The relationship between COPD and lung cancer

被引:334
作者
Durham, A. L. [1 ]
Adcock, I. M. [1 ]
机构
[1] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Airway Dis Sect, London, England
基金
英国惠康基金; 英国生物技术与生命科学研究理事会; 英国医学研究理事会;
关键词
COPD; Cancer; ROS; OBSTRUCTIVE PULMONARY-DISEASE; RECEPTOR TYROSINE KINASE; OXIDATIVE STRESS; DNA METHYLATION; TELOMERE DYSFUNCTION; CELLS; INHIBITORS; RISK; INFLAMMATION; PATHOGENESIS;
D O I
10.1016/j.lungcan.2015.08.017
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Both COPD and lung cancer are major worldwide health concerns owing to cigarette smoking, and represent a huge, worldwide, preventable disease burden. Whilst the majority of smokers will not develop either COPD or lung cancer, they are closely related diseases, occurring as co-morbidities at a higher rate than if they were independently triggered by smoking. Lung cancer and COPD may be different aspects of the same disease, with the same underlying predispositions, whether this is an underlying genetic predisposition, telomere shortening, mitochondrial dysfunction or premature aging. In the majority of smokers, the burden of smoking may be dealt with by the body's defense mechanisms: anti-oxidants such as superoxide dismutases, anti-proteases and DNA repair mechanisms. However, in the case of both diseases these fail, leading to cancer if mutations occur or COPD if damage to the cell and proteins becomes too great. Alternatively COPD could be a driving factor in lung cancer, by increasing oxidative stress and the resulting DNA damage, chronic exposure to pro-inflammatory cytokines, repression of the DNA repair mechanisms and increased cellular proliferation. Understanding the mechanisms that drive these processes in primary cells from patients with these diseases along with better disease models is essential for the development of new treatments. (C) 2015 The Authors. Published by Elsevier Ireland Ltd. This is an open access article under the CC BY-NC-ND license.
引用
收藏
页码:121 / 127
页数:7
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