Evidence map›Paper›PMID 24843010›Full record

ArticleeLife2014

Epidermal barrier defects link atopic dermatitis with altered skin cancer susceptibility.

Sara Cipolat, Esther Hoste, Ken Natsuga, Sven R Quist, Fiona M Watt

Open access · goldAbstract read
In one paragraph

Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
6.8field-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

37 citing papers in PubMed, 60 citations in OpenAlex.

  1. Trial
  2. Psoriasis-like disease prevents squamous skin tumor development by neutrophil-driven inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Caspase-8-dependent autophagy regulates neutrophil infiltration in oral squamous cell carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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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

5 authors at 3 institutions in 3 countries.

Sara CipolatCentre for Stem Cells and Regenerative Medicine, King's College London, London, United Kingdom Cancer Research UK Cambridge Research Institute, Cambridge, United Kingdom.
Esther HosteCentre for Stem Cells and Regenerative Medicine, King's College London, London, United Kingdom Cancer Research UK Cambridge Research Institute, Cambridge, United Kingdom.
Ken NatsugaCancer Research UK Cambridge Research Institute, Cambridge, United Kingdom Department of Dermatology, Hokkaido University, Sapporo, Japan.
Sven R QuistCancer Research UK Cambridge Research Institute, Cambridge, United Kingdom Department of Dermatology and Venereology, Otto von Guericke University Magdeburg, Magdeburg, Germany.
Fiona M WattCentre for Stem Cells and Regenerative Medicine, King's College London, London, United Kingdom fiona.watt@kcl.ac.uk.
Cancer Research UK Cambridge Center · GBKing's College London · GBHokkaido University · JP

Funding

Medical Research CouncilWellcome Trust 096540
6 · The paper itself

Abstract

Atopic dermatitis can result from loss of structural proteins in the outermost epidermal layers, leading to a defective epidermal barrier. To test whether this influences tumour formation, we chemically induced tumours in EPI-/- mice, which lack three barrier proteins-Envoplakin, Periplakin, and Involucrin. EPI-/- mice were highly resistant to developing benign tumours when treated with 7,12-dimethylbenz(a)anthracene (DMBA) and 12-O-tetradecanoylphorbol-13-acetate (TPA). The DMBA response was normal, but EPI-/- skin exhibited an exaggerated atopic response to TPA, characterised by abnormal epidermal differentiation, a complex immune infiltrate and elevated serum thymic stromal lymphopoietin (TSLP). The exacerbated TPA response could be normalised by blocking TSLP or the immunoreceptor NKG2D but not CD4+ T cells. We conclude that atopy is protective against skin cancer in our experimental model and that the mechanism involves keratinocytes communicating with cells of the immune system via signalling elements that normally protect against environmental assaults.DOI: http://dx.doi.org/10.7554/eLife.01888.001.

Indexed as

9,10-Dimethyl-1,2-benzanthraceneAnimalsCarcinoma, Squamous CellCell CommunicationCell DifferentiationCell Transformation, NeoplasticCytokinesDermatitis, AtopicDisease Models, AnimalEpidermisKeratinocytesMembrane ProteinsMice, 129 StrainMice, Inbred BALB CMice, Inbred C57BLMice, Knockout9,10-Dimethyl-1,2-benzanthraceneCytokinesenvoplakininvolucrinKlrk1 protein, mouseMembrane ProteinsNK Cell Lectin-Like Receptor Subfamily KPlakinsPpl protein, mouseProtein PrecursorsTetradecanoylphorbol AcetateThymic Stromal LymphopoietinTSLP protein, mousecancereczemaskin

Identifiers

PMID24843010
PMCPMC4007207
OpenAlexW2153454205

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.