{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T00:42:43Z","timestamp":1791247363672,"version":"4.1.0"},"reference-count":27,"publisher":"Rockefeller University Press","issue":"1","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,1,13]]},"abstract":"<jats:p>MLL-fusion proteins are potent inducers of oncogenic transformation, and their expression is considered to be the main oncogenic driving force in \u223c10% of human acute myeloid leukemia (AML) patients. These oncogenic fusion proteins are responsible for the initiation of a downstream transcriptional program leading to the expression of factors such as MEIS1 and HOXA9, which in turn can replace MLL-fusion proteins in overexpression experiments. To what extent MLL fusion proteins act on their own during tumor initiation, or if they collaborate with other transcriptional regulators, is unclear. Here, we have compared gene expression profiles from human MLL-rearranged AML to normal progenitors and identified the myeloid tumor suppressor C\/EBP\u03b1 as a putative collaborator in MLL-rearranged AML. Interestingly, we find that deletion of Cebpa rendered murine hematopoietic progenitors completely resistant to MLL-ENL\u2013induced leukemic transformation, whereas C\/EBP\u03b1 was dispensable in already established AMLs. Furthermore, we show that Cebpa-deficient granulocytic-monocytic progenitors were equally resistant to transformation and that C\/EBP\u03b1 collaborates with MLL-ENL in the induction of a transcriptional program, which is also apparent in human AML. Thus, our studies demonstrate a key role of C\/EBP\u03b1 in MLL fusion\u2013driven transformation and find that it sharply demarcates tumor initiation and maintenance.<\/jats:p>","DOI":"10.1084\/jem.20130932","type":"journal-article","created":{"date-parts":[[2013,12,24]],"date-time":"2013-12-24T04:20:57Z","timestamp":1387858857000},"page":"5-13","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":68,"title":["Initiation of MLL-rearranged AML is dependent on C\/EBP\u03b1"],"prefix":"10.1084","volume":"211","author":[{"given":"Ewa","family":"Ohlsson","sequence":"first","affiliation":[{"name":"The Finsen Laboratory, Rigshospitalet, Faculty of Health Sciences 1 ; 2 ; 3 ; 4"},{"name":"Biotech Research and Innovation Center (BRIC) 1 ; 2 ; 3 ; 4"},{"name":"Danish Stem Cell Centre (DanStem) Faculty of Health Sciences 1 ; 2 ; 3 ; 4"},{"name":"The Bioinformatic Centre, Department of Biology, Faculty of Natural Sciences, University of Copenhagen, 2200 Copenhagen, Denmark 1 ; 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