In OSAS, an episodic hypoxia-reoxygenation cycle occurs during intermittent nocturnal hypoxias that causes the production of reactive oxygen metabolites [10]. These metabolites are responsible for the activation of inflammatory cells in OSAS [11, 12], and their increased levels eventually cause ischemia-reperfusion injury [13], and cellular and DNA damage [14, 15]. The latter, is also a significant contributor of LC progression. The DNA damage in the presence of reactive oxygen metabolites yields carcinogenesis by several mechanisms. Some of them are single or double-stranded DNA breaks, and modifications in purines or pyrimidines. Nevertheless, OS is not the only susceptible factor for carcinogenesis, there are also many other pathological mechanisms contributing to cancer development, such as reactive nitrogen species, and involvement of mitochondrial DNA mutations [16] in inflammatory conditions. Previous studies reported that LC occurs two-to-five times higher in patients with moderate-to-severe COPD [17, 18]. OS is also the main etiological factor of COPD, which is particularly important in the acute exacerbations of the disease [19]. The parenchymal damage in COPD includes some mechanisms such as chronic inflammation, OS, deteriorations in the balance of protease and antiprotease activities, and apoptosis [20]. The major etiological factor that suspected to play role in the progression of LC in COPD is reported as chronic inflammation, which causes induction of several interleukins and cyclooxygenase-2 activity. The inflammatory micro-environment is a potential medium for contributing the neoproliferative process, which interacts with regulatory mechanism such as apoptosis and angiogenesis [21].