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Cancers
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Epstein–Barr Virus (EBV) Associated Cancers
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Epstein–Barr Virus (EBV) Associated Cancers

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Infectious Agents and Cancer".

Deadline for manuscript submissions: 20 August 2024 | Viewed by 7311

Special Issue Editors

Dr. Mário Henrique Magalhães Barros

E-Mail Website
Guest Editor
Institute for Pathology, Klinikum Chemnitz, Flemmingstraße 2, 09116 Chemnitz, Germany
Interests: hematopathology; EBV-associated neoplasia; classical Hodgkin lymphoma
Dr. Paola A. Chabay

E-Mail Website
Guest Editor
Laboratory of Molecular Biology, Pathology Division, Multidisciplinary Institute for Investigation in Pediatric Pathologies (IMIPP-CONICET-GCBA), Ricardo Gutiérrez Children’s Hospital, Gallo 1330, Buenos Aires C1425EFD, Argentina
Interests: EBV-positive DLBCL lymphomas; plasmablastic lymphomas
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It has been almost 60 years since the initial discovery that the Epstein-Barr virus (EBV) could be related to the pathogenesis of Burkitt's lymphoma in sub-Saharan Africa. However, despite all this time, many questions related to the pathogenesis of EBV-associated neoplasms still remain unanswered.

The association of EBV with some neoplasms, in particular classical Hodgkin lymphoma, plasmablastic lymphoma, EBV-positive nodal NK/T-cell lymphoma and nasopharyngeal carcinoma, has been well described.

Although EBV infects more than 90% of the world's population, only a few individuals will develop a neoplasm associated with this virus. It is estimated that approximately 200,000 new cases of EBV-associated tumours are diagnosed globally each year, which has led the International Agency for Research on Cancer (IARC) to consider it as a  group 1 carcinogen.

This Special Issue welcomes original articles and reviews related to EBV-associated neoplasms, including but not limited to viral pathogenesis, tissue microenvironment modulation, molecular epidemiology, treatment and prognosis. Articles regarding EBV-associated lymphomas, nasopharyngeal carcinoma and gastric carcinoma are greatly appreciated.

We look forward to receiving your contributions.

Dr. Mário Henrique Magalhães Barros
Dr. Paola A. Chabay
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Epstein–Barr Virus (EBV)
  • cancers
  • lymphoma
  • nasopharyngeal carcinoma
  • gastric carcinoma

Published Papers (6 papers)

