前列腺癌发生发展过程中的分子机制  

Molecular mechanism in the development and progression of prostate cancer

作　　者：林吉[1] 侯建国[2] 苏彤[1] 张宏伟[1] 

机构地区：[1]第二军医大学热带医学与公共卫生学系流行病学教研室,上海200433 [2]第二军医大学长海医院泌尿外科,上海200433

出　　处：《第二军医大学学报》2014年第12期1310-1314,共5页Academic Journal of Second Military Medical University

基　　金：国家自然科学基金(81072377)~~

摘　　要：近年来,前列腺癌在我国发病率显著增长,已位于我国男性恶性肿瘤发病第5位。环境因素的持续刺激将导致慢性前列腺炎的发生,γ干扰素(INF-γ)、肿瘤坏死因子-α(TNF-α)、抗炎因子转化细胞生长因子-β(TGF-β)等的持续浸润,促进前列腺组织的损伤及修复,进而导致增生性炎性萎缩症的出现,部分增生细胞出现基因组改变,MYC基因的过表达,NKX3.1、PTEN基因的缺失促进增生性炎性萎缩症转化为上皮内瘤变。雄激素受体(androgen receptor,AR)突变和ERG-TMPRSS2融合等又将驱动前列腺癌的进展。The incidence of prostate cancer has been greatly increased in China and it has ranked the 5＇h of the malignant tumors in Chinese males. Continuous environment stimulation causes chronic prostatic inflammation, and infiltration of inflammatory cytokines such as INF-γ, TNF-α, and TGF-β can cause damage and repair of prostatic tissues, leading to proliferative inflammatory atrophy（HA）. Then a small subset of cells will develop somatic genome alterations, including overexpression of MYC and the loss of NKX3. 1 and PTEN, which can promote PIA into prostatic intraepithelial neoplasia. Androgen receptor mutation and ERC-TMPRSS2 fusion will drive progression of prostatic cancer.

关 键 词：前列腺肿瘤 分子机制 慢性前列腺炎 突变 

分 类 号：R737.25[医药卫生—肿瘤]