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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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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