骨髓增殖性肿瘤血栓形成机制研究进展

摘要
图/表
参考文献(31)
相关文章 (5)

全文: PDF (651 KB) HTML (1 KB)
输出: BibTeX | EndNote (RIS)

摘要经典Ph染色体阴性的骨髓增殖性肿瘤（MPN）是造血干细胞克隆性疾病。血栓是影响MPN患者生存的最主要并发症。MPN血栓形成机制可能与以下多种机制相关，包括血细胞数量增多及活化、内皮细胞异常、凝血系统激活、微颗粒与炎性细胞因子增多、JAK2V617F基因突变等。本文对MPN并发血栓形成机制的研究进展进行了综述，阐明这些机制有助于临床寻找新的预测血栓的生物学标志，为MPN患者血栓预防和治疗提供参考。

	服务

	把本文推荐给朋友
	加入我的书架
	加入引用管理器
	E-mail Alert
	RSS
	作者相关文章
	刘严慈孙鹏慧卢朝阳惠吴函▲

关键词 ：血栓形成, 骨髓增殖性肿瘤, 细胞活化, 基因突变

Abstract：Classic negative Ph chromosome of myeloproliferative neoplasms (MPN) is a clonal disease of hematopoietic stem cells. Thrombus is the most important complication that affects the survival of MPN patients. The mechanism of thrombosis of MPN may be related to a variety of mechanisms including increased blood cell counts and activation, abnormal endothelial cells, activation of the blood coagulation system, increased microparticles and inflammatory cytokines, and JAK2V617F gene mutation. This paper reviews the research progress of MPN complicated thrombosis mechanism, elucidates that these mechanisms are helpful for clinical search new biological markers to predict thrombosis, so as to provide reference for thrombus prevention and treatment in MPN patients.

Key words： Thrombosis Myeloproliferative neoplasms Activation of cells Gene mutation

基金资助:国家自然科学基金青年科学基金项目（814000 94）；
人力资源和社会保障部留学人员科技活动项目择优资助（人社厅函[2016]176号）。

通讯作者: ▲通讯作者

引用本文:

刘严慈孙鹏慧卢朝阳惠吴函▲. 骨髓增殖性肿瘤血栓形成机制研究进展[J]. 中国医药导报, 2019, 16(24): 32-35.
LIU Yanci SUN Penghui LU Chaoyang HUI Wuhan▲. Research progress on mechanism of thrombosis for myeloproliferative neoplasms. 中国医药导报, 2019, 16(24): 32-35.

链接本文:

http://www.yiyaodaobao.com.cn/CN/ 或 http://www.yiyaodaobao.com.cn/CN/Y2019/V16/I24/32

