Evidence map›Paper›PMID 29642420›Full record

ReviewCancers2018

EBNA1: Oncogenic Activity, Immune Evasion and Biochemical Functions Provide Targets for Novel Therapeutic Strategies against Epstein-Barr Virus- Associated Cancers.

Joanna B Wilson, Evelyne Manet, Henri Gruffat, Pierre Busson, Marc Blondel, Robin Fahraeus

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
3.1field-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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

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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

6 authors at 4 institutions in 2 countries.

Joanna B WilsonSchool of Life Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK. joanna.wilson@glasgow.ac.uk.
Evelyne ManetCIRI, Centre International de Recherche en Infectiologie, Team Oncogenic Herpesviruses, Inserm, Université Claude Bernard Lyon 1, CNRS, ENS-Lyon, Université de Lyon, F-69007 Lyon, France. evelyne.manet@ens-lyon.fr.
Henri GruffatCIRI, Centre International de Recherche en Infectiologie, Team Oncogenic Herpesviruses, Inserm, Université Claude Bernard Lyon 1, CNRS, ENS-Lyon, Université de Lyon, F-69007 Lyon, France. henri.gruffat@ens-lyon.fr.ORCID 0000-0002-4735-6894
Pierre BussonCNRS, UMR 8126, Gustave Roussy, Université Paris Sud, Université Paris-Saclay, F-94805 Villejuif, France. pierre.busson@gustaveroussy.fr.
Marc BlondelUMR1078 "Génétique, Génomique Fonctionnelle et Biotechnologies", Inserm, Université de Brest, EFS, IBSAM, CHU, F-29200 Brest, France. marc.blondel@univ-brest.fr.ORCID 0000-0003-4897-2995
Robin FahraeusInserm UMR1162, Université Paris 7, Institut de Génétique Moléculaire, 27 rue Juliette Dodu, F-75010 Paris, France. robin.fahraeus@inserm.fr.
Inserm · FRUniversité Claude Bernard Lyon 1 · FRUniversité Paris-Sud · FRUniversity of Glasgow · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The presence of the Epstein-Barr virus (EBV)-encoded nuclear antigen-1 (EBNA1) protein in all EBV-carrying tumours constitutes a marker that distinguishes the virus-associated cancer cells from normal cells and thereby offers opportunities for targeted therapeutic intervention. EBNA1 is essential for viral genome maintenance and also for controlling viral gene expression and without EBNA1, the virus cannot persist. EBNA1 itself has been linked to cell transformation but the underlying mechanism of its oncogenic activity has been unclear. However, recent data are starting to shed light on its growth-promoting pathways, suggesting that targeting EBNA1 can have a direct growth suppressing effect. In order to carry out its tasks, EBNA1 interacts with cellular factors and these interactions are potential therapeutic targets, where the aim would be to cripple the virus and thereby rid the tumour cells of any oncogenic activity related to the virus. Another strategy to target EBNA1 is to interfere with its expression. Controlling the rate of EBNA1 synthesis is critical for the virus to maintain a sufficient level to support viral functions, while at the same time, restricting expression is equally important to prevent the immune system from detecting and destroying EBNA1-positive cells. To achieve this balance EBNA1 has evolved a unique repeat sequence of glycines and alanines that controls its own rate of mRNA translation. As the underlying molecular mechanisms for how this repeat suppresses its own rate of synthesis in

Indexed as

cancerdrug developmentEBNA1EBV

Identifiers

PMID29642420
PMCPMC5923364
OpenAlexW2795709906

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.