PTEN和EGFR与子宫内膜癌发生和发展研究的最新进展  

The current advancement in the research of the relationship between PTEN and EGFR and the generation and progression of endometrial carcinorma

作　　者：孟丽荣[1] 李田[2] 李小毛[2] 

机构地区：[1]澳门理工学院高等卫生学校,澳门999078 [2]中山大学附属第三医院妇产科,广州510630

出　　处：《肿瘤》2010年第5期447-449,共3页Tumor

基　　金：澳门科学技术发展基金资助项目(编号:002/2009/A)

摘　　要：10号染色体同源丢失性磷酸酶与张力蛋白(phosphatase and tensin homology deleted on chromosome ten,PTEN)基因在子宫内膜癌中的严重丢失,是探讨子宫内膜癌发病机制的研究热点。PTEN基因通过影响下游磷脂酰肌醇3激酶/蛋白激酶B(phosphatidylinositol 3-kinase/protein kinase B,PI3K/Akt)/哺乳动物雷帕霉素靶向(mammalian target of rapamycin,mTOR)、黏着斑激酶(focal adhesion kinase,FAK)和丝裂原激活蛋白激酶(mitogen-activated protein kinase,MAPK)这3条信号途径来调节细胞的生长、增殖、凋亡以及血管生长等,该基因发生丢失或突变均可导致肿瘤的发生。本文就PTEN基因和表皮生长因子受体(epidermal growth factor receptor,EGFR)信号通路及其下游信号通路的联系与子宫内膜癌发生发展研究的最新进展进行综述,为子宫内膜癌的基因诊断和治疗提供理论参考。The phosphatase and tensin homology deleted on chromosome ten（PTEN） gene is severely lost in tissues of endometrial carcinorma,which is a hot topic in research of the tumorigenetic mechanism of endometrial carcinoma.PTEN regulated cell growth,proliferation,apoptosis and angiogenesis by regulating three down stream signaling pathways such as 3-kinase phosphatidylinositol/protein kinase B/mammalian target of rapamycin（PI3K/Akt/mTOR）,focal adhesion kinase（FAK） and mitogen-activated protein kinase（MAPK） pathways.The loss or mutation of PTEN causes tumorigenesis.This review summarizes the current research on association of PTEN and epidermal growth factor receptor（EGFR） and their downstream signaling pathways with tumorigenesis and development of endometrial carcinoma to provide theoretical evidence for gene diagnosis and gene therapy of endometrial carcinorma.

关 键 词：子宫内膜肿瘤 10号染色体同源丢失性磷酸酶与张力蛋白 PTEN 受体 表皮生长因子 信号转导 

分 类 号：R737.33[医药卫生—肿瘤]