Extract
Cigarette smoke exposure is the major driver of chronic obstructive pulmonary disease (COPD) and lung cancer in the developed world [1]. COPD affects over 450 million people worldwide whilst lung cancer is the biggest cause of death in people with cancer [2, 3]. Cigarette smoke-mediated DNA damage causes apoptosis, cellular senescence, inflammation and mutagenesis, which have all been implicated in the pathogenesis of COPD [4, 5]. Reduced components of DNA damage and repair pathways have previously been reported in COPD lung tissues (with or without associated pulmonary emphysema) and blood (including stem cells), and airway epithelium and lung fibroblast primary cells [6–10]. A failure to correctly repair cigarette smoke-induced DNA damage has also been reported in COPD [8] and a genetic link to COPD susceptibility noted [9, 11]. Evidence has also implicated DNA damage and repair mechanisms with lung cancer and response to therapy [12, 13]. However, the precise mechanisms of DNA damage and repair that are associated with these diseases are unclear.
Abstract
Defective DNA damage and repair processes are important in COPD http://ow.ly/edRb30lTF2J
Footnotes
Conflict of interest: None declared.
- Received September 8, 2018.
- Accepted September 10, 2018.
- Copyright ©ERS 2018