ReviewFrontiers in genetics2013
EBV finds a polycomb-mediated, epigenetic solution to the problem of oncogenic stress responses triggered by infection.
Review in Frontiers in genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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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.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Epstein-Barr virus-infected tonsillar marginal zone B cellsJournal of virology · 2025Article
- The Research Progress on Immortalization of Human B Cells.Microorganisms · 2023Review
- The Epstein-Barr virus noncoding RNA EBER2 transactivates the UCHL1 deubiquitinase to accelerate cell growth.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- DNA methylation enzymes and PRC1 restrict B-cell Epstein-Barr virus oncoprotein expression.Nature microbiology · 2020Article
- LTRs activated by Epstein-Barr virus-induced transformation of B cells alter the transcriptome.Genome research · 2018Article
- Epigenetic crossroads of the Epstein-Barr virus B-cell relationship.Current opinion in virology · 2018Review
- The Cooperative Functions of the EBNA3 Proteins Are Central to EBV Persistence and Latency.Pathogens (Basel, Switzerland) · 2018Review
- CRISPR-Cas9 Genetic Analysis of Virus-Host Interactions.Viruses · 2018Review
- EBV epigenetically suppresses the B cell-to-plasma cell differentiation pathway while establishing long-term latency.PLoS biology · 2017Article
- Article
- Core binding factor (CBF) is required for Epstein-Barr virus EBNA3 proteins to regulate target gene expression.Nucleic acids research · 2017Article
- Epigenetic Impact on EBV Associated B-Cell Lymphomagenesis.Biomolecules · 2016Review
- Key Characteristics of Carcinogens as a Basis for Organizing Data on Mechanisms of Carcinogenesis.Environmental health perspectives · 2016Article
- Epigenetics and Genetics of Viral Latency.Cell host & microbe · 2016Review
- Metabolic stress is a barrier to Epstein-Barr virus-mediated B-cell immortalization.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The role of the polycomb repressive complex pathway in T and NK cell lymphoma: biological and prognostic implications.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Epstein-Barr virus latency: current and future perspectives.Current opinion in virology · 2015Review
- Epstein-Barr Virus Proteins EBNA3A and EBNA3C Together Induce Expression of the Oncogenic MicroRNA Cluster miR-221/miR-222 and Ablate Expression of Its Target p57KIP2.PLoS pathogens · 2015Article
- Genome diversity of Epstein-Barr virus from multiple tumor types and normal infection.Journal of virology · 2015Article
- An epigenetic view of B-cell disorders.Immunology and cell biology · 2015Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Viruses that establish a persistent infection, involving intracellular latency, commonly stimulate cellular DNA synthesis and sometimes cell division early after infection. However, most cells of metazoans have evolved "fail-safe" responses that normally monitor unscheduled DNA synthesis and prevent cell proliferation when, for instance, cell proto-oncogenes are "activated" by mutation, amplification, or chromosomal rearrangements. These cell intrinsic defense mechanisms that reduce the risk of neoplasia and cancer are collectively called oncogenic stress responses (OSRs). Mechanisms include the activation of tumor suppressor genes and the so-called DNA damage response that together trigger pathways leading to cell cycle arrest (e.g., cell senescence) or complete elimination of cells (e.g., apoptosis). It is not surprising that viruses that can induce cellular DNA synthesis and cell division have the capacity to trigger OSR, nor is it surprising that these viruses have evolved countermeasures for inactivating or bypassing OSR. The main focus of this review is how the human tumor-associated Epstein-Barr virus manipulates the host polycomb group protein system to control - by epigenetic repression of transcription - key components of the OSR during the transformation of normal human B cells into permanent cell lines.
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Registered trials
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.