Inflammation-induced cancer: crosstalk between tumours, immune cells and microorganisms

被引:1613
作者
Elinav, Eran [1 ]
Nowarski, Roni [2 ]
Thaiss, Christoph A. [1 ]
Hu, Bo [2 ,3 ]
Jin, Chengcheng [2 ,4 ]
Flavell, Richard A. [2 ,5 ]
机构
[1] Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel
[2] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT 06520 USA
[3] Yale Univ, Sch Med, Dept Mol Biophys & Biochem, New Haven, CT 06520 USA
[4] Yale Univ, Sch Med, Dept Cell Biol, New Haven, CT 06520 USA
[5] Howard Hughes Med Inst, New Haven, CT 06520 USA
关键词
NF-KAPPA-B; INTESTINAL EPITHELIAL-CELLS; CYTIDINE DEAMINASE LINKS; TOLL-LIKE RECEPTOR-4; BREAST-CANCER; STAT3; ACTIVATION; COLORECTAL CARCINOGENESIS; GROWTH-FACTOR; MOUSE MODEL; T-CELLS;
D O I
10.1038/nrc3611
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Inflammation is a fundamental innate immune response to perturbed tissue homeostasis. Chronic inflammatory processes affect all stages of tumour development as well as therapy. In this Review, we outline the principal cellular and molecular pathways that coordinate the tumour-promoting and tumour-antagonizing effects of inflammation and we discuss the crosstalk between cancer development and inflammatory processes. In addition, we discuss the recently suggested role of commensal microorganisms in inflammation-induced cancer and we propose that understanding this microbial influence will be crucial for targeted therapy in modern cancer treatment.
引用
收藏
页码:759 / 771
页数:13
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