ArticleThe Journal of clinical investigation2008
Csf3r mutations in mice confer a strong clonal HSC advantage via activation of Stat5.
Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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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
47 citing papers in PubMed, 85 citations in OpenAlex.
- CSF3R Mutations Imply Adverse Prognostic Impact in Adult Acute Myeloid Leukemia Patients: A Single-Center Retrospective Study.Cancer medicine · 2025Article
- Colony-Stimulating Factor 3 Receptor Mutations and Variants in Hematological Malignancies.Cancers · 2025Review
- Research progress on the mechanisms of CSF3R mutations in leukemogenesis and treatment strategies.Cancer cell international · 2025Review
- JAK/STAT: Why choose a classical or an alternative pathway when you can have both?Journal of cellular and molecular medicine · 2022Review
- Leukemia-associated truncation of granulocyte colony-stimulating factor receptor impacts granulopoiesis throughout the life-course.Frontiers in immunology · 2022Article
- A review of granulocyte colony-stimulating factor receptor signaling and regulation with implications for cancer.Frontiers in oncology · 2022Review
- Impaired myelopoiesis in congenital neutropenia: insights into clonal and malignant hematopoiesis.Hematology. American Society of Hematology. Education Program · 2021Article
- The molecular basis of mammary gland development and epithelial differentiation.Seminars in cell & developmental biology · 2021Review
- Review
- Cooperating, congenital neutropenia-associated Csf3r and Runx1 mutations activate pro-inflammatory signaling and inhibit myeloid differentiation of mouse HSPCs.Annals of hematology · 2020Article
- Review
- Mechanisms of leukemic transformation in congenital neutropenia.Current opinion in hematology · 2019Review
- Peering through zebrafish to understand inherited bone marrow failure syndromes.Haematologica · 2019Review
- Article
- Gain-of-function mutations in granulocyte colony-stimulating factor receptor (CSF3R) reveal distinct mechanisms of CSF3R activation.The Journal of biological chemistry · 2018Article
- Chronic neutrophilic leukemia: new science and new diagnostic criteria.Blood cancer journal · 2018Review
- Article
- Unpaired Extracellular Cysteine Mutations of CSF3R Mediate Gain or Loss of Function.Cancer research · 2017Article
- Severe congenital neutropenias.Nature reviews. Disease primers · 2017Review
- A Truncated Granulocyte Colony-stimulating Factor Receptor (G-CSFR) Inhibits Apoptosis Induced by Neutrophil Elastase G185R Mutant: IMPLICATION FOR UNDERSTANDING CSF3R GENE MUTATIONS IN SEVERE CONGENITAL NEUTROPENIA.The Journal of biological chemistry · 2017Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
A fundamental property of leukemic stem cells is clonal dominance of the bone marrow microenvironment. Truncation mutations of CSF3R, which encodes the G-CSF receptor (G-CSFR), are implicated in leukemic progression in patients with severe congenital neutropenia. Here we show that expression of a truncated mutant Csf3r in mice confers a strong clonal advantage at the HSC level that is dependent upon exogenous G-CSF. G-CSF-induced proliferation, phosphorylation of Stat5, and transcription of Stat5 target genes were increased in HSCs isolated from mice expressing the mutant Csf3r. Conversely, the proliferative advantage conferred by the mutant Csf3r was abrogated in myeloid progenitors lacking both Stat5A and Stat5B, and HSC function was reduced in mice expressing a truncated mutant Csf3r engineered to have impaired Stat5 activation. These data indicate that in mice, inappropriate Stat5 activation plays a key role in establishing clonal dominance by stem cells expressing mutant Csf3r.
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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.