Oxidative DNA damage caused by inflammation may link to stress-induced non-targeted effects

被引:51
|
作者
Sprung, Carl N. [1 ]
Ivashkevich, Alesia [1 ]
Forrester, Helen B. [1 ]
Redon, Christophe E. [2 ]
Georgakilas, Alexandros [3 ]
Martin, Olga A. [4 ,5 ,6 ]
机构
[1] Monash Univ, Ctr Innate Immun & Infect Dis, Monash Inst Med Res, Clayton, Vic 3168, Australia
[2] NCI, Mol Pharmacol Lab, Ctr Canc Res, Bethesda, MD 20892 USA
[3] Natl Tech Univ Athens, Dept Phys, Sch Appl Math & Phys Sci, GR-15773 Athens, Greece
[4] Peter MacCallum Canc Ctr, Dept Radiat Oncol, Melbourne, Vic, Australia
[5] Peter MacCallum Canc Ctr, Mol Radiat Biol Lab, Melbourne, Vic, Australia
[6] Univ Melbourne, Sir Peter MacCallum Dept Oncol, Melbourne, Vic 3010, Australia
基金
英国医学研究理事会;
关键词
Bystander effect; Non-targeted effects; Abscopal effects; Radiation induced bystander effects; DNA damage; Ionizing radiation; RAT LUNG IRRADIATION; MONOCYTE CHEMOATTRACTANT PROTEIN-1; INDUCED ADAPTIVE RESPONSE; DOUBLE-STRAND BREAKS; MEDIATED INTERCELLULAR COMMUNICATION; EFFECTS IN-VIVO; IONIZING-RADIATION; HUMAN FIBROBLASTS; HYDROGEN-PEROXIDE; GENE-EXPRESSION;
D O I
10.1016/j.canlet.2013.09.008
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
A spectrum of radiation-induced non-targeted effects has been reported during the last two decades since Nagasawa and Little first described a phenomenon in cultured cells that was later called the "bystander effect". These non-targeted effects include radiotherapy-related abscopal effects, where changes in organs or tissues occur distant from the irradiated region. The spectrum of non-targeted effects continue to broaden over time and now embrace many types of exogenous and endogenous stressors that induce a systemic genotoxic response including a widely studied tumor microenvironment. Here we discuss processes and factors leading to DNA damage induction in non-targeted cells and tissues and highlight similarities in the regulation of systemic effects caused by different stressors. Crown Copyright (C) 2013 Published by Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:72 / 81
页数:10
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