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儿童急性淋巴细胞白血病核转录因子κB的表达及其意义 被引量:3

Expression of Nuclear Transcription Factor κB in Childhood Acute Lymphoblastic Leukemia and Its Significance
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摘要 为了探讨儿童急性淋巴细胞白血病(ALL)NF-κB P65蛋白的表达及意义,应用SP免疫组织化学法检测32例ALL患儿和40例非血液病的对照儿童NF-κBP65蛋白的表达。结果表明:32例ALL患儿的NF-κB P65蛋白的阳性表达率为87.50%(28/32),表达定位于ALL细胞的胞核及胞浆中,阳性表达率明显高于对照组12.50%(5/40),两者比较有显著性差异(χ2=40.28,p<0.01)。在28例ALL患儿组阳性表达者中,弱阳性表达(+)占10.71%(3/28),阳性表达(++)占42.86%(12/28),强阳性表达(+++)占46.43%(13/28)。正常对照组均为弱阳性表达(5/5),两者表达程度经Ridit分析差异有显著意义(p<0.01)。ALL病程间(初发或复发)、免疫表型间(T系ALL与B系ALL)、各细胞形态学间的表达程度差异均无显著意义(p>0.05,四格表精确概率法)。结论:NF-κB P65蛋白表达于儿童ALL细胞中,抑制NF-κB信号传导途径可能在儿童ALL治疗中有重大价值,这为临床寻求以NF-κB为靶点的治疗手段提供了科学依据。 To investigate the expression of nuclear transcription factor κB (NF-κB) in childhood acute lymphoblastic leukemia (ALL) and its significance, the biotin-streptavidin method and microscopy were used to detect NF-κB P65 protein in cells from 32 childhood ALL patients and 40 children without hematologic malignancies as control. The results showed that the positive expression rate of NF-κB P65 protein in cells from 32 childhood ALL patients was 87.50%, obviously higher than that in control group (12.50%) (X^2 =40.56, p 〈 0.01 ). In 28 childhood ALL patients with positive expression, the ratio of weakly positive( + ) cases to all positive cases was 10.71% (3/28) ; the ratio of generally positive( ++ ) case was 42.86% ( 12/28 ), and the ratio of strongly positive( +++ ) cases was 46.43% ( 13/28 ). While in the control group the of NF-KB P65 protein showed low expression with 100% (5/5). There was significant difference in the level of NF-κB P65 protein between ALL patients and control group. While the level of NF-κB P65 protein had no significent difference in morphology, immunophenotype (T-lineage ALL and B-lineage ALL) and the courses in the de novo and the relaspsed cases. It is concluded that NF-κB P65 protein expresses in cells of childhood ALL, the inhibition of NF-κB transduction pathway may have significant value in childhood ALL treatment. This study provides experimental basis concerning clinical treatment for ALL, when NF-κB is taken as a target.
出处 《中国实验血液学杂志》 CAS CSCD 2007年第4期767-771,共5页 Journal of Experimental Hematology
关键词 核转录因子-ΚB 核转录因子-ΚB P65蛋白 急性淋巴细胞白血病 NF-κB NF-κB P65 protein acute lymphocytic leukemia
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参考文献11

  • 1顾龙君.儿童急性淋巴细胞白血病诊疗建议(第三次修订草案)[J].中华儿科杂志,2006,44(5):392-395. 被引量:481
  • 2Sen R,Baltimore D.Multiple nuclear factors interact with the immunoglobulin enhancer sequences.Cell,1986; 46:705 -716
  • 3Attar RM,Caamano J,Carrasco D,et al.Genetic approaches to study Rel/NF-kappa B/I kappa B function in mice.Semin Cancer Biol,1997 ;8:93-101
  • 4崔龙,陈雪华,林言箴,孟荣贵,喻德洪,朱正纲,郁宝铭.腺病毒载体介导的自杀基因对MFC小鼠前胃癌细胞的体外杀伤作用[J].外科理论与实践,2000,5(3):167-169. 被引量:3
  • 5Kordes U,Krappmann D,Heissmeyer V,et al.Transcription factor NF-kappa B is constitutively activated in acute lymphoblastic leukemia cells.Leukemia,2000;14:399 -402
  • 6Jo H,Zhang R,Zhang H,et al.NF-kappa B is required for H-ras oncogene induced abnormal cell proliferation and tumorigenesis.Oncogene,2000; 19:841 -849
  • 7Barkett M,Gilmore TD.Control of apoptosis by Rel / NF-kappaB transcriptuon factors.Oncogene,1999;18:6910-6924
  • 8Wang CY,Mayo MW,Korneluk RG,et al.NF-kappaB antiapoptosis:induction of TRAF 1 and TRAF 2 and c-IAP 1 and c-IAP 2 to suppress caspase-8 activation.Science,1998; 281 (5383):1680 -1683
  • 9Bargou RC,Emmerich F,Krappmann D,et al.Constitutive nuclear factor-kappaB-RelA activation is required for proliferation and survival of Hodgkin's disease tumor cells.J Clin Invest,1997; 100:2961-2969
  • 10Teicher BA,Ara G,Herbst R,et al.The protisome inhibitor PS-341 in cancer therapy.Clin Cancer Res,1999; 59:2638 -2645

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  • 1孙国敬,钱俊杰,孟祥兵,宋宜,张枫,梅柱中,董燕,孙志贤.蛋白酶体抑制剂MG132诱导HL-60细胞凋亡前G_2/M期阻滞及机制[J].癌症,2004,23(10):1144-1148. 被引量:12
  • 2高吉照,许伟,薛天阳,安琪.吡柔比星对HL-60细胞NF-κB p65活性及细胞凋亡的影响[J].徐州医学院学报,2006,26(4):326-329. 被引量:2
  • 3安琪,薛天阳,许伟,高吉照,武怡,徐春萍.胰凝乳蛋白酶和地塞米松对儿童急性淋巴细胞白血病核转录因子-κB表达的影响及其意义[J].中国实验血液学杂志,2007,15(2):399-403. 被引量:5
  • 4吴瑞萍 胡亚美.实用儿科学[M].北京:人民卫生出版社,1995.1825-1827.
  • 5An WG, Hwang SG, Trepel JB, et al. Protease inhibitor - induced apoptosis: accumulalation of wt p53, p21WAFI/CIP1 and induction of apoptosis are independent markers of proteasome inhibition[J]. Leukemia,2000,14(7) :1276 - 1283.
  • 6Glickman MH, Ciechanover A. The ubiquitin - proteasome proteolytic pathway : destruction for the sake of construction [ J ]. Physiol Rev, 2002,82(2) :373 -482.
  • 7Nawaz Z, O'Malley BW. Urban renewal in the nucleus: is protein turnover by proteasomes absolutely required fornuclear receptor - regulated transcription [ J ]. Mol Endocrinol,2004,18 ( 3 ) : 493 - 499.
  • 8Guzman ML, Neefing SJ, Upchurch D, et al. Nuclear factor - κB is constitutively activated in primitive human acute myelogenous leukemia cells [ J ]. Blood,2001,98 ( 8 ) :2301 - 2307.
  • 9Kordes U, Krappmann D, Hessmeyer V, et al. Transcription factor NF - κB is constitutively activated in acute lymphoblastic leukemia ceils [ J ]. Leukemia, 2000,14 (3) :399 - 402.
  • 10Kim SH, Oh SM, Kim TS. Induction of human leukemia HL - 60 cell differentiation via a PKC/ERK pathway by helenalin, a pseudoguainolide lactone [ J ]. Eur J Pharmacol, 2005,511 ( 2 - 3 ) : 89 - 97.

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