ArticleNature genetics2011
Mutant nucleophosmin and cooperating pathways drive leukemia initiation and progression in mice.
Article in Nature genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers.
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Who cites it
150 citing papers in PubMed, 226 citations in OpenAlex.
- Genetically distinct leukemic stem cells in human CD34- acute myeloid leukemia are arrested at a hemopoietic precursor-like stage.The Journal of experimental medicine · 2016Trial
- Article
- Ziftomenib with venetoclax and azacitidine for relapsed/refractory NPM1-mutated acute myeloid leukemia.Blood · 2026Article
- Very Long Chain Fatty Acid Synthesis is a Targetable Dependency in RAS Pathway Mutant Leukemia.Blood cancer discovery · 2026Article
- Two Decades ofCancers · 2026Review
- Stromal cell senescence augments haematopoietic cell fitness in clonal haematopoiesis.Nature cell biology · 2026Article
- Treatment of acute myeloid leukemia models by targeting a cell surface RNA-binding protein.Nature biotechnology · 2026Article
- Characterization of the clonal hierarchy and immunophenotype of PTPN11 mutations in acute myeloid leukemia.JCI insight · 2026Article
- Nucleophosmin supports WNT-driven hyperproliferation and tumor initiation.Nature genetics · 2026Article
- Rapid epigenomic classification of acute leukemia.Nature genetics · 2025Article
- Enforcement of stem-cell dormancy by nucleophosmin mutation is a critical determinant of unrestricted self-renewal during myeloid leukemogenesis.Haematologica · 2025Article
- Review
- MutantProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Menin: from molecular insights to clinical impact.Epigenomics · 2025Review
- Pbx3-mediated suppression of type I interferon response contributes to leukemia progression driven by MLL-AF9.Cancer gene therapy · 2025Article
- Molecular measurable residual disease monitoring and transplant indications in NPM1 mutated acute myeloid leukemia.Bone marrow transplantation · 2025Review
- Review
- Bone marrow mesenchymal stromal cells support translation in refractory acute myeloid leukemia.Cell reports · 2025Article
- Advances in the application of patient-derived xenograft models in acute leukemia resistance.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- In vivo models of subclonal oncogenesis and dependency in hematopoietic malignancy.Cancer cell · 2024Article
90 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
Acute myeloid leukemia (AML) is a molecularly diverse malignancy with a poor prognosis whose largest subgroup is characterized by somatic mutations in NPM1, which encodes nucleophosmin. These mutations, termed NPM1c, result in cytoplasmic dislocation of nucleophosmin and are associated with distinctive transcriptional signatures, yet their role in leukemogenesis remains obscure. Here we report that activation of a humanized Npm1c knock-in allele in mouse hemopoietic stem cells causes Hox gene overexpression, enhanced self renewal and expanded myelopoiesis. One third of mice developed delayed-onset AML, suggesting a requirement for cooperating mutations. We identified such mutations using a Sleeping Beauty transposon, which caused rapid-onset AML in 80% of mice with Npm1c, associated with mutually exclusive integrations in Csf2, Flt3 or Rasgrp1 in 55 of 70 leukemias. We also identified recurrent integrations in known and newly discovered leukemia genes including Nf1, Bach2, Dleu2 and Nup98. Our results provide new pathogenetic insights and identify possible therapeutic targets in NPM1c+ AML.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.