ArticleNature communications2021
Biological and therapeutic implications of a unique subtype of NPM1 mutated AML.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 43 citations in OpenAlex.
- Targeting programmed cell death: a novel therapeutic paradigm for cancer based on mode-of-death classification.Apoptosis : an international journal on programmed cell death · 2026Review
- Integrated proteogenomic and metabolomic profiling of acute myeloid leukemias to identify molecular subtypes and associated therapy targets.Nature cancer · 2026Article
- Resolving inter- and intra-patient heterogeneity in NPM1-mutated AML at single-cell resolution.Leukemia · 2025Article
- The AML cellular state space unveils NPM1 immune evasion subtypes with distinct clinical outcomes.Nature communications · 2025Article
- Enforcement of stem-cell dormancy by nucleophosmin mutation is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis.Haematologica · 2025Article
- Discovery of candidate functional non-coding mutations in acute myeloid leukemia using single-cell chromatin accessibility sequencing.Communications biology · 2025Article
- Pan-cancer convergence of tumour-immune microenvironment motifs revealed by CyTOF and imaging mass cytometry.Frontiers in immunology · 2025Review
- The Clinical Impact of NPM1 Mutations and the Effect of Concurrent Mutations in Acute Myeloid Leukemia: Unraveling the Prognostic Significance.Health science reports · 2024Article
- Current knowledge about FLT3 gene mutations, exploring the isoforms, and protein importance in AML.Molecular biology reports · 2024Review
- Mapping AML heterogeneity - multi-cohort transcriptomic analysis identifies novel clusters and divergent ex-vivo drug responses.Leukemia · 2024Article
- Aging and comprehensive molecular profiling in acute myeloid leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- Baseline immunophenotypic profile of bone marrow leukemia cells in acute myeloid leukemia with nucleophosmin-1 gene mutation: a EuroFlow study.Blood cancer journal · 2023Article
- A Phase Ib/II Study of Ivosidenib with Venetoclax ± Azacitidine in IDH1-Mutated Myeloid Malignancies.Blood cancer discovery · 2023Article
- Genetic, Phenotypic, and Clinical Heterogeneity of NPM1-Mutant Acute Myeloid Leukemias.Biomedicines · 2023Review
- Targeting C/EBPα overcomes primary resistance and improves the efficacy of FLT3 inhibitors in acute myeloid leukaemia.Nature communications · 2023Article
- Verification of prognostic expression biomarkers is improved by examining enriched leukemic blasts rather than mononuclear cells from acute myeloid leukemia patients.Biomarker research · 2023Article
- Immune checkpoint gene VSIR predicts patient prognosis in acute myeloid leukemia and myelodysplastic syndromes.Cancer medicine · 2023Article
- Transcriptome-based molecular subtypes and differentiation hierarchies improve the classification framework of acute myeloid leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Hematopoietic differentiation at single-cell resolution in NPM1-mutated AML.Blood cancer journal · 2022Article
Corrections and comments
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Authors and funding
21 authors at 7 institutions in 3 countries.
Funding
Abstract
In acute myeloid leukemia (AML), molecular heterogeneity across patients constitutes a major challenge for prognosis and therapy. AML with NPM1 mutation is a distinct genetic entity in the revised World Health Organization classification. However, differing patterns of co-mutation and response to therapy within this group necessitate further stratification. Here we report two distinct subtypes within NPM1 mutated AML patients, which we label as primitive and committed based on the respective presence or absence of a stem cell signature. Using gene expression (RNA-seq), epigenomic (ATAC-seq) and immunophenotyping (CyToF) analysis, we associate each subtype with specific molecular characteristics, disease differentiation state and patient survival. Using ex vivo drug sensitivity profiling, we show a differential drug response of the subtypes to specific kinase inhibitors, irrespective of the FLT3-ITD status. Differential drug responses of the primitive and committed subtype are validated in an independent AML cohort. Our results highlight heterogeneity among NPM1 mutated AML patient samples based on stemness and suggest that the addition of kinase inhibitors to the treatment of cases with the primitive signature, lacking FLT3-ITD, could have therapeutic benefit.
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