GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE291nnn/GSE291525/suppl/GSE291525_MOLM13_8p.txt.gzftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE291nnn/GSE291525/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE291525GEOGSEfalseMechanistic Insights into the Epigenetic Regulation and Therapeutic Targeting of RET Receptor Tyrosine Kinase in KMT2A-Rearranged Pediatric Acute Myeloid LeukemiaPediatric 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.2026/04/01GSE291525GSM8837068GSM8837067GSM8837069GSM8837066GSM8837071GSM883707024676291525Homo sapiens[40976985]