{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T16:24:40Z","timestamp":1789575880943,"version":"build-2803163510"},"reference-count":48,"publisher":"American Society of Hematology","issue":"18","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,5,1]]},"abstract":"<jats:sec>\n                  <jats:title>Abstract<\/jats:title>\n                  <jats:p>A mixed phenotype (MP) is a characteristic of de novo MP acute leukemia (MPAL), but it can also be found in other leukemias. It poses substantial classification and management dilemmas. Herein, we report a large cohort of acute leukemia with MP and define acute myeloid leukemia with MP (AML-MP) and MPAL as 2 distinct groups by characterizing clinical, genetic, and transcriptomic features. Clinically, patients with AML-MP and MPAL were both treated with either AML- or acute lymphoblastic leukemia (ALL)\u2013directed induction regimens. AML-MP has inferior responses (hazard ratio, 12.5; 95% confidence interval, 2.72-57.8; P\u00a0=\u00a0.001), whereas MPAL has better responses to ALL-directed treatment. Genetically, AML-MP harbors more frequent RUNX1 (23\/52 [44%]) and TP53 (12\/52 [23.1%]) mutations. In contrast, RUNX1 mutations are less frequent in MPAL (8\/35 [23%]; P\u00a0=\u00a0.01 vs AML-MP) and TP53 mutations as a driver are virtually absent in MPAL. Transcriptionally, AML-MP shows enrichment for stemness signatures and a relative deficit of transcription factors critical for myeloid and lymphoid differentiation. Furthermore, AML-MP rarely switches to a lymphoid immunophenotype after treatment, in contrast to MPAL (1\/40 [2.5%] vs 10\/28 [35.7%]; P\u00a0=\u00a0.0003). Last, a genomic classification framework is proposed for future studies. Together, these data support the designation of AML-MP as a diagnosis distinct from MPAL and provide novel insights into the pathogenesis and therapies of acute leukemia with MP.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1182\/blood.2024026273","type":"journal-article","created":{"date-parts":[[2025,1,15]],"date-time":"2025-01-15T21:56:06Z","timestamp":1736978166000},"page":"2056-2069","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":10,"title":["Defining 2 biologically and clinically distinct groups in acute leukemia with a mixed phenotype"],"prefix":"10.1182","volume":"145","author":[{"given":"Pallavi","family":"Galera","sequence":"first","affiliation":[{"name":"1Hematopathology Service Department of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, 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Kettering Cancer Center, New York, NY"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher","family":"Famulare","sequence":"additional","affiliation":[{"name":"7Center for Hematologic Malignancies, Memorial Sloan Kettering Cancer Center, New York, NY"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qi","family":"Gao","sequence":"additional","affiliation":[{"name":"1Hematopathology Service Department of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, NY"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8059-8668","authenticated-orcid":false,"given":"Douglas A.","family":"Mata","sequence":"additional","affiliation":[{"name":"6Department of Pathology and Laboratory Medicine, Diagnostic Molecular Laboratory, Memorial Sloan Kettering Cancer Center, New York, 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