<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/GSE338nnn/GSE338360/</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=GSE338360</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>The ratio of RUNX1-ETO oncoprotein to normal RUNX1 expression determines the balance between endothelial reprogramming and hematopoietic cell growth</name><description>In t(8;21) acute myeloid leukemia (AML) the RUNX1 DNA binding domain is fused to the RUNX1T1 protein producing the RUNX1-ETO onco-fusion protein. Here, we employed a human embryonic stem cell (ESC) line expressing an inducible RUNX1-ETO transgene to determine whether RUNX1-ETO directly induces endothelial signalling pathways or whether it is dependent on AML progression. Using single cell analyses we show that RUNX1-ETO induction reprograms ESC-derived myeloid progenitors towards endothelial cells. Our experiments provide important insights into the earliest stages of epigenetic reprogramming by oncogenic transcription factors in AML.</description><dates><publication>2026/09/23</publication></dates><accession>GSE338360</accession><cross_references><GSM>GSM9872152</GSM><GSM>GSM9872154</GSM><GSM>GSM9872153</GSM><GPL>24676</GPL><GSE>338360</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>