HPV8 Reverses the Transcriptional Output in Lrig1 Positive Cells to Drive Skin Tumorigenesis.

Adnan Shahzad Syed, Gian Paolo Marcuzzi, Daliborka Miller-Lazic, Jochen Hess, Martin Hufbauer, Baki Akgül

Open access · goldAbstract read

In one paragraph

Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing papers in PubMed

0.3field-weighted citation impact, top 44% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

Human Papillomavirus Carcinogenicity and the Need of New Perspectives: Thoughts from a Retrospective Analysis on Human Papillomavirus Outcomes Conducted at the Hospital University of Bari, Apulia, Italy, between 2011 and 2022.Diagnostics (Basel, Switzerland) · 2024
Article

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

6 authors at 2 institutions in 1 country.

Adnan Shahzad SyedFaculty of Medicine and University Hospital of Cologne, Institute of Virology, University of Cologne, Fürst-Pückler-Str. 56, 50935 Cologne, Germany.

Gian Paolo MarcuzziFaculty of Medicine and University Hospital of Cologne, Institute of Virology, University of Cologne, Fürst-Pückler-Str. 56, 50935 Cologne, Germany.

Daliborka Miller-LazicFaculty of Medicine and University Hospital of Cologne, Institute of Virology, University of Cologne, Fürst-Pückler-Str. 56, 50935 Cologne, Germany.

Jochen HessResearch Group Molecular Mechanisms of Head and Neck Tumors, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.ORCID 0000-0003-3493-1711

Martin HufbauerFaculty of Medicine and University Hospital of Cologne, Institute of Virology, University of Cologne, Fürst-Pückler-Str. 56, 50935 Cologne, Germany.ORCID 0000-0003-4106-0520

Baki AkgülFaculty of Medicine and University Hospital of Cologne, Institute of Virology, University of Cologne, Fürst-Pückler-Str. 56, 50935 Cologne, Germany.ORCID 0000-0002-6564-9412

University of Cologne · DEGerman Cancer Research Center · DE

Funding

Deutsche Forschungsgemeinschaft AK 42/7-1German Cancer Aid 70112727

6 · The paper itself

Abstract

K14-HPV8-CER transgenic mice express the complete early genome region of human papillomavirus type 8 (HPV8) and develop skin tumours attributed to the expansion of the Lrig1+ stem cell population. The correlation between HPV8-induced changes in transcriptional output in the stem cell compartment remains poorly understood. To further understand the oncogenic pathways underlying skin tumour formation we examined the gene expression network in skin tumours of K14-HPV8-CER mice and compared the differentially expressed genes (DEG) with those of the Lrig1-EGFP-ires-CreERT2 mice. Here, we report 397 DEGs in skin tumours of K14-HPV8-CER mice, of which 181 genes were up- and 216 were down-regulated. Gene ontology and KEGG pathway enrichment analyses suggest that the 397 DEGs are acting in signalling pathways known to be involved in skin homeostasis. Interestingly, we found that HPV8 early gene expression subverts the expression pattern of 23 cellular genes known to be expressed in Lrig1+ keratinocytes. Furthermore, we identified putative upstream regulating transcription factors as well as miRNAs in the control of these genes. These data provide strong evidence that HPV8 mediated transcriptional changes may contribute to skin tumorigenesis, offering new insights into the mechanism of HPV8 driven oncogenesis.

Indexed as

differentially regulated geneshuman papillomavirus type 8 (HPV8)skin tumour developmenttransgenic mouse models

Identifiers

PMID35406439

DOI10.3390/cancers14071662

PMCPMC8997052

OpenAlexW4220848595

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.