Open Access
Issue
Med Sci (Paris)
Volume 35, Number 8-9, Août–Septembre 2019
Page(s) 651 - 658
Section M/S Revues
DOI https://doi.org/10.1051/medsci/2019133
Published online 18 September 2019
  1. James C, Ugo V, Le Couédic JP, et al. A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera. Nature 2005 ; 434 : 5. [CrossRef] [Google Scholar]
  2. Scott LM, Tong W, Levine RL, et al. JAK2 Exon 12 mutations in polycythemia vera and idiopathic erythrocytosis. N Engl J Med 2007 ; 356 : 459–468. [CrossRef] [Google Scholar]
  3. Klampfl T, Gisslinger H, Harutyunyan AS, et al. Somatic mutations of calreticulin in myeloproliferative neoplasms. N Engl J Med 2013 ; 369 : 2379–2390. [CrossRef] [Google Scholar]
  4. Nangalia J, Massie CE, Baxter EJ, et al. Somatic CALR mutations in myeloproliferative neoplasms with nonmutated JAK2. N Engl J Med 2013 ; 369 : 2391–2405. [CrossRef] [Google Scholar]
  5. Pikman Y, Lee BH, Mercher T, et al. MPLW515L Is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia. PLoS Med 2006 ; 3 : e270. [CrossRef] [PubMed] [Google Scholar]
  6. Barbui T, Vannucchi AM, Carobbio A, et al. Patterns of presentation and thrombosis outcome in patients with polycythemia vera strictly defined by WHO-criteria and stratified by calendar period of diagnosis. Am J Hematol 2015 ; 90 : 434–437. [CrossRef] [PubMed] [Google Scholar]
  7. Carobbio A, Thiele J, Passamonti F, et al. Risk factors for arterial and venous thrombosis in WHO-defined essential thrombocythemia: an international study of 891 patients. Blood 2011 ; 117 : 5857–5859. [CrossRef] [Google Scholar]
  8. Marchioli R, Finazzi G, Specchia G, et al. Cardiovascular events and intensity of treatment in polycythemia vera. N Engl J Med 2013 ; 368 : 22–33. [CrossRef] [Google Scholar]
  9. Landolfi R, Roberto M, Jack K, et al. Efficacy and safety of low-dose aspirin in polycythemia vera. N Engl J Med 2004 ; 350 : 114–124. [CrossRef] [Google Scholar]
  10. Palandri F, Catani L, Testoni N, et al. Long-term follow-up of 386 consecutive patients with essential thrombocythemia: Safety of cytoreductive therapy. Am J Hematol 2008 ; 84 : 215–220. [CrossRef] [Google Scholar]
  11. Tefferi A, Vannucchi AM, Barbui T. Polycythemia vera treatment algorithm 2018. Blood Cancer J 2018 ; 8 : 3. [CrossRef] [PubMed] [Google Scholar]
  12. Tefferi A, Vannucchi AM, Barbui T. Essential thrombocythemia treatment algorithm 2018. Blood Cancer J 2018 ; 8 : 2. [CrossRef] [PubMed] [Google Scholar]
  13. De Stefano V, Finazzi G, Barbui T. Antithrombotic therapy for venous thromboembolism in myeloproliferative neoplasms. Blood Cancer J 2018 ; 8 : 65. [CrossRef] [PubMed] [Google Scholar]
  14. Borowczyk M, Wojtaszewska M, Lewandowski K, et al. The JAK2 V617F mutational status and allele burden may be related with the risk of venous thromboembolic events in patients with Philadelphia-negative myeloproliferative neoplasms. Thromb Res 2015 ; 135 : 272–280. [CrossRef] [PubMed] [Google Scholar]
  15. Vannucchi AM, Guglielmelli P, Longo G, et al. Prospective identification of high-risk polycythemia vera patients based on JAK2V617F allele burden. Leukemia 2007 ; 21 : 1952–1959. [CrossRef] [PubMed] [Google Scholar]
  16. Silver RT, Vandris K, Wang YL, et al. JAK2V617F allele burden in polycythemia vera correlates with grade of myelofibrosis, but is not substantially affected by therapy. Leuk Res 2011 ; 35 : 177–182. [CrossRef] [PubMed] [Google Scholar]
