Evidence map›Paper›PMID 32641866›Full record

ArticleBritish journal of cancer2020

Cancer-associated fibroblasts mediate cancer progression and remodel the tumouroid stroma.

Judith Pape, Tarig Magdeldin, Katerina Stamati, Agata Nyga, Marilena Loizidou, Mark Emberton, Umber Cheema

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
5.2field-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

60 citing papers in PubMed, 100 citations in OpenAlex.

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  9. Cells · 2025
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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.

Judith PapeInstitute of Orthopaedics and Musculoskeletal Sciences, Division of Surgery and Interventional Science, University College London, Stanmore Campus, Brockley Hill, HA7 4LP, London, UK.
Tarig MagdeldinInstitute of Orthopaedics and Musculoskeletal Sciences, Division of Surgery and Interventional Science, University College London, Stanmore Campus, Brockley Hill, HA7 4LP, London, UK.
Katerina StamatiResearch Department of Surgical Biotechnology, Division of Surgery and Interventional Sciences, University College London, Royal Free Hospital Campus, Pond Street, NW3 2QG, London, UK.
Agata NygaResearch Department of Surgical Biotechnology, Division of Surgery and Interventional Sciences, University College London, Royal Free Hospital Campus, Pond Street, NW3 2QG, London, UK.
Marilena LoizidouResearch Department of Surgical Biotechnology, Division of Surgery and Interventional Sciences, University College London, Royal Free Hospital Campus, Pond Street, NW3 2QG, London, UK.
Mark EmbertonFaculty of Medical Sciences, University College London, Bloomsbury Campus Maple House, 149 Tottenham Court Road, W1T 7NF, London, UK.
Umber CheemaInstitute of Orthopaedics and Musculoskeletal Sciences, Division of Surgery and Interventional Science, University College London, Stanmore Campus, Brockley Hill, HA7 4LP, London, UK. u.cheema@ucl.ac.uk.
University College London · GBThe Royal Free Hospital · GB

Funding

Department of Health II-LA-0813-20002
6 · The paper itself

Abstract

backgroundCancer-associated fibroblasts (CAFs) are highly differentiated and heterogeneous cancer-stromal cells that promote tumour growth, angiogenesis and matrix remodelling.

methodsWe utilised an adapted version of a previously developed 3D in vitro model of colorectal cancer, composed of a cancer mass and the surrounding stromal compartment. We compared cancer invasion with an acellular stromal surround, a "healthy" or normal cellular stroma and a cancerous stroma. For the cancerous stroma, we incorporated six patient-derived CAF samples to study their differential effects on cancer growth, vascular network formation and remodelling.

resultsCAFs enhanced the distance and surface area of the invasive cancer mass whilst inhibiting vascular-like network formation. These processes correlated with the upregulation of hepatocyte growth factor (HGF), metallopeptidase inhibitor 1 (TIMP1) and fibulin-5 (FBLN5). Vascular remodelling of previously formed endothelial structures occurred through the disruption of complex networks, and was associated with the upregulation of vascular endothelial growth factor (VEGFA) and downregulation in vascular endothelial cadherin (VE-Cadherin).

conclusionsThese results support, within a biomimetic 3D, in vitro framework, the direct role of CAFs in promoting cancer invasion, and their key function in driving vasculogenesis and angiogenesis.

Indexed as

Cancer-Associated FibroblastsCell Line, TumorColorectal NeoplasmsDisease ProgressionHumansNeoplasm InvasivenessStromal CellsVascular Endothelial Growth Factor AVascular RemodelingVascular Endothelial Growth Factor A

Identifiers

PMID32641866
PMCPMC7524802
OpenAlexW3042047307

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.