Current Progress in EBV-Associated B-Cell Lymphomas

Pei, Yue‐Hu; Lewis, Alexandria

doi:10.1007/978-981-10-5765-6_5

Cited by 20 publications

(12 citation statements)

References 113 publications

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“…Overexpression of JAK1 and STAT4 in BLCL was observed in the present study, which may be involved in the JAK/STAT signaling pathway that has been reported to be activated in DLBCL (37). MYC oncogene has been reported to be overexpressed in Burkitt's lymphoma, and the present study identified increased MYCL proto-oncogene transcription factor in BLCL, which may be involved in cell proliferation (37). CDK4 and CDK6 gene expression was also increased in BLCL, consistent with results of previous studies that used RNAseq (16,29).…”

Section: Discussionsupporting

confidence: 66%

Cellular expression profiles of Epstein-Barr virus-transformed B-lymphoblastoid cell lines

et al. 2020

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Epstein-Barr virus (EBV) can infect human B cells and is associated with various types of B cell lymphomas. Studies on the global alterations of the cellular pathways mediated by EBV-induced B cell transformation are limited. In the present study, microarray analysis was performed following generation of two EBV-infected B-lymphoblastoid cell lines (BLCL), in which normal B cells obtained from two healthy Thai individuals and transcriptomic profiles were compared with their respective normal B cells. The two EBV-transformed BLCL datasets exhibited a high degree of similarity between their RNA expression profiles, whereas the two normal B-cell datasets did not exhibit the same degree of similarity in their RNA expression profiles. Differential gene expression analysis was performed, and the results showed that EBV infection was able to dysregulate several cellular pathways in the human B-cell genes involved in cancer and cell activation, such as the MAPK, WNT and PI3K-Akt signaling pathways, which were upregulated in the BLCL and were associated with increased cellular proliferation and immortalization of EBV-infected B cells. Expression of proteins located in the plasma membrane, which initiate a biological response to ligand binding, were also notably upregulated. Expression of genes involved in cell cycle control, the p53 signaling pathway and cellular senescence were downregulated. In conclusion, genes that were markedly upregulated by EBV included those involved in the acquisition of a tumorigenic phenotype of BLCL, which was positively correlated with several hallmarks of cancer.

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Section: Discussionsupporting

confidence: 66%

Cellular expression profiles of Epstein-Barr virus-transformed B-lymphoblastoid cell lines

et al. 2020

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“…More importantly, the lack of EBV-specific inhibitors is still a major bottleneck of anti-viral therapies. For example, the R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) commonly used for the treatment of non-Hodgkin lymphomas is not related to EBV infection, despite the fact that it is currently used to treat EBV-associated lymphomas [ 89 , 139 ]. Furthermore, the inducers of EBV lytic reactivation are mostly too toxic to be used in clinical trials.…”

Section: Discussionmentioning

confidence: 99%

Targeted Therapies for Epstein-Barr Virus-Associated Lymphomas

Pei

Wong

Robertson

2020

Cancers

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The Epstein-Barr virus (EBV) is the first human tumor virus identified that can transform quiescent B lymphocytes into lymphoblastoid cell lines (LCLs) in vitro. EBV can establish asymptomatic life-long persistence and is associated with multiple human malignancies, including non-Hodgkin lymphoma and Hodgkin lymphoma, as well as infectious mononucleosis. Although EBV-associated lymphomagenesis has been investigated for over 50 years, viral-mediated transformation is not completely understood, and the development of EBV-specific therapeutic strategies to treat the associated cancers is still a major challenge. However, the rapid development of several novel therapies offers exciting possibilities to target EBV-induced lymphomas. This review highlights targeted therapies with potential for treating EBV-associated lymphomas, including small molecule inhibitors, immunotherapy, cell therapy, preventative and therapeutic vaccines, and other potent approaches, which are novel strategies for controlling, preventing, and treating these viral-induced malignances.

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“…In vivo , EBV instead switches to latency II in immunocompetent hosts upon germinal center entry, where EBNA1, LMP1/2A and ncRNA are expressed. Upon memory cell differentiation, EBV restricts expression to EBNA1 and ncRNAs by the latency I program [2,9,10]. This progression is thought to result from the accumulation of epigenetic silencing marks on viral promoters [11,12] (Figure 1).…”

Section: Introductionmentioning

confidence: 99%

Epigenetic crossroads of the Epstein-Barr virus B-cell relationship

Frost

Gewurz

2018

Current Opinion in Virology

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Epstein-Barr virus (EBV) is a gamma-herpesvirus that establishes lifelong infection in the majority of people worldwide. EBV uses epigenetic reprogramming to switch between multiple latency states in order to colonize the memory B-cell compartment and to then periodically undergo lytic reactivation upon plasma cell differentiation. This review focuses on recent advances in the understanding of epigenetic mechanisms that EBV uses to control its lifecycle and to subvert the growth and survival pathways that underly EBV-driven B-cell differentiation versus B-cell growth transformation, a hallmark of the first human tumor virus. These include the formation of viral super enhancers that drive expression of key host dependency factors, evasion of tumor suppressor responses, prevention of plasmablast differentiation, and regulation of the B-cell lytic switch.

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Current Progress in EBV-Associated B-Cell Lymphomas

Cited by 20 publications

References 113 publications

Cellular expression profiles of Epstein-Barr virus-transformed B-lymphoblastoid cell lines

Cellular expression profiles of Epstein-Barr virus-transformed B-lymphoblastoid cell lines

Targeted Therapies for Epstein-Barr Virus-Associated Lymphomas

Epigenetic crossroads of the Epstein-Barr virus B-cell relationship

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