  17. Falanga A, Marchetti M, Vignoli A, et al. Leukocyte-platelet interaction in patients with essential thrombocythemia and polycythemia vera. Exp Hematol 2005 ; 33 : 523–530. [CrossRef] [PubMed] [Google Scholar]
  18. Arellano-Rodrigo E, Alvarez-Larrán A, Reverter JC, et al. Increased platelet and leukocyte activation as contributing mechanisms for thrombosis in essential thrombocythemia and correlation with the JAK2 mutational status. Haematologica 2006 ; 91 : 169–175. [PubMed] [Google Scholar]
  19. Falanga A, Marchetti M, Vignoli A, et al. V617F JAK-2 mutation in patients with essential thrombocythemia: relation to platelet, granulocyte, and plasma hemostatic and inflammatory molecules. Exp Hematol 2007 ; 35 : 702–711. [CrossRef] [PubMed] [Google Scholar]
  20. Alvarez-Larrán A, Arellano-Rodrigo E, Reverter JC, et al. Increased platelet, leukocyte, and coagulation activation in primary myelofibrosis. Ann Hematol 2008 ; 87 : 269–276. [CrossRef] [PubMed] [Google Scholar]
  21. Tong D, Yu M, Guo L, et al. Phosphatidylserine-exposing blood and endothelial cells contribute to the hypercoagulable state in essential thrombocythemia patients. Ann Hematol 2018 ; 97 : 605–616. [CrossRef] [PubMed] [Google Scholar]
  22. Panova-Noeva M, Marchetti M, Buoro S, et al. JAK2V617F mutation and hydroxyurea treatment as determinants of immature platelet parameters in essential thrombocythemia and polycythemia vera patients. Blood 2011 ; 118 : 2599–2601. [CrossRef] [Google Scholar]
  23. Lamrani L, Lacout C, Ollivier V, et al. Hemostatic disorders in a JAK2V617F-driven mouse model of myeloproliferative neoplasm. Blood 2014 ; 124 : 1136–1145. [CrossRef] [Google Scholar]
  24. Etheridge SL, Roh ME, Cosgrove ME, et al. JAK2V617F-positive endothelial cells contribute to clotting abnormalities in myeloproliferative neoplasms. Proc Natl Acad Sci USA 2014 ; 111 : 2295–2300. [CrossRef] [Google Scholar]
  25. Hobbs CM, Manning H, Bennett C, et al. JAK2V617F leads to intrinsic changes in platelet formation and reactivity in a knock-in mouse model of essential thrombocythemia. Blood 2013 ; 122 : 3787–3797. [CrossRef] [Google Scholar]
  26. Strassel C, Kubovcakova L, Mangin PH, et al. Haemorrhagic and thrombotic diatheses in mouse models with thrombocytosis. Thromb Haemost 2015 ; 113 : 414–425. [CrossRef] [PubMed] [Google Scholar]
  27. Falanga A, Marchetti M, Evangelista V, et al. Polymorphonuclear leukocyte activation and hemostasis in patients with essential thrombocythemia and polycythemia vera. Blood 2000 ; 96 : 4261–4266. [Google Scholar]
  28. Wang W, Liu W, Fidler T, et al. Macrophage inflammation, erythrophagocytosis, and accelerated atherosclerosis in Jak2V617F mice. Circ Res 2018 ; 23 : e35–e47. [Google Scholar]
  29. Gupta N, Edelmann B, Schnoeder TM, et al. JAK2-V617F activates β1-integrin-mediated adhesion of granulocytes to vascular cell adhesion molecule 1. Leukemia 2017 ; 31 : 1223–1226. [CrossRef] [PubMed] [Google Scholar]
  30. Edelmann B, Gupta N, Schnöder TM, et al. JAK2-V617F promotes venous thrombosis through β1/β2 integrin activation. J. Clin. Invest. 2018 ; 128 : 4359–4371. [CrossRef] [PubMed] [Google Scholar]
  31. Fuchs TA, Brill A, Duerschmied D, et al. Extracellular DNA traps promote thrombosis. Proc Natl Acad Sci USA 2010 ; 107 : 15880–15885. [CrossRef] [Google Scholar]
  32. Massberg S, Grahl L, von Bruehl M-L, et al. Reciprocal coupling of coagulation and innate immunity via neutrophil serine proteases. Nat Med 2010 ; 16 : 887–896. [CrossRef] [PubMed] [Google Scholar]
