Evidence map›Paper›PMID 15542628›Full record

ArticleJournal of virology2004

Conserved methylation patterns of human papillomavirus type 16 DNA in asymptomatic infection and cervical neoplasia.

Mina Kalantari, Itzel E Calleja-Macias, Devansu Tewari, Bjørn Hagmar, Kathrine Lie, Hugo A Barrera-Saldana, Dorothy J Wiley, Hans-Ulrich Bernard

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

68 citing papers in PubMed, 180 citations in OpenAlex.

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  15. Methylation of High-Risk Human Papillomavirus Genomes Are Associated with Cervical Precancer in HIV-Positive Women.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018
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8 more citing papers are in PubMed but not listed here.

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

8 authors at 5 institutions in 4 countries.

Mina KalantariDepartment of Molecular Biology and Biochemistry, 114 Sprague Hall, University of California, Irvine, Irvine, CA 92697-3900, USA.
Itzel E Calleja-Macias
Devansu Tewari
Bjørn Hagmar
Kathrine Lie
Hugo A Barrera-Saldana
Dorothy J Wiley
Hans-Ulrich Bernard
University of California, Irvine · USNational Hospital · INNorwegian Cancer Society · NOUniversidad Autónoma de Nuevo León · MXUniversity of California, Los Angeles · US

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

DNA methylation contributes to the chromatin conformation that represses transcription of human papillomavirus type16 (HPV-16), which is prevalent in the etiology of cervical carcinoma. In an effort to clarify the role of this phenomenon in the regulation and carcinogenicity of HPV-16, 115 clinical samples were studied to establish the methylation patterns of the 19 CpG dinucleotides within the long control region and part of the L1 gene by bisulfite modification, PCR amplification, DNA cloning, and sequencing. We observed major heterogeneities between clones from different samples as well as between clones from individual samples. The methylation frequency of CpGs was measured at 14.5%. In addition, 0.21 and 0.23%, respectively, of the CpA and CpT sites, indicators of de novo methylation, were methylated. Methylation frequencies exceeded 30% in the CpGs overlapping with the L1 gene and were about 10% for most other positions. A CpG site located in the linker between two nucleosomes positioned over the enhancer and promoter of HPV-16 had minimal methylation. This region forms part of the HPV replication origin and is close to binding sites of master-regulators of transcription during epithelial differentiation. Methylation of most sites was highest in carcinomas, possibly due to tandem repetition and chromosomal integration of HPV-16 DNA. Methylation was lowest in dysplasia, likely reflecting the transcriptional activity in these infections. Our data document the efficient targeting of HPV genomes by the epithelial methylation machinery, possibly as a cellular defense mechanism, and suggest involvement of methylation in HPV oncogene expression and the early-late switch.

Indexed as

DNA MethylationCell Line, TumorCpG IslandsDNA, ViralFemaleGenome, ViralHumansPapillomaviridaePapillomavirus InfectionsUterine Cervical NeoplasmsDNA, Viral

Identifiers

PMID15542628
PMCPMC525027
OpenAlexW2131459766

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.