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骨髓增殖性肿瘤研究进展：JAK2 V617F基因突变发现后10年 被引量：2

Myeloproliferative neoplasms：ten years after the discovery of JAK2 V617F gene mutation
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摘要 结合大量的临床实践和近10年来对骨髓增殖性肿瘤（MPN）[骨髓增殖性疾病（MPD）]在JAK2 V617F基因突变等分子水平的大量研究,更加深了对MPN（MPD）的分子发病机制和临床价值的认识.研究者们探讨了JAK2 V617F基因突变如何促进MPN（MPD）发病的机制,分析了JAK2 V617F基因突变的分子机制和JAK2 V617F基因突变如何引起MPN（MPD）不同临床表型,以及MPN（MPD）基因组突变图谱及其生物学意义,指出了MPN（MPD）病理克隆的复杂性.JAK2 V617F基因突变在研究和诊治MPN（MPD）的过程中发挥着重大作用,其促使MPN（MPD）的研究和应用深入到基因/分子水平,治疗更趋于靶向性,更加精确,特别是使那些常规检验无法明确诊断的患者获得了及时诊治,避免了合并疾病的发生.MPN（MPD）的防治焦点是及时诊治,预防并避免血栓/出血性并发症的发生.推荐首选干扰素α（IFN-α）治疗,对于年龄大于60岁的患者,羟基脲是可以采用的.MPN（MPD）患者的预后大多数良好,发生恶变的风险不高,这是反复建议对中国MPD患者避免使用MPN称谓的主要理由. This article focuses on the rapidly evolving understanding of the molecular pathogenetic mechanisms of the bcr-abl-negative myeloproliferative neoplasms （MPN） [myeloproliferative disorders （MPD）],such as polycythemia vera （PV）,essential thrombocythemia （ET）,and primary myelofibrosis （MF）.The amplify therapies were reviewed and IFN-α is an effective agent for these MPN （MPD）.Also,the article emphasize once again avoidance MPN and select MPD for such chinese patients.
作者 田丁
机构地区 首都医科大学宣武医院血液科
出处 《白血病．淋巴瘤》 CAS 2015年第7期385-387,共3页 Journal of Leukemia & Lymphoma
关键词 骨髓增殖性肿瘤 骨髓增殖性疾病 JAK2 V617F基因突变 干扰素Α Myeloproliferative neoplasms,MPN Myeloproliferative disorders,MPD JAK2 V617F gene mutation Interferon-alpha
分类号 R733.3 [医药卫生—肿瘤]
  • 相关文献

参考文献16

  • 1James C, Ugo V, Le Cou6dic JP, et al. A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera [ J ]. Nature, 2005, 434 ( 7037 ) : 1 144-1148.
  • 2Baxter EJ, Scott LM, Campbell PJ, et al. Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders [ J ]. Lancet, 2005, 365 ( 9464 ) : 1054-1061.
  • 3Levine RL, Wadleigh M, Cools J, et al. Activiting mutation in thetyrosine kinase JAK2 polycythaemia vera, essential thrombythemia, and myeloid metaplasia with myelofibrosis [ J ]. Cancer Cell, 2005, 7 ( 4 ) : 387-397.
  • 4Kralavics R, Passamonti F, Buser AS, et al. A gain-of-function mutation of JAK2 in myeloproliferative disorde [ J]. N Engl J Med, 2005, 352( 17 ) : 1779-1790.
  • 5Harrison C, Kiladjian JJ, A1-Ali HK, et al. JAK inhibition with ruxolitinib versus best available therapy for myelofibrosis [ J]. N Engl J Med, 2012, 366 (9): 787-798.
  • 6Chen E, Mullally A. How does JAK2V617F contribute to the pathogenesis of myeloproliferative neoplasms? [ J ]. Hematology Am Soc Hematol Educ Program, 2014, 2014 ( 1 ) : 268-276.
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  • 8Klampfl T, Gisslinger H, Harutyunyan AS, et al. Somatic mutations of calreticulin in myeloproliferative neoplasms [ J ]. N Engl J Med, 2013, 369( 25 ): 2379-2390.
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二级参考文献69

  • 1那立军,马洪.30例骨髓增生性疾病JAK2V617F基因突变检测分析[J].黑龙江医学,2013,37(6):401-402. 被引量：1
  • 2申徐良,陈方平,魏武,张梅香,史文芝,秦小琪,徐洪亮.bcr-abl阴性骨髓增生性疾病患者JAK2V617F点突变检测的临床意义[J].白血病．淋巴瘤,2008,17(2). 被引量：1
  • 3James C, Ugo V, Le Cou e dic JP, et al. A unique clonal JAK2 mutation leading to constitutive signaling causes polycythaemi a vera. Nature, 2005, 434:1144-1148.
  • 4Baxter EJ, Scott LM, Campbell PJ, et al. Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. Lancet, 2005, 365: 1054-1061.
  • 5Levine RL, Wadleigh M, Cools J, et al. Aetiviting mutation in the tyrosine kinase JAK2 polyeythaemia vera,essential thromboeythemia, and myeloid metaplasia with myelofibrosis. Cancer Cell, 2005, 7: 387- 397.
  • 6Kralovics R, Passamonti F, Buser AS, et al. A gain-of-function mutation of JAK2 in myeloproliferative disorders. N Engl J Med, 2005, 352: 1779-1790.
  • 7Tefferi A. Classification, diagnosis and magagemant of myeloproliferative disorders in the JAK2617F era. Hematology Am Soc Hematol Educ Program, 2006: 240-245.
  • 8Skoda R. The genec basis ofmyeloproliferative disorders. Hematology Am Soc Hematol Educ Program, 2007: 1-10.
  • 9Prchal JT. Philadelphia chromosome-negativemyeloproliferative disorders: an historical perspective. Hematology Am Soc Hematol Educ Program, 2008: 68.
  • 10James C. The JAK2V617F mutation in polycythemia vera and other myeloproliferative disorders: one mutatio for three Diseases? Hematology Am Soc Hematol Educ Program, 2008: 69-75.

共引文献13

同被引文献16

引证文献2

二级引证文献6

白血病．淋巴瘤
2015年 第7期

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