ArticleExperimental hematology2011
A truncation mutant of Csf3r cooperates with PML-RARα to induce acute myeloid leukemia in mice.
Article in Experimental hematology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Colony-Stimulating Factor 3 Receptor Mutations and Variants in Hematological Malignancies.Cancers · 2025Review
- A case of chronic neutrophilic leukemia and multiple myeloma showing the benefits of lenalidomide and cyclophosphamide therapy in treating both conditions.American journal of hematology · 2022Article
- Leukemia-associated truncation of granulocyte colony-stimulating factor receptor impacts granulopoiesis throughout the life-course.Frontiers in immunology · 2022Article
- Mechanisms of leukemic transformation in congenital neutropenia.Current opinion in hematology · 2019Review
- Chronic neutrophilic leukemia: new science and new diagnostic criteria.Blood cancer journal · 2018Review
- Article
- Recent Progress in Chronic Neutrophilic Leukemia and Atypical Chronic Myeloid Leukemia.Current hematologic malignancy reports · 2017Review
- Genomics of chronic neutrophilic leukemia.Blood · 2017Review
- Granulocyte colony-stimulating factor receptor signaling in severe congenital neutropenia, chronic neutrophilic leukemia, and related malignancies.Experimental hematology · 2017Review
- Validation is a dish oft served cold.Blood · 2014Article
- Article
- Aberrant regulation of FBW7 in cancer.Oncotarget · 2014Review
- Granulocyte colony-stimulating factor receptor mutations in myeloid malignancy.Frontiers in oncology · 2014Review
- Article
- CSF3R T618I is a highly prevalent and specific mutation in chronic neutrophilic leukemia.Leukemia · 2013Article
- Oncogenic CSF3R mutations in chronic neutrophilic leukemia and atypical CML.The New England journal of medicine · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Severe congenital neutropenia is associated with a marked propensity to develop myelodysplasia or acute myeloid leukemia (AML). Truncation mutations of CSF3R, encoding the granulocyte colony-stimulating factor receptor (G-CSFR), are associated with development of myelodysplasia/AML in severe congenital neutropenia. However, a causal relationship between CSF3R mutations and leukemic transformation has not been established. Herein, we show that truncated G-CSFR cooperates with the PML-RARα oncogene to induce AML in mice. Expression of truncated G-CSFR significantly shortens the latency of AML in a G-CSF-dependent fashion and it is associated with a distinct AML presentation characterized by higher blast counts and more severe myelosuppression. Basal and G-CSF-induced signal transducer and activator of transcription 3, signal transducer and activator of transcription 5, and extracellular signal-regulated kinase 1/2 phosphorylation were highly variable but similar in leukemic blasts expressing wild-type and truncated G-CSFR. These data provide new evidence suggesting a causative role for CSF3R mutations in human AML.
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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.