期刊文献+

凋亡及凋亡相关基因表达在食管鳞癌发生发展中的意义 被引量:2

Significance of apoptosis and expression of the genes related to apoptosis in esophageal squamous cell carcinogenesis
下载PDF
导出
摘要 目的 探讨食管鳞癌发生发展过程中凋亡及凋亡相关基因表达的变化规律及意义。方法 采用免疫组化染色 (s- p法 )和细胞凋亡原位检测技术 (TUNEL染色 )检测食管鳞癌、非典型增生和正常食管粘膜各 72例中bcl- 2、P5 3的表达及细胞凋亡的变化。结果 bcl- 2和P5 3在非典型增生和浸润癌中的表达显著高于正常粘膜上皮 (P <0 .0 1) ,并与食管鳞癌的淋巴结转移密切相关 (P <0 .0 5 ) ,P5 3还与食管鳞癌浸润深度和患者年龄密切相关 (P分别 <0 .0 1和 0 .0 5 )。TUNEL染色结果显示 :凋亡指数在非典型增生和浸润癌中显著增高(P <0 .0 5或P <0 .0 1) ;bcl- 2、P5 3阳性组凋亡指数分别低于同一阶段其阴性组凋亡指数(P <0 .0 5 )。结论 凋亡及凋亡相关基因 (bcl- 2 ,P5 3 )表达与食管鳞癌的发生发展和恶性表型密切相关。 Objective To investigate the regulation of changes and significance of apoptosis and expression of the genes related to apoptosis in esophageal squamous cell carcinogenesis.Methods Immunohistochemical staining and TUNEL staining were used to detect the expression of bcl-2,p53 and the changes of apoptosis for 72 patients with esophageal squamous cell carcinoma (including normal mucosal epithelium, dysplasia and invasive carcinoma), respectively.Results The expression of bcl-2 and p53 in dysplasia and invasive carcinoma was significantly higher than normal mucosal epithelium(P<0.01),and it was correlated closely with the metastasis of lymph node(P<0.05).The expression of p53 correlated with the depth of invasion and the age of patients. TUNEL staining results showed apoptotic index in dysplasia and invasive carcinoma increased markedly(P<0.05 or P<0.01).Bcl-2 and p53 positive lesions had lower apoptotic index than its negative lesions in the same stage, respectively(P<0.05).Conclusions There is close relation between apoptosis and expression of the genes related to apoptosis and esophageal squamous cell carcinogenesis. Immunohistochemical method in situ detection technique may be used as important molecular markers in early diagnosis and prognosis of esophageal squamous cell carcinoma.
出处 《新乡医学院学报》 CAS 2003年第1期1-4,共4页 Journal of Xinxiang Medical University
关键词 食管鳞癌 BCL-2 P53 凋亡 esophageal squamous cell carcinoma bcl-2 p53 apoptosis
  • 相关文献

参考文献3

二级参考文献6

共引文献28

同被引文献8

引证文献2

二级引证文献2

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