Evidence map›Paper›PMID 28595997›Full record

ArticleThe Journal of investigative dermatology2017

HPV8 Field Cancerization in a Transgenic Mouse Model Is due to Lrig1+ Keratinocyte Stem Cell Expansion.

Simone Lanfredini, Carlotta Olivero, Cinzia Borgogna, Federica Calati, Kathryn Powell, Kelli-Jo Davies, Marco De Andrea, Sarah Harries, Hiu Kwan Carolyn Tang, Herbert Pfister and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 26 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 2 countries.

Simone LanfrediniEuropean Cancer Stem Cell Research Institute, School of Biosciences, Cardiff University, Cardiff, UK.
Carlotta OliveroVirology Unit, Department of Translational Medicine, Novara Medical School, Novara, Italy.
Cinzia BorgognaVirology Unit, Department of Translational Medicine, Novara Medical School, Novara, Italy.
Federica CalatiVirology Unit, Department of Translational Medicine, Novara Medical School, Novara, Italy.
Kathryn PowellEuropean Cancer Stem Cell Research Institute, School of Biosciences, Cardiff University, Cardiff, UK.
Kelli-Jo DaviesEuropean Cancer Stem Cell Research Institute, School of Biosciences, Cardiff University, Cardiff, UK.
Marco De AndreaVirology Unit, Department of Translational Medicine, Novara Medical School, Novara, Italy; Viral Pathogenesis Unit, Department of Public Health and Pediatric Sciences, Turin Medical School, Turin, Italy.
Sarah HarriesEuropean Cancer Stem Cell Research Institute, School of Biosciences, Cardiff University, Cardiff, UK.
Hiu Kwan Carolyn TangEuropean Cancer Stem Cell Research Institute, School of Biosciences, Cardiff University, Cardiff, UK.
Herbert PfisterInstitute of Virology, University of Cologne, Cologne, Germany.
Marisa GariglioVirology Unit, Department of Translational Medicine, Novara Medical School, Novara, Italy.
Girish K PatelEuropean Cancer Stem Cell Research Institute, School of Biosciences, Cardiff University, Cardiff, UK. Electronic address: patelgk@cardiff.ac.uk.
Cardiff University · GBUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

β-Human papillomaviruses (HPVs) cause near ubiquitous latent skin infection within long-lived hair follicle (HF) keratinocyte stem cells. In patients with epidermodysplasia verruciformis, β-HPV viral replication is associated with skin keratosis and cutaneous squamous cell carcinoma. To determine the role of HF keratinocyte stem cells in β-HPV-induced skin carcinogenesis, we utilized a transgenic mouse model in which the keratin 14 promoter drives expression of the entire HPV8 early region (HPV8tg). HPV8tg mice developed thicker skin in comparison with wild-type littermates consistent with a hyperproliferative epidermis. HF keratinocyte proliferation was evident within the Lrig1+ keratinocyte stem cell population (69 vs. 55%, P < 0.01, n = 7), and not in the CD34+, LGR5+, and LGR6+ keratinocyte stem cell populations. This was associated with a 2.8-fold expansion in Lrig1+ keratinocytes and 3.8-fold increased colony-forming efficiency. Consistent with this, we observed nuclear p63 expression throughout this population and the HF infundibulum and adjoining interfollicular epidermis, associated with a switch from p63 transcriptional activation isoforms to ΔNp63 isoforms in HPV8tg skin. Epidermodysplasia verruciformis keratosis and in some cases actinic keratoses demonstrated similar histology associated with β-HPV reactivation and nuclear p63 expression within the HF infundibulum and perifollicular epidermis. These findings would suggest that β-HPV field cancerization arises from the HF junctional zone and predispose to squamous cell carcinoma.

Indexed as

Neoplasms, ExperimentalAnimalsCell ProliferationKeratinocytesKeratosis, ActinicMembrane GlycoproteinsMiceMice, TransgenicNeoplastic Stem CellsNerve Tissue ProteinsPapillomaviridaeSkin NeoplasmsLrig1 protein, mouseMembrane GlycoproteinsNerve Tissue Proteins

Identifiers

PMID28595997
PMCPMC5613749
OpenAlexW2623999651

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.