Open Access
Med Sci (Paris)
Volume 35, Number 8-9, Août–Septembre 2019
Page(s) 651 - 658
Section M/S Revues
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. [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. [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. [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. [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. [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. [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. [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. [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. [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. [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. [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. [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. [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]

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