ArticleBlood2013
The CSF3R T618I mutation causes a lethal neutrophilic neoplasia in mice that is responsive to therapeutic JAK inhibition.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 119 citations in OpenAlex.
- Efficacy of Ruxolitinib in Patients With Chronic Neutrophilic Leukemia and Atypical Chronic Myeloid Leukemia.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2020Trial
- Atypical chronic myeloid leukemia: From diagnosis to molecular features and therapeutic options.HemaSphere · 2025Review
- 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
- Dual ASXL1 and CSF3R mutations drive myeloid-biased stem cell expansion and enhance neutrophil differentiation.Blood advances · 2025Article
- Chronic Neutrophilic Leukemia: Advances in Diagnosis, Genetic Insights, and Management Strategies.Cancers · 2025Review
- Distribution of different classes of CSF3R mutations and co-mutational pattern in 360 myeloid neoplasia.Annals of hematology · 2025Article
- Research progress of additional pathogenic mutations in chronic neutrophilic leukemia.Annals of hematology · 2024Review
- Enhanced MAPK signaling induced by CSF3R mutants confers dependence to DUSP1 for leukemic transformation.Blood advances · 2024Article
- Article
- CSF3R as a potential prognostic biomarker and immunotherapy target in glioma.Central-European journal of immunology · 2024Article
- Case report: Safety and efficacy of synergistic treatment using selinexor and azacitidine in patients with atypical chronic myeloid leukemia with resistance to decitabine.Frontiers in oncology · 2024Article
- Definitions, Biology, and Current Therapeutic Landscape of Myelodysplastic/Myeloproliferative Neoplasms.Cancers · 2023Review
- CNL and aCML should be considered as a single entity based on molecular profiles and outcomes.Blood advances · 2023Article
- Extremely rare chronic neutrophilic leukemia characterized by unrelieved abdominal distention and swollen painful limbs: new clinical insight.American journal of translational research · 2023Article
- Avapritinib treatment of KIT D816V-mutant atypical chronic myeloid leukemia.Leukemia research reports · 2023Article
- Co-Occurring CSF3R W791* Germline and Somatic T618I Driver Mutations Induce Early CNL and Clonal Progression to Mixed Phenotype Acute Leukemia.Current oncology (Toronto, Ont.) · 2022Article
- Chronic Neutrophilic Leukemia: A Comprehensive Review of Clinical Characteristics, Genetic Landscape and Management.Frontiers in oncology · 2022Review
- Atypical Chronic Myeloid Leukemia: New Developments from Molecular Diagnosis to Treatment.Medicina (Kaunas, Lithuania) · 2021Review
- Current Management of Chronic Neutrophilic Leukemia.Current treatment options in oncology · 2021Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
We have recently identified targetable mutations in CSF3R (GCSFR) in 60% of chronic neutrophilic leukemia (CNL) and atypical (BCR-ABL-negative) chronic myeloid leukemia (aCML) patients. Here we demonstrate that the most prevalent, activating mutation, CSF3R T618I, is sufficient to drive a lethal myeloproliferative disorder in a murine bone marrow transplantation model. Mice transplanted with CSF3R T618I-expressing hematopoietic cells developed a myeloproliferative disorder characterized by overproduction of granulocytes and granulocytic infiltration of the spleen and liver, which was uniformly fatal. Treatment with the JAK1/2 inhibitor ruxolitinib lowered the white blood count and reduced spleen weight. This demonstrates that activating mutations in CSF3R are sufficient to drive a myeloproliferative disorder resembling aCML and CNL that is sensitive to pharmacologic JAK inhibition. This murine model is an excellent tool for the further study of neutrophilic myeloproliferative neoplasms and implicates the clinical use of JAK inhibitors for this disease.
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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.