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      EBV based cancer prevention and therapy in nasopharyngeal carcinoma

      , 1 , 2 , 3 , 4

      NPJ Precision Oncology

      Nature Publishing Group UK

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          Abstract

          Epstein–Barr virus is an important cancer causing virus. Nasopharyngeal carcinoma is an infection-related cancer strongly driven by Epstein–Barr virus. In this cancer model, we identified the major host targets of latent membrane protein 1 which is a driving oncogene encoded by Epstein–Barr virus in latency infection. latent membrane protein 1 activates several oncogenic signaling axes causing multiple malignant phenotypes and therapeutic resistance. Also, Epstein–Barr virus up-regulates DNA methyltransferase 1 and mediates onco-epigenetic effects in the carcinogenesis. The collaborating pathways activated by latent membrane protein 1 constructs an oncogenic signaling network, which makes latent membrane protein 1 an important potential target for effective treatment or preventive intervention. In Epstein–Barr virus lytic phase, the plasma level of Epstein–Barr virus DNA is considered as a distinguishing marker for nasopharyngeal carcinoma in subjects from healthy high-risk populations and is also a novel prognostic marker in Epstein–Barr virus-positive nasopharyngeal carcinoma. Now the early detection and screening of the lytic proteins and Epstein–Barr virus DNA have been applied to clinical and high-risk population. The knowledge generated regarding Epstein–Barr virus can be used in Epstein–Barr virus based precision cancer prevention and therapy in the near future.

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          Most cited references 64

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          Epstein-Barr virus: more than 50 years old and still providing surprises.

          It is more than 50 years since the Epstein-Barr virus (EBV), the first human tumour virus, was discovered. EBV has subsequently been found to be associated with a diverse range of tumours of both lymphoid and epithelial origin. Progress in the molecular analysis of EBV has revealed fundamental mechanisms of more general relevance to the oncogenic process. This Timeline article highlights key milestones in the 50-year history of EBV and discusses how this virus provides a paradigm for exploiting insights at the molecular level in the diagnosis, treatment and prevention of cancer.
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            Host shutoff during productive Epstein-Barr virus infection is mediated by BGLF5 and may contribute to immune evasion.

            Relatively little is known about immune evasion during the productive phase of infection by the gamma(1)-herpesvirus Epstein-Barr virus (EBV). The use of a unique system to isolate cells in lytic cycle allowed us to identify a host shutoff function operating in productively EBV-infected B cells. This impairment of protein synthesis results from mRNA degradation induced upon expression of the early lytic-cycle gene product BGLF5. Recently, a gamma(2)-herpesvirus, Kaposi sarcoma herpesvirus, has also been shown to encode a host shutoff function, indicating that host shutoff appears to be a general feature of gamma-herpesviruses. One of the consequences of host shutoff is a block in the synthesis of HLA class I and II molecules, reflected by reduced levels of these antigen-presenting complexes at the surface of cells in EBV lytic cycle. This effect could lead to escape from T cell recognition and elimination of EBV-producing cells, thereby allowing generation of viral progeny in the face of memory T cell responses.
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              Regulation of the latent-lytic switch in Epstein-Barr virus.

              Epstein-Barr virus (EBV) infection contributes to the development of several different types of human malignancy, including Burkitt lymphoma, Hodgkin lymphoma, and nasopharyngeal carcinoma. As a herpesvirus, EBV can establish latent or lytic infection in cells. EBV-positive tumors are composed almost exclusively of cells with latent EBV infection. Strategies for inducing the lytic form of EBV infection in tumor cells are being investigated as a potential therapy for EBV-positive tumors. In this article, we review how cellular and viral proteins regulate the latent-lytic EBV switch in infected B cells and epithelial cells, and discuss how harnessing lytic viral reactivation might be used therapeutically. Copyright © 2014 Elsevier Ltd. All rights reserved.
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                Author and article information

                Contributors
                ycao98@vip.sina.com
                Journal
                NPJ Precis Oncol
                NPJ Precis Oncol
                NPJ Precision Oncology
                Nature Publishing Group UK (London )
                2397-768X
                15 May 2017
                15 May 2017
                2017
                : 1
                : 1
                Affiliations
                [1 ]GRID grid.216417.7, Key Laboratory of Carcinogenesis and Invasion, Ministry of Education, Xiangya Hospital, , Central South University, ; Changsha, 410008 China
                [2 ]GRID grid.216417.7, Cancer Research Institute, Xiangya School of Medicine, , Central South University, ; Changsha, 410078 China
                [3 ]Key Laboratory of Carcinogenesis, Chinese Ministry of Health, Changsha, 410078 China
                [4 ]Research Center for Technologies of Nucleic Acid-Based Diagnostics and Therapeutics Hunan Province, Changsha, 410078 China
                Article
                18
                10.1038/s41698-017-0018-x
                5871899
                © The Author(s) 2017

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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