Evidence map›Paper›PMID 21123375›Full record

ArticleJournal of virology2011

Human papillomavirus type 16 (HPV-16) genomes integrated in head and neck cancers and in HPV-16-immortalized human keratinocyte clones express chimeric virus-cell mRNAs similar to those found in cervical cancers.

Michael J Lace, James R Anson, Jens P Klussmann, Dong Hong Wang, Elaine M Smith, Thomas H Haugen, Lubomir P Turek

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
3.8field-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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
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  13. Modelling human papillomavirus biology in oropharyngeal keratinocytes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019
    Review
  14. A Review of HPV-Related Head and Neck Cancer.Journal of clinical medicine · 2018
    Review
  15. Article
  16. Review
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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

7 authors at 2 institutions in 2 countries.

Michael J LaceDepartment of Pathology, University of Iowa Roy J and Lucille A Carver College ofMedicine, Veterans Affairs Medical Center, Iowa City, Iowa 52242, USA. michael-lace@uiowa.edu
James R Anson
Jens P Klussmann
Dong Hong Wang
Elaine M Smith
Thomas H Haugen
Lubomir P Turek
University of Iowa · USUniversity of Giessen · DE

Funding

Transcripitonal and Genetic Profiles in HNSCCsR01DE015944 · NIDCR · UNIVERSITY OF IOWA · PI SMITH, ELAINE M · 2004 to 2008
$1.5M
International Collaborative HNC ResearchR21DE017212 · NIDCR · UNIVERSITY OF IOWA · PI SMITH, ELAINE M · 2006 to 2007
$291k
NIDCR NIH HHS R01 DE015944NIDCR NIH HHS R21 DE017212
6 · The paper itself

Abstract

Many human papillomavirus (HPV)-positive high-grade lesions and cancers of the uterine cervix harbor integrated HPV genomes expressing the E6 and E7 oncogenes from chimeric virus-cell mRNAs, but less is known about HPV integration in head and neck cancer (HNC). Here we compared viral DNA status and E6-E7 mRNA sequences in HPV-16-positive HNC tumors to those in independent human keratinocyte cell clones derived from primary tonsillar or foreskin epithelia immortalized with HPV-16 genomes. Three of nine HNC tumors and epithelial clones containing unintegrated HPV-16 genomes expressed mRNAs spliced from HPV-16 SD880 to SA3358 and terminating at the viral early gene p(A) signal. In contrast, most integrated HPV genomes in six HNCs and a set of 31 keratinocyte clones expressed HPV-16 major early promoter (MEP)-initiated mRNAs spliced from viral SD880 directly to diverse cellular sequences, with a minority spliced to SA3358 followed by a cellular DNA junction. Sequence analysis of chimeric virus-cell mRNAs from HNC tumors and keratinocyte clones identified viral integration sites in a variety of chromosomes, with some located in or near growth control genes, including the c-myc protooncogene and the gene encoding FAP-1 phosphatase. Taken together, these findings support the hypothesis that HPV integration in cancers is a stochastic process resulting in clonal selection of aggressively expanding cells with altered gene expression of integrated HPV genomes and potential perturbations of cellular genes at or near viral integration sites. Furthermore, our results demonstrate that this selection also takes place and can be studied in primary human keratinocytes in culture.

Indexed as

Recombination, GeneticVirus IntegrationCells, CulturedCell Transformation, ViralClone CellsFemaleGenome, ViralHead and Neck NeoplasmsHuman papillomavirus 16HumansKeratinocytesMaleOncogene Proteins, ViralPapillomavirus E7 ProteinsRepressor ProteinsRNA, MessengerE6 protein, Human papillomavirus type 16oncogene protein E7, Human papillomavirus type 16Oncogene Proteins, ViralPapillomavirus E7 ProteinsRepressor ProteinsRNA, MessengerRNA, Viral

Identifiers

PMID21123375
PMCPMC3028875
OpenAlexW2040423351

What OpenQuestion holds

Textmetadata
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.