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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2025,5,20]]},"abstract":"<jats:p>\n                    In human acute myeloid leukemia (AML), mutations of isocitrate dehydrogenase-1 (\n                    <jats:italic toggle=\"yes\">IDH1<\/jats:italic>\n                    ) often co-occur with\n                    <jats:italic toggle=\"yes\">NPM1<\/jats:italic>\n                    mutations, and less frequently with\n                    <jats:italic toggle=\"yes\">FLT3<\/jats:italic>\n                    mutations. To investigate whether the effects of\n                    <jats:italic toggle=\"yes\">IDH1<\/jats:italic>\n                    mutation differ according to the specific co-occurring mutation, we generated two strains of double knock-in mutant mice.\n                    <jats:italic toggle=\"yes\">Idh1<\/jats:italic>\n                    <jats:sup>R132H<\/jats:sup>\n                    combined with\n                    <jats:italic toggle=\"yes\">Npm1c<\/jats:italic>\n                    induced overt AML, whereas\n                    <jats:italic toggle=\"yes\">Idh1<\/jats:italic>\n                    <jats:sup>R132H<\/jats:sup>\n                    plus\n                    <jats:italic toggle=\"yes\">Flt3<\/jats:italic>\n                    <jats:sup>ITD<\/jats:sup>\n                    resulted in\n                    <jats:italic toggle=\"yes\">Flt3<\/jats:italic>\n                    <jats:sup>ITD<\/jats:sup>\n                    -driven myelo- or lymphoproliferation that was minimally affected by\n                    <jats:italic toggle=\"yes\">Idh1<\/jats:italic>\n                    <jats:sup>R132H<\/jats:sup>\n                    and rarely generated AML. Gene expression profiling revealed differences between\n                    <jats:italic toggle=\"yes\">Idh1<\/jats:italic>\n                    <jats:sup>R132H<\/jats:sup>\n                    ;\n                    <jats:italic toggle=\"yes\">Npm1c<\/jats:italic>\n                    cells and\n                    <jats:italic toggle=\"yes\">Idh1<\/jats:italic>\n                    <jats:sup>R132H<\/jats:sup>\n                    ;\n                    <jats:italic toggle=\"yes\">Flt3<\/jats:italic>\n                    <jats:sup>ITD<\/jats:sup>\n                    cells and suggested altered heme metabolism and immune responses in the former. The profile of\n                    <jats:italic toggle=\"yes\">Idh1<\/jats:italic>\n                    <jats:sup>R132H<\/jats:sup>\n                    ;\n                    <jats:italic toggle=\"yes\">Npm1c<\/jats:italic>\n                    cells corresponded to that of human\n                    <jats:italic toggle=\"yes\">IDH<\/jats:italic>\n                    -mutated AML cells, particularly those resistant to inhibitors of mutant IDH. Compared to treatment with a menin inhibitor, IDH1-targeted therapy of\n                    <jats:italic toggle=\"yes\">Idh1<\/jats:italic>\n                    <jats:sup>R132H<\/jats:sup>\n                    ;\n                    <jats:italic toggle=\"yes\">Npm1c<\/jats:italic>\n                    AML-bearing mice was less efficacious in improving cell differentiation and extending survival. The differential cooperation of\n                    <jats:italic toggle=\"yes\">Idh1<\/jats:italic>\n                    <jats:sup>R132H<\/jats:sup>\n                    with\n                    <jats:italic toggle=\"yes\">Npm1c<\/jats:italic>\n                    vs.\n                    <jats:italic toggle=\"yes\">Flt3<\/jats:italic>\n                    <jats:sup>ITD<\/jats:sup>\n                    may have implications for the devising of subtype-specific treatments for human AML.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2415779122","type":"journal-article","created":{"date-parts":[[2025,5,16]],"date-time":"2025-05-16T11:59:56Z","timestamp":1747396796000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":8,"title":["Mutant\n                    <i>IDH1<\/i>\n                    cooperates with\n                    <i>NPM1c<\/i>\n                    or\n                    <i>FLT3<\/i>\n                    <sup>ITD<\/sup>\n                    to drive distinct myeloid diseases and molecular outcomes"],"prefix":"10.1073","volume":"122","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8868-1661","authenticated-orcid":false,"given":"Takashi","family":"Sakamoto","sequence":"first","affiliation":[{"name":"Princess Margaret Cancer Centre, University Health Network","place":["Toronto, Canada"]},{"name":"Department of Hematology, Graduate School of Medicine, Kyoto University","place":["Kyoto, Japan"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie","family":"Leca","sequence":"additional","affiliation":[{"name":"Princess Margaret Cancer Centre, University Health Network","place":["Toronto, Canada"]},{"name":"BMP, Ecosystem, stemness and dynamic in cancer Laboratory, Centre de Recherche en Cancerologie de Lyon, UMR INSERM 1052 CNRS 5286, Centre L\u00e9on B\u00e9rard, Universit\u00e9 Claude Bernard Lyon 1","place":["Lyon, France"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin","family":"Zhang","sequence":"additional","affiliation":[{"name":"Princess Margaret Cancer Centre, University Health Network","place":["Toronto, Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cem","family":"Meydan","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, Weill Cornell Medicine","place":["New York"]},{"name":"The HRH Prince Alwaleed Bin Talal Bin Abdulaziz Alsaud Institute for Computational Biomedicine, Weill Cornell Medicine","place":["New York"]},{"name":"WorldQuant Initiative for Quantitative Prediction, Weill Cornell Medicine","place":["New York"]},{"name":"Department of Medicine, Division of Hematology and Medical Oncology, Weill Cornell Medicine","place":["New York"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonathan","family":"Foox","sequence":"additional","affiliation":[{"name":"Department of Physiology and 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