Evidence map›Paper›PMID 31221668›Full record

ArticleDisease models & mechanisms2019

Development of mouse models of angiosarcoma driven by p53.

Donald M Salter, Meredyth Griffin, Morwenna Muir, Katy Teo, Jayne Culley, James R Smith, Laura Gomez-Cuadrado, Kylie Matchett, Andrew H Sims, Larry Hayward and 2 more

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Donald M SalterCentre for Genomic & Experimental Medicine, Institute of Genetics & Molecular Medicine, University of Edinburgh, Crewe Road South, Edinburgh EH4 2XR, UK.
Meredyth GriffinEdinburgh Cancer Research UK Centre, Institute of Genetics & Molecular Medicine, University of Edinburgh, Crewe Road South, Edinburgh EH4 2XR, UK.
Morwenna MuirEdinburgh Cancer Research UK Centre, Institute of Genetics & Molecular Medicine, University of Edinburgh, Crewe Road South, Edinburgh EH4 2XR, UK.
Katy TeoEdinburgh Cancer Research UK Centre, Institute of Genetics & Molecular Medicine, University of Edinburgh, Crewe Road South, Edinburgh EH4 2XR, UK.
Jayne CulleyEdinburgh Cancer Research UK Centre, Institute of Genetics & Molecular Medicine, University of Edinburgh, Crewe Road South, Edinburgh EH4 2XR, UK.
James R SmithCentre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, Little France Crescent, Edinburgh EH16 4TJ, UK.
Laura Gomez-CuadradoEdinburgh Cancer Research UK Centre, Institute of Genetics & Molecular Medicine, University of Edinburgh, Crewe Road South, Edinburgh EH4 2XR, UK.
Kylie MatchettCentre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, Little France Crescent, Edinburgh EH16 4TJ, UK.
Andrew H SimsEdinburgh Cancer Research UK Centre, Institute of Genetics & Molecular Medicine, University of Edinburgh, Crewe Road South, Edinburgh EH4 2XR, UK.
Larry HaywardEdinburgh Cancer Research UK Centre, Institute of Genetics & Molecular Medicine, University of Edinburgh, Crewe Road South, Edinburgh EH4 2XR, UK.
Neil C HendersonCentre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, Little France Crescent, Edinburgh EH16 4TJ, UK.
Valerie G BruntonEdinburgh Cancer Research UK Centre, Institute of Genetics & Molecular Medicine, University of Edinburgh, Crewe Road South, Edinburgh EH4 2XR, UK v.brunton@ed.ac.uk.ORCID 0000-0002-7778-8794
Edinburgh Cancer Research · GBCentre for Inflammation Research · GB

Funding

Cancer Research UK 15703Cancer Research UK C157/A15703Cancer Research UK C157/A9148Cancer Research UK C6088/A12063Wellcome Trust 103749
6 · The paper itself

Abstract

Angiosarcomas are a rare group of tumours which have poor prognosis and limited treatment options. The development of new therapies has been hampered by a lack of good preclinical models. Here, we describe the development of an autochthonous mouse model of angiosarcoma driven by loss of p53 in VE-cadherin-expressing endothelial cells. Using

Indexed as

Disease Models, AnimalAnimalsAntigens, CDCadherin 5CadherinsCell DifferentiationEndothelial CellsHemangiosarcomaIntegrasesMiceReceptor, Platelet-Derived Growth Factor betaRecombination, GeneticTumor Suppressor Protein p53Antigens, CDCadherin 5CadherinsCre recombinaseIntegrasesReceptor, Platelet-Derived Growth Factor betaTrp53 protein, mouseTumor Suppressor Protein p53AngiosarcomaGenetically engineered mouse modelLymphomasTrp53Tumour

Identifiers

PMID31221668
PMCPMC6679377
OpenAlexW2952458507

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.