期刊文献+

人肝癌组织GGT异常表达与逆转录巢式PCR分析 被引量:1

Abnormal Expression and RT-PCR Analysis of γ-Glutamyl Transpeptidase Genes in the Tissues of Human Hepatocelullar Carcinoma
下载PDF
导出
摘要 为探讨肝癌组织中γ-谷氨酰转肽酶(GGT)的表达与改变,将自身配对的肝癌、癌周及远癌组织总RNA纯化,分析不同分子形式GGT表达,并以逆转录巢式PCR(RT-PCR)扩增GGT5’-末端非编码区基因。结果:肝癌、癌周和远癌组总RNA浓度呈明显的梯度升高趋势(P<0.05);肝癌组总GGT比活性和不同分子形式GGT均明显高于癌周和远癌组(P<0.05);RT-PCR扩增GGT基因片段,在肝癌、癌周和远癌组阳性率分别为95.8%、87.5%和79.2%。提示肝癌组织中GGT呈异常表达,GGT基因分析可望成为监测肝细胞癌变的灵敏方法。 To explore the situation of expression of yg1utamyl transpeptidase (GGT) genes in thetissues of hepatocellular carcinoma, The t0tal RNA were purifled and quantified, the different molecu-lar forms of GGT were analyzed, The 5'-non coding (5'-NC) regions of the GGT genes were amplifiedusing reverse transcription nest po1ymerase chain reaction (RT-PCR) in the self-paired samples of hepa-tocellular carcinoma, adjacent paracancerous and distal cancerous tissues. Total RNA quantitationshowed an increasing tendency from carcinoma to distal cancerous. The specific activities (U/g) of totalGGT and the amount of different molecular forms of GGT were significantly higher in carcinoma tissuesthan those in paracancerous and distal cancerous tissues (P<0.O5). The positive rates of GGT genefragment amplified by RT-PCR were 95. 8% in hepatocellular carcinoma, 87. 5% in paracancerous tis-sue, and 79. 2% in distal cancerous tissues- The present data suggest that GGT gene in the tissues ofhepatocellular carcinoma was overexpressed and the analysis of GGT gene fragments may play a r01e inmonitoring the ear1y events 0f hepatocellular carcinoma.
出处 《江苏医药》 CAS CSCD 1999年第6期399-401,共3页 Jiangsu Medical Journal
基金 国家教委留学回国人员课题 南通市科委课题
关键词 肝癌 表达 GGT RNA RT-PCR 聚合酶链反应 Hepatocellular carcinoma γ-glutamyl transpeptidase gene Expression Total RNA RT-PCR
  • 相关文献

参考文献6

  • 1姚登福.-[J].国外医学:内科学分册,1997,24(2):59-59.
  • 2姚登福.-[J].胃肠病学和肝脏病学杂志,1997,6(1):78-78.
  • 3姚登福,国外医学.内科学分册,1997年,24卷,2期,59页
  • 4姚登福,胃肠病学和肝脏病学杂志,1997年,6卷,1期,78页
  • 5Peng S Y,Hepatology,1993年,17卷,1期,35页
  • 6Xu K C,Am J Gastroent,1992年,87卷,8期,991页

同被引文献32

引证文献1

二级引证文献1

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