Journal
EXPERT OPINION ON THERAPEUTIC TARGETS
Volume 23, Issue 6, Pages 539-553Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/14728222.2019.1615884
Keywords
COPD; lung cancer; smoking; squamous cell carcinoma
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Funding
- National Health and Medical Research Council of Australia [1079187]
- British Heart Foundation [PG/14/27/30679]
- Dunhill Medical Trust [R368/0714]
- Wellcome Trust [093080/Z/10/Z]
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Introduction: COPD and lung cancer are leading causes of morbidity and mortality worldwide, and they share a common environmental risk factor in cigarette smoke exposure and a genetic predisposition represented by their incidence in only a fraction of smokers. This reflects the ability of cigarette smoke to induce an inflammatory response in the airways of susceptible smokers. Moreover, COPD could be a driving factor in lung cancer, by increasing oxidative stress and the resulting DNA damage and repression of the DNA repair mechanisms, chronic exposure to pro-inflammatory cytokines, repression of innate immunity and increased cellular proliferation. Areas covered: We have focused our review on the potential pathogenic molecular links between tobacco smoking-related COPD and lung cancer and the potential molecular targets for new drug development by understanding the common signaling pathways involved in COPD and lung cancer. Expert commentary: Research in this field is mostly limited to animal models or small clinical trials. Large clinical trials are needed but mostly combined models of COPD and lung cancer are necessary to investigate the processes caused by chronic inflammation, including genetic and epigenetic alteration, and the expression of inflammatory mediators that link COPD and lung cancer, to identify new molecular therapeutic targets.
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