{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Txt":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE291nnn/GSE291525/suppl/GSE291525_MOLM13_8p.txt.gz"],"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE291nnn/GSE291525/"]},"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=GSE291525"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Mechanistic Insights into the Epigenetic Regulation and Therapeutic Targeting of RET Receptor Tyrosine Kinase in KMT2A-Rearranged Pediatric Acute Myeloid Leukemia","description":"Pediatric acute myeloid leukemia (pAML) driven by KMT2A gene rearrangements (KMT2A-r; 11q23 translocations) is a high-risk leukemia with limited treatment options and a poor prognosis. Previously, we reported (PMID: 38226414) that the RET receptor tyrosine kinase is epigenetically upregulated in major KMT2A-r subgroups. In this study, we utilized a synthetic drug, 8p, which serves as a dual inhibitor of RET and cyclin-dependent kinase 8 (CDK8). We conducted RNA sequencing analysis on 8p-treated KMT2A-MLLT3 fusion-positive MOLM-13 cells to profile genome-wide gene expression changes. This study enhances our understanding of the major pathways affected by the dual inhibition of RET and CDK8 in KMT2A-r AML.","dates":{"publication":"2026/04/01"},"accession":"GSE291525","cross_references":{"GSM":["GSM8837068","GSM8837067","GSM8837069","GSM8837066","GSM8837071","GSM8837070"],"GPL":["24676"],"GSE":["291525"],"taxon":["Homo sapiens"],"PMID":["[40976985]"]}}