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Epigenetic Impact on EBV Associated B-Cell Lymphomagenesis

Epigenetic modifications leading to either transcriptional repression or activation, play an indispensable role in the development of human cancers. Epidemiological study revealed that approximately 20% of all human cancers are associated with tumor viruses. Epstein-Barr virus (EBV), the first human...

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Detalles Bibliográficos
Autores principales: Ghosh Roy, Shatadru, Robertson, Erle S., Saha, Abhik
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5197956/
https://www.ncbi.nlm.nih.gov/pubmed/27886133
http://dx.doi.org/10.3390/biom6040046
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author Ghosh Roy, Shatadru
Robertson, Erle S.
Saha, Abhik
author_facet Ghosh Roy, Shatadru
Robertson, Erle S.
Saha, Abhik
author_sort Ghosh Roy, Shatadru
collection PubMed
description Epigenetic modifications leading to either transcriptional repression or activation, play an indispensable role in the development of human cancers. Epidemiological study revealed that approximately 20% of all human cancers are associated with tumor viruses. Epstein-Barr virus (EBV), the first human tumor virus, demonstrates frequent epigenetic alterations on both viral and host genomes in associated cancers—both of epithelial and lymphoid origin. The cell type-dependent different EBV latent gene expression patterns appear to be determined by the cellular epigenetic machinery and similarly viral oncoproteins recruit epigenetic regulators in order to deregulate the cellular gene expression profile resulting in several human cancers. This review elucidates the epigenetic consequences of EBV–host interactions during development of multiple EBV-induced B-cell lymphomas, which may lead to the discovery of novel therapeutic interventions against EBV-associated B-cell lymphomas by alteration of reversible patho-epigenetic markings.
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spelling pubmed-51979562017-01-04 Epigenetic Impact on EBV Associated B-Cell Lymphomagenesis Ghosh Roy, Shatadru Robertson, Erle S. Saha, Abhik Biomolecules Review Epigenetic modifications leading to either transcriptional repression or activation, play an indispensable role in the development of human cancers. Epidemiological study revealed that approximately 20% of all human cancers are associated with tumor viruses. Epstein-Barr virus (EBV), the first human tumor virus, demonstrates frequent epigenetic alterations on both viral and host genomes in associated cancers—both of epithelial and lymphoid origin. The cell type-dependent different EBV latent gene expression patterns appear to be determined by the cellular epigenetic machinery and similarly viral oncoproteins recruit epigenetic regulators in order to deregulate the cellular gene expression profile resulting in several human cancers. This review elucidates the epigenetic consequences of EBV–host interactions during development of multiple EBV-induced B-cell lymphomas, which may lead to the discovery of novel therapeutic interventions against EBV-associated B-cell lymphomas by alteration of reversible patho-epigenetic markings. MDPI 2016-11-24 /pmc/articles/PMC5197956/ /pubmed/27886133 http://dx.doi.org/10.3390/biom6040046 Text en © 2016 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Ghosh Roy, Shatadru
Robertson, Erle S.
Saha, Abhik
Epigenetic Impact on EBV Associated B-Cell Lymphomagenesis
title Epigenetic Impact on EBV Associated B-Cell Lymphomagenesis
title_full Epigenetic Impact on EBV Associated B-Cell Lymphomagenesis
title_fullStr Epigenetic Impact on EBV Associated B-Cell Lymphomagenesis
title_full_unstemmed Epigenetic Impact on EBV Associated B-Cell Lymphomagenesis
title_short Epigenetic Impact on EBV Associated B-Cell Lymphomagenesis
title_sort epigenetic impact on ebv associated b-cell lymphomagenesis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5197956/
https://www.ncbi.nlm.nih.gov/pubmed/27886133
http://dx.doi.org/10.3390/biom6040046
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