Common pathogenic mechanisms and pathways in the development of COPD and lung cancer

• Published in: Expert opinion on therapeutic targets Vol. 15; no. 4; p. 439
• Main Authors: Yang, Ian A, Relan, Vandana, Wright, Casey M, Davidson, Morgan R, Sriram, Krishna B, Savarimuthu Francis, Santiyagu M, Clarke, Belinda E, Duhig, Edwina E, Bowman, Rayleen V, Fong, Kwun M
• Format: Journal Article
• Language: English
• Published: England 01.04.2011
• Subjects: Adenocarcinoma - drug therapy; Adenocarcinoma - epidemiology; Adenocarcinoma - genetics; Adenocarcinoma - pathology; Adenocarcinoma of Lung; Epigenesis, Genetic; Female; Humans; Lung Neoplasms - drug therapy; Lung Neoplasms - epidemiology; Lung Neoplasms - genetics; Lung Neoplasms - pathology; Male; Molecular Targeted Therapy; Polymorphism, Single Nucleotide; Pulmonary Disease, Chronic Obstructive - drug therapy; Pulmonary Disease, Chronic Obstructive - epidemiology; Pulmonary Disease, Chronic Obstructive - genetics; Pulmonary Disease, Chronic Obstructive - pathology; Smoking; Smoking Cessation
• ISSN: 1744-7631
• DOI: 10.1517/14728222.2011.555400

Lung cancer and COPD commonly coexist in smokers, and the presence of COPD increases the risk of developing lung cancer. In addition to smoking cessation and preventing smoking initiation, understanding the shared mechanisms of these smoking-related lung diseases is critical, in order to develop new methods of prevention, diagnosis and treatment of lung cancer and COPD. This review discusses the common mechanisms for susceptibility to lung cancer and COPD, which in addition to cigarette smoke, may involve inflammation, epithelial-mesenchymal transition, abnormal repair, oxidative stress, and cell proliferation. Furthermore, we discuss the underlying genomic and epigenomic changes (single nucleotide polymorphisms (SNPs), copy number variation, promoter hypermethylation and microRNAs) that are likely to alter biological pathways, leading to susceptibility to lung cancer and COPD (e.g., altered nicotine receptor biology). Strategies to study genomics, epigenomics and gene-environment interaction will yield greater insight into the shared pathogenesis of lung cancer and COPD, leading to new diagnostic and therapeutic modalities.