Evidence map›Paper›PMID 26013585›Full record

ReviewBritish journal of pharmacology2016

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

Steven Bozinovski, Ross Vlahos, Desiree Anthony, Jonathan McQualter, Gary Anderson, Louis Irving, Daniel Steinfort

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in British journal of pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 2 pooled it
10.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

79 citing papers in PubMed, 2 syntheses or guidelines pooled it, 129 citations in OpenAlex.

  1. Pooled it
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  13. The Current Roadmap of Lung Cancer Biology, Genomics and Racial Disparity.International journal of molecular sciences · 2025
    Review
  14. Article
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  20. Mechanisms Contributing to the Comorbidity of COPD and Lung Cancer.International journal of molecular sciences · 2023
    Review

19 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Steven BozinovskiSchool of Health Sciences and Health Innovations Research Institute, RMIT University, Melbourne, Vic., Australia.
Ross VlahosSchool of Health Sciences and Health Innovations Research Institute, RMIT University, Melbourne, Vic., Australia.
Desiree AnthonyLung Health Research Centre, Department of Pharmacology & Therapeutics, The University of Melbourne, Parkville, Vic., Australia.
Jonathan McQualterLung Health Research Centre, Department of Pharmacology & Therapeutics, The University of Melbourne, Parkville, Vic., Australia.
Gary AndersonLung Health Research Centre, Department of Pharmacology & Therapeutics, The University of Melbourne, Parkville, Vic., Australia.
Louis IrvingDepartment of Respiratory Medicine, The Royal Melbourne Hospital, Parkville, Vic., Australia.
Daniel SteinfortDepartment of Respiratory Medicine, The Royal Melbourne Hospital, Parkville, Vic., Australia.
University of Melbourne · AUThe Royal Melbourne Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Carcinoma, Squamous CellHumansImmunityInflammationLung NeoplasmsPulmonary Disease, Chronic Obstructive

Identifiers

PMID26013585
PMCPMC4742298
OpenAlexW1516195360

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.