Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016 Feb;173(4):635-48.
doi: 10.1111/bph.13198. Epub 2015 Jul 8.

COPD and squamous cell lung cancer: aberrant inflammation and immunity is the common link

Steven Bozinovski  1   2 , Ross Vlahos  1   2 , Desiree Anthony  2 , Jonathan McQualter  2 , Gary Anderson  2 , Louis Irving  3 , Daniel Steinfort  3
Affiliations
Review

COPD and squamous cell lung cancer: aberrant inflammation and immunity is the common link

Steven Bozinovski et al. Br J Pharmacol. 2016 Feb.

Abstract

Cigarette smoking has reached epidemic proportions within many regions of the world and remains the highest risk factor for chronic obstructive pulmonary disease (COPD) and lung cancer. Squamous cell lung cancer is commonly detected in heavy smokers, where the risk of developing lung cancer is not solely defined by tobacco consumption. Although therapies that target common driver mutations in adenocarcinomas are showing some promise, they are proving ineffective in smoking-related squamous cell lung cancer. Since COPD is characterized by an excessive inflammatory and oxidative stress response, this review details how aberrant innate, adaptive and systemic inflammatory processes can contribute to lung cancer susceptibility in COPD. Activated leukocytes release increasing levels of proteases and free radicals as COPD progresses and tertiary lymphoid aggregates accumulate with increasing severity. Reactive oxygen species promote formation of reactive carbonyls that are not only tumourigenic through initiating DNA damage, but can directly alter the function of regulatory proteins involved in host immunity and tumour suppressor functions. Systemic inflammation is also markedly increased during infective exacerbations in COPD and the interplay between tumour-promoting serum amyloid A (SAA) and IL-17A is discussed. SAA is also an endogenous allosteric modifier of FPR2 expressed on immune and epithelial cells, and the therapeutic potential of targeting this receptor is proposed as a novel strategy for COPD-lung cancer overlap.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Inflammatory and oxidative mechanisms prominent in COPD that can promote lung cancer by causing genomic instability, suppressing tumour immuno‐surveillance mechanisms and promoting inflammation that is beneficial to tumour growth and migration.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Agusti A, Edwards LD, Rennard SI, MacNee W, Tal‐Singer R, Miller BE et al (2012). Persistent systemic inflammation is associated with poor clinical outcomes in COPD: a novel phenotype. PLoS ONE 7: e37483. - PMC - PubMed
    1. Alexander SPH, Benson HE, Faccenda E, Pawson AJ, Sharman JL, Spedding M et al (2013a). The Concise Guide to PHARMACOLOGY 2013/14: G protein‐coupled receptors. Br J Pharmacol 170: 1459–1581. - PMC - PubMed
    1. Alexander SPH, Benson HE, Faccenda E, Pawson AJ, Sharman JL, Spedding M et al (2013b). The Concise Guide to PHARMACOLOGY 2013/14: catalytic receptors. Br J Pharmacol 170: 1676–1705. - PMC - PubMed
    1. Alexander SPH, Benson HE, Faccenda E, Pawson AJ, Sharman JL, Spedding M et al (2013c). The Concise Guide to PHARMACOLOGY 2013/14: enzymes. Br J Pharmacol 170: 1797–1867. - PMC - PubMed
    1. Allavena P, Sica A, Solinas G, Porta C, Mantovani A (2008). The inflammatory micro‐environment in tumor progression: the role of tumor‐associated macrophages. Crit Rev Oncol Hematol 66: 1–9. - PubMed

MeSH terms