Evidence map›Paper›PMID 28190296›Full record

ReviewOral diseases2018

Epstein-Barr virus in the pathogenesis of oral cancers.

J T Guidry, C E Birdwell, R S Scott

Open access · bronzeAbstract readReview
In one paragraph

Review in Oral diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 3 pooled it
2.7field-weighted citation impact, top 8% 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

59 citing papers in PubMed, 3 syntheses or guidelines pooled it, 117 citations in OpenAlex.

  1. A Rare Synchronous Existence of Warthin's Tumour and Oral Cancer:Sultan Qaboos University medical journal · 2025
    Pooled it
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  19. Crosstalk Between Oral Microbiome and Cancer: Emerging Trends and Insights.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2025
    Article
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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

3 authors at 1 institution in 1 country.

J T GuidryDepartment of Microbiology and Immunology, Center for Tumor and Molecular Virology, and Feist-Weiller Cancer Center, Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA, USA.
C E BirdwellDepartment of Microbiology and Immunology, Center for Tumor and Molecular Virology, and Feist-Weiller Cancer Center, Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA, USA.
R S ScottDepartment of Microbiology and Immunology, Center for Tumor and Molecular Virology, and Feist-Weiller Cancer Center, Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA, USA.ORCID http://orcid.org/0000-0003-3840-9189
Louisiana State University Health Sciences Center Shreveport · US

Funding

COBRE Center for Molecular and Tumor VirologyP30GM110703 · NIGMS · LOUISIANA STATE UNIV HSC SHREVEPORT · PI SAPP, MARTIN · 2014 to 2018
$4.8M
Epigenetic Effects of Epstein-Barr Virus Infection in Oral Squamous Cell CarcinomaR01DE025565 · NIDCR · LOUISIANA STATE UNIV HSC SHREVEPORT · PI SCOTT, RONA S · 2015 to 2019
$1.8M
NIDCR NIH HHS R01 DE025565NIGMS NIH HHS P30 GM110703
6 · The paper itself

Abstract

Epstein-Barr virus (EBV) is a ubiquitous gamma-herpesvirus that establishes a lifelong persistent infection in the oral cavity and is intermittently shed in the saliva. EBV exhibits a biphasic life cycle, supported by its dual tropism for B lymphocytes and epithelial cells, which allows the virus to be transmitted within oral lymphoid tissues. While infection is often benign, EBV is associated with a number of lymphomas and carcinomas that arise in the oral cavity and at other anatomical sites. Incomplete association of EBV in cancer has questioned if EBV is merely a passenger or a driver of the tumorigenic process. However, the ability of EBV to immortalize B cells and its prevalence in a subset of cancers has implicated EBV as a carcinogenic cofactor in cellular contexts where the viral life cycle is altered. In many cases, EBV likely acts as an agent of tumor progression rather than tumor initiation, conferring malignant phenotypes observed in EBV-positive cancers. Given that the oral cavity serves as the main site of EBV residence and transmission, here we review the prevalence of EBV in oral malignancies and the mechanisms by which EBV acts as an agent of tumor progression.

Indexed as

Herpesvirus 4, HumanLife Cycle StagesCarcinoma, Squamous CellEpstein-Barr Virus InfectionsHumansLeukoplakia, HairyLymphomaMouth NeoplasmsSalivary Gland NeoplasmscarcinomaEpstein-Barr virus (EBV)lymphomatumor

Identifiers

PMID28190296
PMCPMC5554094
OpenAlexW2587457530

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.