Detection of Antitumor Promoting Activity in Raji Cells Carrying Epstein-Barr Virus Genome by Immunoblotting Analysis

1998 ◽  
Vol 62 (2) ◽  
pp. 377-379 ◽  
Author(s):  
Akira KONDO ◽  
Tetsuhiro MORIMOTO ◽  
Katsuichiro OKAZAKI
The Lancet ◽  
1989 ◽  
Vol 333 (8652) ◽  
pp. 1458 ◽  
Author(s):  
Stefania Uccini ◽  
Francesca Monardo ◽  
LuigiP. Ruco ◽  
CarloD. Baroni ◽  
Alberto Faggioni ◽  
...  

2001 ◽  
Vol 75 (13) ◽  
pp. 6235-6241 ◽  
Author(s):  
Barbara Wensing ◽  
Albert Stühler ◽  
Peter Jenkins ◽  
Martine Hollyoake ◽  
Claudio Elgueta Karstegl ◽  
...  

ABSTRACT Most of the Epstein-Barr virus genome in latently infected cells is in a standard nucleosomal structure, but the region encompassingoriP and the Epstein-Barr virus-encoded small RNA (EBER) genes shows a distinctive pattern when digested with micrococcal nuclease. This pattern corresponds to a previously mapped nuclear matrix attachment region. Although the EBER genes are adjacent to oriP, there is only a two- to fourfold effect oforiP on EBER expression. However, sequences containing a consensus ATF site upstream of EBER1 are important for EBER1 expression.


Author(s):  
P. J. Farrell ◽  
J. Dyson ◽  
P. Tuffnell ◽  
M. Biggin ◽  
T. Gibson ◽  
...  

2020 ◽  
Author(s):  
Aditya Thandoni ◽  
Andrew Zloza ◽  
Devora Schiff ◽  
Malay Rao ◽  
Kwok-wai Lo ◽  
...  

AbstractNasopharyngeal carcinoma (NPC) is a malignancy endemic to East Asia and is caused by Epstein-Barr Virus (EBV)-mediated cancerous transformation of epithelial cells. The standard of care treatment for NPC involves radiation and chemotherapy. While treatment outcomes continue to improve, up to 50% of patients can be expected to recur by five years, and additional innovative treatment options are needed. We posit that a potential way to do this is by targeting the underlying cause of malignant transformation, namely EBV. One method by which EBV escapes immune surveillance is by undergoing latent phase replication, during which EBV expression of immunogenic proteins is reduced. However, chemoradiation is known to drive conversion of EBV from a latent to a lytic phase. This creates an opportunity for the targeting of EBV-infected cells utilizing anti-viral drugs. Indeed, we found that combining acyclovir with cisplatin and radiation significantly decreases the viability of the EBV-infected C666-1 cell line. Western blot quantification revealed a resultant increase of thymidine kinase (TK) and apoptosis-inducing mediators, cleaved PARP (cPARP) and phosphorylated ERK (pERK). These studies suggest that the addition of anti-viral drugs to frontline chemoradiation may improve outcomes in patients treated for EBV-related NPC and future in vivo and clinical studies are needed.


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