Evidence map›Paper›PMID 33758004›Full record

ArticleGut2022

Activation of the GPR35 pathway drives angiogenesis in the tumour microenvironment.

Ester Pagano, Joshua E Elias, Georg Schneditz, Svetlana Saveljeva, Lorraine M Holland, Francesca Borrelli, Tom H Karlsen, Arthur Kaser, Nicole C Kaneider

Open access · hybridAbstract read
In one paragraph

Article in Gut, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
9.6field-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

45 citing papers in PubMed, 72 citations in OpenAlex.

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  18. TME-Related Biomimetic Strategies Against Cancer.International journal of nanomedicine · 2024
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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

9 authors at 3 institutions in 3 countries.

Ester PaganoCambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Cambridge, UK.
Joshua E EliasCambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Cambridge, UK.
Georg SchneditzCambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Cambridge, UK.
Svetlana SaveljevaCambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Cambridge, UK.
Lorraine M HollandCambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Cambridge, UK.
Francesca BorrelliDepartment of Pharmacy, School of Medicine and Surgery, University of Naples Federico II, Naples, Italy.ORCID 0000-0002-2695-3294
Tom H KarlsenNorwegian PSC Research Center, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway.ORCID 0000-0002-8289-9931
Arthur KaserCambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Cambridge, UK.
Nicole C KaneiderCambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus, University of Cambridge, Cambridge, UK nk428@cam.ac.uk.ORCID 0000-0002-6079-4389
University of Cambridge · GBOslo University Hospital · NOUniversity of Naples Federico II · IT

Funding

Department of HealthWellcome TrustWellcome Trust 103077/Z/13/ZWellcome Trust 106260/Z/14/ZWellcome Trust 216630/Z/19/Z
6 · The paper itself

Abstract

objectivePrimary sclerosing cholangitis (PSC) is in 70% of cases associated with inflammatory bowel disease. The hypermorphic T108M variant of the orphan G protein-coupled receptor GPR35 increases risk for PSC and ulcerative colitis (UC), conditions strongly predisposing for inflammation-associated liver and colon cancer. Lack of GPR35 reduces tumour numbers in mouse models of spontaneous and colitis associated cancer. The tumour microenvironment substantially determines tumour growth, and tumour-associated macrophages are crucial for neovascularisation. We aim to understand the role of the GPR35 pathway in the tumour microenvironment of spontaneous and colitis-associated colon cancers.

designMice lacking GPR35 on their macrophages underwent models of spontaneous colon cancer or colitis-associated cancer. The role of tumour-associated macrophages was then assessed in biochemical and functional assays.

resultsHere, we show that GPR35 on macrophages is a potent amplifier of tumour growth by stimulating neoangiogenesis and tumour tissue remodelling. Deletion of

conclusionsActivation of the GPR35 pathway promotes tumour growth via two separate routes, by directly augmenting proliferation in epithelial cells that express the receptor, and by coordinating macrophages' ability to create a tumour-permissive environment.

Indexed as

AnimalsCholangitis, SclerosingColitis, UlcerativeColonic NeoplasmsDisease Models, AnimalMacrophagesMiceNeovascularization, PathologicReceptors, G-Protein-CoupledTumor MicroenvironmentGPR35 protein, mouseReceptors, G-Protein-Coupledangiogenesiscolorectal cancerprimary sclerosing cholangitisreceptor characterisationulcerative colitis

Identifiers

PMID33758004
PMCPMC8862021
OpenAlexW3136792458

What OpenQuestion holds

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LicenceCC BY
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.