ArticleProceedings of the National Academy of Sciences of the United States of America2006
Granulocyte colony-stimulating factor preferentially stimulates proliferation of monosomy 7 cells bearing the isoform IV receptor.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 115 citations in OpenAlex.
- Treatment optimization and genomic outcomes in refractory severe aplastic anemia treated with eltrombopag.Blood · 2019Trial
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- Alemtuzumab treatment of intermediate-1 myelodysplasia patients is associated with sustained improvement in blood counts and cytogenetic remissions.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2010Trial
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- Busulfan-cyclophosphamide vs fludarabine-busulfan for allogeneic transplant in acute myeloid leukemia.Future oncology (London, England) · 2025Article
- Kmt2c restricts G-CSF-driven HSC mobilization and granulocyte production in a methyltransferase-independent manner.Cell reports · 2024Article
- First report of familial mixed phenotype acute leukemia: shared clinical characteristics, Philadelphia translocation, and germline variants.International journal of hematology · 2024Article
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- A review of granulocyte colony-stimulating factor receptor signaling and regulation with implications for cancer.Frontiers in oncology · 2022Review
- Risk factors associated with poor response to immunosuppressive therapy in acquired aplastic anemia: A meta-analysis of retrospective studies.Experimental and therapeutic medicine · 2020Article
- Cytokine receptor splice variants in hematologic diseases.Cytokine · 2020Review
- Altered expression of CSF3R splice variants impacts signal response and is associated with SRSF2 mutations.Leukemia · 2020Article
- Improving Treatment for Myelodysplastic Syndromes Patients.Current treatment options in oncology · 2018Review
- Mathematical modeling of the impact of cytokine response of acute myeloid leukemia cells on patient prognosis.Scientific reports · 2018Article
- Recent advances in understanding clonal haematopoiesis in aplastic anaemia.British journal of haematology · 2017Review
- Hematopoietic Cell Transplantation Outcomes in Monosomal Karyotype Myeloid Malignancies.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2016Article
- miR-155 is associated with the leukemogenic potential of the class IV granulocyte colony-stimulating factor receptor in CD34⁺ progenitor cells.Molecular medicine (Cambridge, Mass.) · 2015Article
- [Acquired aplastic anemia developing myelodysplastic syndrome/acute myeloid leukemia: clinical analysis of nineteen patients and literatures review].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2015Review
- Alternatively spliced, truncated GCSF receptor promotes leukemogenic properties and sensitivity to JAK inhibition.Leukemia · 2014Article
- Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Granulocyte colony-stimulating factor (GCSF) administration has been linked to the development of monosomy 7 in severe congenital neutropenia and aplastic anemia. We assessed the effect of pharmacologic doses of GCSF on monosomy 7 cells to determine whether this chromosomal abnormality developed de novo or arose as a result of favored expansion of a preexisting clone. Fluorescence in situ hybridization (FISH) of chromosome 7 was used to identify small populations of aneuploid cells. When bone marrow mononuclear cells from patients with monosomy 7 were cultured with 400 ng/ml GCSF, all samples showed significant increases in the proportion of monosomy 7 cells. In contrast, bone marrow from karyotypically normal aplastic anemia, myelodysplastic syndrome, or healthy individuals did not show an increase in monosomy 7 cells in culture. In bone marrow CD34 cells of patients with myelodysplastic syndrome and monosomy 7, GCSF receptor (GCSFR) protein was increased. Although no mutation was found in genomic GCSFR DNA, CD34 cells showed increased expression of the GCSFR class IV mRNA isoform, which is defective in signaling cellular differentiation. GCSFR signal transduction via the Jak/Stat system was abnormal in monosomy 7 CD34 cells, with increased phosphorylated signal transducer and activation of transcription protein, STAT1-P, and increased STAT5-P relative to STAT3-P. Our results suggest that pharmacologic doses of GCSF increase the proportion of preexisting monosomy 7 cells. The abnormal response of monosomy 7 cells to GCSF would be explained by the expansion of undifferentiated monosomy 7 clones expressing the class IV GCSFR, which is defective in signaling cell maturation.
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