Chronic Obstructive Pulmonary Disease and Lung Cancer: New Molecular Insights
Abstract
Both chronic obstructive pulmonary disease (COPD) and lung cancer are major causes of death worldwide. In most cases this reflects cigarette smoke exposure which is able to induce an inflammatory response in the airways of smokers. Indeed, COPD is characterized by lower airway inflammation, and importantly, the presence of COPD is by far the greatest risk factor for lung cancer amongst smokers. Cigarette smoke induces the release of many inflammatory mediators and growth factors including TGF-β, EGFR, IL-1, IL-8 and G-CSF through oxidative stress pathways and this inflammation may persist for decades after smoking cessation. Mucus production is also increased by these inflammatory mediators, further linking airway inflammation to an important mechanism of lung cancer. A greater understanding of the molecular and cellular pathobiology that distinguishes smokers with lung cancer from smokers with and without COPD is needed to unravel the complex molecular interactions between COPD and lung cancer. By understanding the common signalling pathways involved in COPD and lung cancer the hope is that treatments will be developed that not only treat the underlying disease process in COPD, but also reduce the currently high risk of developing lung cancer in these patients.
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The impaired DNA repair and resulting oxidative stress in COPD patients explain a higher prevalence of lung cancer compared to smokers without airway obstruction.
“The impaired DNA repair and resulting oxidative stress in patients suffering from COPD explain a higher prevalence of lung cancer compared to smokers without airway obstruction (Adcock et al. 2011).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Adcock et al. 2011
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- Authors
- Adcock, I. M., Caramori, G., & Barnes, P. J.
- Affiliations
- Imperial College London (GB)
- University of Ferrara (IT)
- Venue
- Respiration
- Publisher
- S. Karger AG
- Published
- 2011
- Volume
- 81
- Issue
- 4
- Pages
- 265-284
- ISSN
- 0025-7931 (ISSN-L)
- 1423-0356
- OpenAlex
- W2007328352
- Cited by
- 257
- References
- 225
- Citations by year
- 2026: 5 · 2025: 11 · 2024: 13 · 2023: 16 · 2022: 16 · 2021: 8 · 2020: 11 · 2019: 11 · 2018: 15 · 2017: 20 · 2016: 18 · 2015: 21 · 2014: 22 · 2013: 31 · 2012: 32
- FWCI
- 4.80
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Respiration (publishedVersion)
- PubMed (publishedVersion)
- Institutional Research Information System University of Ferrara (University of Ferrara) (submittedVersion)
- Funders
- Pfizer
- GlaxoSmithKline
- Wellcome Trust
- Medical Research Council
- Biotechnology and Biological Sciences Research Council
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Health Sciences › Medicine › Oncology › Lung Cancer Research Studies
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Keywords
- chronic obstructive pulmonary disease, lung cancer, cigarette smoking, airway inflammation, oxidative stress, TGF-beta, EGFR, interleukin-1, interleukin-8, granulocyte colony-stimulating factor, mucus overproduction, molecular pathobiology, smoking cessation, inflammatory mediators
- MeSH terms
- Carcinoma, Squamous Cell, Disease Susceptibility, DNA Damage, DNA Repair, Humans, Lung Neoplasms, Polymorphism, Genetic, Prostaglandins, Smoking, Stem Cells, Signal Transduction, Gene Expression, Apoptosis, Oxidative Stress, Pulmonary Disease, Chronic Obstructive, MicroRNAs, Epigenesis, Genetic
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