ReviewLeukemia2015
Mouse models of NPM1-mutated acute myeloid leukemia: biological and clinical implications.
Review in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- Targeting SMC3 deacetylation synergizes with XPO1 inhibition to reprogram the epigenetic landscape and suppress NPM1-mutated acute myeloid leukemia.Nature communications · 2026Article
- Homoharringtonine Promotes FTO Degradation to Suppress LILRB4-Mediated Immune Evasion in Acute Monocytic Leukaemia.Cell proliferation · 2026Article
- Identification and experimental validation of mitochondria pathway related genes in acute myeloid leukemia.Frontiers in immunology · 2026Article
- Review
- Exploration of ETV6::ABL1-positive AML with concurrent NPM1 and FLT3-ITD mutations.Annals of hematology · 2024Article
- The discovery ofHaematologica · 2024Article
- Review
- Comprehensive analysis of genetic factors predicting overall survival in Myelodysplastic syndromes.Scientific reports · 2022Article
- Diagnostic Workup of Acute Myeloid Leukemia: What Is Really Necessary? An Italian Survey.Frontiers in oncology · 2022Article
- Molecular Targeted Therapy and Immunotherapy for Myelodysplastic Syndrome.International journal of molecular sciences · 2021Review
- Bcor deficiency perturbs erythro-megakaryopoiesis and cooperates with Dnmt3a loss in acute erythroid leukemia onset in mice.Leukemia · 2021Article
- The Role of Somatic Mutations in Acute Myeloid Leukemia Pathogenesis.Cold Spring Harbor perspectives in medicine · 2021Review
- Mouse Models of Myeloid Malignancies.Cold Spring Harbor perspectives in medicine · 2021Review
- Review
- The Clinicopathological Impact of Granulocyte-Macrophage Colony-Stimulating Factor Gene Expression and Different Molecular Prognostic Biomarkers in Egyptian Acute Myeloid Leukemia Patients.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- Enhanced expression of the sphingosine-1-phosphate-receptor-3 causes acute myelogenous leukemia in mice.Leukemia · 2020Article
- Nucleophosmin1 (NPM1) abnormality in hematologic malignancies, and therapeutic targeting of mutant NPM1 in acute myeloid leukemia.Therapeutic advances in hematology · 2020Review
- Cooperation of Dnmt3a R878H with Nras G12D promotes leukemogenesis in knock-in mice: a pilot study.BMC cancer · 2019Article
- New insights into the biology of acute myeloid leukemia with mutated NPM1.International journal of hematology · 2019Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Acute myeloid leukemia (AML) carrying nucleophosmin (NPM1) mutations displays distinct biological and clinical features that led to its inclusion as a provisional disease entity in the 2008 World Health Organization (WHO) classification of myeloid neoplasms. Studies of the molecular mechanisms underlying the pathogenesis of NPM1-mutated AML have benefited greatly from several mouse models of this leukemia developed over the past few years. Immunocompromised mice xenografted with NPM1-mutated AML served as the first valuable tool for defining the biology of the disease in vivo. Subsequently, genetically engineered mouse models of the NPM1 mutation, including transgenic and knock-in alleles, allowed the generation of mice with a constant genotype and a reproducible phenotype. These models have been critical for investigating the nature of the molecular effects of these mutations, defining the function of leukemic stem cells in NPM1-mutated AML, identifying chemoresistant preleukemic hemopoietic stem cells and unraveling the key molecular events that cooperate with NPM1 mutations to induce AML in vivo. Moreover, they can serve as a platform for the discovery and validation of new antileukemic drugs in vivo. Advances derived from the analysis of these mouse models promise to greatly accelerate the development of new molecularly targeted therapies for patients with NPM1-mutated 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.