Evidence map›Paper›PMID 27343048›Full record

ArticleInternational journal of cancer2016

Genomic characterization of viral integration sites in HPV-related cancers.

Clara Bodelon, Michael E Untereiner, Mitchell J Machiela, Svetlana Vinokurova, Nicolas Wentzensen

Open access · greenAbstract read
In one paragraph

Article in International journal of cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 1 pooled it
6.7field-weighted citation impact, top 3% 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

95 citing papers in PubMed, 1 synthesis or guideline pooled it, 162 citations in OpenAlex.

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35 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

5 authors at 2 institutions in 2 countries.

Clara BodelonDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD.
Michael E UntereinerDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD.
Mitchell J MachielaDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD.
Svetlana VinokurovaLaboratory of Molecular Biology of Viruses, NN Blokhin Russian Cancer Research Center, Moscow, Russia.
Nicolas WentzensenDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD.
Division of Cancer Epidemiology and GeneticsRussian Cancer Research Center NN Blokhin · RU

Funding

Human papillomavirus (HPV) infection and cervical and anal cancersZIACP010124 · NCI · DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS · PI WENTZENSEN, NICOLAS · 2009 to 2025
$17.3M
Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

Persistent infection with carcinogenic human papillomaviruses (HPV) causes the majority of anogenital cancers and a subset of head and neck cancers. The HPV genome is frequently found integrated into the host genome of invasive cancers. The mechanisms of how it may promote disease progression are not well understood. Thoroughly characterizing integration events can provide insights into HPV carcinogenesis. Individual studies have reported limited number of integration sites in cell lines and human samples. We performed a systematic review of published integration sites in HPV-related cancers and conducted a pooled analysis to formally test for integration hotspots and genomic features enriched in integration events using data from the Encyclopedia of DNA Elements (ENCODE). Over 1,500 integration sites were reported in the literature, of which 90.8% (N = 1,407) were in human tissues. We found 10 cytobands enriched for integration events, three previously reported ones (3q28, 8q24.21 and 13q22.1) and seven additional ones (2q22.3, 3p14.2, 8q24.22, 14q24.1, 17p11.1, 17q23.1 and 17q23.2). Cervical infections with HPV18 were more likely to have breakpoints in 8q24.21 (p = 7.68 × 10(-4) ) than those with HPV16. Overall, integration sites were more likely to be in gene regions than expected by chance (p = 6.93 × 10(-9) ). They were also significantly closer to CpG regions, fragile sites, transcriptionally active regions and enhancers. Few integration events occurred within 50 Kb of known cervical cancer driver genes. This suggests that HPV integrates in accessible regions of the genome, preferentially genes and enhancers, which may affect the expression of target genes.

Indexed as

Virus IntegrationAlphapapillomavirusChromosome BreakpointsChromosome Fragile SitesCpG IslandsFemaleGenome, HumanHead and Neck NeoplasmsHumansMalePapillomavirus InfectionsProto-OncogenesUrogenital NeoplasmsHPVintegration

Identifiers

PMID27343048
PMCPMC6749823
OpenAlexW2473141600

What OpenQuestion holds

Textmetadata
LicenceTDM
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.