Evidence map›Paper›PMID 34295679›Full record

ReviewTranslational lung cancer research2021

Emerging and multifaceted role of neutrophils in lung cancer.

Christian Aloe, Hao Wang, Ross Vlahos, Louis Irving, Daniel Steinfort, Steven Bozinovski

Open access · diamondAbstract readReview
In one paragraph

Review in Translational lung cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 69 citations in OpenAlex.

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  10. Tumor-educated cells in tumor microenvironment: Key drivers of immunotherapy resistance.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025
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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

6 authors at 2 institutions in 1 country.

Christian AloeSchool of Health & Biomedical Sciences, RMIT University, Bundoora, Victoria, Australia.
Hao WangSchool of Health & Biomedical Sciences, RMIT University, Bundoora, Victoria, Australia.
Ross VlahosSchool of Health & Biomedical Sciences, RMIT University, Bundoora, Victoria, Australia.
Louis IrvingDepartment of Respiratory Medicine, Royal Melbourne Hospital, Melbourne, Australia.
Daniel SteinfortDepartment of Respiratory Medicine, Royal Melbourne Hospital, Melbourne, Australia.
Steven BozinovskiSchool of Health & Biomedical Sciences, RMIT University, Bundoora, Victoria, Australia.
RMIT University · AUThe Royal Melbourne Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has long been recognized that cigarette smoking is a shared risk factor for lung cancer and the debilitating lung disease, chronic obstructive pulmonary disease (COPD). As the severity of COPD increases, so does the risk for developing lung cancer, independently of pack years smoked. Neutrophilic inflammation increases with COPD severity and anti-inflammatories such as non-steroidal anti-inflammatory drugs (NSAIDs) can modulate neutrophil function and cancer risk. This review discusses the biology of tumour associated neutrophils (TANs) in lung cancer, which increase in density with tumour progression, particularly in smokers with non-small cell lung cancer (NSCLC). It is now increasingly recognized that neutrophils are responsive to the tumour microenvironment (TME) and polarize into distinct phenotypes that operate in an anti- (N1) or pro-tumorigenic (N2) manner. Intriguingly, the emergence of the pro-tumorigenic N2 phenotype increases with tumour growth, to suggest that cancer cells and the surrounding stroma can re-educate neutrophils. The neutrophil itself is a potent source of reactive oxygen species (ROS), arginase, proteases and cytokines that paradoxically can exert a potent immunosuppressive effect on lymphocytes including cytotoxic T cells (CTLs). Indeed, the neutrophil to lymphocyte ratio (NLR) is a systemic biomarker that is elevated in lung cancer patients and prognostic for poor survival outcomes. Herein, we review the molecular mechanisms by which neutrophil derived mediators can suppress CTL function. Selective therapeutic strategies designed to suppress pathogenic neutrophils in NSCLC may cooperate with immune checkpoint inhibitors (ICI) to increase CTL killing of cancer cells in the TME.

Indexed as

chronic obstructive pulmonary disease (COPD)immunotherapyLung cancerneutrophils

Identifiers

PMID34295679
PMCPMC8264329
OpenAlexW3155437431

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.