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
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
相关论文
共 159 条
[51]   A DOMINANT-NEGATIVE MUTANT OF 2-5A-DEPENDENT RNASE SUPPRESSES ANTIPROLIFERATIVE AND ANTIVIRAL EFFECTS OF INTERFERON [J].
HASSEL, BA ;
ZHOU, A ;
SOTOMAYOR, C ;
MARAN, A ;
SILVERMAN, RH .
EMBO JOURNAL, 1993, 12 (08) :3297-3304
[52]   Macrophage scavenger receptor 1 999C>T (R293X) mutation and risk of prostate cancer [J].
Hope, Q ;
Bullock, S ;
Evans, C ;
Meitz, J ;
Hamel, N ;
Edwards, SM ;
Severi, G ;
Dearnaley, D ;
Jhavar, S ;
Southgate, C ;
Falconer, A ;
Dowe, A ;
Muir, K ;
Houlston, RS ;
Engert, JC ;
Roquis, D ;
Sinnett, D ;
Simard, J ;
Heimdal, K ;
Moller, P ;
Maehle, L ;
Badzioch, M ;
Eeles, RA ;
Easton, DF ;
English, DR ;
Southey, MC ;
Hopper, JL ;
Foulkes, WD ;
Giles, GG .
CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION, 2005, 14 (02) :397-402
[53]  
Hsing AW, 2000, INT J CANCER, V85, P60, DOI 10.1002/(SICI)1097-0215(20000101)85:1<60::AID-IJC11>3.0.CO
[54]  
2-B
[55]   The role of Fgf10 signaling in branching morphogenesis and gene expression of the rat prostate gland:: lobe-specific suppression by neonatal estrogens [J].
Huang, LW ;
Pu, YB ;
Alam, S ;
Birch, L ;
Prins, GS .
DEVELOPMENTAL BIOLOGY, 2005, 278 (02) :396-414
[56]  
Huang LW, 2004, J ANDROL, V25, P330
[57]   High susceptibility of the ACI and spontaneously hypertensive rat (SHR) strains to 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhlP) prostate carcinogenesis [J].
Inaguma, S ;
Takahashi, S ;
Ohnishi, H ;
Suzuki, S ;
Cho, YM ;
Shirai, T .
CANCER SCIENCE, 2003, 94 (11) :974-979
[58]   PROSTATIC STRUCTURE AND FUNCTION IN RELATION TO THE ETIOLOGY OF PROSTATIC-CANCER [J].
ISAACS, JT .
PROSTATE, 1983, 4 (04) :351-366
[59]   A large cohort study of aspirin and other nonsteroidal anti-inflammatory drugs and prostate cancer incidence [J].
Jacobs, EJ ;
Rodriguez, C ;
Mondul, AM ;
Connell, CJ ;
Henley, SJ ;
Calle, EE ;
Thun, MJ .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 2005, 97 (13) :975-980
[60]   Innate immune recognition [J].
Janeway, CA ;
Medzhitov, R .
ANNUAL REVIEW OF IMMUNOLOGY, 2002, 20 :197-216