ArticleLeukemia2017
Enhanced MAPK signaling is essential for CSF3R-induced leukemia.
Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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
22 citing papers in PubMed, 36 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
- 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
- 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
- Rare case of simultaneous occurrence of chronic neutrophil leukemia and T lymphoblastic lymphoma: case report and literature review.Annals of hematology · 2024Review
- Enhanced MAPK signaling induced by CSF3R mutants confers dependence to DUSP1 for leukemic transformation.Blood advances · 2024Article
- Evaluating biomarkers in canine cytotoxic interface dermatitis reactions to account for clinical and histopathological similarities and differences.Frontiers in veterinary science · 2024Article
- MAPK-negative feedback regulation confers dependence to JAK2Leukemia · 2023Article
- A novel colony stimulating factor 3 receptor activating mutation identified in a patient with chronic neutrophilic leukemia.Haematologica · 2023Article
- Article
- Current Management of Chronic Neutrophilic Leukemia.Current treatment options in oncology · 2021Review
- Chronic Neutrophilic Leukemia: A Literature Review of the Rare Myeloproliferative Pathology.Cureus · 2021Review
- Atypical Chronic Myelogenous Leukemia,Frontiers in oncology · 2021Review
- Article
- A Novel Germline Variant in CSF3R Reduces N-Glycosylation and Exerts Potent Oncogenic Effects in Leukemia.Cancer research · 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
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Both membrane-proximal and truncation mutations in CSF3R have recently been reported to drive the onset of chronic neutrophilic leukemia (CNL). Here we show that although truncation mutation alone cannot induce leukemia, both proximal and compound mutations (proximal and truncation mutations on same allele) are leukemogenic with a disease latency of 90 and 23 days, respectively. Comparative whole-genome expression profiling and biochemical experiments revealed that induced expression of Mapk adaptor protein Ksr1 and enhanced Mapk signaling are crucial to leukemogenesis by CSF3R proximal and compound mutants. Moreover, inhibition of Mek1/2 by trametinib alone is sufficient to suppress leukemia induced by both CSF3R proximal and ruxolitinib-resistant compound mutations. Together, these findings elucidate a Mapk-dependent mechanism of CSF3R-induced pathogenesis, and they establish the rationale for clinical evaluation of MEK1/2 inhibition in CNL.
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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.