{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T18:56:09Z","timestamp":1788893769063,"version":"build-2803163510"},"reference-count":28,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2025,2,8]],"date-time":"2025-02-08T00:00:00Z","timestamp":1738972800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100007313","name":"University of Texas MD Anderson Cancer Center","doi-asserted-by":"publisher","award":["CA016672"],"award-info":[{"award-number":["CA016672"]}],"id":[{"id":"10.13039\/100007313","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["American J Hematol"],"published-print":{"date-parts":[[2025,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Ontogeny of acute myeloid leukemia (AML) provides prognostic information, however closer interrogation with respect to AML characteristics, genomics, and various treatments are warranted. We defined untreated clinical secondary (CS) AML as AML with a diagnosis of antecedent myelodysplastic syndrome (MDS) or MDS\/myeloproliferative neoplasm (MDS\u2010MPN) without exposure to hypomethylating agents or chemotherapy; genomic secondary (GS) AML included patients with myelodysplasia related cytogenetics (MRC) or myelodysplasia related mutations (MRM) without a known antecedent myeloid neoplasm or prior chemo\u2010radiotherapy for non\u2010myeloid neoplasms. Among newly diagnosed AML patients classified as untreated CS\u2010AML (<jats:italic>n<\/jats:italic>\u2009=\u2009133) or GS\u2010AML (<jats:italic>n<\/jats:italic>\u2009=\u2009389), median relapse\u2010free survival (RFS) (11.9 vs. 12.4\u2009months, <jats:italic>p<\/jats:italic>\u2009=\u20090.36) and overall survival (OS) (11.6 vs. 14.4\u2009months, <jats:italic>p<\/jats:italic>\u2009=\u20090.75) were similar. No difference in RFS and OS between these groups treated with low\u2010intensity therapy (LIT) and venetoclax regimens was seen, but both were inferior to <jats:italic>de novo<\/jats:italic> (DN) AML without secondary\u2010type genomics (pure DN\u2010AML). GS\u2010AML defined by the presence of only MRM had superior OS compared with MRM\u2009\u00b1\u2009MRC with LIT+ venetoclax therapy (RFS 19.5 vs. 6.8\u2009months [<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.01] and OS 29.6 vs. 8.4 [<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.01]) and had similar RFS (29.8\u2009months, <jats:italic>p<\/jats:italic>\u2009=\u20090.48) and OS (32.0\u2009months, <jats:italic>p<\/jats:italic>\u2009=\u20090.48) to pure DN\u2010AML treated with LIT+ venetoclax. On multivariate analysis in patients treated with LIT+ venetoclax, untreated CS\u2010AML (vs. GS\u2010AML), adverse cytogenetics and ELN 2024 adverse\u2010risk disease (mutated <jats:italic>TP53<\/jats:italic>) were associated with higher hazard of death. Adverse cytogenetics was the strongest prognostic variable predicting survival. Mutation\u2010driven genomic ontogeny of newly diagnosed AML with MRM appears less prognostic than cytogenetic\u2010driven ontogeny with venetoclax\u2010based therapy.<\/jats:p>","DOI":"10.1002\/ajh.27628","type":"journal-article","created":{"date-parts":[[2025,2,11]],"date-time":"2025-02-11T13:41:37Z","timestamp":1739281297000},"page":"758-769","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Clinico\u2010Genomic Interrogation of Secondary\u2010Type Acute Myeloid Leukemia: Response and Outcomes to\u00a0Contemporary Therapies"],"prefix":"10.1002","volume":"100","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6831-2567","authenticated-orcid":false,"given":"Jayastu","family":"Senapati","sequence":"first","affiliation":[{"name":"Department of Leukemia The University of Texas MD Anderson Cancer Center  Houston Texas 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