scholarly journals The Role of Epstein-Barr Virus LMP-1 Immunohistochemical Staining in Childhood Hodgkin Lymphoma

2015 ◽  
Vol 25 (6) ◽  
Author(s):  
Hikmet Gulsah Tanyildiz ◽  
Inci Yildiz ◽  
Nuray Bassullu ◽  
Nukhet Tuzuner ◽  
Alp Ozkan ◽  
...  
Author(s):  
Victor Pereira ◽  
Sabah Boudjemaa ◽  
Caroline Besson ◽  
Thierry Leblanc ◽  
Charlotte Rigaud ◽  
...  

To analyze the role of Epstein-Barr virus (EBV) in the biological and clinical characteristics of patients treated for classic Hodgkin lymphoma (cHL) in France. Bio-pathological data of 301 patients treated for a cHL in or according to the protocol of the EuroNet PHL-C1 trial between November 2008 and February 2013 were centrally reviewed. Median age at diagnosis was 14 [3-18] years and the F/M ratio 0.86, 0.47 before 10 years and 0.9 from 11 to 18. CHL subtypes were nodular sclerosis for 266/301 (88%) patients, mixed cellularity for 22/301 (7%), lymphocyte rich for 2/301 (1%), and 11/301 were unclassified. EBV expression in situ (EBV cHL) was observed for 68/301 (23%) patients, significantly associated with MC subtype and male gender, and there was a trend with age <10 years, it was particularly overrepresented in boys below 10 years: 15/23 (65%) vs 28/139 among other male patients (20%). Event-free and overall survival were equivalent between EBV and non-EBV cHL patients. EBV viral load was tested for 108/301 patients and detectable in 22/108 (22%) cases. A positive viral load was overrepresented in EBV cHL versus non-EBV cHL patients: 13/28 (46%) vs 9/80 (11%). Detailed semi-quantitative histological analysis showed a high number of B-cell residual follicles in EBV cHL and no significant association with CD 20 or PAX 5 immunostaining in tumoral cells relative to EBV-negative HL. Distribution of EBV cHL in children and adolescents is associated with young age and male gender, suggesting a specific physiopathology and may require a differential therapeutic approach.


Blood ◽  
2019 ◽  
Vol 134 (7) ◽  
pp. 591-596 ◽  
Author(s):  
Paul G. Murray ◽  
Lawrence S. Young

Abstract Although a pathogenic role for the Epstein-Barr virus (EBV) is largely undisputed for tumors that are consistently EBV genome positive (eg, nasopharyngeal carcinoma, endemic Burkitt lymphoma), this is not the case for classical Hodgkin lymphoma (cHL), a tumor with only a variable EBV association. In light of recent developments in immunotherapeutics and small molecules targeting EBV, we believe it is now timely to reevaluate the role of EBV in cHL pathogenesis.


2017 ◽  
Vol 1 (17) ◽  
pp. 1324-1334 ◽  
Author(s):  
Amy S. Duffield ◽  
Maria Libera Ascierto ◽  
Robert A. Anders ◽  
Janis M. Taube ◽  
Alan K. Meeker ◽  
...  

Key Points CHL broadly expresses the PD-1/PD-L1 pathway, but EBV+ CHL displays a Th1 profile, whereas EBV− tumors have a pathogenic Th17 profile. These findings support further studies to define the role of the IL-23/IL-17 axis in CHL response/resistance to anti-PD-1 therapy.


Life ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 593
Author(s):  
Srikanth Umakanthan ◽  
Maryann M Bukelo

Global genomic studies have detected the role of genomic alterations in the pathogenesis of Epstein–Barr virus (EBV)-associated tumors. EBV oncoproteins cause a vital shift of EBV from an infectious virus to an oncogenic form during the latent and lytic phase within the lymphoid B cells and epithelial cells. This epigenetic alteration modulates the virus and host genomes and inactivates and disrupts numerous tumor suppressors and signaling pathways. Genomic profiling has played the main role in identifying EBV cancer pathogenesis and its related targeted therapies. This article reviews the role of genetic changes in EBV-associated lymphomas and carcinomas. This includes the prolific molecular genesis, key diagnostic tools, and target-specific drugs that have been in recent clinical use.


Lupus ◽  
2021 ◽  
pp. 096120332110103
Author(s):  
Anna Truszewska ◽  
Agnieszka Wirkowska ◽  
Kamila Gala ◽  
Piotr Truszewski ◽  
Łucja Krzemień-Ojak ◽  
...  

Background For long Epstein–Barr virus (EBV) has been suspected to be involved in the pathogenesis of systemic lupus erythematosus (SLE). The aim of this study was to verify the association between EBV, cell-free DNA (cfDNA) and kidney disease in SLE. Methods Blood samples were obtained from 43 SLE patients and 50 healthy individuals. EBV load was measured via real-time PCR assay. Sizing and quantification of plasma cfDNA was performed on Bioanalyzer. We proposed that the uniformity of cfDNA fragmentation can be described using cfDNA fragmentation index. Results SLE patients with chronic kidney disease (CKD +) had higher EBV load compared to CKD(–) patients (P = 0.042). Patients with high cfDNA level had higher EBV load (P = 0.041) and higher cfDNA fragmentation index (P < 0.001) compared to patients with low cfDNA level. Among patients with high cfDNA level, EBV load was higher in CKD(+) group compared to CKD(–) group (P = 0.035). EBV load was positively correlated with the fragmentation index in all SLE patients (P = 0.028, R2 = 0.13), and the correlation was even more pronounced in CKD (+) patients (P < 0.001, R2 = 0.20). Conclusions We showed that EBV load was associated with non-uniform cfDNA fragmentation, higher cfDNA levels, and kidney disease in SLE patients. Although the causality of this relationship could not be determined with the current study, it brings rationale for further investigations on the role of EBV and cfDNA interplay in SLE pathogenesis.


Sign in / Sign up

Export Citation Format

Share Document