ArticleBlood2013
JAK2V617F leads to intrinsic changes in platelet formation and reactivity in a knock-in mouse model of essential thrombocythemia.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.
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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
74 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Jak2 V617F clonal hematopoiesis promotes arterial thrombosis via platelet activation and cross talk.Blood · 2024Pooled it
- Anti-Platelet Factor 4/Heparin Antibody Formation Occurs Endogenously and at Unexpected High Frequency in Polycythemia Vera.BioMed research international · 2017Trial
- The effects of JAK inhibitor therapy upon novel markers of thrombosis In myeloproliferative neoplasms.Haematologica · 2015Trial
- JAK2 V617F, MPL, and CALR mutations in essential thrombocythaemia and major thrombotic complications: a single-institute retrospective analysis.Pathology oncology research : POR · 2015Trial
- Prevalence of the JAK2 V617F Mutation in Patients with Non-Cardioembolic Stroke.Journal of atherosclerosis and thrombosis · 2026Article
- Characterizing mouse platelet heterogeneity across diverse disease models using spectral flow cytometry and high-dimensional analysis.Research and practice in thrombosis and haemostasis · 2026Article
- JAK inhibitors and adverse cardiovascular events: Class effect or molecule-specific risk?Frontiers in pharmacology · 2026Review
- Human plasma proteomic profile of clonal hematopoiesis.Nature communications · 2025Article
- Review
- Clonal Hematopoiesis of Intermediate Potential in Atrial Fibrillation: A Critical View of Current Knowledge as a Springboard for Future Research.Diagnostics (Basel, Switzerland) · 2025Review
- Clonal hematopoiesis of indeterminate potential: contribution to disease and promising interventions.Molecular and cellular biochemistry · 2025Review
- Clonal Hematopoiesis of Indeterminate Potential and Atrial Fibrillation: Insights into Pathophysiology and Clinical Implications.International journal of molecular sciences · 2025Review
- Obliteration of liver sinusoids through platelet aggregates associated to extramedullary haematopoiesis in myeloid neoplasms.Virchows Archiv : an international journal of pathology · 2025Article
- Repeated Ischemic Stroke due to in situ Thrombus at the Middle Cerebral Artery in a Patient with Essential Thrombocythemia.Internal medicine (Tokyo, Japan) · 2025Article
- Newly diagnosed essential thrombocythemia leading to cardiogenic shock: a case report.BMC cardiovascular disorders · 2024Article
- Clonal hematopoiesis of indeterminate potential and the risk of pulmonary embolism: an observational study.EClinicalMedicine · 2024Article
- Neutrophil-specific expression of JAK2-V617F or CALRmut induces distinct inflammatory profiles in myeloproliferative neoplasia.Journal of hematology & oncology · 2024Article
- Cancer-associated thrombosis in hematologic malignancies.International journal of hematology · 2024Review
- Multiomic profiling reveals metabolic alterations mediating aberrant platelet activity and inflammation in myeloproliferative neoplasms.The Journal of clinical investigation · 2024Article
- TLR2 Derangements Likely Play a Significant Role in the Inflammatory Response and Thrombosis in Patients withMediators of inflammation · 2024Article
14 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors.
Funding
Abstract
The principal morbidity and mortality in patients with essential thrombocythemia (ET) and polycythemia rubra vera (PV) stems from thrombotic events. Most patients with ET/PV harbor a JAK2V617F mutation, but its role in the thrombotic diathesis remains obscure. Platelet function studies in patients are difficult to interpret because of interindividual heterogeneity, reflecting variations in the proportion of platelets derived from the malignant clone, differences in the presence of additional mutations, and the effects of medical treatments. To circumvent these issues, we have studied a JAK2V617F knock-in mouse model of ET in which all megakaryocytes and platelets express JAK2V617F at a physiological level, equivalent to that present in human ET patients. We show that, in addition to increased differentiation, JAK2V617F-positive megakaryocytes display greater migratory ability and proplatelet formation. We demonstrate in a range of assays that platelet reactivity to agonists is enhanced, with a concomitant increase in platelet aggregation in vitro and a reduced duration of bleeding in vivo. These data suggest that JAK2V617F leads to intrinsic changes in both megakaryocyte and platelet biology beyond an increase in cell number. In support of this hypothesis, we identify multiple differentially expressed genes in JAK2V617F megakaryocytes that may underlie the observed biological differences.
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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.