期刊文献+

bcl-2及MDR-1基因产物在肾癌组织中的表达及其意义

The expression of bcl-2 and MDR in renal cell carcinoma
暂未订购
导出
摘要 目的 :探讨基因 bcl- 2和 MDR- 1产物在肾癌组织中表达的意义及相关关系 ,了解肿瘤增殖与耐药的特点。方法 :采用免疫组织化学 SABC法对 48例肾癌和 10例正常肾组织的石蜡包埋标本切片进行 bcl- 2和MDR- 1基因产物表达的统计研究。结果 :bcl- 2在肾癌组织中阳性表达率为 77.1% ,与正常肾组织 (4 0 .0 % )相比 ,差异有显著性意义 (P <0 .0 5 ) ,但其表达与肿瘤分级、分期及预后无关 (P >0 .0 5 )。 MDR- 1在肾癌组织和正常肾组织中均有阳性表达 ,与其它肾癌组织类型比较 ,颗粒型中显示高表达 (P <0 .0 5 ) ,但 MDR- 1表达与肿瘤病理分级及预后无关 (P>0 .0 5 )。结论 :bcl- 2蛋白在大多数肾癌组织中呈高表达 ,其表达在肾肿瘤形成中可能起作用 ;进一步证实 MDR- 1基因在肾细胞癌抵抗化疗中起作用 ,与 bcl- 2无显著相关性 ;肾癌化疗、放疗不敏感可能涉及 MDR- 1和 bcl- 2的双重作用。 Purpose:To study bcl 2 and MDR expressions in renal cell carcinoma and to evaluate its clinical significance.Methods:blc 2 and MDR expression were studied by immunohistochemical technique in 48 specimens of renal cell carcinoma tissues and in 10 normal renal tissues and their clinical significance was analyzed.Results:The positive rate of expression of bcl 2 in the renal cell carcinoma tissue was 77.1 %, while it was 40.0 % in the normal renal tissue(P< 0.05 ). However, it was not related to the tumor grade and tumor stage(P> 0.05 ). On the other hand, There was a positive expression of MDR1 in renal cell carcinoma and normal renal tissue. MDR1 was positively related to tumor cell type(P< 0.05 ). Compared with the other types of renal cell carcinoma. The granular existed higher expression. Both have no relationship with prognosis.Conclusions: bcl 2 Protein is overexpressed in the majority of renal cell carcinomas. The overexpression of bcl 2 may have a role in tumorigenesis. MDR1, an established predictor for chemo-resistance, however, has no significant correlation with bcl 1. The multidrug resistant of renal cell cancer is probably induced by double-functions of bcl and MDR1.
出处 《临床泌尿外科杂志》 2001年第2期77-79,共3页 Journal of Clinical Urology
关键词 肾肿瘤 耐药性 BCL-2基因 MDR-1基因 基因表达 Kidney neoplasm Carcinoma Genes Drug resistant
  • 相关文献

参考文献2

二级参考文献1

  • 1夏红,肿瘤防治研究,1995年,22卷,54页

共引文献14

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