The Microenvironment in Epstein–Barr Virus-Associated Malignancies

The Epstein–Barr virus (EBV) can cause a wide variety of cancers upon infection of different cell types and induces a highly variable composition of the tumor microenvironment (TME). This TME consists of both innate and adaptive immune cells and is not merely an aspecific reaction to the t...

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Main Authors: Geok Wee Tan, Lydia Visser, Lu Ping Tan, Anke van den Berg, Arjan Diepstra
Format: Article
Language:English
Published: MDPI AG 2018-04-01
Series:Pathogens
Subjects:
Online Access:http://www.mdpi.com/2076-0817/7/2/40
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spelling doaj-f835057de35543a5b2d17ac7c3169b432020-11-24T21:20:52ZengMDPI AGPathogens2076-08172018-04-01724010.3390/pathogens7020040pathogens7020040The Microenvironment in Epstein–Barr Virus-Associated MalignanciesGeok Wee Tan0Lydia Visser1Lu Ping Tan2Anke van den Berg3Arjan Diepstra4Molecular Pathology Unit, Cancer Research Centre, Institute for Medical Research, Jalan Pahang, 50588 Kuala Lumpur, MalaysiaDepartment of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, code EA10, P.O. Box 30.001, 9700 RB Groningen, The NetherlandsMolecular Pathology Unit, Cancer Research Centre, Institute for Medical Research, Jalan Pahang, 50588 Kuala Lumpur, MalaysiaDepartment of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, code EA10, P.O. Box 30.001, 9700 RB Groningen, The NetherlandsDepartment of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, code EA10, P.O. Box 30.001, 9700 RB Groningen, The NetherlandsThe Epstein–Barr virus (EBV) can cause a wide variety of cancers upon infection of different cell types and induces a highly variable composition of the tumor microenvironment (TME). This TME consists of both innate and adaptive immune cells and is not merely an aspecific reaction to the tumor cells. In fact, latent EBV-infected tumor cells utilize several specific mechanisms to form and shape the TME to their own benefit. These mechanisms have been studied largely in the context of EBV+ Hodgkin lymphoma, undifferentiated nasopharyngeal carcinoma, and EBV+ gastric cancer. This review describes the composition, immune escape mechanisms, and tumor cell promoting properties of the TME in these three malignancies. Mechanisms of susceptibility which regularly involve genes related to immune system function are also discussed, as only a small proportion of EBV-infected individuals develops an EBV-associated malignancy.http://www.mdpi.com/2076-0817/7/2/40Epstein-Barr virustumor microenvironmentHodgkin lymphomaundifferentiated nasopharyngeal carcinomagastric carcinomaimmune escapesusceptibility
collection DOAJ
language English
format Article
sources DOAJ
author Geok Wee Tan
Lydia Visser
Lu Ping Tan
Anke van den Berg
Arjan Diepstra
spellingShingle Geok Wee Tan
Lydia Visser
Lu Ping Tan
Anke van den Berg
Arjan Diepstra
The Microenvironment in Epstein–Barr Virus-Associated Malignancies
Pathogens
Epstein-Barr virus
tumor microenvironment
Hodgkin lymphoma
undifferentiated nasopharyngeal carcinoma
gastric carcinoma
immune escape
susceptibility
author_facet Geok Wee Tan
Lydia Visser
Lu Ping Tan
Anke van den Berg
Arjan Diepstra
author_sort Geok Wee Tan
title The Microenvironment in Epstein–Barr Virus-Associated Malignancies
title_short The Microenvironment in Epstein–Barr Virus-Associated Malignancies
title_full The Microenvironment in Epstein–Barr Virus-Associated Malignancies
title_fullStr The Microenvironment in Epstein–Barr Virus-Associated Malignancies
title_full_unstemmed The Microenvironment in Epstein–Barr Virus-Associated Malignancies
title_sort microenvironment in epstein–barr virus-associated malignancies
publisher MDPI AG
series Pathogens
issn 2076-0817
publishDate 2018-04-01
description The Epstein–Barr virus (EBV) can cause a wide variety of cancers upon infection of different cell types and induces a highly variable composition of the tumor microenvironment (TME). This TME consists of both innate and adaptive immune cells and is not merely an aspecific reaction to the tumor cells. In fact, latent EBV-infected tumor cells utilize several specific mechanisms to form and shape the TME to their own benefit. These mechanisms have been studied largely in the context of EBV+ Hodgkin lymphoma, undifferentiated nasopharyngeal carcinoma, and EBV+ gastric cancer. This review describes the composition, immune escape mechanisms, and tumor cell promoting properties of the TME in these three malignancies. Mechanisms of susceptibility which regularly involve genes related to immune system function are also discussed, as only a small proportion of EBV-infected individuals develops an EBV-associated malignancy.
topic Epstein-Barr virus
tumor microenvironment
Hodgkin lymphoma
undifferentiated nasopharyngeal carcinoma
gastric carcinoma
immune escape
susceptibility
url http://www.mdpi.com/2076-0817/7/2/40
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