{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T10:49:26Z","timestamp":1785408566446,"version":"3.56.0"},"reference-count":67,"publisher":"American Society of Hematology","issue":"13","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,3,26]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>NUTM1 rearrangement defines a significant subset of B-cell acute lymphoblastic leukemia (B-ALL), particularly in infants lacking KMT2A rearrangements, yet its underlying molecular characteristics remain poorly understood. Here, we establish that NUTM1-rearranged (NUTM1-r) leukemia is a discrete entity characterized by a unique transcriptional and epigenetic landscape, notably featuring global DNA hypomethylation, irrespective of the 5\u2032 fusion partner. Functional interrogation of NUTM1 fusions reveals a dual oncogenic role: they drive commitment toward the B-lymphoid lineage while concurrently conferring potent leukemic stem cell properties. Strikingly, expression of a representative fusion, BRD9-NUTM1, is sufficient to induce serially transplantable B-cell progenitor, prepro\u2013B-like leukemia in vivo, faithfully recapitulating the key molecular and immunophenotypic features of human NUTM1-r B-ALL. Mechanistically, NUTM1 fusions establish an aberrant chromatin state, marked by global enhancement of H3K27 acetylation and the creation of distinctive open chromatin regions that co-opt both B-lineage and stemness-related transcriptional programs, including those involving NF-\u03baB and posterior HoxA genes. In stark contrast to resistant KMT2A-rearranged leukemias, NUTM1-r leukemic cells exhibit a profound sensitivity to chemotherapy. This vulnerability is mechanistically linked to the leukemia's dependence on active transcription. Our findings delineate the unique molecular profile of NUTM1-r leukemias, revealing specific vulnerabilities that rationalize their favorable clinical outcomes and suggest opportunities for modified therapeutic strategies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1182\/blood.2024026928","type":"journal-article","created":{"date-parts":[[2025,12,29]],"date-time":"2025-12-29T19:04:21Z","timestamp":1767035061000},"page":"1395-1411","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":4,"title":["Comprehensive molecular and functional analysis of\n                    <i>NUTM1<\/i>\n                    -rearranged leukemia"],"prefix":"10.1182","volume":"147","author":[{"given":"Koutarou","family":"Nishimura","sequence":"first","affiliation":[{"name":"1Department of Cancer Pathology, Graduate School of Medicine, The University of Osaka, Suita, Japan"},{"name":"2Laboratory of Cancer Pathology, Graduate School of Frontier Biosciences, The University of Osaka, Suita, Japan"},{"name":"3Department of Hematology-Oncology, Institute of Biomedical Research and Innovation, Foundation for Biomedical Research and Innovation at Kobe, Kobe, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3487-3307","authenticated-orcid":false,"given":"Tomoya","family":"Isobe","sequence":"additional","affiliation":[{"name":"4Department of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan"},{"name":"5Department of Hematology, Wellcome-MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5286-5108","authenticated-orcid":false,"given":"Tsukasa","family":"Shigehiro","sequence":"additional","affiliation":[{"name":"6Division of Immunology and Allergy, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda, 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