Role of chronic obstructive pulmonary disease in lung cancer pathogenesis

Abstract

Chronic obstructive pulmonary disease (COPD) and lung cancer are two important smoking related conditions. However, COPD has been shown to be an independent risk factor for lung cancer regardless of smoking history, suggesting that COPD and lung cancer may share a common pathogenesis. This review summarizes the epidemiology of lung cancer and COPD briefly, as well as discussing the potential for shared genetic risk, and shared genomic mechanisms, such as epigenetic changes or DNA damage induced by smoking. How key areas of COPD pathogenesis, such as inflammation, oxidative stress and protease imbalance may contribute to subsequent development of cancer will also be covered. Finally the possibility that consequences of COPD, such as hypoxia, influence carcinogenesis will be reviewed. By understanding the pathogenesis of COPD and lung cancer in detail it is possible that new treatments may be developed and the risk of lung cancer in COPD may be reduced.

Keywords: Chronic obstructive pulmonary disease, Non-small cell lung carcinoma, Smoking, Oxidative stress, Inflammation

Core tip: Chronic obstructive pulmonary disease (COPD) has been shown to be an independent risk factor for lung cancer regardless of smoking history, suggesting that COPD and lung cancer may share a common pathogenesis. Chronic inflammation and oxidative stress are the most likely mechanistic links between COPD and lung cancer. Further analysis and elucidation of the molecular mechanisms involved in the pathogenesis of COPD and lung cancer should provide us with new treatment modalities and perhaps a key to understanding how the risk of lung cancer in COPD patients may be reduced.