Evidence map›Paper›PMID 29281816›Full record

ArticleCell reports2017

Tumor-Associated Macrophages Derived from Circulating Inflammatory Monocytes Degrade Collagen through Cellular Uptake.

Daniel Hargbøl Madsen, Henrik Jessen Jürgensen, Majken Storm Siersbæk, Dorota Ewa Kuczek, Loretta Grey Cloud, Shihui Liu, Niels Behrendt, Lars Grøntved, Roberto Weigert, Thomas Henrik Bugge

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% 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

87 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.

  1. Pooled it
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  13. Targeting collagen to optimize cancer immunotherapy.Experimental hematology & oncology · 2025
    Review
  14. FOLR2Cell communication and signaling : CCS · 2025
    Review
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27 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

10 authors at 5 institutions in 2 countries.

Daniel Hargbøl MadsenProteases and Tissue Remodeling Section , Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA; Center for Cancer Immune Therapy, Department of Haematology, Copenhagen University Hospital, 2730 Herlev, Denmark; Department of Oncology, Copenhagen University Hospital, 2730 Herlev, Denmark; The Finsen Laboratory, Rigshospitalet/Biotech Research and Innovation Centre (BRIC), University of Copenhagen, 2200 Copenhagen, Denmark. Electronic address: daniel.hargboel.madsen@regionh.dk.
Henrik Jessen JürgensenProteases and Tissue Remodeling Section , Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA; The Finsen Laboratory, Rigshospitalet/Biotech Research and Innovation Centre (BRIC), University of Copenhagen, 2200 Copenhagen, Denmark.
Majken Storm SiersbækDepartment of Biochemistry and Molecular Biology, University of Southern Denmark, 5230 Odense, Denmark.
Dorota Ewa KuczekCenter for Cancer Immune Therapy, Department of Haematology, Copenhagen University Hospital, 2730 Herlev, Denmark.
Loretta Grey CloudProteases and Tissue Remodeling Section , Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.
Shihui LiuProteases and Tissue Remodeling Section , Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.
Niels BehrendtThe Finsen Laboratory, Rigshospitalet/Biotech Research and Innovation Centre (BRIC), University of Copenhagen, 2200 Copenhagen, Denmark.
Lars GrøntvedDepartment of Biochemistry and Molecular Biology, University of Southern Denmark, 5230 Odense, Denmark.
Roberto WeigertIntracellular Membrane Trafficking Unit , Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA; Laboratory of Cellular and Molecular Biology, CCR, National Cancer Research Bethesda, MD 20892, USA.
Thomas Henrik BuggeProteases and Tissue Remodeling Section , Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: thomas.bugge@nih.gov.
National Institutes of Health · USUniversity of Southern Denmark · DKCopenhagen University Hospital · DKNational Institute of Dental and Craniofacial Research · USRigshospitalet · DK

Funding

Cell surface serine proteases in development, tissue repair, and malignancyZIADE000699 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI BUGGE, THOMAS H · 2009 to 2025
$34.1M
Molecular mechanisms of membrane remodelingZIABC011682 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WEIGERT, ROBERTO · 2016 to 2025
$17.5M
Serine Proteases In Remodeling Of The Extracellular MatrZ01DE000699 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI BUGGE, THOMAS H · 2000 to 2008
$3.2M
Intramural NIH HHS Z01 DE000699
6 · The paper itself

Abstract

Physiologic turnover of interstitial collagen is mediated by a sequential pathway in which collagen is fragmented by pericellular collagenases, endocytosed by collagen receptors, and routed to lysosomes for degradation by cathepsins. Here, we use intravital microscopy to investigate if malignant tumors, which are characterized by high rates of extracellular matrix turnover, utilize a similar collagen degradation pathway. Tumors of epithelial, mesenchymal, or neural crest origin all display vigorous endocytic collagen degradation. The cells engaged in this process are identified as tumor-associated macrophage (TAM)-like cells that degrade collagen in a mannose receptor-dependent manner. Accordingly, mannose-receptor-deficient mice display increased intratumoral collagen. Whole-transcriptome profiling uncovers a distinct extracellular matrix-catabolic signature of these collagen-degrading TAMs. Lineage-ablation studies reveal that collagen-degrading TAMs originate from circulating CCR2+ monocytes. This study identifies a function of TAMs in altering the tumor microenvironment through endocytic collagen turnover and establishes macrophages as centrally engaged in tumor-associated collagen degradation.

Indexed as

Cell MovementEndocytosisProteolysisAnimalsCell PolarityCollagenExtracellular MatrixInflammationLectins, C-TypeMacrophagesMannose-Binding LectinsMannose ReceptorMice, Inbred C57BLMonocytesNeoplasmsRatsCollagenLectins, C-TypeMannose-Binding LectinsMannose ReceptorReceptors, CCR2Receptors, Cell Surfacecancer invasioncathepsinsCCR2-derived TAMscollagenasescollagen endocytosisendocytic matrix turnoverextracellular matrix remodelingM2-polarized macrophagestumor-associated macrophagestumor microenvironment

Identifiers

PMID29281816
PMCPMC5753792
OpenAlexW2779884587

What OpenQuestion holds

Textmetadata
LicenceTDM
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.