ArticleBlood2010
Expression of the cytoplasmic NPM1 mutant (NPMc+) causes the expansion of hematopoietic cells in zebrafish.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 76 citations in OpenAlex.
- Vulnerability of SRSF2-mutated chronic myelomonocytic leukemia to perturbation of the cGAS-STING pathway.Blood advances · 2026Article
- Influence of Nucleophosmin (Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2025Article
- Infrequent Presentations of ChronicCancers · 2024Review
- Depletion ofFrontiers in hematology · 2023Article
- The antagonistic duality of NPM1 mutations in AML.Blood advances · 2022Article
- Zebrafish models of acute leukemias: Current models and future directions.Wiley interdisciplinary reviews. Developmental biology · 2021Review
- Dhx15 regulates zebrafish definitive hematopoiesis through the unfolded protein response pathway.Cancer science · 2021Article
- Article
- Preferential transcription of the mutated allele in NPM1 mutated acute myeloid leukaemia.Scientific reports · 2020Article
- Adaptation to low parasite abundance affects immune investment and immunopathological responses of cavefish.Nature ecology & evolution · 2020Article
- Article
- Zebrafish Models of Cancer-New Insights on Modeling Human Cancer in a Non-Mammalian Vertebrate.Genes · 2019Review
- Modeling hematopoietic disorders in zebrafish.Disease models & mechanisms · 2019Review
- Review
- Article
- A tale of two genes: a new connection betweenHaematologica · 2019Article
- Disruption ofDisease models & mechanisms · 2019Article
- Genetic Models of Leukemia in Zebrafish.Frontiers in cell and developmental biology · 2018Review
- Role of Nucleophosmin Gene Mutation in Leukemogenesis of Acute Myeloid Leukemia.Journal of hematology · 2018Article
- NPM1 directs PIDDosome-dependent caspase-2 activation in the nucleolus.The Journal of cell biology · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 4 countries.
Funding
Abstract
Mutations in the human nucleophosmin (NPM1) gene are the most frequent genetic alteration in adult acute myeloid leukemias (AMLs) and result in aberrant cytoplasmic translocation of this nucleolar phosphoprotein (NPMc+). However, underlying mechanisms leading to leukemogenesis remain unknown. To address this issue, we took advantage of the zebrafish model organism, which expresses 2 genes orthologous to human NPM1, referred to as npm1a and npm1b. Both genes are ubiquitously expressed, and their knockdown produces a reduction in myeloid cell numbers that is specifically rescued by NPM1 expression. In zebrafish, wild-type human NPM1 is nucleolar while NPMc+ is cytoplasmic, as in human AML, and both interact with endogenous zebrafish Npm1a and Npm1b. Forced NPMc+ expression in zebrafish causes an increase in pu.1(+) primitive early myeloid cells. A more marked perturbation of myelopoiesis occurs in p53(m/m) embryos expressing NPMc+, where mpx(+) and csf1r(+) cell numbers are also expanded. Importantly, NPMc+ expression results in increased numbers of definitive hematopoietic cells, including erythromyeloid progenitors in the posterior blood island and c-myb/cd41(+) cells in the ventral wall of the aorta. These results are likely to be relevant to human NPMc+ AML, where the observed NPMc+ multilineage expression pattern implies transformation of a multipotent stem or progenitor cell.
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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.