期刊文献+
任意字段
题名或关键词
题名
关键词
文摘
作者
第一作者
机构
刊名
分类号
参考文献
作者简介
基金资助
栏目信息

髓系白血病患者中血管生成素及受体酪氨酸激酶的表达及其意义

The Significance of Expression Angs/Tie-2 System in Myeloid Leukemia
下载PDF
导出
摘要 目的:探讨血管生成素及受体酪氨酸激酶(Angs及Tie-2)与髓系白血病的关系,以及与血管内皮生长因子(VEGF)的相互关系。方法:应用半定量RT-PCR检测80例急性髓系白血病(AML)、10例慢性髓系白血病(CML)和10例正常人骨髓单个核细胞(BMNCs)中Ang-1、Ang-2、Tie-2和VEGF mRNA的表达。用流式细胞术检测白血病细胞增殖指数(PI)。结果:与正常对照相比,除Ang-1外,Ang-2、Tie-2和VEGF mRNA在初治的髓系白血病中表达均增高,缓解后降低。在Ang-2与VEGF双阳性白血病组,髓外浸润率明显增高(P<0.05);Ang-2/Tie-2双阳性组缓解率低(P<0.05)、PI增高(P<0.05)并与CML的发展阶段有关。结论:髓系白血病患者高表达Angs/Tie-2,同时其与VEGF之间相互作用,与白血病的发展阶段相关。 Objective：To investigate the expression level of Angs/Tie-2 and VEGF mRNA and their significance in myeloid leukemia. Methods：The expression of Ang-1, Ang-2, Tie-2 and VEGF mRNA in 80 AML patients, 10 CML patients and 10 healthy controls were detected by RT PCR. The Proliferation Index （PI） of leukemia ceils was assayed by flow cytometry （FCM）. Results： The expression levels of Ang-2, Tie-2 and VEGF mRNA, except Ang-1 mRNA, were statistically significant higher in untreated myeloid leukemia patients than those in complete remission （CR） patients. The percentage of extra-medullary infiltrations were significant higher in both Ang-2 and VEGF positive group （P〈0.05）. Patients with both Ang-2 and Tie- 2 positive had a lower CR rate （P〈0.05） but a higher PI （P〈0.05）. The expression levels of Ang-2 and Tie-2 increased significantly with the progressing of CML. Conclusion： Angs/Tie-2 mRNA are over-expressed in myeloid leukemia. The over-expressed Angs/Tie-2 may have synergistic effect with VEGF in the pathogenesis of leukemia.
作者 成志勇 潘崚 杨琳 薛芳 杨敬慈 姚丽 董作仁
机构地区 河北医科大学第二医院血液内科
出处 《中国临床医学》 北大核心 2008年第4期518-521,共4页 Chinese Journal of Clinical Medicine
关键词 髓系白血病 血管生成素 受体酪氨酸激酶 血管内皮生长因子 Myeloid leukemia Angiopoietins Tie-2 receptor Vascular endothelial growth factor
分类号 R733.7 [医药卫生—肿瘤]
  • 相关文献

参考文献13

  • 1Watarai M, Miwa H, Shikami M, et al. Expression of endothe lial cell-associated molecules in AML cells [J]. Leukemia, 2002,16:112-119.
  • 2Hayashibara T, Yamada Y, Miyanishi T, et al. Vascular endothelial growth factor and cellular chemotaxis: a possible autocrine pathway in adult T-Cell leukemia cell invasion[J]. Clinical Cancer Research ,2001,7: 2719 2726.
  • 3Padro T, Ruiz S, Bieker R, et al. Increased angiogenesis in the bone marrow of patients with acute myeloid leukemia [J]. Blood, 2000,95, (8) : 2637-2644.
  • 4Malsonpiewe PC, Suri C, Jones PF, et al. Angiopoietin-2, a natural antagonist for tie-2 that disrupt sin vivo angiogenesis [J]. Science, 1997, 277 (5322): 55-60.
  • 5Yancopoulos GD, Davis S, Gale NW, et al. Vascularspecific growth factors and blood vessel formation[J]. Nature, 2000, 407:242 248.
  • 6Chung YC, Hou YC, Chang CN, et al. Expression and prognostic significance of angiopoietin in colorectal carcinoma[J]. J Surg Oncol. 2006,94(7) ;631-638.
  • 7Sugimachi K, Tanaka S, Taguchi K, et al. Angiopoietin switching regulates angiogenesis and progression of human hepatocellular carcinoma[J]. J Clin Pathol, 2003,56 (11) : 854-860.
  • 8Muller A, Lange K, Gaiser T, et al. Expression of angiopoie tin-1 and its receptor TEK in hematopoietic cells from patients with myeloid leukemia[J]. Leuk Res, 2002,26: 163-168.
  • 9Nicola G, Simona C, Mirca L. Pro-angiogenetic properties of human myeloma cells: production of angiopoietin-1 and its potential relationship with myeloma induced angiogenesis [J]. Blood, 2003,(10) : 1182-2002.
  • 10Schliemann C, Bieker R, Padro T, et al. Expression of angio poietins and their receptor Tie2 in the bone marrow of patients with acute myeloid leukemia[J]. Haematologica, 2006,91(9): 1203-1211.

二级参考文献14

  • 1Fialkow PJ, Jacobmn RJ, Papayannopoulou T. Chronic myelocytic leukemia: clonal origin in a stem cell common to the granulocyte, erythrocyte plateletand monocyte/macrophage[J]. Am J Med, 1977,63(1):125-130.
  • 2Folkman J. Tumor angiogenesis: therapeutic implications[J]. N Engl J Med, 1971,18,285(21):1182-1186.
  • 3Bussolino F, Alhini A, (hmussi G, et al. Role of soluble mediators in angiogenesis[J]. Eur J Cancer, 1996,32A(14) :2401 2412.
  • 4Toi M, Taniguchi T,YamamotoY, et al. Clinical significance of the determination of angiogenic factors[J]. Eur J Cancer, 1996,32A(14):2513-2519.
  • 5Ferrara N. Vascular endothelial growth factor[J]. Eur J Cancer,1996,32A(14): 2413-2422.
  • 6Keyt BA, Nguyen HV, Berleau LT,et al. Identification of vascular endothelial growth factor determinants for binding KDR and FLT-1 receptors. Generation of receptor-selective VEGF variants by site-directed mutagenesis[J]. J Biol Chem, 1996,271(10) :5638-5646.
  • 7Park JE, Keller GA, Ferrara N. The vascular endothelial growth factor (VEGF) isoforms, differential deposition into the subepithelial extracellular matrix and bioaetivity of extracellular matrix-bound VEGFF[J] Mol Biol Ce11,1993,4(12):1317-1326.
  • 8Keyt BA, Berleau LT, Nguyen Hv,et al. The carboxyl-terrninal domain (111 - 165) of vascular endothelial growth factor is critical for its mitogenic potency[J]. J Biol Chem,1996,271(13):7788-7795.
  • 9Shweiki D, Itin A, Softer D, et al. Vascular endothelial growth factor induced by hypoxia may mediate hypoxia-initiated angiogenesis[J].Nature, 1992,359(6398):843-845.
  • 10Forsythe JA, Jiang BH, Iyer NV,et al. Activation of vascular endothelial growth [actor gene transcription by hypoxia-inducible factor 1[J]. Mol Cell Biol, 1996,16(9) :4604-4613.

共引文献1

中国临床医学
2008年 第4期

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