V617F mutation in JAK2 is associated with poorer survival in idiopathic myelofibrosis
Open accessAbstract
Most patients with polycythemia vera and half with idiopathic myelofibrosis and essential thrombocythemia have an acquired V617F mutation in JAK2. Using sensitive polymerase chain reaction (PCR)-based methods, we genotyped 152 patients with idiopathic myelofibrosis to establish whether there were differences in presentation and outcome between those with and those without the mutation. Patients positive for V617F had higher neutrophil and white cell counts (P = .02) than did patients negative for V617F, but other diagnostic features were comparable between the 2 groups. Patients positive for V617F were less likely to require blood transfusion during follow-up (P = .03). Despite this, patients positive for V617F had poorer overall survival, even after correction for confounding factors (P = .01).
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Activation of JAK2 caused by the V617F mutation leads to constitutive activation of STAT3 and is associated with reduced survival in idiopathic myelofibrosis.
“Activation of JAK2 caused by this mutation leads to constitutive activation of STAT3 and is associated with reduced survival in idiopathic myelofibrosis.54,55”
From Critical analysis of the potential for targeting STAT3 in human malignancy (2013) · cites this paper as [54]
The Results and discussion report significantly poorer survival among patients with idiopathic myelofibrosis who were V617F-positive than among those who were V617F-negative (adjusted hazard ratio 3.30). The paper does not report that the mutation causes constitutive STAT3 activation; a search for STAT3 found no supporting passage. Page numbers were not available in our copy. (LLM, conf=0.88)
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Research works printed but not linked: 9
- Baxter EJ, Scott LM, Campbell PJ, et al. Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. Lancet. 2005;365: 1054-1061.
- James C, Ugo V, Le Couedic JP, et al. A unique clonal JAK2 mutation leading to constitutive sig- nalling causes polycythaemia vera. Nature. 2005; 434:1144-1148.
- Levine RL, Wadleigh M, Cools J, et al. Activating mutation in the tyrosine kinase JAK2 in polycy- themia vera, essential thrombocythemia, and my- eloid metaplasia with myelofibrosis. Cancer Cell. 2005;7:387-397.
- Kralovics R, Passamonti F, Buser AS, et al. A gain-of-function mutation of JAK2 in myeloprolif- erative disorders. N Engl J Med. 2005;352:1779- 1790.
- Barosi G, Ambrosetti A, Finelli C, et al. The Italian Consensus Conference on Diagnostic Criteria for Myelofibrosis with Myeloid Metaplasia. Br J Haematol. 1999;104:730-737.
- Dupriez B, Morel P, Demory JL, et al. Prognostic factors in agnogenic myeloid metaplasia: a report on 195 cases with a new scoring system. Blood. 1996;88:1013-1018.
- Campbell PJ, Scott LM, Buck G, et al. Definition of subtypes of essential thrombocythaemia and relation to polycythaemia vera based on JAK2 V617F mutation status: a prospective study. Lan- cet. 2005;366:1945-1953.
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“Activation of JAK2 caused by this mutation leads to constitutive activation of STAT3 and is associated with reduced survival in idiopathic myelofibrosis.(54,55) Another mechanism of kinase-driven STAT3 activation in cancer is genomic amplification of kinase genes or RTK ligands with subsequent protein overexpression,…”
- Authors
- Campbell, P. J.
- Affiliations
- University of Cambridge (GB)
- Corresponding author
- Campbell, P. J.
- ORCID
- Campbell, P. J.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2006-03-01
- Volume
- 107
- Issue
- 5
- Pages
- 2098-2100
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2148101855
- Cited by
- 224
- References
- 0
- Citations by year
- 2026: 1 · 2024: 2 · 2023: 3 · 2022: 1 · 2021: 4 · 2020: 7 · 2019: 3 · 2018: 3 · 2017: 7 · 2016: 9 · 2015: 10 · 2014: 6 · 2013: 14 · 2012: 23
- FWCI
- 12.81
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- University of Southern Denmark Research Portal (University of Southern Denmark) (publishedVersion)
- HAL (submittedVersion)
- Funders
- Wellcome Trust (088340)
- Topics
- Health Sciences › Medicine › Genetics › Myeloproliferative Neoplasms: Diagnosis and Treatment
- Health Sciences › Medicine › Hematology › Platelet Disorders and Treatments
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Keywords
- JAK2 V617F mutation, primary myelofibrosis, overall survival, prognostic factors, transfusion requirements, neutrophil count, white blood cell count, essential thrombocythemia, polycythemia vera, myeloproliferative neoplasms
- MeSH terms
- Aged, Blood Transfusion, Female, Follow-Up Studies, Humans, Male, Middle Aged, Polycythemia Vera, Protein-Tyrosine Kinases, Proto-Oncogene Proteins, Thrombocythemia, Essential, Point Mutation, Disease-Free Survival, Amino Acid Substitution, Janus Kinase 2, Primary Myelofibrosis
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