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Moreover, the gene expression profile in\n                    <jats:italic>NUTM1<\/jats:italic>\n                    \u2010R infant ALL characteristically reveals upregulation of the genes that are involved in\n                    <jats:italic>KMT2A<\/jats:italic>\n                    \u2010R infant ALL development, including\n                    <jats:italic>HOXA9<\/jats:italic>\n                    and\n                    <jats:italic>HOXA10<\/jats:italic>\n                    . However, the direct association of\n                    <jats:italic>NUTM1<\/jats:italic>\n                    \u2010fusion with this gene expression remains unexplored. Clinically, in sharp contrast to\n                    <jats:italic>KMT2A<\/jats:italic>\n                    \u2010R infant ALL, the prognosis of\n                    <jats:italic>NUTM1<\/jats:italic>\n                    \u2010R infant ALL is excellent, although its drug sensitivity profile remains unclear. Here, we newly identified an\n                    <jats:italic>ACIN1::NUTM1<\/jats:italic>\n                    \u2010positive ALL cell line, KOPN32, which was previously established from a relapsed infant\u2010ALL case, as the only cell line with\n                    <jats:italic>NUTM1<\/jats:italic>\n                    \u2010fusion. KOPN32 had fewer copy number alterations, like\n                    <jats:italic>KMT2A<\/jats:italic>\n                    \u2010R ALL cell lines. Both KOPN32 and an ACIN1::NUTM1\u2010inducible ALL model, which was established using the\n                    <jats:italic>ACIN1::NUTM1<\/jats:italic>\n                    fusion cDNA subcloned from KOPN32, revealed upregulation of\n                    <jats:italic>HOXA9, HOXA10<\/jats:italic>\n                    ,\n                    <jats:italic>SKIDA1<\/jats:italic>\n                    and\n                    <jats:italic>BMI1<\/jats:italic>\n                    , indicating direct involvement of ACIN1::NUTM1 fusion in the upregulation of these genes. In the drug sensitivity to eight standard agents, KOPN32 showed high sensitivity to both daunorubicin and vincristine; both are crucial agents in the induction therapy for infant ALL.\n                  <\/jats:p>","DOI":"10.1111\/bjh.70130","type":"journal-article","created":{"date-parts":[[2025,8,30]],"date-time":"2025-08-30T06:05:49Z","timestamp":1756533949000},"page":"1842-1854","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["A characteristic gene expression profile regulated by\n                    <i>ACIN1::NUTM1<\/i>\n                    fusion in a newly identified infant leukaemic cell line and an\n                    <scp>ACIN1<\/scp>\n                    ::\n                    <scp>NUTM1<\/scp>\n                    \u2010inducible model"],"prefix":"10.1111","volume":"207","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6905-4582","authenticated-orcid":false,"given":"Minori","family":"Tamai","sequence":"first","affiliation":[{"name":"Department of Paediatrics, School of Medicine University of Yamanashi  Chuo Yamanashi Japan"},{"name":"Global Leukemia Cell\u2010Line Assembly Network (Glean), University of Yamanashi  Chuo Yamanashi Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chiaki","family":"Komatsu","sequence":"additional","affiliation":[{"name":"Department of Paediatrics, School of Medicine University of Yamanashi  Chuo Yamanashi Japan"},{"name":"Global Leukemia Cell\u2010Line Assembly Network (Glean), University of Yamanashi  Chuo Yamanashi Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keiko","family":"Kagami","sequence":"additional","affiliation":[{"name":"Department of Paediatrics, School of Medicine University of Yamanashi  Chuo Yamanashi 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