ArticleBlood2025
Defining 2 biologically and clinically distinct groups in acute leukemia with a mixed phenotype.
Article in Blood, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- AML, Myelodysplasia-Related With B/Myeloid MPAL Immunophenotype, Normal Karyotype, and SRSF2/ASXL1/FLT3 Co-Mutations.International journal of laboratory hematology · 2026Article
- A lower-intensity, venetoclax-containing protocol is effective in adults with newly diagnosed mixedphenotype acute leukemia.Haematologica · 2026Article
- Acute leukemia of ambiguous lineage: the known and the uncertain.Haematologica · 2026Review
- Case Report: Successful treatment of mixed-phenotype acute leukemia with cauda equina syndrome as the initial manifestation.Frontiers in oncology · 2026Article
- Clinical Outcomes of Adult Patients With Newly Diagnosed Mixed Phenotype Acute Leukemia.JCO precision oncology · 2025Article
- Lower-intensity chemo-immunotherapy with cladribine, low-dose cytarabine, venetoclax and blinatumomab produces high response rates in patients withHaematologica · 2025Article
- Review
- Mixed phenotype acute leukemia, the dissection of an enigmatic disease in the era of novel therapies.Frontiers in pediatrics · 2025Review
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21 authors.
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Abstract
abstractA 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)-directed induction regimens. AML-MP has inferior responses (hazard ratio, 12.5; 95% confidence interval, 2.72-57.8; P = .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 = .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 = .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.
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