期刊文献+

急性白血病患者JAK家族基因的表达及临床意义 被引量:3

Clinical Significance of the Expression of JAKs Genes in Cells of Acute Leukemia Patients
下载PDF
导出
摘要 目的探讨不同时期急性白血病(AL)细胞中JAKs基因的表达情况及其临床意义。方法将入选患者分为初治组、复发组、完全缓解组(CR组)和正常对照组(NC组),RT-PCR方法检测AL患者和正常对照者骨髓MNC中JAK1~3和TYK2 mRNA的表达。结果(1)AL患者JAK2、JAK3、TYK2 mRNA平均表达水平较CR组和NC组差异有统计学意义(P<0.05)。初治AL患者JAK1 mRNA表达水平较NC组略增高,但差异无统计学(P>0.05),复发AL患者JAK1 mRNA表达水平较NC组差异有统计学意义(P<0.05);(2)TYK2阳性组的AL患者缓解率较TYK2阴性患者差异有统计学意义(P<0.05)。结论JAK家族基因在白血病患者的高表达可能在白血病的发生发展中起重要作用。急性髓性白血病(AML)和急性淋巴细胞白血病(ALL)在激活JAK/STAT信号传导通路的方式有所不同。 Objective To investigate the expressions of JAKs gene in cells of patients with acute leukemia (AL) in different stages and their clinical significance. Methods The patients enrolled were divided as initial treatment group, relapse group and complete remission (CR) group, with a normal control (NC) group. RT - PCR was used in assay of expressions of JAK1 - 3 and TYK2 mRNA of bone marrow mononuclear ceils ( BM - MNCs). Results The average expression levels of JAK2, JAK3 and TYK2 mRNA in the initial treatment and relapse groups were significantly higher than those in the CR and NC groups ( P 〈0. 05). The expression level of JAK1 mRNA was slightly higher in the initial group than in the NC group, but with no significant difference ( P 〉0.05). The expression level of JAK1 mRNA was higher in the relapse group than in the NC group, with a significant difference ( P 〈 0. 05). There was significant difference in remission rate of AL between the patients with positive TYK2 expression and with negative TYK2 expression ( P 〈 0. 05). Conclusion The high expression of JAKs may play an important role in development of leukemia. Acute myeloid leukemia and acute lamphoblastic leukemia have different modes of JAK/ STAT signaling pathway.
出处 《中国全科医学》 CAS CSCD 2008年第21期1946-1948,共3页 Chinese General Practice
基金 河北省自然科学基金资助项目(C2005000744)
关键词 JAKs基因 白血病 预后 JAKs genes Leukemia Prognosis
  • 相关文献

参考文献7

  • 1Yamaoka K, Saharinen P, Pesu M, et al. The Janus kinases (Jaks) [J]. Genome Siol, 2004, 5 (12): 253-257.
  • 2Biethahn S, Alves F, Wilde S, et al. Expression of granulocyte colony - stimulating factor - and granulocyte - macrophage colony - stimulating factor - associated signal transduction proteins of the JAK/STAT pathway in normal granulopoiesis and in blast cells of acute myelogenous leukemia [J].Exp Hematol, 1999, 27:885-894.
  • 3Ingley E, Klinken SP. Cross -regulation of JAK and Src kinases [ J ]. Growth Factors, 2006, 24 : 89 - 95.
  • 4Schade AE, Wlodarski MW, Maciejewski JP. Pathophysiology defined by altered signal transduction pathways: the role of JAK - STAT and PBK signaling in leukemic large granular lymphocytes [J]. Cell Cycle [J]. 2006, 5: 2571-2574.
  • 5Wu C, Guan Q, Wang Y, et al. SHP - 1 suppresses cancer cell growth by promating degradation of JAK kinase [ J ]. J Cell Biochem, 2003, 90 (5) : 1026 -1037.
  • 6Han Y, Amin H, Franko B, et al. Loss of SHP1 enhances JAK3/ STAT3 signaling and decreases proteosome degradation of JAK3 and NPM - ALK in ALK - positive anaplastic large - cell lymphoma [ J]. Blood 2006, 108 (8): 2796-2803.
  • 7Nagy ZS, Rui H, Stepkowski SM, et al. A preferential role, for STAT5, not constitutively active STAT3, in promoting survival of a human lymphoid tumor [J]. J Immunol, 2006, 177:5032 -5040.

同被引文献39

  • 1张国建,李猛,王天阳,石铖,王晨宇,闫庆辉.去甲斑蝥素通过JAK-STAT3途径诱导结肠癌LS-174T细胞凋亡[J].肿瘤防治研究,2014,41(1):16-21. 被引量:12
  • 2潘湘涛,吴锦昌.JAK2基因突变与骨髓增殖性疾病[J].中国医学文摘(内科学),2006,27(4):305-308. 被引量:6
  • 3宫本法,王建祥.JAK2 V617F突变与真性红细胞增多症发生[J].国际输血及血液学杂志,2006,29(5):403-406. 被引量:5
  • 4李英华,罗建民.白血病形成中JAK/STAT信号通路的持续激活[J].国际病理科学与临床杂志,2006,26(5):398-402. 被引量:6
  • 5DEININGER M W,GOLDMAN J M,MELO J V.The mo-lecular biology of chronic myeloid leukemia[J].Blood,2000,96(10):3343-3356.
  • 6LEVINE R L,WADLEIGH M,COOLS J,et al.Activatingmutation in the tyrosinekinase JAK2in polysythemia vera,es-sential thrombocythemia,and myeloid metaplasia with myelo-fibrosis[J].Cancer Cell,2005,7:387-397.
  • 7KRALOVICS R,PASSAMONTI F,BUSER A S,et al.Again of function mutation in JAK2is frequently foundingatients with myeloprofiferative disorders[J].N Engl J Med,2005,352:1779-1790.
  • 8BAXTER E J,SCOTT L M,CAMPBEL P J,et al.Acquiredmutation of the tyrosine kinase JAK2in human myeloprolifer-ative disorders[J].Lancet,2005,365:1054-1061.
  • 9KAUSHANSKY K.On the molecular origins of the chronicmyeloproliferative disorders:it all makes sense[J].Blood,2005,105(11):4187-4190.
  • 10PARGANAS E,WANG D,STRAVOPODIS D,et al.Jak2isessential for signaling through a variety of cytokine receptors[J].Cell,1998,93(3):385-395.

引证文献3

二级引证文献3

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部