[1] Barbui T，Thiele J，Gisslinger H，et al. The 2016 WHO classification and diagnostic criteria for myeloproliferative neoplasms：document summary and in-depth discussion [J]. Blood Cancer J，2018，8（2）：15.
[2] Hultcrantz M，Bj?觟rkholm M，Dickman PW，et al. Risk for Arterial and Venous Thrombosis in Patients With Myeloproliferative Neoplasms：A Population-Based Cohort Study [J]. Ann Intern Med，2018，168（5）：317-325.
[3] Reikvam H，Tiu RV. Venous thromboembolism in patients with essential thrombocythemia and polycythemia vera [J]. Leukemia，2012，26（4）：563-571.
[4] Shin DW，Gu JY，Kim JS，et al. Increased plasma viscosity in plasma cell dyscrasia and whole blood viscosity in polycythemia vera [J]. Clin Hemorheol Microcirc，2018，70（1）：59-67.
[5] Chen H，Angerer JI，Napoleone M，et al. Hematocrit and flow rate regulate the adhesion of platelets to von Willebrand factor [J]. Biomicrofluidics，2013，7（6）：64113.
[6] De Grandis M，Cambot M，Wautier MP，et al. JAK2V617F activates Lu/BCAM-mediated red cell adhesion in polycythemia vera through an EpoR-independent Rap1/Akt pathway [J]. Blood，2013，121（4）：658-665.
[7] Buxhofer-Ausch V，Steurer M，Sormann S，et al. Impact of white blood cells on thrombotic risk in patients with optimized platelet count in essential thrombocythemia [J]. Eur J Haematol，2018. doi：10.1111/ejh.13070.
[8] Alvarez-Larrán A，Arellano-Rodrigo E，Reverter JC，et al. Increased platelet，leukocyte，and coagulation activation in primary myelofibrosis [J]. Ann Hematol，2008，87（4）：269-276.
[9] Afshar-Kharghan V，Thiagarajan P. Leukocyte adhesion and thrombosis [J]. Curr Opin Hematol，2006，13（1）：34-39.
[10] Marin Oyarzún CP，Carestia A，Lev PR，et al. Neutrophil extracellular trap formation and circulating nucleosomes in patients with chronic myeloproliferative neoplasms [J]. Sci Rep，2016，6：38738.
[11] Robertson B，Urquhart C，Ford I，et al. Platelet and coagulation activation markers in myeloproliferative diseases：relationships with JAK2 V6I7 F status，clonality，and antiphospholipid antibodies [J]. J Thromb Haemost，2007，5（8）：1679-1685.
[12] Masselli E，Carubbi C，Pozzi G，et al. Platelet expression of PKCepsilon oncoprotein in myelofibrosis is associated with disease severity and thrombotic risk [J]. Ann Transl Med，2017，5（13）：273.
[13] 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 [J]. Am J Hematol，2011，86（4）：337-342.
[14] Treliński J，Wierzbowska A，Krawczyńska A，et al. Circulating endothelial cells in essential thrombocythemia and polycythemia vera：correlation with JAK2-V617F mutational status，angiogenic factors and coagulation activation markers [J]. Int J Hematol，2010，91（5）：792-798.
[15] Guadall A，Lesteven E，Letort G，et al. Endothelial Cells Harbouring the JAK2V617F Mutation Display Pro-Adherent and Pro-Thrombotic Features [J]. Thromb Haemost，2018，118（9）：1586-1599.
[16] Cella G，Marchetti M，Vianello F，et al. Nitric oxide derivatives and soluble plasma selectins in patients with myeloproliferative neoplasms [J]. Thromb Haemost，2010， 104（1）：151-156.
[17] 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 [J]. Haematologica，2018. [Epub ahead of print]. doi：10.3324/haematol.2018.195321.
[18] Tong D，Yu M，Guo L，et al. Phosphatidylserine-exposing blood and endothelial cells contribute to the hypercoagulable state in essential thrombocythemia patients [J]. Ann Hematol，2018，97（4）：605-616.
[19] Brinkman HJ，Mertens K，van Mourik JA. Proteolytic cleavage of protein S during the hemostatic response [J]. J Thromb Haemost，2005，3（12）：2712-2720.
[20] Marchetti M，Castoldi E，Spronk HM，et al. Thrombin generation and activated protein C resistance in patients with essential thrombocythemia and polycythemia vera [J]. Blood，2008，112（10）：4061-4068.
[21] Pourcelot E，Trocme C，Mondet J，et al. Cytokine profiles in polycythemia vera and essential thrombocythemia patients：clinical implications [J]. Exp Hematol，2014，42（5）：360-368.
[22] Gadomska G，Stankowska K，Boinska J，et al. Activation of the tissue factor-dependent extrinsic pathway and its relation to JAK2 V617F mutation status in patients with essential thrombocythemia [J]. Blood Coagul Fibrinolysis，2016，27（7）：817-821.
[23] Barbui T，Carobbio A，Finazzi G，et al. Inflammation and thrombosis in essential thrombocythemia and polycythemia vera：different role of C-reactive protein and pentraxin 3 [J]. Haematologica，2011，96（2）：315-318.
[24] Charpentier A，Lebreton A，Rauch A，et al. Microparticle phenotypes are associated with driver mutations and distinct thrombotic risks in essential thrombocythemia [J]. Haematologica，2016，101（9）：e365-e368.
[25] Taniguchi Y，Tanaka H，Luis EJ，et al. Elevated plasma levels of procoagulant microparticles are a novel risk factor for thrombosis in patients with myeloproliferative neoplasms [J]. Int J Hematol，2017，106（5）：691-703.
[26] Dahabreh IJ，Zoi K，Giannouli S，et al. Is JAK2 V617F mutation more than a diagnostic index? A meta-analysis of clinical outcomes in essential thrombocythemia [J]. Leuk Res，2009，33（1）：67-73.
[27] Bertozzi I，Bogoni G，Biagetti G，et al. Thromboses and hemorrhages are common in MPN patients with high JAK2V617F allele burden [J]. Ann Hematol，2017，96（8）：1297-1302.
[28] Dentali F，Squizzato A，Brivio L，et al. JAK2V617F mutation for the early diagnosis of Ph- myeloproliferative neoplasms in patients with venous thromboembolism：a meta-analysis [J]. Blood，2009，113（22）：5617-5623.
[29] Palandri F，Latagliata R，Polverelli N，et al. Mutations and long-term outcome of 217 young patients with essential thrombocythemia or early primary myelofibrosis [J]. Leukemia，2015，29（6）：1344-1349.
[30] Torregrosa JM，Ferrer-Marin F，Lozano ML，et al. Impaired leucocyte activation is underlining the lower thrombotic risk of essential thrombocythaemia patients with CALR mutations as compared with those with the JAK2 mutation [J]. Br J Haematol，2016，172（5）：813-815.
[31] Vannucchi AM，Antonioli E，Guglielmelli P，et al. Characteristics and clinical correlates of MPL 515W＞L/K mutation in essential thrombocythemia [J]. Blood，2008，112（3）：844-847.