Evidence map›Paper›PMID 35315360›Full record

ArticleJCI insight2022

CSF1/CSF1R signaling mediates malignant pleural effusion formation.

Chrysavgi N Kosti, Photene C Vaitsi, Apostolos G Pappas, Marianthi P Iliopoulou, Katherina K Psarra, Sophia F Magkouta, Ioannis T Kalomenidis

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
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  4. CXCL2/CXCR2 pathway regulates CD169Frontiers in medicine · 2026
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  16. International journal of molecular sciences · 2022
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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

7 authors at 2 institutions in 1 country.

Chrysavgi N KostiMarianthi Simou Laboratory, 1st Department of Critical Care and Pulmonary Medicine, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Photene C VaitsiMarianthi Simou Laboratory, 1st Department of Critical Care and Pulmonary Medicine, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Apostolos G PappasMarianthi Simou Laboratory, 1st Department of Critical Care and Pulmonary Medicine, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Marianthi P IliopoulouMarianthi Simou Laboratory, 1st Department of Critical Care and Pulmonary Medicine, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Katherina K PsarraDepartment of Immunology - Histocompatibility, Evangelismos Hospital, Athens, Greece.
Sophia F MagkoutaMarianthi Simou Laboratory, 1st Department of Critical Care and Pulmonary Medicine, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Ioannis T KalomenidisMarianthi Simou Laboratory, 1st Department of Critical Care and Pulmonary Medicine, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
National and Kapodistrian University of Athens · GREvangelismos Hospital · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant pleural effusion (MPE) is an incurable common manifestation of many malignancies. Its formation is orchestrated by complex interactions among tumor cells, inflammatory cells, and the vasculature. Tumor-associated macrophages present the dominant inflammatory population of MPE, and M2 macrophage numbers account for dismal prognosis. M2 polarization is known to be triggered by CSF1/CSF1 receptor (CSF1R) signaling. We hypothesized that CSF1R+ M2 macrophages favor MPE formation and could be therapeutically targeted to limit MPE. We generated mice with CSF1R-deficient macrophages and induced lung and colon adenocarcinoma-associated MPE. We also examined the therapeutic potential of a clinically relevant CSF1R inhibitor (BLZ945) in lung and colon adenocarcinoma-induced experimental MPE. We showed that CSF1R+ macrophages promoted pleural fluid accumulation by enhancing vascular permeability, destabilizing tumor vessels, and favoring immune suppression. We also showed that CSF1R inhibition limited MPE in vivo by reducing vascular permeability and neoangiogenesis and impeding tumor progression. This was because apart from macrophages, CSF1R signals in cancer-associated fibroblasts leading to macrophage inflammatory protein 2 secretion triggered the manifestation of suppressive and angiogenic properties in macrophages upon CXCR2 paracrine activation. Pharmacological targeting of the CSF1/CSF1R axis can therefore be a vital strategy for limiting MPE.

Indexed as

Colonic NeoplasmsMacrophage Colony-Stimulating FactorPleural Effusion, MalignantReceptors, Granulocyte-Macrophage Colony-Stimulating FactorAnimalsMacrophagesMiceReceptor, Macrophage Colony-Stimulating FactorReceptor Protein-Tyrosine KinasesCSF1 protein, mouseCsf1r protein, mouseMacrophage Colony-Stimulating FactorReceptor, Macrophage Colony-Stimulating FactorReceptor Protein-Tyrosine KinasesReceptors, Granulocyte-Macrophage Colony-Stimulating FactorAngiogenesisCancerMacrophagesOncology

Identifiers

PMID35315360
PMCPMC8986064
OpenAlexW4220723098

What OpenQuestion holds

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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.