摘要
目的探讨食管肿瘤癌变的机制。方法对1998年食管内镜普查诊断为食管异型增生的57例患者随访2 a,40例仍为异型增生(未癌变组),17例进展为早期癌(癌变组)。对2次活检组织标本分别采用免疫组化SP法行信号转导子和转录激活子3(Stat3)和Ki-67蛋白检测。结果1998年标本Stat3和Ki-67在两组表达差异无统计学意义(P>0.05);2000年标本二者表达均升高,但癌变组高于非癌变组(P<0.05)。癌变组Stat3和Ki-67 2 a中由阴性变为阳性的比率均分别高于非癌变组(P<0.05)。17例食管早期癌标本中Stat3和Ki-67的相关分析示二者存在正相关(P<0.05)。结论Stat3和Ki-67尤其是Stat3可能在食管癌变中起关键作用,阻断Stat3的表达可能阻断Ki-67表达,从而阻断食管癌变进程;此可能为食管癌的基因治疗提供理想靶点。
Objective To observe the expression of Star3 and Ki-67 gene dynamicly and to explore their roles in the process of esophageal carcinogenesis. Methods Biopsy specimens were collected from 57 cases with esophageal epithelial dysplasia detected in endoscopic surveys in 1998. The 57 cases were followed up for two years and second biopsy specimens were obtained in 2000. Out of them, 40 cases remained the dysplasia of the esophagus and were defined as non- carcinogenesis group. Other 17 cases developed into early stage carcinoma and were defined as cancerous group. Stat3 and Ki-67 protein were detected respectively in two groups by immunohistoehemistry( S-P method). Results The expression of Star3 and Ki-67 in two groups had no statistically difference in 1998 (P 〉 0.05 ). The expression of Star3 and Ki-67 in two groups both increased, and which in carcinogenesis group were significantly higher than that in non-carcinogenesis group in 2000 (P 〈 0.05 ). The ratio of variation from negative to positive expression of Star3 and Ki-67 during two years in carcinogenesis group was respectively higher than that in non-carcinogenesis group, and there was significant differece between the two groups( P 〈 0.05 ). The expression of Stat3 and Ki-67 in the carcinogenesis had positive correlation (P 〈 0.05 ). Conclusions Stat3 and Ki-67 gene may play a critical role in the process of esophageal carcinogenesis.
出处
《山东医药》
CAS
北大核心
2008年第26期29-31,共3页
Shandong Medical Journal