Correction: Frequent traces of EBV infection in Hodgkin and non-Hodgkin lymphomas classified as EBV-negative by routine methods: expanding the landscape of EBV-related lymphomas

Mundo, Lucia; Porro, Leonardo Del; Granai, Massimo; Siciliano, Maria Chiara; Mancini, Virginia; Santi, Raffaella; Marcar, Lynnette; Vrzalikova, Katerina; Vergoni, Federica; Stefano, Gioia Di; Schiavoni, Gianluca; Segreto, Giovanna; Onyango, Noel; Nyagol, Joshua; Amato, Teresa; Bellan, Cristiana; Anagnostopoulos, Ioannis; Falini, Brunangelo; Leoncini, Lorenzo; Tiacci, Enrico; Lazzi, Stefano

doi:10.1038/s41379-020-0608-y

Cited by 4 publications

(4 citation statements)

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“…EBV-positive samples were identified according to the strong nuclear expression of EBV-encoded small RNA genes EBER-1 and -2. A control slide prepared from a paraffin-embedded tissue block containing EBV-positive metastatic nasopharyngeal carcinoma in a lymph node accompanied each hybridization run [ 45 ].…”

Section: Methodsmentioning

confidence: 99%

Epigenetic Alteration of the Cancer-Related Gene TGFBI in B Cells Infected with Epstein–Barr Virus and Exposed to Aflatoxin B1: Potential Role in Burkitt Lymphoma Development

Manara

Jay

Odongo

et al. 2022

Cancers

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Burkitt lymphoma (BL) is a malignant B cell neoplasm that accounts for almost half of pediatric cancers in sub-Saharan African countries. Although the BL endemic prevalence is attributable to the combination of Epstein–Barr virus (EBV) infection with malaria and environmental carcinogens exposure, such as the food contaminant aflatoxin B1 (AFB1), the molecular determinants underlying the pathogenesis are not fully understood. Consistent with the role of epigenetic mechanisms at the interface between the genome and environment, AFB1 and EBV impact the methylome of respectively leukocytes and B cells specifically. Here, we conducted a thorough investigation of common epigenomic changes following EBV or AFB1 exposure in B cells. Genome-wide DNA methylation profiling identified an EBV–AFB1 common signature within the TGFBI locus, which encodes for a putative tumor suppressor often altered in cancer. Subsequent mechanistic analyses confirmed a DNA-methylation-dependent transcriptional silencing of TGFBI involving the recruitment of DNMT1 methyltransferase that is associated with an activation of the NF-κB pathway. Our results reveal a potential common mechanism of B cell transformation shared by the main risk factors of endemic BL (EBV and AFB1), suggesting a key determinant of disease that could allow the development of more efficient targeted therapeutic strategies.

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Section: Methodsmentioning

confidence: 99%

Epigenetic Alteration of the Cancer-Related Gene TGFBI in B Cells Infected with Epstein–Barr Virus and Exposed to Aflatoxin B1: Potential Role in Burkitt Lymphoma Development

Manara

Jay

Odongo

et al. 2022

Cancers

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“…EBV’s relation to such cells has long been known [ 116 ]. Indeed, it is estimated that approximately 30% of classical Hodgkin lymphoma (cHL) cases in the Western world are associated with EBV [ 117 ], and recent research has shown that the lymphomagenesis of a subset of EBV − lymphomas may in fact be related to EBV [ 118 ]. Notably, this statistic does not reflect the nodular lymphocyte-predominant variant of Hodgkin lymphoma, which can have EBV + lymphocyte-predominant cells, but is not typically EBV-associated [ 119 ].…”

Section: Ebv and Oncogenesismentioning

confidence: 99%

EBV and Lymphomagenesis

Sausen

Basith

Muqeemuddin³

2023

Cancers

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The clinical significance of Epstein–Barr virus (EBV) cannot be understated. Not only does it infect approximately 90% of the world’s population, but it is also associated with numerous pathologies. Diseases linked to this virus include hematologic malignancies such as diffuse large B-cell lymphoma, Hodgkin lymphoma, Burkitt lymphoma, primary CNS lymphoma, and NK/T-cell lymphoma, epithelial malignancies such as nasopharyngeal carcinoma and gastric cancer, autoimmune diseases such as multiple sclerosis, Graves’ disease, and lupus. While treatment for these disease states is ever evolving, much work remains to more fully elucidate the relationship between EBV, its associated disease states, and their treatments. This paper begins with an overview of EBV latency and latency-associated proteins. It will then review EBV’s contributions to select hematologic malignancies with a focus on the contribution of latent proteins as well as their associated management.

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“…Once the cells acquired a stable and heritable malignant feature, the virus may not be a critical factor for cell propagation; therefore, the transformed cells will steadily lose the EBV accompanied with the continuously proliferation (Ambinder, 2000;Mundo et al, 2020). However, there is only a limited direct evidence to support this idea.…”

Section: Ebv Infection In Tumorigenesismentioning

confidence: 99%

EBV Infection and Its Regulated Metabolic Reprogramming in Nasopharyngeal Tumorigenesis

Yang

You

Meng³

et al. 2022

Front. Cell. Infect. Microbiol.

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Viral oncogenes may drive cellular metabolic reprogramming to modulate the normal epithelia cell malignant transformation. Understanding the viral oncogene–mediated signaling transduction dysregulation that involves in metabolic reprogramming may provide new therapeutic targets for virus-associated cancer treatment. Latent EBV infection and expression of viral oncogenes, including latent membrane proteins 1 and 2 (LMP1/2), and EBV-encoded BamH I-A rightward transcripts (BART) microRNAs (miR-BARTs), have been demonstrated to play fundamental roles in altering host cell metabolism to support nasopharyngeal carcinoma (NPC) pathogenesis. Yet, how do EBV infection and its encoded oncogenes facilitated the metabolic shifting and their roles in NPC carcinogenesis remains unclear. In this review, we will focus on delineating how EBV infection and its encoded oncoproteins altered the metabolic reprograming of infected cells to support their malignances. Furthermore, based on the understanding of the host’s metabolic signaling alterations induced by EBV, we will provide a new perspective on the interplay between EBV infection and these metabolic pathways and offering a potential therapeutic intervention strategy in the treatment of EBV-associated malignant diseases.

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Correction: Frequent traces of EBV infection in Hodgkin and non-Hodgkin lymphomas classified as EBV-negative by routine methods: expanding the landscape of EBV-related lymphomas

Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Cited by 4 publications

References 0 publications

Epigenetic Alteration of the Cancer-Related Gene TGFBI in B Cells Infected with Epstein–Barr Virus and Exposed to Aflatoxin B1: Potential Role in Burkitt Lymphoma Development

Epigenetic Alteration of the Cancer-Related Gene TGFBI in B Cells Infected with Epstein–Barr Virus and Exposed to Aflatoxin B1: Potential Role in Burkitt Lymphoma Development

EBV and Lymphomagenesis

EBV Infection and Its Regulated Metabolic Reprogramming in Nasopharyngeal Tumorigenesis

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