Evidence map›Paper›PMID 34876407›Full record

ArticleJournal for immunotherapy of cancer2021

Uncoupled biological and chronological aging of neutrophils in cancer promotes tumor progression.

Laura A Mittmann, Florian Haring, Johanna B Schaubächer, Roman Hennel, Bojan Smiljanov, Gabriele Zuchtriegel, Martin Canis, Olivier Gires, Fritz Krombach, Lesca Holdt and 5 more

Open access · goldAbstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

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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

15 authors at 3 institutions in 3 countries.

Laura A MittmannDepartment of Otorhinolaryngology, LMU München, Munich, Germany.
Florian HaringDepartment of Otorhinolaryngology, LMU München, Munich, Germany.
Johanna B SchaubächerDepartment of Otorhinolaryngology, LMU München, Munich, Germany.
Roman HennelDepartment of Radiotherapy and Radiation Oncology, LMU München, Munich, Germany.
Bojan SmiljanovDepartment of Otorhinolaryngology, LMU München, Munich, Germany.
Gabriele ZuchtriegelDepartment of Otorhinolaryngology, LMU München, Munich, Germany.
Martin CanisDepartment of Otorhinolaryngology, LMU München, Munich, Germany.
Olivier GiresDepartment of Otorhinolaryngology, LMU München, Munich, Germany.
Fritz KrombachWalter Brendel Centre of Experimental Medicine, LMU München, Munich, Germany.
Lesca HoldtInstitute for Laboratory Medicine, LMU München, Munich, Germany.
Sven BrandauDepartment of Otorhinolaryngology, University Hospital Essen, Essen, Germany.ORCID 0000-0002-2702-4163
Thomas VoglInstitute for Immunology, University of Munster, Munster, Germany.
Kirsten LauberDepartment of Radiotherapy and Radiation Oncology, LMU München, Munich, Germany.
Bernd UhlDepartment of Otorhinolaryngology, LMU München, Munich, Germany.
Christoph A ReichelDepartment of Otorhinolaryngology, LMU München, Munich, Germany christoph.reichel@med.uni-muenchen.de.ORCID 0000-0003-2145-0388
LMU Klinikum · DEEssen University Hospital · DEUniversity of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBeyond their fundamental role in homeostasis and host defense, neutrophilic granulocytes (neutrophils) are increasingly recognized to contribute to the pathogenesis of malignant tumors. Recently, aging of mature neutrophils in the systemic circulation has been identified to be critical for these immune cells to properly unfold their homeostatic and anti-infectious functional properties. The role of neutrophil aging in cancer remains largely obscure.

methodsEmploying advanced in vivo microscopy techniques in different animal models of cancer as well as utilizing pulse-labeling and cell transfer approaches, various

resultsHere, we show that signals released during early tumor growth accelerate biological aging of circulating neutrophils, hence uncoupling biological from chronological aging of these immune cells. This facilitates the accumulation of highly reactive neutrophils in malignant lesions and endows them with potent protumorigenic functions, thus promoting tumor progression. Counteracting uncoupled biological aging of circulating neutrophils by blocking the chemokine receptor CXCR2 effectively suppressed tumor growth.

conclusionsOur data uncover a self-sustaining mechanism of malignant neoplasms in fostering protumorigenic phenotypic and functional changes in circulating neutrophils. Interference with this aberrant process might therefore provide a novel, already pharmacologically targetable strategy for cancer immunotherapy.

Indexed as

AgingNeovascularization, PathologicAnimalsCarcinoma, Squamous CellChemokine CXCL2FemaleInflammationMaleMiceMice, Inbred BALB CMice, Inbred C3HNeutrophilsReceptors, CXCR4Receptors, Formyl PeptideReceptors, Interleukin-8BChemokine CXCL2Cxcl2 protein, mouseCxcr2 protein, mouseCXCR4 protein, mouseFpr1 protein, mouseReceptors, CXCR4Receptors, Formyl PeptideReceptors, Interleukin-8Bcellularhead and neck neoplasmsimmunityinflammationinnateneutrophil infiltration

Identifiers

PMID34876407
PMCPMC8655594
OpenAlexW4200081731

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Registered trials

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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.