ArticleLeukemia2017
Characterization of the leukemogenic potential of distal cytoplasmic CSF3R truncation and missense mutations.
Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- AML with t(16;21)(p11.2;q22)/FUS::ERG rearrangement presenting with hemophagocytes and multinucleated cells: a case report and literature review.Annals of hematology · 2026Review
- Genotype-environment interaction drives the onset of riboflavin-responsive multiple acyl-CoA dehydrogenase deficiency in carriers of single heterozygous ETFDH variants.Cell communication and signaling : CCS · 2026Article
- Article
- Analysis and Interpretation of Somatic NMD-Escaping Variants in Oncogenes and Dual-Function Genes across Adult and Pediatric Cancer Cohorts.medRxiv : the preprint server for health sciences · 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
- Expanding the Spectrum ofJournal of clinical medicine · 2025Article
- The spectrum of Ph-negative disease: CNL and CSF3R-related disorders.Hematology. American Society of Hematology. Education Program · 2024Review
- Article
- Article
- 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
- Leukemia-associated truncation of granulocyte colony-stimulating factor receptor impacts granulopoiesis throughout the life-course.Frontiers in immunology · 2022Article
- Synoptic Diagnostics of Myeloproliferative Neoplasms: Morphology and Molecular Genetics.Cancers · 2021Review
- Colony-stimulating factor 3 receptor (CSF3R) M696T mutation does not impact on clinical outcomes of a Ph+ acute lymphoblastic leukemia patient.Blood science (Baltimore, Md.) · 2021Article
- Current Management of Chronic Neutrophilic Leukemia.Current treatment options in oncology · 2021Review
- Functional characterization of two rare BCR-FGFR1Cold Spring Harbor molecular case studies · 2020Article
- Next-generation sequencing reveals unique combination of mutations in cis of CSF3R in atypical chronic myeloid leukemia.Journal of clinical laboratory analysis · 2020Article
- Two myeloid leukemia cases with rareCold Spring Harbor molecular case studies · 2018Article
- 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
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
An increasing number of variants of unknown significance are being identified in leukemia patients with the application of deep sequencing and these include CSF3R cytoplasmic mutations. Previous studies have demonstrated oncogenic potential of certain CSF3R truncation mutations prior to internalization motifs. However, the oncogenic potential of truncating the more distal region of CSF3R cytoplasmic domain as well as cytoplasmic missense mutations remains uncharacterized. Here we identified that CSF3R distal cytoplasmic truncation mutations (Q793-Q823) also harbored leukemogenic potential. Mechanistically, these distal cytoplasmic truncation mutations demonstrated markedly decreased receptor degradation, probably owing to loss of the de-phosphorylation domain (residues N818-F836). Furthermore, all truncations prior to Q823 demonstrated increased expression of the higher molecular weight CSF3R band, which is shown to be essential for the receptor surface expression and the oncogenic potential. We further demonstrated that sufficient STAT5 activation is essential for oncogenic potential. In addition, CSF3R K704A demonstrated transforming capacity due to interruption of receptor ubiquitination and degradation. In summary, we have expanded the region of the CSF3R cytoplasmic domain in which truncation or missense mutations exhibit leukemogenic capacity, which will be useful for evaluating the relevance of CSF3R mutations in patients and helpful in defining targeted therapy strategies.
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