Inflammation and immune surveillance in cancer

被引:156
作者
Chow, Melvyn T. [1 ,2 ,3 ]
Moeller, Andreas [2 ,3 ,4 ]
Smyth, Mark J. [1 ,2 ,3 ]
机构
[1] Peter MacCallum Canc Inst, Canc Immunol Program, Melbourne, Vic 3002, Australia
[2] Univ Melbourne, Sir Peter MacCallum Dept Oncol, Parkville, Vic 3010, Australia
[3] Univ Melbourne, Dept Pathol, Parkville, Vic 3010, Australia
[4] Peter MacCallum Canc Inst, Canc Genom & Genet Lab, Melbourne, Vic 3002, Australia
基金
英国医学研究理事会;
关键词
Inflammation; Immunoediting; Danger signal; Toll-like receptor; Inflammasome; TOLL-LIKE RECEPTOR-4; MOBILITY GROUP BOX-1; REGULATORY T-CELLS; NEONATALLY THYMECTOMIZED MICE; NASOPHARYNGEAL CARCINOMA RISK; MELANOMA INHIBITORY-ACTIVITY; ENDOGENOUS DANGER SIGNAL; PROMOTE TUMOR-GROWTH; NATURAL-KILLER-CELLS; END-PRODUCTS RAGE;
D O I
10.1016/j.semcancer.2011.12.004
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Chronic inflammation is a risk factor for tumor development. However, understanding the effect of the immune system on tumor development has only been significantly advanced over the past two decades. We now appreciate that the immune system, in addition to tumor-suppressive function by eliminating nascent transformed tumor cells, can also exert selection pressure on tumor cells and facilitate tumor growth by providing a favorable tumor microenvironment. Yet, the distinctions between tumor-promoting inflammation and tumor-suppressive immunity are still not clear due to the dual role of some cytokines and other molecules in the immune system. The danger signal hypothesis has shaped our view of the role of immunity in cancer development, but still little is known about the exact role of danger signal receptors in cancer progression. In this review, we introduce the processes of cancer immunoediting and inflammation-induced cancer and discuss what is currently known about the role of danger signal receptors in cancer development and progression. (C) 2011 Elsevier Ltd. All rights reserved.
引用
收藏
页码:23 / 32
页数:10
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