{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T20:26:57Z","timestamp":1790713617031,"version":"4.1.0"},"reference-count":56,"publisher":"American Society of Hematology","issue":"14","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,4,3]]},"abstract":"<jats:sec>\n                  <jats:title>Abstract<\/jats:title>\n                  <jats:p>Pediatric acute myeloid leukemia frequently harbors fusion oncogenes associated with poor prognosis, including KMT2A, NUP98, and GLIS2 rearrangements. Although murine models have demonstrated their leukemogenic activities, the steps from a normal human cell to leukemic blasts remain unclear. Here, we precisely reproduced the inversion of chromosome 16 resulting in the ETO2::GLIS2 fusion in human induced pluripotent stem cells (iPSCs). iPSC-derived ETO2::GLIS2-expressing hematopoietic cells showed differentiation alterations in\u00a0vitro and efficiently induced in\u00a0vivo development of leukemia that closely phenocopied human acute megakaryoblastic leukemia (AMKL), reflected by flow cytometry and single-cell transcriptomes. Comparison of iPS-derived cells with patient-derived cells revealed altered chromatin accessibility at early and later bona fide leukemia stages, with aberrantly higher accessibility and expression of the osteogenic homeobox factor DLX3 that preceded increased accessibility to ETS factors. DLX3 overexpression in normal CD34+ cells increased accessibility to ETS motifs and reduced accessibility to GATA motifs. A DLX3 transcriptional module was globally enriched in both ETO2::GLIS2 AMKL and some aggressive pediatric osteosarcoma. Importantly, DLX3 knockout abrogated leukemia initiation in this ETO2::GLIS2 iPSC model. Collectively, the characterization of a novel human iPSC-derived AMKL model revealed that hijacking of the osteogenic homeobox transcription factor DLX3 is an essential early step in chromatin changes and leukemogenesis driven by the ETO2::GLIS2 fusion oncogene.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1182\/blood.2024024505","type":"journal-article","created":{"date-parts":[[2024,12,10]],"date-time":"2024-12-10T19:59:48Z","timestamp":1733860788000},"page":"1510-1525","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":3,"title":["Progressive chromatin rewiring by ETO2::GLIS2 revealed in a genome-edited human iPSC model of pediatric leukemia initiation"],"prefix":"10.1182","volume":"145","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3156-504X","authenticated-orcid":false,"given":"Fabien","family":"Boudia","sequence":"first","affiliation":[{"name":"1Gustave Roussy, PEDIAC program, INSERM U1170, Universit\u00e9 Paris-Saclay, Villejuif, France"},{"name":"2Equipe labellis\u00e9e Ligue Contre le Cancer, Paris, France"},{"name":"3Universit\u00e9 Paris Cit\u00e9, Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5736-5559","authenticated-orcid":false,"given":"Marie","family":"Baille","sequence":"additional","affiliation":[{"name":"1Gustave Roussy, PEDIAC program, INSERM U1170, Universit\u00e9 Paris-Saclay, Villejuif, France"},{"name":"2Equipe labellis\u00e9e Ligue Contre le Cancer, Paris, France"},{"name":"3Universit\u00e9 Paris Cit\u00e9, Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lo\u00e9lia","family":"Babin","sequence":"additional","affiliation":[{"name":"4Laboratory of the Genome Dynamics in the Immune System, Institut Imagine, Universit\u00e9 de Paris, Universit\u00e9 Paris Saclay, INSERM UMR 1163, Paris, 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