Evidence map›Paper›PMID 18688866›Full record

ArticleInternational journal of cancer2008

Human papillomavirus-16 and -18 in penile carcinomas: DNA methylation, chromosomal recombination and genomic variation.

Mina Kalantari, Luisa L Villa, Itzel E Calleja-Macias, Hans-Ulrich Bernard

Open access · greenAbstract readComparative Study
In one paragraph

Article in International journal of cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 61 citations in OpenAlex.

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  17. Epigenetic mechanisms in penile carcinoma.International journal of molecular sciences · 2013
    Review
  18. Article
  19. Human papillomavirus DNA methylation as a potential biomarker for cervical cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2012
    Review
  20. 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

4 authors at 2 institutions in 2 countries.

Mina KalantariDepartment of Molecular Biology and Biochemistry, University of California Irvine, Irvine, CA 92697, USA.
Luisa L Villa
Itzel E Calleja-Macias
Hans-Ulrich Bernard
University of California, Irvine · USInstituto Paulo Gontijo · BR

Funding

Control of Human Papillomavirus-16 TranscriptionR01CA091964 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI BERNARD, HANS-ULRICH ULRICH · 2002 to 2006
$1.6M
NCI NIH HHS R01 CA091964NCI NIH HHS R01 CA-91964
6 · The paper itself

Abstract

Penile carcinomas are frequently associated with high risk human papillomavirus (HPV) types. Because little is known about the molecular biology of this association, we investigated three properties of HPV genomes in penile carcinomas from Brazilian patients: (i) HPV DNA methylation, (ii) junctions between HPV and cellular DNA and (iii) genomic variation. In cervical carcinogenesis, recombination between HPV and chromosomal DNA is frequent and likely necessary for progression, and DNA hypermethylation-specifically of the L1 gene-is a biomarker for cancerous progression. The same mechanisms apparently occur during penile carcinogenesis, because 95 HPV-16 molecules derived from 19 penile lesions had 58% of the CpGs in L1 and 22% in the 5' part of the long control region methylated, more than the percentages found in cervical carcinomas. In addition, 2 out of 3 HPV-18 infections, all present in double infections with HPV-16, showed L1 specific methylation typical of malignant cervical lesions. In 11 out of 15 HPV-16 lesions, we confirmed chromosomal integration by reverse ligation inverted PCR, while 4 samples had concatemeric integrations or episomes. Nine of 17 penile carcinomas contained HPV-16 AA variants, and 8 E variants. As AA variants are relatively rare in Brazilian cohorts of asymptomatic women, the high prevalence in penile carcinomas may indicate a higher risk of progression of AA lesions, as suspected for cervical infections. Our observations of frequent viral DNA methylation, chromosomal integration and the prevalence of high risk variants suggest that HPV-dependent carcinogenesis of the penis and cervix follows similar etiological and epidemiological parameters.

Indexed as

Capsid ProteinsDNA MethylationDNA, ViralGenetic VariationGenome, ViralHuman papillomavirus 16Human papillomavirus 18HumansMaleOncogene Proteins, ViralPapillomavirus InfectionsPenile NeoplasmsPolymerase Chain ReactionPromoter Regions, GeneticRecombination, GeneticVirus IntegrationCapsid ProteinsDNA, ViralL1 protein, Human papillomavirus type 16Oncogene Proteins, Viral

Identifiers

PMID18688866
PMCPMC2750853
OpenAlexW2040918948

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.