Evidence map›Paper›PMID 30054470›Full record

ArticleNature communications2018

Macrophages are exploited from an innate wound healing response to facilitate cancer metastasis.

Tamara Muliaditan, Jonathan Caron, Mary Okesola, James W Opzoomer, Paris Kosti, Mirella Georgouli, Peter Gordon, Sharanpreet Lall, Desislava M Kuzeva, Luisa Pedro and 7 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 1 pooled it
4.6field-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

76 citing papers in PubMed, 1 synthesis or guideline pooled it, 135 citations in OpenAlex.

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  19. Myeloid cell-derived apCAFs promote HNSCC progression by regulating proportion of CD4Journal of experimental & clinical cancer research : CR · 2025
    Article
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16 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

17 authors at 4 institutions in 2 countries.

Tamara MuliaditanSchool of Cancer and Pharmaceutical Sciences, King's College London, Faculty of Life Sciences and Medicine, Guy's Campus, London, SE1 1UL, UK.
Jonathan CaronSchool of Cancer and Pharmaceutical Sciences, King's College London, Faculty of Life Sciences and Medicine, Guy's Campus, London, SE1 1UL, UK.
Mary OkesolaSchool of Cancer and Pharmaceutical Sciences, King's College London, Faculty of Life Sciences and Medicine, Guy's Campus, London, SE1 1UL, UK.
James W OpzoomerSchool of Cancer and Pharmaceutical Sciences, King's College London, Faculty of Life Sciences and Medicine, Guy's Campus, London, SE1 1UL, UK.
Paris KostiSchool of Cancer and Pharmaceutical Sciences, King's College London, Faculty of Life Sciences and Medicine, Guy's Campus, London, SE1 1UL, UK.
Mirella GeorgouliTumour Plasticity Laboratory, Randall Centre for Cell and Molecular Biophysics, King's College London, Guy's Campus, London, SE1 1UL, UK.
Peter GordonSchool of Cancer and Pharmaceutical Sciences, King's College London, Faculty of Life Sciences and Medicine, Guy's Campus, London, SE1 1UL, UK.
Sharanpreet LallSchool of Cancer and Pharmaceutical Sciences, King's College London, Faculty of Life Sciences and Medicine, Guy's Campus, London, SE1 1UL, UK.
Desislava M KuzevaSchool of Cancer and Pharmaceutical Sciences, King's College London, Faculty of Life Sciences and Medicine, Guy's Campus, London, SE1 1UL, UK.
Luisa PedroMedical Research Council Cancer Cell Unit, Hutchison/Medical Research Council Research Centre, Cambridge, CB2 0XZ, UK.
Jacqueline D ShieldsMedical Research Council Cancer Cell Unit, Hutchison/Medical Research Council Research Centre, Cambridge, CB2 0XZ, UK.
Cheryl E GillettSchool of Cancer and Pharmaceutical Sciences, King's College London, Faculty of Life Sciences and Medicine, Guy's Campus, London, SE1 1UL, UK.
Sandra S DieboldNational Institute for Biological Standards and Control, Potters Bar, Hertfordshire, EN6 3QG, UK.
Victoria Sanz-MorenoTumour Plasticity Laboratory, Randall Centre for Cell and Molecular Biophysics, King's College London, Guy's Campus, London, SE1 1UL, UK.ORCID http://orcid.org/0000-0002-5096-9456
Tony NgSchool of Cancer and Pharmaceutical Sciences, King's College London, Faculty of Life Sciences and Medicine, Guy's Campus, London, SE1 1UL, UK.
Esther HosteUnit for Cellular and Molecular Pathophysiology, VIB Center for Inflammation Research, B-9052, Ghent-Zwijnaarde, Belgium.ORCID http://orcid.org/0000-0002-3181-431X
James N ArnoldSchool of Cancer and Pharmaceutical Sciences, King's College London, Faculty of Life Sciences and Medicine, Guy's Campus, London, SE1 1UL, UK. james.n.arnold@kcl.ac.uk.ORCID http://orcid.org/0000-0002-6949-0613
King's College London · GBHutchison/MRC Research Centre · GBGhent University · BENational Institute for Biological Standards and Control · GB

Funding

Cancer Research UK 12065Cancer Research UK 24478European Research Council 335326Medical Research Council MC_UP_1101/2Medical Research Council MC_UU_12022/5Wellcome Trust
6 · The paper itself

Abstract

Tumour-associated macrophages (TAMs) play an important role in tumour progression, which is facilitated by their ability to respond to environmental cues. Here we report, using murine models of breast cancer, that TAMs expressing fibroblast activation protein alpha (FAP) and haem oxygenase-1 (HO-1), which are also found in human breast cancer, represent a macrophage phenotype similar to that observed during the wound healing response. Importantly, the expression of a wound-like cytokine response within the tumour is clinically associated with poor prognosis in a variety of cancers. We show that co-expression of FAP and HO-1 in macrophages results from an innate early regenerative response driven by IL-6, which both directly regulates HO-1 expression and licenses FAP expression in a skin-like collagen-rich environment. We show that tumours can exploit this response to facilitate transendothelial migration and metastatic spread of the disease, which can be pharmacologically targeted using a clinically relevant HO-1 inhibitor.

Indexed as

Neoplasm MetastasisAnimalsBreast NeoplasmsCell Line, TumorCell SurvivalCollagenCytokinesEndopeptidasesFemaleFibroblast Activation Protein AlphaGelatinasesGene Expression Regulation, NeoplasticHeme Oxygenase-1HumansInterleukin-6MacrophagesCollagenCytokinesEndopeptidasesFibroblast Activation Protein AlphaGelatinasesHeme Oxygenase-1Interleukin-6interleukin-6, mouseMembrane ProteinsSerine Endopeptidases

Identifiers

PMID30054470
PMCPMC6063977
OpenAlexW2884310345

What OpenQuestion holds

Textmetadata
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.