ArticleLeukemia2014
Alternatively spliced, truncated GCSF receptor promotes leukemogenic properties and sensitivity to JAK inhibition.
Article in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
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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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Effectiveness and safety of primary prophylaxis with G-CSF after induction therapy for acute myeloid leukemia: a systematic review and meta-analysis of the clinical practice guidelines for the use of G-CSF 2022 from the Japan society of clinical oncology.International journal of clinical oncology · 2024Pooled it
- Expanding the Spectrum ofJournal of clinical medicine · 2025Article
- Neutrophils: a new target for postoperative cognitive dysfunction.Apoptosis : an international journal on programmed cell death · 2025Review
- Multiomics Integration and Machine Learning Reveal Colony Stimulating Factor 3 Receptor as a Key Gene and Therapeutic Target in Crohn's Disease.Mediators of inflammation · 2025Article
- Distribution of different classes of CSF3R mutations and co-mutational pattern in 360 myeloid neoplasia.Annals of hematology · 2025Article
- Article
- JAK/STAT: Why choose a classical or an alternative pathway when you can have both?Journal of cellular and molecular medicine · 2022Review
- A review of granulocyte colony-stimulating factor receptor signaling and regulation with implications for cancer.Frontiers in oncology · 2022Review
- Contrasting Immunopathogenic and Therapeutic Roles of Granulocyte Colony-Stimulating Factor in Cancer.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Inducible expression of a disease-associatedThe Journal of biological chemistry · 2020Article
- Cytokine receptor splice variants in hematologic diseases.Cytokine · 2020Review
- Altered expression of CSF3R splice variants impacts signal response and is associated with SRSF2 mutations.Leukemia · 2020Article
- Review
- Characterization of the leukemogenic potential of distal cytoplasmic CSF3R truncation and missense mutations.Leukemia · 2017Article
- A t(1;9) translocation involvingHaematologica · 2017Article
- G-CSF and GM-CSF in Neutropenia.Journal of immunology (Baltimore, Md. : 1950) · 2015Review
- miR-155 is associated with the leukemogenic potential of the class IV granulocyte colony-stimulating factor receptor in CD34⁺ progenitor cells.Molecular medicine (Cambridge, Mass.) · 2015Article
- The cell survival pathways of the primordial RNA-DNA complex remain conserved in the extant genomes and may function as proto-oncogenes.European journal of microbiology & immunology · 2015Review
- Systems approach to phagocyte production and activation: neutrophils and monocytes.Advances in experimental medicine and biology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
Granulocyte colony-stimulating factor (GCSF) drives the production of myeloid progenitor and precursor cells toward neutrophils via the GCSF receptor (GCSFR, gene name CSF3R). Children with severe congenital neutropenia chronically receive pharmacologic doses of GCSF, and ∼30% will develop myelodysplasia/acute myeloid leukemia (AML) associated with GCSFR truncation mutations. In addition to mutations, multiple isoforms of CSF3R have also been reported. We found elevated expression of the alternatively spliced isoform, class IV CSF3R in adult myelodysplastic syndrome/AML patients. Aside from its association with monosomy 7 and higher rates of relapse in pediatric AML patients, little is known about the biology of the class IV isoform. We found developmental regulation of CSF3R isoforms with the class IV expression more representative of a progenitor cell stage. Striking differences were found in phosphoprotein signaling involving Janus kinase (JAK)-signal transducer and activator of transcription (STAT) and cell cycle gene expression. Enhanced proliferation by class IV GCSFR was associated with diminished STAT3 and STAT5 activation, yet showed sensitivity to JAK2 inhibitors. Alterations in the C-terminal domain of the GCSFR result in leukemic properties of enhanced growth, impaired differentiation and resistance to apoptosis, suggesting that they can behave as oncogenic drivers, sensitive to JAK2 inhibition.
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Identifiers
What OpenQuestion holds
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.