4.5 Review

The relationship between COPD and lung cancer

Journal

LUNG CANCER
Volume 90, Issue 2, Pages 121-127

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.lungcan.2015.08.017

Keywords

COPD; Cancer; ROS

Funding

  1. Biotechnology and Biological Sciences Research Council
  2. Medical Research Council [G1001367/1]
  3. Royal Society
  4. Wellcome Trust [093080/Z/10/Z]
  5. GlaxoSmithKline
  6. Pfizer
  7. NIHR Respiratory Disease Biomedical Research Unit at the Royal Brompton NHS Foundation Trust and Imperial College London

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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.

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