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Research

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19 pages, 4859 KiB  
Article
Activation of Epstein–Barr Virus’ Lytic Cycle in Nasopharyngeal Carcinoma Cells by NEO212, a Conjugate of Perillyl Alcohol and Temozolomide
by Hannah Hartman-Houstman, Steve Swenson, Radu O. Minea, Uttam K. Sinha, Ming-Fu Chiang, Thomas C. Chen and Axel H. Schönthal
Cancers 2024, 16(5), 936; https://doi.org/10.3390/cancers16050936 - 26 Feb 2024
Viewed by 870
Abstract
The Epstein–Barr virus (EBV) is accepted as a primary risk factor for certain nasopharyngeal carcinoma (NPC) subtypes, where the virus persists in a latent stage which is thought to contribute to tumorigenesis. Current treatments are sub-optimal, and recurrence occurs in many cases. An [...] Read more.
The Epstein–Barr virus (EBV) is accepted as a primary risk factor for certain nasopharyngeal carcinoma (NPC) subtypes, where the virus persists in a latent stage which is thought to contribute to tumorigenesis. Current treatments are sub-optimal, and recurrence occurs in many cases. An alternative therapeutic concept is aimed at triggering the lytic cycle of EBV selectively in tumor cells as a means to add clinical benefit. While compounds able to stimulate the lytic cascade have been identified, their clinical application so far has been limited. We are developing a novel anticancer molecule, NEO212, that was generated by covalent conjugation of the alkylating agent temozolomide (TMZ) to the naturally occurring monoterpene perillyl alcohol (POH). In the current study, we investigated its potential to trigger the lytic cycle of EBV in NPC cells in vitro and in vivo. We used the established C666.1 cell line and primary patient cells derived from the brain metastasis of a patient with NPC, both of which harbored latent EBV. Upon treatment with NEO212, there was an increase in EBV proteins Zta and Ea-D, key markers of the lytic cycle, along with increased levels of CCAAT/enhancer-binding protein homologous protein (CHOP), a marker of endoplasmic reticulum (ER) stress, followed by the activation of caspases. These effects could also be confirmed in tumor tissue from mice implanted with C666.1 cells. Towards a mechanistic understanding of these events, we used siRNA-mediated knockdown of CHOP and inclusion of anti-oxidant compounds. Both approaches blocked lytic cycle induction by NEO212. Therefore, we established a sequence of events, where NEO212 caused reactive oxygen species (ROS) production, which triggered ER stress and elevated the levels of CHOP, which was required to stimulate the lytic cascade of EBV. Inclusion of the antiviral agent ganciclovir synergistically enhanced the cytotoxic impact of NEO212, pointing to a potential combination treatment for EBV-positive cancers which should be explored further. Overall, our study establishes NEO212 as a novel agent able to stimulate EBV’s lytic cycle in NPC tumors, with implications for other virus-associated cancers. Full article
(This article belongs to the Special Issue Epstein–Barr Virus (EBV) Associated Cancers)
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31 pages, 8372 KiB  
Article
Could Immune Checkpoint Disorders and EBV Reactivation Be Connected in the Development of Hematological Malignancies in Immunodeficient Patients?
by Paulina Mertowska, Sebastian Mertowski, Konrad Smolak, Gabriela Kita, Katarzyna Guz, Aleksandra Kita, Marcin Pasiarski, Jolanta Smok-Kalwat, Stanisław Góźdź and Ewelina Grywalska
Cancers 2023, 15(19), 4786; https://doi.org/10.3390/cancers15194786 - 29 Sep 2023
Viewed by 1054
Abstract
Primary immunodeficiencies (PIDs) and secondary immunodeficiencies (SIDs) are characterized by compromised immune function, rendering individuals susceptible to infections and potentially influencing cancer development. Epstein–Barr virus (EBV), a widespread herpesvirus, has been linked to cancer, particularly in those with weakened immune systems. This study [...] Read more.
Primary immunodeficiencies (PIDs) and secondary immunodeficiencies (SIDs) are characterized by compromised immune function, rendering individuals susceptible to infections and potentially influencing cancer development. Epstein–Barr virus (EBV), a widespread herpesvirus, has been linked to cancer, particularly in those with weakened immune systems. This study aims to compare selected immune parameters, focusing on immune checkpoint molecules (PD-1/PD-L1, CTLA-4/CD86, CD200R/CD200), and EBV reactivation in patients with chronic lymphocytic leukemia (CLL, a representative of SIDs) and common variable immunodeficiency (CVID, a representative of PIDs). We performed a correlation analysis involving patients diagnosed with CLL, CVID, and a healthy control group. EBV reactivation was assessed using specific antibody serology and viral load quantification. Peripheral blood morphology, biochemistry, and immunophenotyping were performed, with emphasis on T and B lymphocytes expressing immune checkpoints and their serum concentrations. Our findings revealed elevated EBV reactivation markers in both CLL and CVID patients compared with healthy controls, indicating increased viral activity in immunodeficient individuals. Furthermore, immune checkpoint expression analysis demonstrated significantly altered percentages of T and B lymphocytes expressing PD-1/PD-L1, CTLA-4/CD86, and CD200R/CD200 in CLL and CVID patients. This suggests a potential interplay between immune checkpoint dysregulation and EBV reactivation in the context of immunodeficiency. In conclusion, our study underscores the intricate relationship between immune dysfunction, EBV reactivation, and immune checkpoint modulation in the context of immunodeficiency-associated cancers. The altered expression of immune checkpoints, along with heightened EBV reactivation, suggests a potential mechanism for immune evasion and tumor progression. These findings provide insights into the complex interactions that contribute to cancer development in immunocompromised individuals, shedding light on potential therapeutic targets for improved management and treatment outcomes. Further investigations are warranted to elucidate the underlying mechanisms and to explore potential interventions to mitigate cancer risk in these patient populations. Full article
(This article belongs to the Special Issue Epstein–Barr Virus (EBV) Associated Cancers)
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Review

