检索规则说明:AND代表“并且”;OR代表“或者”;NOT代表“不包含”;(注意必须大写,运算符两边需空一格)
检 索 范 例 :范例一: (K=图书馆学 OR K=情报学) AND A=范并思 范例二:J=计算机应用与软件 AND (U=C++ OR U=Basic) NOT M=Visual
机构地区:[1]西安交通大学第一医院肿瘤放疗科,陕西西安710061
出 处:《肿瘤防治杂志》2005年第20期1535-1538,共4页China Journal of Cancer Prevention and Treatment
摘 要:目的:研究VEGF、cyclin D1和p27kip1在小鼠前胃癌组织形成过程中的表达及意义,初步探讨维甲酸对小鼠前胃癌的干预机制。方法:建立ICR小鼠前胃癌模型,SABC法测定VEGF、cyclin D1和p27kip1表达。结果:cyclin D1在小鼠前胃癌组织中的表达(64·7%)明显高于癌前期病变(29·4%),χ2=4·3447,P=0·0371;VEGF表达在癌前期病变(47·1%)高于增生期病变(33·3%),χ2=4·836,P=0·0381;cyclinD1、p27kip1和VEGF阳性表达与小鼠胃癌组织学分级无相关性。维甲酸抑制组癌及癌前期病变发生率(23·5%)低于单纯诱导组(76·9%),χ2=14·3549,P=0·0002。结论:VEGF、cyclin D1和p27kip1是小鼠前胃癌组织形成过程中重要的分子事件;维甲酸对亚硝胺类致癌物诱发的小鼠前胃鳞状上皮癌及癌前期病变具有抑制作用,但与对VEGF、cyclin D1和p27kip1表达的调控无明显相关。OBJECTIVE: To investigate expressions of VEGF, cyclin D1 and p27^kip1 and mechanisms by retinoic acid intervention in progressing forestornach carcinoma of mice. METHODS: Forestornach carcinoma model of ICR mice was established, and VEGF, cyclin D1 and p27^kip1 expressions were assayed by SABC immunohistochemical method. RESULTS: Cyclin D1 expression was significantly higher in forestomach carcinoma (64. 7%) than in precancerous lesions (29.4%), X^2=4. 344 7,P=0. 0371; VEGF expression was higher in precancerous lesions (47. 1%) than in proliferative lesions (33.3%), X^2=4. 836, P=0. 038 1;cyclin D1, p27^kip1 and VEGF expressions had no relation ship among mice gastric carcinoma histology grades; carcinoma and precancerous lesions obviously decreased in retinoic acid intervention group (23. 5 %) than in induce-carcinoma group (76. 9%), X^2=14. 354 9,P=0. 000 2. CONCLUSION: VEGF, cyclin D1 and p27^kip1 play key roles in developing mice carcinoma and precancerous lesions; retinoic acid can inhibit squamous epithelium carcinoma and precancerous lesions of mice induced by nitrosamines carcinogen. However, this inhibition is irrele vant to the controller of VEGF, cyclin D1 and p27^kip1 expressions.
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在链接到云南高校图书馆文献保障联盟下载...
云南高校图书馆联盟文献共享服务平台 版权所有©
您的IP:216.73.216.145