{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T15:52:45Z","timestamp":1792252365604,"version":"4.4.0"},"reference-count":31,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2025,3,17]],"date-time":"2025-03-17T00:00:00Z","timestamp":1742169600000},"content-version":"vor","delay-in-days":2,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["acsjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cancer"],"published-print":{"date-parts":[[2025,3,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>FMS\u2010like tyrosine kinase 3 (<jats:italic>FLT3<\/jats:italic>) mutations, either internal tandem duplications (<jats:italic>FLT3<\/jats:italic>\u2010ITD) or tyrosine kinase domain (<jats:italic>FLT3<\/jats:italic>\u2010TKD), are common in acute myeloid leukemia (AML). <jats:italic>FLT3<\/jats:italic>\u2010ITD confers an adverse prognosis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The authors performed a retrospective study including 619 patients to evaluate outcomes in newly diagnosed <jats:italic>FLT3<\/jats:italic>\u2010mutated AML across treatment regimens.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In patients with <jats:italic>FLT3<\/jats:italic>\u2010ITD\u2013mutated AML who received intensive chemotherapy (IC), the addition of a FLT3 inhibitor (FLT3i) was associated with trends toward improved relapse\u2010free survival (median 32.3 vs. 14.3 months with vs. without a FLT3i; <jats:italic>p<\/jats:italic>\u00a0=\u00a0.055) and overall survival (OS; 35.5 vs. 18.9 months with vs. without a FLT3i; <jats:italic>p<\/jats:italic>\u00a0=\u00a0.098). In patients with <jats:italic>FLT3<\/jats:italic>\u2010ITD mutations who received low\u2010intensity (LIT) regimens, triplets (LIT plus a FLT3i plus venetoclax) were associated with significantly longer OS (19.1 months) compared with those who received other treatment combinations (11.2 months with LIT alone, 9.2 months with LIT plus FLT3i, and 10.3 months with LIT plus venetoclax). Patients with <jats:italic>FLT3<\/jats:italic>\u2010ITD plus <jats:italic>NPM1<\/jats:italic> co\u2010mutations who received any therapy had a trend toward improved OS (2\u2010year OS: 47% vs. 33%; <jats:italic>p<\/jats:italic>\u00a0=\u00a0.087). The <jats:italic>FLT3<\/jats:italic>\u2010ITD allelic ratio; <jats:italic>IDH1<\/jats:italic>, <jats:italic>IDH2<\/jats:italic>, <jats:italic>WT1<\/jats:italic>, <jats:italic>RUNX1<\/jats:italic>, and myelodysplastic syndrome\u2010related mutations; and adverse cytogenetics had no significant impact on OS. In landmark analyses, allogeneic stem cell transplantation was associated with a trend toward improved OS in patients with <jats:italic>FLT3<\/jats:italic>\u2010ITD mutations who received IC (52.6 vs. 22.7 months with versus without allogeneic stem cell transplantation; <jats:italic>p<\/jats:italic>\u00a0=\u00a0.076) and a marked improvement in OS in those who received LIT (38.6 vs. 14.0 months with vs. without allogeneic stem cell transplantation; <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a0.0001).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>A FLT3i and allogeneic stem cell transplantation are key treatment modalities for patients who have <jats:italic>FLT3<\/jats:italic>\u2010mutated AML. LIT\u2010based triplets are promising in IC\u2010ineligible patients.<\/jats:p><\/jats:sec>","DOI":"10.1002\/cncr.35813","type":"journal-article","created":{"date-parts":[[2025,3,18]],"date-time":"2025-03-18T00:15:02Z","timestamp":1742256902000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["A retrospective study of outcomes across time and treatment regimens in newly diagnosed, FMS\u2010like tyrosine kinase 3 (<i>FLT3<\/i>)\u2010mutated acute myeloid leukemia"],"prefix":"10.1002","volume":"131","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5538-4943","authenticated-orcid":false,"given":"Alexandre","family":"Bazinet","sequence":"first","affiliation":[{"name":"Department of Leukemia The University of Texas MD Anderson Cancer Center  Houston Texas 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