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28 pages, 2428 KiB  
Review
Epigenetic Mechanisms in Latent Epstein-Barr Virus Infection and Associated Cancers
by Atharva S. Torne and Erle S. Robertson
Cancers 2024, 16(5), 991; https://doi.org/10.3390/cancers16050991 - 29 Feb 2024
Viewed by 1144
Abstract
The Epstein–Barr Virus (EBV) is a double-stranded DNA-based human tumor virus that was first isolated in 1964 from lymphoma biopsies. Since its initial discovery, EBV has been identified as a major contributor to numerous cancers and chronic autoimmune disorders. The virus is particularly [...] Read more.
The Epstein–Barr Virus (EBV) is a double-stranded DNA-based human tumor virus that was first isolated in 1964 from lymphoma biopsies. Since its initial discovery, EBV has been identified as a major contributor to numerous cancers and chronic autoimmune disorders. The virus is particularly efficient at infecting B-cells but can also infect epithelial cells, utilizing an array of epigenetic strategies to establish long-term latent infection. The association with histone modifications, alteration of DNA methylation patterns in host and viral genomes, and microRNA targeting of host cell factors are core epigenetic strategies that drive interactions between host and virus, which are necessary for viral persistence and progression of EBV-associated diseases. Therefore, understanding epigenetic regulation and its role in post-entry viral dynamics is an elusive area of EBV research. Here, we present current outlooks of EBV epigenetic regulation as it pertains to viral interactions with its host during latent infection and its propensity to induce tumorigenesis. We review the important epigenetic regulators of EBV latency and explore how the strategies involved during latent infection drive differential epigenetic profiles and host-virus interactions in EBV-associated cancers. Full article
(This article belongs to the Special Issue Epstein–Barr Virus (EBV) Associated Cancers)
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23 pages, 1738 KiB  
Review
Precision Medicine for Nasopharyngeal Cancer—A Review of Current Prognostic Strategies
by Luvita Suryani, Hazel P. Y. Lee, Wei Keat Teo, Zhi Kang Chin, Kwok Seng Loh and Joshua K. Tay
Cancers 2024, 16(5), 918; https://doi.org/10.3390/cancers16050918 - 24 Feb 2024
Viewed by 987
Abstract
Nasopharyngeal carcinoma (NPC) is an Epstein–Barr virus (EBV) driven malignancy arising from the nasopharyngeal epithelium. Current treatment strategies depend on the clinical stage of the disease, including the extent of the primary tumour, the extent of nodal disease, and the presence of distant [...] Read more.
Nasopharyngeal carcinoma (NPC) is an Epstein–Barr virus (EBV) driven malignancy arising from the nasopharyngeal epithelium. Current treatment strategies depend on the clinical stage of the disease, including the extent of the primary tumour, the extent of nodal disease, and the presence of distant metastasis. With the close association of EBV infection with NPC development, EBV biomarkers have shown promise in predicting treatment outcomes. Among the omic technologies, RNA and miRNA signatures have been widely studied, showing promising results in the research setting to predict treatment response. The transformation of radiology images into measurable features has facilitated the use of radiomics to generate predictive models for better prognostication and treatment selection. Nonetheless, much of this work remains in the research realm, and challenges remain in clinical implementation. Full article
(This article belongs to the Special Issue Epstein–Barr Virus (EBV) Associated Cancers)
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15 pages, 845 KiB  
Review
Modulation of Epstein-Barr-Virus (EBV)-Associated Cancers by Co-Infections
by Christian Münz
Cancers 2023, 15(24), 5739; https://doi.org/10.3390/cancers15245739 - 07 Dec 2023
Viewed by 1295
Abstract
The oncogenic and persistent Epstein Barr virus (EBV) is carried by more than 95% of the human adult population. While asymptomatic in most of these, EBV can cause a wide variety of malignancies of lymphoid or epithelial cell origin. Some of these are [...] Read more.
The oncogenic and persistent Epstein Barr virus (EBV) is carried by more than 95% of the human adult population. While asymptomatic in most of these, EBV can cause a wide variety of malignancies of lymphoid or epithelial cell origin. Some of these are also associated with co-infections that either increase EBV-induced tumorigenesis or weaken its immune control. The respective pathogens include Kaposi-sarcoma-associated herpesvirus (KSHV), Plasmodium falciparum and human immunodeficiency virus (HIV). In this review, I will discuss the respective tumor entities and possible mechanisms by which co-infections increase the EBV-associated cancer burden. A better understanding of the underlying mechanisms could allow us to identify crucial features of EBV-associated malignancies and defects in their immune control. These could then be explored to develop therapies against the respective cancers by targeting EBV and/or the respective co-infections with pathogen-specific therapies or vaccinations. Full article
(This article belongs to the Special Issue Epstein–Barr Virus (EBV) Associated Cancers)
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18 pages, 12444 KiB  
Review
A Clinicopathology Review and Update of Epstein–Barr Virus-Associated Mesenchymal Tumors
by Oswald Zhao Jian Lee, Noorjehan Omar, Joshua K. Tay and Victor Kwan Min Lee
Cancers 2023, 15(23), 5563; https://doi.org/10.3390/cancers15235563 - 24 Nov 2023
Viewed by 1454
Abstract
The Epstein–Barr virus (EBV) is associated with various tumor types, including nasopharyngeal carcinoma and lymphoproliferative disorders. While much is known about EBV-related epithelial and lymphoid tumors, there is a paucity of knowledge concerning EBV-associated mesenchymal tumors. This review aims to provide a comprehensive [...] Read more.
The Epstein–Barr virus (EBV) is associated with various tumor types, including nasopharyngeal carcinoma and lymphoproliferative disorders. While much is known about EBV-related epithelial and lymphoid tumors, there is a paucity of knowledge concerning EBV-associated mesenchymal tumors. This review aims to provide a comprehensive overview of EBV-associated mesenchymal tumors, encompassing their clinical features, pathological characteristics, pathophysiology, prognostic factors, and current treatment approaches. Through an extensive literature search using the PubMed database, we were able to identify three distinct EBV-associated mesenchymal tumors: EBV-associated smooth muscle tumors, inflammatory pseudotumor-like follicular dendritic cell sarcomas, and EBV-associated osteosarcomas. Although this review extensively explored the different aspects of these mesenchymal tumors, our comprehension of the underlying pathophysiology in this context is still incomplete. Therefore, we hope that this review paper will not only serve as a valuable repository of information but also serve as a catalyst for prospective in vitro and in vivo research studies to bridge the existing knowledge gap surrounding pathophysiology, ultimately making an important contribution to shaping future therapeutic approaches. Full article
(This article belongs to the Special Issue Epstein–Barr Virus (EBV) Associated Cancers)
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