Evidence map›Paper›PMID 27923803›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2017

Whole-Exome Sequencing Validates a Preclinical Mouse Model for the Prevention and Treatment of Cutaneous Squamous Cell Carcinoma.

Elena V Knatko, Brandon Praslicka, Maureen Higgins, Alan Evans, Karin J Purdie, Catherine A Harwood, Charlotte M Proby, Aikseng Ooi, Albena T Dinkova-Kostova

Open access · bronzeAbstract readComparative StudyValidation Study
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

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  2. International journal of molecular sciences · 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

9 authors at 1 institution in 1 country.

Elena V Knatko *Division of Cancer Research, School of Medicine, University of Dundee, Scotland, United Kingdom.
Brandon Praslicka *Department of Toxicology and Pharmacology, College of Pharmacy, University of Arizona. Tucson, Arizona, USA.
Maureen HigginsDivision of Cancer Research, School of Medicine, University of Dundee, Scotland, United Kingdom.
Alan EvansDepartment of Pathology, Ninewells Hospital and Medical School, Dundee, Scotland, United Kingdom.
Karin J PurdieCentre for Cutaneous Research, Barts and the London Queen Mary University of London, London, United Kingdom.
Catherine A HarwoodCentre for Cutaneous Research, Barts and the London Queen Mary University of London, London, United Kingdom.
Charlotte M ProbyDivision of Cancer Research, School of Medicine, University of Dundee, Scotland, United Kingdom.
Aikseng OoiDepartment of Toxicology and Pharmacology, College of Pharmacy, University of Arizona. Tucson, Arizona, USA.
Albena T Dinkova-KostovaDivision of Cancer Research, School of Medicine, University of Dundee, Scotland, United Kingdom.
Johns Hopkins University · US

Funding

Cancer Research UK 10270Cancer Research UK 18644
6 · The paper itself

Abstract

Cutaneous squamous cell carcinomas (cSCC) are among the most common and highly mutated human malignancies. Solar UV radiation is the major factor in the etiology of cSCC. Whole-exome sequencing of 18 microdissected tumor samples (cases) derived from SKH-1 hairless mice that had been chronically exposed to solar-simulated UV (SSUV) radiation showed a median point mutation (SNP) rate of 155 per Mb. The majority (78.6%) of the SNPs are C.G>T.A transitions, a characteristic UVR-induced mutational signature. Direct comparison with human cSCC cases showed high overlap in terms of both frequency and type of SNP mutations. Mutations in Trp53 were detected in 15 of 18 (83%) cases, with 20 of 21 SNP mutations located in the protein DNA-binding domain. Strikingly, multiple nonsynonymous SNP mutations in genes encoding Notch family members (Notch1-4) were present in 10 of 18 (55%) cases. The histopathologic spectrum of the mouse cSCC that develops in this model resembles very closely the spectrum of human cSCC. We conclude that the mouse SSUV cSCCs accurately represent the histopathologic and mutational spectra of the most prevalent tumor suppressors of human cSCC, validating the use of this preclinical model for the prevention and treatment of human cSCC. Cancer Prev Res; 10(1); 67-75. ©2016 AACR.

Indexed as

AnimalsCarcinogenesisCarcinoma, Squamous CellDNA Mutational AnalysisExomeFemaleHumansMiceMice, HairlessNeoplasms, ExperimentalPoint MutationPolymorphism, Single NucleotideProtein DomainsReceptors, NotchSkin NeoplasmsTumor Suppressor Protein p53Receptors, NotchTumor Suppressor Protein p53

Identifiers

PMID27923803
PMCPMC5408961
OpenAlexW2559955417

What OpenQuestion holds

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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.