基因芯片分析比较基因敲入和转基因小鼠前列腺癌模型  

cDNA microarray analysis of transgenic and knock-in prostate cancer mouse models

作　　者：武国军[1,2] 朱李兵[1] 李晓武[1] 袁建林[1] 王禾[1] 刘贺亮[1] 于磊[1] 张更[1] 邵晨[1] 

机构地区：[1]第四军医大学西京医院泌尿外科,陕西西安710032 [2]加拿大西安大略大学维多利亚医院外科

出　　处：《中国现代医学杂志》2009年第14期2117-2122,共6页China Journal of Modern Medicine

基　　金：军队医药卫生"十一五"科研项目(No:06H040);第四军医大学优秀博士学位论文课题资助项目

摘　　要：目的利用基因芯片技术分析比较基因敲入(KIMAP)和转基因(TGMAP)小鼠前列腺癌模型。方法对于来自KIMAP和TGMAP的肿瘤标本进行了基因芯片分析和比较。结果基因芯片分析证明,在KIMAP中免疫应答基因高表达,而TGMAP晚期肿瘤(26～32周)中与神经内分泌肿瘤(NE)分化相关的基因占主体,而NE肿瘤在人类前列腺癌中少于10%。人类前列腺癌的几个肿瘤标记物基因在KIMAP中均可检测到(在TGMAP中缺乏),包括hepsin、maspin、Nkx3.1、CD10和PSP94等。结论由于KIMAP模型成功地模仿了人类前列腺癌特征,在前列腺癌临床前期研究中具有潜在的应用价值。[Objectives] This study used eDNA mieroarray analysis to measure and compare the new knock-in mouse adenocarcinoma prostate model （KIMAP） with transgenic mouse adenocarcinoma prostate model （TGMAP）. [Method] cDNA microarray analysis was performed on malignant prostate tissues obtained from both TGMAP and KIMAP models and compared with each other. [Results] Global molecular profiling by cDNA microarray analysis demonstrated that higher contents of immunoresponse genes in KIMAP, whereas in TGMAP neuroendocrine carcinoma differentiation constituted the majority of tumors identified in late stages （26-32 weeks）, which represents less than 10 % in human prostate cancer （CAP） structure. Several tumor marker genes characteristic of human CaP were uniquely identified in KIMAP （absence in the TGMAP）, including hepsin, maspin, Nkx3.1, CD10 and PSP94, etc. [Conclusion] Due to the effective mimicry of human Cap tumors demonstrated by the KIMAP model, this study advocates its use in the clinical study of human Cap.

关 键 词：前列腺 肿瘤 小鼠模型 

分 类 号：R737.25[医药卫生—肿瘤] Q789[医药卫生—临床医学]