胰腺癌中p33^(ING1b)基因变化及其表达研究  

Genetic alteration and reduced expression of tumor suppressor p33^(ING1b) in human exocrine pancreatic carcinoma

作　　者：于观贞[1] 朱明华[1] 祝峙[1] 倪灿荣[1] 陈颖[1] 李芳梅[1] 

机构地区：[1]第二军医大学长海医院病理科,上海200433

出　　处：《肿瘤》2005年第1期33-36,共4页Tumor

摘　　要：目的　检测胰腺癌中p33ING1b蛋白表达及基因变化情况,以了解p33ING1b在肿瘤发生过程中的作用。方法　采用免疫组化、聚合酶链反应单链构象多态性技术(PCR SSCP)和杂合型缺失(LOH)技术,检测胰腺癌中p33ING1b表达及p33ING1b基因变化情况。结果　ING1b蛋白的阳性表达率为85% (34/40),SSCP显示在40例病例中仅1例突变,LOH率为60.9% (14/23)。结论　突变与缺失表达并不是p33ING1b的主要失活形式,染色体改变可能导致p33ING1b功能下降,从而引发肿瘤发生。Objective To detect the expression of p33 ING1b protein and the change of p33 ING1b gene in pancreatic carcinoma and investigate the significance of p33 ING1b in pancreatic cell carcinogenesis. Methods Pathological specimens from pancreatic carcinoma and matched non-tumor pancreatic tissue were examined for p33 ING1b expression and mutation by immunohistochemistry, polymerase chain reaction single-strand conformation polymorphisms(PCR-SSCP) and loss of heterozygosity(LOH). Results The rate of p33 ING1b protein expression was 85% (34/40). A single germline missense mutation was detected in 1 of 40 tumors analyzed located at codon 215:TGC-TCC(Cys-Ser). Fourteen of 23 (60.9%) tumour samples showed LOH in all of the informative markers tested, but no mutation was detected in these tumours and only two of the informative tumours lack expressions of p33 ING1b protein. Conclusion Mutation and loss of expression are not the main reasons for the disfunction of p33 ING1b in pancreatic carcinoma, abnormity at the level of chromosome and/or transcription may inhibit their normal functions, which then contribute to pancreatic cell carcinogenesis.

关 键 词：胰腺肿瘤 p33^ING1b基因 p33^ING1b蛋白 免疫组织化学 聚合酶链式反应 单链构象多态性 杂合型缺失 

分 类 号：R735.9[医药卫生—肿瘤] R730.231[医药卫生—临床医学]