ArticleThe Journal of clinical investigation1991
Polycythemia vera blood burst-forming units-erythroid are hypersensitive to interleukin-3.
Article in The Journal of clinical investigation, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 93 citations in OpenAlex.
- Serum Inflammatory Factor Profiles in the Pathogenesis of High-Altitude Polycythemia and Mechanisms of Acclimation to High Altitudes.Mediators of inflammation · 2021Article
- Complex oncogene dependence in microRNA-125a-induced myeloproliferative neoplasms.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Current outlook on molecular pathogenesis and treatment of myeloproliferative neoplasms.Molecular diagnosis & therapy · 2012Review
- CREB in the pathophysiology of cancer: implications for targeting transcription factors for cancer therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Article
- Review
- JAK2 inhibitor therapy in myeloproliferative disorders: rationale, preclinical studies and ongoing clinical trials.Leukemia · 2008Review
- The JAK2(V617F) tyrosine kinase mutation in myeloproliferative disorders: Summary of published literature and a perspective.Current hematologic malignancy reports · 2006Review
- Diagnostic and prognostic value of colony formation of hematopoietic progenitor cells in myeloid malignancies.Wiener klinische Wochenschrift · 2003Review
- Dysregulated hematopoiesis and a progressive neurological disorder induced by expression of an activated form of the human common beta chain in transgenic mice.The Journal of clinical investigation · 1998Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Because polycythemia vera (PV) is a clonal hematopoietic stem cell disease with a trilineage hyperplasia, and interleukin-3 (IL-3) stimulates trilineage hematopoiesis, we have studied the response of highly purified PV blood burst-forming units-erythroid (BFU-E) to recombinant human IL-3 (rIL-3). Whereas the growth of normal blood BFU-E in vitro rapidly declined by 40 and 60% after 24 and 48 h of incubation without 50 U/ml of rIL-3, the growth of PV BFU-E declined by only 10 and 30% under the same conditions, demonstrating a reduced dependence on rIL-3. A reduced dependence of PV BFU-E on recombinant human erythropoietin (rEP) was also present. Dose-response experiments showed a 117-fold increase in PV BFU-E sensitivity to rIL-3, and a 6.5-fold increase in sensitivity to rEP, compared to normal BFU-E, whereas blood BFU-E from patients with secondary polycythemia responded like normal BFU-E. Endogenous erythroid colony (EEC) formation, which is independent of the addition of rEP, was reduced by 50% after erythroid colony-forming cells were generated from PV BFU-E in vitro without rIL-3 for 3 d, whereas rEP-stimulated erythroid colonies were unaffected. These studies demonstrate a striking hypersensitivity of PV blood BFU-E to rIL-3, which may be the major factor in the pathogenesis of increased erythropoiesis without increased EP concentrations.
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