摘要
目的:探讨p16 、 Cyclin D1、 Cdk4 、 Rb 在胰腺癌中的作用及其相互关系。方法:免疫组织化学检测p16 、 Cyclin D1、 Cdk4 、 Rb 蛋白在胰腺癌中的表达,原位杂交检测p16 和 Cyclin D1 在胰腺癌中的存在状况。结果:p16 在胰腺癌中低表达, Cyclin D1 和 Cdk4 过度表达,未发现 Rb 在胰腺癌标本中缺失;p16 与 Cyclin D1,p16 与 Rb 呈负相关关系( P< 0.05) , Cdk4 与 Cyclin D1 呈正相关关系( P< 0 .05) 。结论:胰腺癌发生机制涉及p16 、 Cyclin D1、 Cdk4 和 Rb 调节环路中多个基因的异常,p16 低表达和 Cyclin D1 过度表达可能起在胰腺癌发生中起协同作用。
Objectives:To study the mechanism of p16, CyclinD1, Cdk4, Rb, and their relationship in pancreatic carcinoma. Methods:To examine these proteins and genes by immunchistochemistry and in situ hybridization. Results:Overexpression of cyclin D1 and Cdk4 were revealed in these samples and p16 was undetectable, the Rb deletion was not revealed in these samples. There is a negative relationship between p16 and cyclin D1,p16 and Rb in these samples (P< 0.05); there is a positive relationship between cyclin D1 and Cdk4 (P< 0.05). Conclusions:Abnormality of many genes involved in the regulatory pathway of p16,cyclin D1/Cdk4 and Rb may be involved in the molecular mechanism of pancreatic carcinogenesis, both the lower pression of p16 and the overexpression of cyclin D1 may coexist in the development of pancreatic carcinoma.
出处
《癌症》
SCIE
CAS
CSCD
北大核心
1999年第4期418-421,共4页
Chinese Journal of Cancer