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原发性肝癌细胞核和线粒体DNA微卫星不稳定性研究

Nuclear and mitochondrial microsatellite instability in primary hepatocellular carcinoma
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摘要 目的 探讨细胞核和线粒体DNA微卫星不稳在原发肝癌发生中的作用及两者的关系。方法 采用限制性片段长度多态性 (polymerasechainreaction ,singlestrandconformationalpolymorphism ,PCR SSCP)方法检测原发性肝癌线粒体DNA微卫星不稳 (mitochondrialmicrosatelliteinstability ,mtMSI) ;采用PCR方法检测细胞核BAT2 6微卫星位点不稳定性 (nucle armicrosatelliteinstability ,nMSI)。结果  5 2份肝癌组织检出mtMSI 11例 ( 2 1 2 %) ,其中仅 1个微卫星位点mtMSI阳性者 7份 ( 13 5 %) ,有 2个微卫星位点mtMSI阳性者 4例 ( 7 7%)。有 4份于BAT2 6位点检出nMSI ,阳性率为 7 7%。肝癌mtMSI发生率在患者同性别、年龄、是否合并乙型肝炎病毒感染和肝硬化、AFP是否阳性组无显著性差异 (P >0 .0 5 ) ,亦未发现mtMSI与nMSI有显著相关。结论 mtMSI在部分原发性肝癌的发生中起重要作用 。 Objective To explore the roles of nuclear microsatellite instability (nMSI) at BAT26 and mitochondrial microsatellite instability (mtMSI) in the genesis and development of primary hepatocellular carcinoma. Methods mtMSI was detected using polymerase chain reaction, single strand conformational polymorphism (PCR SSCP) analysis, and nMSI by PCR method. Results Fifty two cases of primary hepatocellular carcinoma were studied for mtMSI and nMSI. The mtMSI in at least one locus was detected in 11 out of 52 (21 2%) cases. Out of the 11 cases with mtSMI, 7 showed mtMSI at one locus (13 5%) and 4 at two loci (7 7%), but none at more than three loci. The nMSI at BAT26 was detected in only 4 out of 52 (7 7%) cases. mtMSI was found not to be associated with sex, age, HBsAg, cirrhosis of liver, AFP level, and nMSI ( P >0 05). Conclusion mtMSI may be involved in the carcinogenesis of some hepatocellular carcinomas, but mtMSI is not associated with nMSI.
作者 方丽 房殿春
出处 《第三军医大学学报》 CAS CSCD 北大核心 2004年第4期346-348,共3页 Journal of Third Military Medical University
基金 国家自然科学基金资助项目 ( 30 0 70 0 4 3)~~
关键词 肝癌 线粒体微卫星不稳 BAT26 hepatocellular carcinoma mitochondrial microsatellite instability BAT26
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  • 1[1]Martinou J C. Apoptosis. Key to the mitochondrial gate[J]. Nature, 1999, 399(6735): 411-412.
  • 2[2]Niranjan B G, Bhat N K, Avadhani N G. Preferential attack of mitochondrial DNA by aflatoxin B1 during hepatocarcinogenesis[J]. Science, 1982, 215(4528): 73-75.
  • 3[3]Green D R, Reed J C. Mitochrondria and apoptosis[J]. Science, 1998, 281(5381): 1309-1312.
  • 4[4]Susin S A, Lorenzo H K, Zamzami N, et al. Molecular characterization of mitochrondrial apoptosis-inducing factor[J]. Nature, 1999, 397(6718): 441-443.
  • 5[5]Shimizu S, Narita M, Tsujimoto Y. Bcl-2 family proteins regulate the releases of apoptogenic cytochrome C by the mitochondrial channel VDAC[J]. Nature, 1999, 399(6735): 483-487.
  • 6[6]Habano W, Nakamura S I, Sugai T. Microsatellite instability in the mitochondrial DNA of colorectal carcinomas: Evidence for mismatch repair systems in mitochondrial genome[J]. Oncogene, 1998, 17(15): 1931-1937.
  • 7[7]Hoang J M, Cottu P H, Thuille B, et al. BAT-26, an indicator of the replication error phenotype in colorectal cancers and cell lines[J]. Cancer Res, 1997, 57(2): 300-303.
  • 8[8]Habano W, Sugai T, Nakamura S I, et al. Microsatellite instability and mutation of mitochondrial and nuclear DNA in gastric carcinoma[J]. Gastroenterology, 2000, 118(5): 835-841.
  • 9[9]Habano W, Sugai T, Yoshida T, et al. Mitochondrial gene mutation, but not large-scale deletion, is a feature of colorectal carcinomas with mitochondrial microsatellite instability[J]. Int J Cancer, 1999, 83(5): 625-629.
  • 10[10]Richard S M, Bailliet G, Paez G L, et al. Nuclear and mitochondrial genome instability in human breast cancer[J]. Cancer Res, 2000, 60(15): 4231-4237.

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