TLR-signaling and proinflammatory cytokines as drivers of tumorigenesis

被引：156

作者：

Korneev, Kirill V. ^{[1
,2
]}

Atretkhany, Kamar-Sulu N. ^{[1
,2
]}

Drutskaya, Marina S. ^{[1
]}

Grivennikov, Sergei I. ^{[1
,3
]}

Kuprash, Dmitry V. ^{[1
,2
]}

Nedospasov, Sergei A. ^{[1
,2
]}

机构：

[1] Russian Acad Sci, Engelhardt Inst Mol Biol, Moscow, Russia

[2] Lomonosov Moscow State Univ, Fac Biol, Moscow, Russia

[3] Fox Chase Canc Ctr, 7701 Burholme Ave, Philadelphia, PA 19111 USA

来源：

CYTOKINE | 2017年 / 89卷

基金：

俄罗斯科学基金会;

关键词：

Innate immunity; Chronic inflammation; Cancer; TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; TOLL-LIKE RECEPTOR-4; CANCER-ASSOCIATED FIBROBLASTS; ISOLATED LIMB PERFUSION; FACTOR-ALPHA INHIBITOR; SOFT-TISSUE SARCOMAS; SUPPRESSOR-CELLS; TNF-ALPHA; COLORECTAL-CANCER;

D O I：

10.1016/j.cyto.2016.01.021

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The link between inflammation and cancer was first proposed by R. Virchow. It was later realized that it is chronic inflammation that may promote cancer, whereas acute inflammation can actually block tumor development or even result in cure. Many molecular mediators of these diverse processes have been characterized only during the past 3 decades thanks to the advances in molecular and cellular techniques, as well as due to technologies of reverse genetics. In this chapter we discuss the role of Toll-like receptor (TLR) 4 signaling in cancer and contributions of proinflammatory cytokine signaling (whose expression may be driven by TLR-mediated signals) to tumor-promoting microenvironment. We also discuss recent clinical advances to target these pro-tumorigenic pathways at distinct stages of tumorigenesis. (C) 2016 Elsevier Ltd. All rights reserved.

引用

页码：127 / 135

页数：9

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