ReviewCurrent hematologic malignancy reports2006
The JAK2(V617F) tyrosine kinase mutation in myeloproliferative disorders: Summary of published literature and a perspective.
Review in Current hematologic malignancy reports, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
3 citing papers in PubMed, 4 citations in OpenAlex.
- Comparability of JAK2 p.V617F allele burden in peripheral blood and that in bone marrow in patients with suspected myeloproliferative neoplasms: a single-center prospective study.American journal of translational research · 2023Article
- Two patterns of thrombopoietin signaling suggest no coupling between platelet production and thrombopoietin reactivity in thrombocytopenia-absent radii syndrome.Haematologica · 2012Article
- The 2008 WHO diagnostic criteria for polycythemia vera, essential thrombocythemia, and primary myelofibrosis.Current hematologic malignancy reports · 2009Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A common somatic point mutation has recently been identified in the Janus kinase 2 (JAK2) gene in virtually all cases of polycythemia vera and in a majority of patients with essential thrombocythemia and idiopathic myelofibrosis. This common mutation in the pseudokinase autoinhibitory domain of the enzyme results in constitutive tyrosine kinase activation, which in turn leads to cytokine hypersensitivity and factor independence in factor-dependent cell lines, and causes polycythemia in mice. This discovery has led to greater understanding of the molecular pathogenesis of the chronic myeloproliferative disorders, which may translate into targeted therapy.
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What OpenQuestion holds
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.