Inflammation in prostate carcinogenesis

被引：1187
作者：
De Marzo, Angelo M.
Platz, Elizabeth A.
Sutcliffe, Siobhan
Xu, Jianfeng
Gronberg, Henrik
Drake, Charles G.
Nakai, Yasutomo
Isaacs, William B.
Nelson, William G.
机构：
[1] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21231 USA
[2] Johns Hopkins Univ, Dept Oncol, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21231 USA
[3] Johns Hopkins Univ, Dept Epidemiol, Bloomberg Sch Publ Hlth, Baltimore, MD 21205 USA
[4] Wake Forest Univ, Sch Med, Ctr Human Genom, Winston Salem, NC 27157 USA
[5] Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden
[6] Osaka Univ, Osaka 565, Japan
[7] Johns Hopkins Univ Hosp, Brady Urol Res Inst, Dept Urol, Baltimore, MD 21287 USA
来源：
NATURE REVIEWS CANCER | 2007年 / 7卷 / 04期
关键词：
MACROPHAGE SCAVENGER RECEPTOR; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; SEXUALLY-TRANSMITTED-DISEASES; COMMON SEQUENCE VARIANTS; TOLL-LIKE RECEPTOR-4; CANCER RISK; INTRAEPITHELIAL NEOPLASIA; POSTATROPHIC HYPERPLASIA; TRICHOMONAS-VAGINALIS; HETEROCYCLIC AMINES;
D O I：
10.1038/nrc2090
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
About 20% of all human cancers are caused by chronic infection or chronic inflammatory states. Recently, a new hypothesis has been proposed for prostate carcinogenesis. It proposes that exposure to environmental factors such as infectious agents and dietary carcinogens, and hormonal imbalances lead to injury of the prostate and to the development of chronic inflammation and regenerative 'risk factor' lesions, referred to as proliferative inflammatory atrophy (PIA). By developing new experimental animal models coupled with classical epidemiological studies, genetic epidemiological studies and molecular pathological approaches, we should be able to determine whether prostate cancer is driven by inflammation, and if so, to develop new strategies to prevent the disease.
引用
收藏
页码：256 / 269
页数：14
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