  33. von Brühl M-L, Stark K, Steinhart A, et al. Monocytes, neutrophils, and platelets cooperate to initiate and propagate venous thrombosis in mice in vivo. J Exp Med 2012 ; 209 : 819–835. [CrossRef] [PubMed] [Google Scholar]
  34. Yang X, Li L, Liu J, et al. Extracellular histones induce tissue factor expression in vascular endothelial cells via TLR and activation of NF-κB and AP-1. Thromb Res 2016 ; 137 : 211–218. [CrossRef] [PubMed] [Google Scholar]
  35. Glaser CB, Morser J, Clarke JH, et al. Oxidation of a specific methionine in thrombomodulin by activated neutrophil products blocks cofactor activity. A potential rapid mechanism for modulation of coagulation. J Clin Invest 1992 ; 90 : 2565–2573. [CrossRef] [PubMed] [Google Scholar]
  36. Oyarzún CP, Carestia A, Lev PR, et al. Neutrophil extracellular trap formation and circulating nucleosomes in patients with chronic myeloproliferative neoplasms. Sci Rep 2016 ; 6 : 38738. [CrossRef] [PubMed] [Google Scholar]
  37. Wolach O, Sellar RS, Martinod K, et al. Increased neutrophil extracellular trap formation promotes thrombosis in myeloproliferative neoplasms. Sci Transl Med 2018; 10. pii: eaan8292. [CrossRef] [PubMed] [Google Scholar]
  38. Guy A, Favre S, Labrouche-Colomer S, et al. High circulating levels of MPO-DNA are associated with thrombosis in patients with MPN. Leukemia 2019 Jun 7. doi : 10.1038/s41375-019-0500-2 [Google Scholar]
  39. Pearson TC, Wetherley-Mein G. Vascular occlusive episodes and venous haematocrit in primary proliferative polycythaemia. Lancet 1978 ; 312 : 1219–1222. [Google Scholar]
  40. Pearson T.. Hemorheologic Considerations in the pathogenesis of vascular occlusive events in polycythemia vera. Semin Thromb Hemost 1997 ; 23 : 433–439. [CrossRef] [PubMed] [Google Scholar]
  41. Zhao B, Mei Y, Cao L, et al. Loss of pleckstrin-2 reverts lethality and vascular occlusions in JAK2V617F-positive myeloproliferative neoplasms. J Clin Invest 2017 ; 128 : 125–140. [CrossRef] [PubMed] [Google Scholar]
  42. Wautier M-P, El Nemer W, Gane P, et al. Increased adhesion to endothelial cells of erythrocytes from patients with polycythemia vera is mediated by laminin 5 chain and Lu/BCAM. Blood 2007 ; 110 : 894–901. [Google Scholar]
  43. De Grandis M, Cambot M, Wautier M-P, et al. JAK2V617F activates Lu/BCAM-mediated red cell adhesion in polycythemia vera through an EpoR-independent Rap1/Akt pathway. Blood 2013 ; 121 : 658–665. [Google Scholar]
  44. Belotti A, Elli E, Speranza T, et al. Circulating endothelial cells and endothelial activation in essential thrombocythemia: Results from CD146+ immunomagnetic enrichment—flow cytometry and soluble E-selectin detection. Am J Hematol 2011 ; 87 : 319–320. [CrossRef] [PubMed] [Google Scholar]
  45. Torres C, Fonseca AM, Leander M, et al. Circulating endothelial cells in patients with venous thromboembolism and myeloproliferative neoplasms. PLoS One 2013 ; 8 : e81574. [CrossRef] [PubMed] [Google Scholar]
  46. Cella G, Marchetti M, Vianello F, et al. Nitric oxide derivatives and soluble plasma selectins in patients with myeloproliferative neoplasms. Thromb Haemost 2010 ; 104 : 151–156. [CrossRef] [PubMed] [Google Scholar]
  47. Kogan I, Chap D, Hoffman R, et al. JAK-2 V617F mutation increases heparanase procoagulant activity. Thromb Haemost 2016 ; 115 : 73–80. [CrossRef] [PubMed] [Google Scholar]
