在携带JAK2 V617F突变的原发性血小板增多症和真性红细胞增多症患者的中性粒细胞中，组织因子活性增加。 - Suppr

Tissue factor activity is increased in neutrophils from JAK2 V617F-mutated essential thrombocythemia and polycythemia vera patients.

作者信息

Reeves Brandi N, Kim Soo Jin, Song Jihyun, Wilson Kathryn J, Henderson Michael W, Key Nigel S, Pawlinski Rafal, Prchal Josef T

机构信息

Division of Hematology, Blood Research Center and Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina, USA.

Division of Hematology, School of Medicine, University of Utah, Salt Lake City, Utah, USA.

出版信息

Am J Hematol. 2022 Feb 1;97(2):E37-E40. doi: 10.1002/ajh.26402. Epub 2021 Nov 14.

DOI:10.1002/ajh.26402

PMID:34748652

Abstract

摘要

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Tissue factor activity is increased in neutrophils from JAK2 V617F-mutated essential thrombocythemia and polycythemia vera patients.在携带JAK2 V617F突变的原发性血小板增多症和真性红细胞增多症患者的中性粒细胞中，组织因子活性增加。

Am J Hematol. 2022 Feb 1;97(2):E37-E40. doi: 10.1002/ajh.26402. Epub 2021 Nov 14.

Narrative review: Thrombocytosis, polycythemia vera, and JAK2 mutations: The phenotypic mimicry of chronic myeloproliferation.综述：血小板增多症、真性红细胞增多症和 JAK2 突变：慢性骨髓增殖性疾病的表型模拟。

Ann Intern Med. 2010 Mar 2;152(5):300-6. doi: 10.7326/0003-4819-152-5-201003020-00008.

Progression to polythythemia vera from familial thrombocytosis with germline JAK2 R867Q mutation.携带种系JAK2 R867Q突变的家族性血小板增多症进展为真性红细胞增多症。

Ann Hematol. 2018 Apr;97(4):737-739. doi: 10.1007/s00277-017-3209-1. Epub 2018 Jan 24.

Molecular pathogenesis and therapy of polycythemia induced in mice by JAK2 V617F.JAK2 V617F 诱导小鼠发生红细胞增多症的分子发病机制与治疗

PLoS One. 2006 Dec 20;1(1):e18. doi: 10.1371/journal.pone.0000018.

Megakaryocytic morphology and clinical parameters in essential thrombocythemia, polycythemia vera, and primary myelofibrosis with and without JAK2 V617F.真性红细胞增多症、原发性血小板增多症以及原发性骨髓纤维化伴或不伴JAK2 V617F突变时的巨核细胞形态及临床参数

Arch Pathol Lab Med. 2014 Sep;138(9):1203-9. doi: 10.5858/arpa.2013-0018-OA.

Hydroxyurea dose impacts hematologic parameters in polycythemia vera and essential thrombocythemia but does not appreciably affect JAK2-V617F allele burden.羟基脲剂量影响真性红细胞增多症和原发性血小板增多症的血液学参数，但对JAK2-V617F等位基因负荷无明显影响。

Haematologica. 2011 Mar;96(3):e18-20. doi: 10.3324/haematol.2010.037846.

Megakaryopoiesis and platelet function in polycythemia vera and essential thrombocythemia patients with JAK2 V617F mutation.真性红细胞增多症和伴有JAK2 V617F突变的原发性血小板增多症患者的巨核细胞生成和血小板功能

Int J Hematol. 2008 Sep;88(2):181-188. doi: 10.1007/s12185-008-0129-9. Epub 2008 Jul 10.

A gain-of-function mutation of JAK2 in myeloproliferative disorders.骨髓增殖性疾病中JAK2的功能获得性突变。

N Engl J Med. 2005 Apr 28;352(17):1779-90. doi: 10.1056/NEJMoa051113.

Circulating endothelial cells in essential thrombocythemia and polycythemia vera: correlation with JAK2-V617F mutational status, angiogenic factors and coagulation activation markers.原发性血小板增多症和真性红细胞增多症患者循环内皮细胞：与 JAK2-V617F 突变状态、血管生成因子和凝血激活标志物的相关性。

Int J Hematol. 2010 Jun;91(5):792-8. doi: 10.1007/s12185-010-0596-7. Epub 2010 May 15.

Loss of Stat1 decreases megakaryopoiesis and favors erythropoiesis in a JAK2-V617F-driven mouse model of MPNs.Stat1 缺失会减少巨核细胞生成，并有利于 JAK2-V617F 驱动的骨髓增殖性肿瘤小鼠模型中的红细胞生成。

Blood. 2014 Jun 19;123(25):3943-50. doi: 10.1182/blood-2013-07-514208. Epub 2014 May 12.

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Increased Transferrin Concentrations Are Not Associated With Thrombosis in People Living at High Altitude.转铁蛋白浓度升高与高原地区人群的血栓形成无关。

J Hematol. 2025 Feb;14(1):20-25. doi: 10.14740/jh1388. Epub 2025 Jan 17.

Blood cell JAKtivation aggravates cerebral venous thrombosis.血细胞JAK激活会加重脑静脉血栓形成。

Blood Adv. 2024 Jun 25;8(12):3327-3329. doi: 10.1182/bloodadvances.2024012977.

TFPI from erythroblasts drives heme production in central macrophages promoting erythropoiesis in polycythemia.红细胞来源的 TFPI 驱动中巨噬细胞的血红素生成，从而促进红细胞生成增多症中的红细胞生成。

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Increased transferrin protects from thrombosis in Chuvash erythrocytosis.转铁蛋白升高可预防楚瓦什红细胞增多症的血栓形成。

Am J Hematol. 2023 Oct;98(10):1532-1539. doi: 10.1002/ajh.27021. Epub 2023 Jul 12.

Machine learning analyses constructed a novel model to predict recurrent thrombosis in adults with essential thrombocythemia.机器学习分析构建了一种新模型，以预测成人原发性血小板增多症患者的复发性血栓形成。

J Thromb Thrombolysis. 2023 Aug;56(2):291-300. doi: 10.1007/s11239-023-02833-7. Epub 2023 May 30.

JAK2 V617F allele burden in polycythemia vera: burden of proof.真性红细胞增多症中 JAK2 V617F 等位基因负担：证据负担。

Blood. 2023 Apr 20;141(16):1934-1942. doi: 10.1182/blood.2022017697.

JAK-STAT inhibition reduces endothelial prothrombotic activation and leukocyte-endothelial proadhesive interactions.JAK-STAT 抑制可减少内皮细胞促血栓形成激活和白细胞-内皮细胞的促黏附相互作用。

J Thromb Haemost. 2023 May;21(5):1366-1380. doi: 10.1016/j.jtha.2023.01.027. Epub 2023 Feb 2.

Downregulated KLF2 in polycythemia vera and essential thrombocythemia induces prothrombotic gene expression.KLF2 在真性红细胞增多症和原发性血小板增多症中下调，诱导促血栓形成基因表达。

Blood Adv. 2023 Mar 14;7(5):712-717. doi: 10.1182/bloodadvances.2022008052.

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Tissue factor activity is increased in neutrophils from JAK2 V617F-mutated essential thrombocythemia and polycythemia vera patients.

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