ArticleBlood2011
Hematopoiesis and leukemogenesis in mice expressing oncogenic NrasG12D from the endogenous locus.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.
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Who cites it
102 citing papers in PubMed, 1 synthesis or guideline pooled it, 151 citations in OpenAlex.
- Molecular Pathogenesis of Chronic Myelomonocytic Leukemia and Potential Molecular Targets for Treatment Approaches.Frontiers in oncology · 2021Pooled it
- Clinical implications of RAS mutations in AML: prognostic significance is based upon the involved gene and mutation complexity.Blood advances · 2026Article
- Succinate receptor 1 restricts hematopoiesis and prevents acute myeloid leukemia progression.Nature communications · 2026Article
- The oncogenic role of ecotropic viral integration site 1 in hematological malignancies: mechanisms of activation and leukemogenesis.Frontiers in immunology · 2026Review
- Targeting O-GlcNAcylated METTL3 impedes MDS/AML progression via diminishing SRSF1 mMolecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Single-cell proteomics characterization of bone marrow hematopoiesis with distinct Ras pathway lesions.Blood advances · 2025Article
- Humanized mouse models in MDS.Cell death & disease · 2025Review
- Identification of GDP as a small inhibitory molecule in HepG2 cells by non‑targeted metabolomics analysis.Oncology letters · 2025Article
- Bone marrow sympathetic neuropathy is a hallmark of hematopoietic malignancies and it involves severe ultrastructural damage.Experimental hematology & oncology · 2025Article
- The Crossroads of Clonal Evolution, Differentiation Hierarchy, and Ontogeny in Leukemia Development.Blood cancer discovery · 2025Review
- scTML: a pan-cancer single-cell landscape of multiple mutation types.Nucleic acids research · 2025Article
- Progression and perspectives in disease modeling for Juvenile myelomonocytic leukemia.Medical oncology (Northwood, London, England) · 2024Review
- Mutational cooperativity of RUNX1::RUNX1T1 isoform 9a and oncogenic NRAS in zebrafish myeloid leukaemia.Biology open · 2024Article
- 5G2 mutant mice model loss of a commonly deleted segment of chromosome 7q22 in myeloid malignancies.Leukemia · 2024Article
- A gain-of-function p53 mutant synergizes with oncogenic NRAS to promote acute myeloid leukemia in mice.The Journal of clinical investigation · 2023Article
- BRD9 determines the cell fate of hematopoietic stem cells by regulating chromatin state.Nature communications · 2023Article
- Article
- Endogenous IL-1 receptor antagonist restricts healthy and malignant myeloproliferation.Nature communications · 2023Article
- A promising new cancer marker: Long noncoding RNA EGFR-AS1.Frontiers in oncology · 2023Review
- Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation.Cancer discovery · 2022Article
42 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
Abstract
NRAS is frequently mutated in hematologic malignancies. We generated Mx1-Cre, Lox-STOP-Lox (LSL)-Nras(G12D) mice to comprehensively analyze the phenotypic, cellular, and biochemical consequences of endogenous oncogenic Nras expression in hematopoietic cells. Here we show that Mx1-Cre, LSL-Nras(G12D) mice develop an indolent myeloproliferative disorder but ultimately die of a diverse spectrum of hematologic cancers. Expressing mutant Nras in hematopoietic tissues alters the distribution of hematopoietic stem and progenitor cell populations, and Nras mutant progenitors show distinct responses to cytokine growth factors. Injecting Mx1-Cre, LSL-Nras(G12D) mice with the MOL4070LTR retrovirus causes acute myeloid leukemia that faithfully recapitulates many aspects of human NRAS-associated leukemias, including cooperation with deregulated Evi1 expression. The disease phenotype in Mx1-Cre, LSL-Nras(G12D) mice is attenuated compared with Mx1-Cre, LSL-Kras(G12D) mice, which die of aggressive myeloproliferative disorder by 4 months of age. We found that endogenous Kras(G12D) expression results in markedly elevated Ras protein expression and Ras-GTP levels in Mac1(+) cells, whereas Mx1-Cre, LSL-Nras(G12D) mice show much lower Ras protein and Ras-GTP levels. Together, these studies establish a robust and tractable system for interrogating the differential properties of oncogenic Ras proteins in primary cells, for identifying candidate cooperating genes, and for testing novel therapeutic strategies.
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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.