Evidence map›Paper›PMID 27877083›Full record

ReviewInternational journal of biological sciences2016

Epstein-Barr virus lytic reactivation regulation and its pathogenic role in carcinogenesis.

Hongde Li, Sufang Liu, Jianmin Hu, Xiangjian Luo, Namei Li, Ann M Bode, Ya Cao

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of biological sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
–field-weighted citation impact
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

89 citing papers in PubMed.

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  12. Dihydrotestosterone-androgen receptor signaling suppresses EBV-positive gastric cancer through DNA demethylation-mediated viral reactivation.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2025
    Article
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29 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

7 authors.

Hongde LiKey Laboratory of Carcinogenesis and Invasion, Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha 410078, China; Cancer Research Institute, Xiangya School of Medicine, Central South University, Changsha 410078, China; Key Laboratory of Carcinogenesis, Chinese Ministry of Health, Changsha 410078, China.
Sufang LiuDivision of Hematology, Institute of Molecular Hematology, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Jianmin HuKey Laboratory of Carcinogenesis and Invasion, Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha 410078, China; Cancer Research Institute, Xiangya School of Medicine, Central South University, Changsha 410078, China; Key Laboratory of Carcinogenesis, Chinese Ministry of Health, Changsha 410078, China.
Xiangjian LuoKey Laboratory of Carcinogenesis and Invasion, Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha 410078, China; Cancer Research Institute, Xiangya School of Medicine, Central South University, Changsha 410078, China; Key Laboratory of Carcinogenesis, Chinese Ministry of Health, Changsha 410078, China.
Namei LiKey Laboratory of Carcinogenesis and Invasion, Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha 410078, China; Cancer Research Institute, Xiangya School of Medicine, Central South University, Changsha 410078, China; Key Laboratory of Carcinogenesis, Chinese Ministry of Health, Changsha 410078, China.
Ann M BodeThe Hormel Institute, University of Minnesota, Austin, MN 55912, USA.
Ya CaoKey Laboratory of Carcinogenesis and Invasion, Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha 410078, China; Cancer Research Institute, Xiangya School of Medicine, Central South University, Changsha 410078, China; Key Laboratory of Carcinogenesis, Chinese Ministry of Health, Changsha 410078, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epstein-Barr virus (EBV) has been associated with several types of human cancers. In the host, EBV can establish two alternative modes of life cycle, known as latent or lytic and the switch from latency to the lytic cycle is known as EBV reactivation. Although EBV in cancer cells is found mostly in latency, a small number of lytically-infected cells promote carcinogenesis through the release of growth factors and oncogenic cytokines. This review focuses on the mechanisms by which EBV reactivation is controlled by cellular and viral factors, and discusses how EBV lytic infection contributes to human malignancies.

Indexed as

AnimalsCarcinogenesisDNA MethylationEpigenesis, GeneticEpstein-Barr Virus InfectionsHerpesvirus 4, HumanHumansImmediate-Early ProteinsOxidative StressSignal TransductionTrans-ActivatorsBZLF1 protein, Herpesvirus 4, HumanIE2 protein, bovine herpesvirus type 4Immediate-Early ProteinsTrans-ActivatorscarcinogenesisEpstein-Barr viruslatencyreactivationRtaZta

Identifiers

PMID27877083
PMCPMC5118777

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.