  48. Teofili L, Martini M, Iachininoto MG, et al. Endothelial progenitor cells are clonal and exhibit the JAK2V617F mutation in a subset of thrombotic patients with Ph-negative myeloproliferative neoplasms. Blood 2011 ; 117 : 2700–2707. [Google Scholar]
  49. Guy A, Gourdou-Latyszenok V, Le-Lay N, et al. Vascular endothelial cell expression of JAK2V617F is sufficient to promote a pro-thrombotic state due to increased P-selectin expression. Haematologica 2019 ; 104 : 70–81. [CrossRef] [PubMed] [Google Scholar]
  50. Guadall A, Lesteven E, Letort G, et al. Endothelial cells harbouring the JAK2V617F mutation display pro-adherent and pro-thrombotic features. Thromb Haemost 2018 ; 118 : 1586–1599. [CrossRef] [PubMed] [Google Scholar]
  51. Bucalossi A, Marotta G, Bigazzi C, et al. Reduction of antithrombin III, protein C, and protein S levels and activated protein C resistance in polycythemia vera and essential thrombocythemia patients with thrombosis. Am J Hematol 1996 ; 52 : 14–20. [CrossRef] [PubMed] [Google Scholar]
  52. Marchetti M, Castoldi E, Spronk HMH, et al. Thrombin generation and activated protein C resistance in patients with essential thrombocythemia and polycythemia vera. Blood 2008 ; 112 : 4061–4068. [Google Scholar]
  53. Dienava-Verdoold I, Marchetti MR, Boome LCJ, et al. Platelet-mediated proteolytic down regulation of the anticoagulant activity of protein S in individuals with haematological malignancies. Thromb Haemost 2012 ; 107 : 468–476. [CrossRef] [PubMed] [Google Scholar]
  54. Wieczorek I, MacGregor IR, Prescott RJ, et al. The fibrinolytic system and proteins C and S in treated polycythaemia rubra vera. Blood Coagul Fibrinolysis 1992 ; 3 : 823–826. [CrossRef] [PubMed] [Google Scholar]
  55. Arellano-Rodrigo E, Alvarez-Larrán A, Reverter JC, et al. Platelet turnover, coagulation factors, and soluble markers of platelet and endothelial activation in essential thrombocythemia: Relationship with thrombosis occurrence and JAK2 V617F allele burden. Am J Hematol 2008 ; 84 : 102–108. [Google Scholar]
  56. Panova-Noeva M, Marchetti M, Spronk HM, et al. Platelet-induced thrombin generation by the calibrated automated thrombogram assay is increased in patients with essential thrombocythemia and polycythemia vera. Am J Hematol 2011 ; 86 : 337–342. [CrossRef] [PubMed] [Google Scholar]
  57. Trappenburg MC, van Schilfgaarde M, Marchetti M, et al. Elevated procoagulant microparticles expressing endothelial and platelet markers in essential thrombocythemia. Haematologica 2009 ; 94 : 911–918. [CrossRef] [PubMed] [Google Scholar]
  58. Charpentier A, Lebreton A, Rauch A, et al. Microparticle phenotypes are associated with driver mutations and distinct thrombotic risks in essential thrombocythemia. Haematologica 2016 ; 101 : e365–e368. [CrossRef] [PubMed] [Google Scholar]
  59. Duchemin J, Ugo V, Ianotto JC, et al. Increased circulating procoagulant activity and thrombin generation in patients with myeloproliferative neoplasms. Thromb Res 2010 ; 126 : 238–242. [CrossRef] [PubMed] [Google Scholar]

Current usage metrics show cumulative count of Article Views (full-text article views including HTML views, PDF and ePub downloads, according to the available data) and Abstracts Views on Vision4Press platform.

Data correspond to usage on the plateform after 2015. The current usage metrics is available 48-96 hours after online publication and is updated daily on week days.

Initial download of the metrics may take a while.