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作 者:陈小贺[1] 孟文格[2] 张国军[3] 袁权利[4] 翟新容 钱娟娟[1] 周伟[1]
机构地区:[1]石家庄市中医院普外科,石家庄050000 [2]石家庄市第一医院急诊科,石家庄050000 [3]石家庄市卫生局,石家庄050000 [4]河北唐山工人医院,唐山063700 [5]河北正定县医院功能科,正定050800
出 处:《中国医药导刊》2011年第6期1038-1040,共3页Chinese Journal of Medicinal Guide
基 金:河北省科技厅指导项目(编号:072761748)
摘 要:目的:探讨细胞周期调控因子在大肠癌中的表达及其与大肠癌临床病理特征的关系。方法:应用免疫组化SP法对70例大肠癌组织及距癌灶3cm以外的癌旁组织、10cm以外的正常组织中CyclinD1和p16进行检测。结果:CyclinD1在大肠癌中过度表达为36/70(51.4%)并与肿瘤的分化程度呈反比,有淋巴结转移的大肠癌,其CyclinD1的阳性率为70.0%,无淋巴结转移的大肠癌阳性率为44.0%,两者相比差异有显著性(P<0.05)。p16在大肠癌中为低表达33/70(47.1%),癌旁组织和正常组织中p16的表达分别为57.1%和71.4%。CyclinD1与p16呈负相关关系(P<0.05)。结论:CyclinD1的过度表达与肿瘤的分化程度、淋巴结转移密切相关;CyclinD1的过度表达和p16的低表达在大肠癌发生中起协同作用;大肠癌的发生机制涉及CyclinD1和p16调节环路中多个基因的异常。Objeelive: To investigate the relationship between the expression of CyclinDl,pl6 and clinical pathological characteristics in colorectal carcinoma.Methods:CyclinDl,pl6 were detected in 70 colorectal carcinomas,tumor-adjacent colorectal carcinoma tissues and normal tissues by method.Results:Overexpression of CyclinD1 revealed in 36/70 samples(51.4%) respectively which showed a negative correlation with tumor differentiation(P〈0.01).The expression percent of CyclinDl was 70.0% respectively in metastatic cancer whereas only 44.0% expression was shown in non-metastatic cancer. The over expression rate of CyclinD1 in cancer tissues was significantly higher than that in tumor-adjacent and normal colorectal carcinoma tissues(P〈0.05).The positive rates of p l 6 expression was 47.1% in samples of colorectal carcinomas. The incidence of p16 was significantly lower in cancer tissues than that in normal tissues(P〈0.01 ).There is a negative relationship between p 16 and CyclinD 1 in this samples(P〈0,05). Conclusions:Over expression of CyclinDl exsist in colorectal carcinoma and show a good relation with tumor differentiation and lymphnode metastasis,Both the over expression of CyclinD 1 and the lower expression of p 16 coexist in the development of colorectal carcinoma.Abnormality of many genes involved in the regulatory pathway ofCyclinDl ,pl 6 may be involved in the molocular mechanism of colorectal carcinogenesis.
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