Abstract

Chronic Obstructive Pulmonary Disease (COPD) and Lung cancer are the major reasons for lung disease-related mortality worldwide. Chronic inflammation is a key attribute of COPD and a potential driver of lung carcinogenesis. Among various environmental risk factors, cigarette smoke plays a crucial role in the development and progression of COPD and lung cancer. Several epidemiological studies show that COPD patients are at a greater risk of developing lung cancer independently of cigarette smoking which suggests the role of genetic predisposition in the disease development. Uncovering the mechanistic link between these two diseases is hampered due to their heterogeneous nature: each is characterized by several sub-phenotypes of diseases. This review focuses on the nature of the link between the two diseases and specific mechanisms that occur in both COPD and lung cancer, some of the therapeutic targets which are currently employed, and the role of gene-editing technology to combat these debilitating lung-inflammatory disorders.

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