scholarly journals Dual blockade of the PI 3K/Akt/ mTOR pathway inhibits posttransplant Epstein‐Barr virus B cell lymphomas and promotes allograft survival

2019 ◽  
Vol 19 (5) ◽  
pp. 1305-1314 ◽  
Author(s):  
Adam X. Sang ◽  
Marla C. McPherson ◽  
Geoffrey T. Ivison ◽  
Xiumei Qu ◽  
Joseph Rigdon ◽  
...  
Keyword(s):  
B Cell ◽  
Epstein Barr Virus ◽  
Mtor Pathway ◽  
Allograft Survival ◽  
B Cell Lymphomas ◽  
Barr Virus ◽  
Dual Blockade ◽  
Epstein Barr

scholarly journals PI3Kδ Inhibition Augments the Efficacy of Rapamycin in Suppressing Proliferation of Epstein−Barr Virus (EBV)+ B Cell Lymphomas

2013 ◽  
Vol 13 (8) ◽  
pp. 2035-2043 ◽  
Author(s):  
S. Furukawa ◽  
L. Wei ◽  
S. M. Krams ◽  
C. O. Esquivel ◽  
O. M. Martinez
Keyword(s):  
B Cell ◽  
Epstein Barr Virus ◽  
B Cell Lymphomas ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Epstein–Barr Virus-Induced Metabolic Rearrangements in Human B-Cell Lymphomas

2018 ◽  
Vol 9 ◽  
Author(s):  
Pier P. Piccaluga ◽  
Alessandra Weber ◽  
Maria R. Ambrosio ◽  
Yonis Ahmed ◽  
Lorenzo Leoncini
Keyword(s):  
B Cell ◽  
Epstein Barr Virus ◽  
B Cell Lymphomas ◽  
Barr Virus ◽  
Epstein Barr ◽  
Human B Cell

Epstein-Barr Virus-positive Diffuse Large B-cell Lymphomas of the Elderly

2011 ◽  
Vol 18 (5) ◽  
pp. 349-355 ◽  
Author(s):  
Patrick Adam ◽  
Irina Bonzheim ◽  
Falko Fend ◽  
Leticia Quintanilla-Martínez
Keyword(s):  
B Cell ◽  
Epstein Barr Virus ◽  
The Elderly ◽  
B Cell Lymphomas ◽  
Barr Virus ◽  
Epstein Barr ◽  
Large B Cell

scholarly journals Virally Induced Cellular MicroRNA miR-155 Plays a Key Role in B-Cell Immortalization by Epstein-Barr Virus

2010 ◽  
Vol 84 (22) ◽  
pp. 11670-11678 ◽  
Author(s):  
Sarah D. Linnstaedt ◽  
Eva Gottwein ◽  
Rebecca L. Skalsky ◽  
Micah A. Luftig ◽  
Bryan R. Cullen
Keyword(s):  
B Cell ◽  
Cell Lines ◽  
Epstein Barr Virus ◽  
B Cell Lymphoma ◽  
Selective Inhibition ◽  
B Cell Lymphomas ◽  
Cell Infection ◽  
Barr Virus ◽  
Epstein Barr

ABSTRACT Infection of resting primary human B cells by Epstein-Barr virus (EBV) results in their transformation into indefinitely proliferating lymphoblastoid cell lines (LCLs). LCL formation serves as a model for lymphomagenesis, and LCLs are phenotypically similar to EBV-positive diffuse large B-cell lymphomas (DLBCLs), which represent a common AIDS-associated malignancy. B-cell infection by EBV induces the expression of several cellular microRNAs (miRNAs), most notably miR-155, which is overexpressed in many tumors and can induce B-cell lymphomas when overexpressed in animals. Here, we demonstrate that miR-155 is the most highly expressed miRNA in LCLs and that the selective inhibition of miR-155 function specifically inhibits the growth of both LCLs and the DLBCL cell line IBL-1. Cells lacking miR-155 are inefficient in progressing through S phase and spontaneously undergo apoptosis. In contrast, three other B-cell lymphoma lines, including two EBV-positive Burkitt's lymphoma cell lines, grew normally in the absence of miR-155 function. These data identify the induction of cellular miR-155 expression by EBV as critical for the growth of both laboratory-generated LCLs and naturally occurring DLBCLs and suggest that targeted inhibition of miR-155 function could represent a novel approach to the treatment of DLBCL in vivo.

scholarly journals Epstein Barr virus-positive B-cell lymphoma is highly vulnerable to MDM2 inhibitors in vivo

2021 ◽  
Author(s):  
Xiaoshan Zhang ◽  
Ran Zhang ◽  
Chenghui Ren ◽  
Yi Xu ◽  
Shuhong Wu ◽  
...  
Keyword(s):  
B Cell ◽  
Epstein Barr Virus ◽  
Cell Lymphoma ◽  
Tumor Regression ◽  
B Cell Lymphoma ◽  
B Cell Lymphomas ◽  
T Cell Therapy ◽  
Barr Virus ◽  
Epstein Barr

Epstein-Barr virus (EBV)-positive B-cell lymphomas are common in immunocompromised patients and remain an unmet medical need. Here we report that MDM2 inhibitors (MDM2i) navtemadlin and idasanutlin have potent in vivo activity in EBV+ B-cell lymphoma established in immunocompromised mice. Tumor regression was observed in all 5 EBV+ xenograft-associated B-cell lymphomas treated with navtemadlin or idasanutlin. Molecular characterization showed that treatment with MDM2i resulted in activation of p53 pathways and downregulation of cell cycle effectors in human lymphoma cell lines that either were EBV+ or had undetectable expression of BCL6, a transcriptional inhibitor of the TP53 gene. Moreover, treatment with navtemadlin resulted in tumor regression and prevented systemic dissemination of EBV+ lymphoma derived from 2 juvenile patients with posttransplant lymphoproliferative diseases, including one whose tumor was resistant to virus-specific T-cell therapy. These results provide proof-of-concept for targeted therapy of EBV+ lymphoma with MDM2i and the feasibility of using EBV infection or loss of BCL6 expression to identify responders to MDM2i.

scholarly journals EBNA2-deleted Epstein-Barr virus (EBV) isolate, P3HR1, causes Hodgkin-like lymphomas and diffuse large B cell lymphomas with type II and Wp-restricted latency types in humanized mice

2020 ◽  
Vol 16 (6) ◽  
pp. e1008590 ◽  
Author(s):  
Chunrong Li ◽  
James C. Romero-Masters ◽  
Shane Huebner ◽  
Makoto Ohashi ◽  
Mitchell Hayes ◽  
...  
Keyword(s):  
B Cell ◽  
Epstein Barr Virus ◽  
Humanized Mice ◽  
Type Ii ◽  
B Cell Lymphomas ◽  
Barr Virus ◽  
Epstein Barr ◽  
Large B Cell

Abstract A16: Epstein-Barr virus encoded EBNA2 alters immune checkpoint PD-L1 expression by downregulating miR-34a in B cell lymphomas

2018 ◽  
Author(s):  
Anastasiadou Eleni ◽  
Stroopinsky Dina ◽  
Stella Alimperti ◽  
Alan Jiao ◽  
Athalia Pyzer ◽  
...  
Keyword(s):  
B Cell ◽  
Immune Checkpoint ◽  
Epstein Barr Virus ◽  
B Cell Lymphomas ◽  
Barr Virus ◽  
Epstein Barr
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