ArticleThe Journal of clinical investigation1998
Increased granulocyte colony-stimulating factor responsiveness but normal resting granulopoiesis in mice carrying a targeted granulocyte colony-stimulating factor receptor mutation derived from a patient with severe congenital neutropenia.
Article in The Journal of clinical investigation, 1998. 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, 121 citations in OpenAlex.
- Trial
- Colony-Stimulating Factor 3 Receptor Mutations and Variants in Hematological Malignancies.Cancers · 2025Review
- Leukemia-associated truncation of granulocyte colony-stimulating factor receptor impacts granulopoiesis throughout the life-course.Frontiers in immunology · 2022Article
- Impaired myelopoiesis in congenital neutropenia: insights into clonal and malignant hematopoiesis.Hematology. American Society of Hematology. Education Program · 2021Article
- Cooperating, congenital neutropenia-associated Csf3r and Runx1 mutations activate pro-inflammatory signaling and inhibit myeloid differentiation of mouse HSPCs.Annals of hematology · 2020Article
- Mechanisms of leukemic transformation in congenital neutropenia.Current opinion in hematology · 2019Review
- Article
- New monogenic disorders identify more pathways to neutropenia: from the clinic to next-generation sequencing.Hematology. American Society of Hematology. Education Program · 2017Review
- MEK/ERK addiction in CNL/aCML.Oncotarget · 2017Article
- Article
- 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
- Granulocyte colony-stimulating factor receptor signaling in severe congenital neutropenia, chronic neutrophilic leukemia, and related malignancies.Experimental hematology · 2017Review
- Granulocyte colony-stimulating factor receptor mutations in myeloid malignancy.Frontiers in oncology · 2014Review
- Severe congenital neutropenia and chronic neutrophilic leukemia: an intriguing molecular connection unveiled by oncogenic mutations in CSF3R.Haematologica · 2013Article
- G-CSF activation of AKT is not sufficient to prolong neutrophil survival.Journal of leukocyte biology · 2013Article
- Hematopoietic stem cell transplantation for severe congenital neutropenia.Current opinion in hematology · 2012Review
- A truncation mutant of Csf3r cooperates with PML-RARα to induce acute myeloid leukemia in mice.Experimental hematology · 2011Article
- Neutrophil elastase downmodulates native G-CSFR expression and granulocyte-macrophage colony formation.Journal of inflammation (London, England) · 2010Article
- An activating mutation in the CSF3R gene induces a hereditary chronic neutrophilia.The Journal of experimental medicine · 2009Article
- Granulocyte colony-stimulating factor: molecular mechanisms of action during steady state and 'emergency' hematopoiesis.Cytokine · 2008Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The role of mutations of the granulocyte colony-stimulating factor receptor (G-CSFR) in the pathogenesis of severe congenital neutropenia (SCN) and the subsequent development of acute myeloid leukemia (AML) is controversial. Mice carrying a targeted mutation of their G-CSFR that reproduces the mutation found in a patient with SCN and AML have been generated. The mutant G-CSFR allele is expressed in a myeloid-specific fashion at levels comparable to the wild-type allele. Mice heterozygous or homozygous for this mutation have normal levels of circulating neutrophils and no evidence for a block in myeloid maturation, indicating that resting granulopoiesis is normal. However, in response to G-CSF treatment, these mice demonstrate a significantly greater fold increase in the level of circulating neutrophils. This effect appears to be due to increased neutrophil production as the absolute number of G-CSF-responsive progenitors in the bone marrow and their proliferation in response to G-CSF is increased. Furthermore, the in vitro survival and G-CSF-dependent suppression of apoptosis of mutant neutrophils are normal. Despite this evidence for a hyperproliferative response to G-CSF, no cases of AML have been detected to date. These data demonstrate that the G-CSFR mutation found in patients with SCN is not sufficient to induce an SCN phenotype or AML in mice.
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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.