ArticleThe New England journal of medicine2013
Oncogenic CSF3R mutations in chronic neutrophilic leukemia and atypical CML.
Article in The New England journal of medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 288 papers, 1 of them a synthesis that pooled it.
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Who cites it
288 citing papers in PubMed, 1 synthesis or guideline pooled it, 562 citations in OpenAlex.
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- A phase II trial of ruxolitinib in combination with azacytidine in myelodysplastic syndrome/myeloproliferative neoplasms.American journal of hematology · 2018Trial
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- A bioinformatic survey of RNA isoform diversity and expression across 9 GTEx tissues using long-read sequencing data.BMC genomics · 2025Article
- CSF3R Mutations Imply Adverse Prognostic Impact in Adult Acute Myeloid Leukemia Patients: A Single-Center Retrospective Study.Cancer medicine · 2025Article
- Corticosterone reprograms splenic responses to avian pathogenic Escherichia coli infection in broiler chickens.Poultry science · 2025Article
- 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
- Expanding the Spectrum ofJournal of clinical medicine · 2025Article
- Dual ASXL1 and CSF3R mutations drive myeloid-biased stem cell expansion and enhance neutrophil differentiation.Blood advances · 2025Article
228 more citing papers are in PubMed but not listed here.
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Authors and funding
19 authors at 10 institutions in 2 countries.
Funding
Abstract
backgroundThe molecular causes of many hematologic cancers remain unclear. Among these cancers are chronic neutrophilic leukemia (CNL) and atypical (BCR-ABL1-negative) chronic myeloid leukemia (CML), both of which are diagnosed on the basis of neoplastic expansion of granulocytic cells and exclusion of genetic drivers that are known to occur in other myeloproliferative neoplasms and myeloproliferative-myelodysplastic overlap neoplasms.
methodsTo identify potential genetic drivers in these disorders, we used an integrated approach of deep sequencing coupled with the screening of primary leukemia cells obtained from patients with CNL or atypical CML against panels of tyrosine kinase-specific small interfering RNAs or small-molecule kinase inhibitors. We validated candidate oncogenes using in vitro transformation assays, and drug sensitivities were validated with the use of assays of primary-cell colonies.
resultsWe identified activating mutations in the gene encoding the receptor for colony-stimulating factor 3 (CSF3R) in 16 of 27 patients (59%) with CNL or atypical CML. These mutations segregate within two distinct regions of CSF3R and lead to preferential downstream kinase signaling through SRC family-TNK2 or JAK kinases and differential sensitivity to kinase inhibitors. A patient with CNL carrying a JAK-activating CSF3R mutation had marked clinical improvement after the administration of the JAK1/2 inhibitor ruxolitinib.
conclusionsMutations in CSF3R are common in patients with CNL or atypical CML and represent a potentially useful criterion for diagnosing these neoplasms. (Funded by the Leukemia and Lymphoma Society and others.).
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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.