子宫内膜癌发生分子机制研究进展  

Progresses of Molecular Mechanisms on Endometrial Cancer

作　　者：王连邦[1] 张丽英[1] 单春华[1] 

机构地区：[1]东北林业大学,黑龙江哈尔滨150040

出　　处：《现代生物医学进展》2009年第14期2791-2793,共3页Progress in Modern Biomedicine

摘　　要：子宫内膜癌(Endometrial cancer,EC)是子宫内膜上皮的恶性肿瘤,可分为Ⅰ型EC和Ⅱ型EC。最近的分子遗传学证据表明EC是由基因表达异常改变及突变引起的,例如Ⅰ型EC中常伴随着pten、k-ras、ctnnb1(β-CATENIN)、runx、etv5/erm、hgf/met、cyr16等基因的异常;Ⅱ型EC通常与p53、erbb2(her2/neu)等基因异常有关,这些异常包括基因突变、缺失、扩增、过量表达等。本文就其相关分子机制的研究进展进行综述。Endometrial cancer is a malignant tumor of the endometrial epithelial tissue. Endometrial carcinomas are classified into two types： type I and type II. Molecular genetic evidence indicates that EC likely develops as the result of specificity alterations or mutation of genetic factors, such as pten, k-ras,ctnnbl （13-CATENIN）,runx,etv5/erm,hgf/met,cyrl6 et al associated with type I tumors; p53,erbb2 （also known as her2/neu） linked to type II tumors. The alterations include mutations, deletions and amplification/over-expression of genes. In this review, we summarize the above progress.

关 键 词：子宫内膜癌 原癌基因 抑癌基因 凋亡基因 

分 类 号：R737[医药卫生—肿瘤] R737.33[医药卫生—临床医学]