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      The relationship between COPD and lung cancer

      * ,

      Lung Cancer (Amsterdam, Netherlands)

      Elsevier Scientific Publishers

      COPD, Cancer, ROS

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          • COPD is a risk factor for lung cancer beyond their shared aetiology.

          • Both are driven by oxidative stress.

          • Both are linked to cellular aging, senescence and telomere shortening.

          • Both have been linked to genetic predisposition.

          • Both show altered epigenetic regulation of gene expression.


          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.

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          Most cited references 88

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          Cancer Statistics, 2017

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            The natural history of chronic airflow obstruction.

            A prospective epidemiological study of the early stages of the development of chronic obstructive pulmonary disease was performed on London working men. The findings showed that forced expiratory volume in one second (FEV1) falls gradually over a lifetime, but in most non-smokers and many smokers clinically significant airflow obstruction never develops. In susceptible people, however, smoking causes irreversible obstructive changes. If a susceptible smoker stops smoking he will not recover his lung function, but the average further rates of loss of FEV1 will revert to normal. Therefore, severe or fatal obstructive lung disease could be prevented by screening smokers' lung function in early middle age if those with reduced function could be induced to stop smoking. Infective processes and chronic mucus hypersecretion do not cause chronic airflow obstruction to progress more rapidly. There are thus two largely unrelated disease processes, chronic airflow obstruction and the hypersecretory disorder (including infective processes).
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              Radical causes of cancer.

              Free radicals are ubiquitous in our body and are generated by normal physiological processes, including aerobic metabolism and inflammatory responses, to eliminate invading pathogenic microorganisms. Because free radicals can also inflict cellular damage, several defences have evolved both to protect our cells from radicals--such as antioxidant scavengers and enzymes--and to repair DNA damage. Understanding the association between chronic inflammation and cancer provides insights into the molecular mechanisms involved. In particular, we highlight the interaction between nitric oxide and p53 as a crucial pathway in inflammatory-mediated carcinogenesis.

                Author and article information

                Lung Cancer
                Lung Cancer
                Lung Cancer (Amsterdam, Netherlands)
                Elsevier Scientific Publishers
                1 November 2015
                November 2015
                : 90
                : 2
                : 121-127
                Airway Disease Section, National Heart and Lung Institute, Imperial College London, Dovehouse Street, London, UK
                Author notes
                [* ]Corresponding author. Airways Disease Section, National Heart & Lung Institute, Dovehouse Street, London, SW3 6LY, UK. Fax: +44 20 7351 8126. a.durham@
                © 2015 The Authors

                This is an open access article under the CC BY-NC-ND license (


                copd, ros, cancer


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