Evidence map›Paper›PMID 18616681›Full record

ReviewCancer science2008

Epstein-Barr virus and gastric carcinoma: virus-host interactions leading to carcinoma.

Masashi Fukayama, Rumi Hino, Hiroshi Uozaki

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 3 pooled it
5.2field-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

77 citing papers in PubMed, 3 syntheses or guidelines pooled it, 175 citations in OpenAlex.

  1. Epstein-Barr Virus and Gastric Cancer Risk: A Meta-analysis With Meta-regression of Case-control Studies.Journal of preventive medicine and public health = Yebang Uihakhoe chi · 2016
    Pooled it
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  15. Viruses in colorectal cancer.Molecular oncology · 2022
    Review
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17 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

3 authors at 1 institution in 1 country.

Masashi FukayamaDepartment of Pathology and Diagnostic Pathology, Graduate School of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-0033, Japan. mfukayama-tky@umin.ac.jp
Rumi Hino
Hiroshi Uozaki
The University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epstein-Barr virus (EBV)-associated gastric carcinoma (GC) is a distinct subgroup of GC, comprising 10% of all cases of GC. EBV-associated carcinoma is the monoclonal growth of EBV-infected epithelial cells, and it represents a model of virus-host interactions leading to carcinoma. EBV-infected cells express several latent proteins (latency I program of viral latent gene expression) in EBV-associated GC. However, latent membrane protein 2A (LMP2A) up-regulates the cellular survivin gene through the NFkB pathway, conferring resistance to apoptotic stimuli on the neoplastic cells. EBV-associated GC also shows characteristic abnormality, that is, global and non-random CpG island methylation of the promoter region of many cancer-related genes. Since the viral genes are also regulated by promoter methylation in the infected cells, the DNA methylation mechanism specific to EBV-associated GC may be an exaggeration of the cellular mechanism, which is primarily for defense against foreign DNA. Production of several immunomodulator molecules, inducing tumor-infiltrating lymphocyte and macrophages, serves to form the characteristic histologic pattern in EBV-associated GC. The proposed sequence of events within the mucosa is as follows: EBV infection of certain gastric stem cells; expression of viral latent genes; abnormality of signal pathways caused by viral gene products; DNA methylation-mediated repression of tumor suppressor genes; and monoclonal growth of EBV-infected cells through interaction with other etiologic factors. Potentially useful therapeutic approaches to EBV-associated GC are those that utilize the virus-host interactions, such as bortezomib-induced and viral enzyme-targeted radiotherapy.

Indexed as

Gene Expression Regulation, ViralEpithelial CellsEpstein-Barr Virus InfectionsHerpesvirus 4, HumanHumansNF-kappaB-Inducing KinasePromoter Regions, GeneticProtein Serine-Threonine KinasesSignal TransductionStomach NeoplasmsNF-kappaB-Inducing KinaseProtein Serine-Threonine Kinases

Identifiers

PMID18616681
PMCPMC11158613
OpenAlexW2016870031

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.