA2T3-GLIS2 (C/G) fusion. To investigate the epigenetic mechanisms contributing to these challenges, we employed multi-epigenomic approaches to identify oncogenic enhancers at cis-regulatory elements (CREs) that drive aberrant gene expression.</description><dates><publication>2026/07/13</publication></dates><accession>GSE290257</accession><cross_references><GSM>GSM8809383</GSM><GSM>GSM8809372</GSM><GSM>GSM8809373</GSM><GSM>GSM8809384</GSM><GSM>GSM8809374</GSM><GSM>GSM8809375</GSM><GSM>GSM8809380</GSM><GSM>GSM8809370</GSM><GSM>GSM8809381</GSM><GSM>GSM8809382</GSM><GSM>GSM8809371</GSM><GSM>GSM8809376</GSM><GSM>GSM8809377</GSM><GSM>GSM8809378</GSM><GSM>GSM8809379</GSM><GPL>24676</GPL><GSE>290257</GSE><taxon>Homo sapiens</taxon><PMID>[41141393]</PMID></cross_references></HashMap>