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脑胶质瘤端粒酶活性的表达及端粒长度的分析 被引量:3

Telomerase activity and telomere lengths in glioma
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摘要 目的 研究分析在不同级别脑胶质瘤细胞端粒酶活性的表达及端粒长度的变化。方法 采集 40例脑胶质瘤手术切除标本、 4例正常脑组织 ,通过半定量端粒重复序列扩增 (telomererepeatamplificationprotocol,TRAP) 银染方法检测端粒酶活性水平 ,应用人的端粒序列特异性探针32 P (CCC TAA) 3 进行Southern杂交检测脑胶质瘤细胞的端粒长度。结果 在 40例胶质瘤标本中的 33例(82 5 % )中均检出端粒酶活性 ,而在正常脑组织中无端粒酶活性的表达 ,不同级别胶质瘤之间端粒酶活性水平有明显差异 ;恶性胶质瘤细胞中端粒的长度明显比正常胶质细胞缩短 ,端粒的长度与端粒酶活性的水平有着显著的的负相关。结论 端粒酶活性可以作为脑胶质瘤的恶性标记之一 ,端粒的缩短可能是脑胶质瘤进展的重要因素 。 Objective To investigate the relationship of telomerase activity and telomere length in different grades of glioma.Methods 40 rapidly specimens of surgical resected glioma and 4 normal brain tissue were used to study the telomerase activity by semi quantitative telomeric repeat amplification protocol (TRAP) silver staining. Telomere length was estimated from southern blots of telomere restriction fragments (TRFs)with 32 P (CCCTAA) 3 probe specific for human telomeric sequences.Results Telomerase activity was detected positively in 33 of 40(82 5%)gliomas specimens, and none of normal brain tissue. The level of telomerase expression was associated with grade of tumor. The length of telomerase in maligant gliomas was shorter than that in normal glia cells. The length of also telomere correlated with telomerase activity. Conclusions Our findings suggest that telomerase activity could be a special marker of gliomas and an index of maligant potential. Telomere reduction is one of the important genetic events during transformation of gliomas. Telomere repair mechanism may be initiated in glioma which may maintain a relative stability of TRFs and permit a constitutive proliferation of these malignant cells.
出处 《中华神经外科杂志》 CSCD 北大核心 2000年第5期316-319,共4页 Chinese Journal of Neurosurgery
关键词 端粒酶 端粒 脑胶质瘤 肿瘤细胞 Telomerase Telomere Glioma Proliferation
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  • 1Allsopp R C,Exp Cell Res,1995年,220期,194页

同被引文献19

  • 1陕声国,张端莲,余瑛,陕光,唐甜,杨勇,熊颜娥,李红.血管瘤组织中端粒酶逆转录酶基因表达与端粒酶活性的关系[J].中华实验外科杂志,2004,21(6):661-663. 被引量:5
  • 2张峰,刘晔,刘三光,谢绍建,李冬斌,李荣琴,蔡建辉.RNA干预研究及其在肿瘤基因治疗中的应用[J].中华实验外科杂志,2006,23(3):381-382. 被引量:26
  • 3马衍刚,傅强,冯晶军,于如同,许崇福,郭常利,杨凤海.脑胶质瘤组织中靶向乏氧诱导因子-1α shRNA表达载体的构建与鉴定[J].山东医药,2007,47(15):30-31. 被引量:1
  • 4DiUin A. The specifics of small interfering RNA specificity [ J ]. Proc Natl Acad Sci USA, 2003,100( 11 ) :6289-6291.
  • 5Kim NW, Piatyszek MA, Prowse KR, et al. Specific association of human telomerase activity with immortal cells and cancer[J]. Science, 1994,266(5193 ): 2011-2015.
  • 6Bouffler SD, Blasco MA, Cox R, et al. Telomeric sequences,radiation sensitivity and genomic instability[J]. Int J Radiat Biol, 2001,77(10) :995-1005.
  • 7Slijepcevic P, Bryant PE. Chromosome healing, telomere capture and mechanisms of radiation-induced chromosome breakage[J]. Int J Radiat Biol, 1998,73(1):1-13.
  • 8Hande MP, Lansdorp PM, Natarajan AT. Induction of telomerase activity by in vivo X-irradiation of mouse splenocytes and its possible role in chromosome healing[J]. Mutat Res, 1998,404(1-2): 205-214.
  • 9Heppner GH. Tumor heterogeneity[J]. Cancer Res, 1984,44 (6): 2259-2265.
  • 10Brown DC, Trott KR. Clonal heterogeneity in the progeny of HeLa cells which survive X-irradiation[J]. Int J Radiat Biol,1994,66(2): 151-155.

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