M1912 Role of Zinc Finger E-Box Binding Factor 1 Modulating Latent-Lytic Switch of Epstein-Barr Virus in Gastric Cancer

2010 ◽  
Vol 138 (5) ◽  
pp. S-438
Author(s):  
Junhong Zhao ◽  
Hongchuan Jin ◽  
Kin-Fai Cheung ◽  
Sui Zhang ◽  
Xiaoxing Li ◽  
...  
Cancer ◽  
2011 ◽  
Vol 118 (4) ◽  
pp. 924-936 ◽  
Author(s):  
Junhong Zhao ◽  
Hongchuan Jin ◽  
Kin Fai Cheung ◽  
Joanna H. M. Tong ◽  
Sui Zhang ◽  
...  

2021 ◽  
Vol 75 (1) ◽  
pp. 611-619
Author(s):  
Magdalena Dzikowiec ◽  
Dorota Pastuszak-Lewandoska

Abstract It is well established that human body is an ecosystem for numerous microorganisms: bacteria, fungi, eukaryotic parasites, and viruses. They form a “microbiome” that under conditions of homeostasis remains in a friendly mutual relationship with the host. However, the composition and diversity of this microbe community is dynamic and can be changed under the influence of environmental factors, such as diet, antibiotic therapy, lifestyle, and the host’s genotype and immunity. The result of gut microbiome dysbiosis can lead even to cancer. The aim of this review is the description of the healthy gastrointestinal microbiome and the role of two infectious agents: Gram-negative bacteria Helicobacter pylori and Epstein-Barr virus in the development of gastric cancer in terms of gut dysbiosis. H. pylori is the most important pathogen of gastric microbiome with clear impact on its diversity. Coinfection with Epstein-Barr virus causes chronic gastritis, and the inflammatory process is significantly increased. The process of carcinogenesis begins with chronic inflammation that causes atrophic gastritis, intestinal metaplasia, dysplasia, and finally cancer. It has been proven that chronic inflammatory infection caused by infectious agents increases the risk of stomach cancer. Molecular methods that are progressively used to explore the human microbiome provide hope that this knowledge will be used for future diagnoses and therapy in the state of its dysbiosis and in cases of gastric cancer.


2017 ◽  
Vol 18 (8) ◽  
pp. 1606 ◽  
Author(s):  
Jun Nishikawa ◽  
Hisashi Iizasa ◽  
Hironori Yoshiyama ◽  
Munetaka Nakamura ◽  
Mari Saito ◽  
...  

2021 ◽  
Author(s):  
Arghavan Zebardast ◽  
Maryam Pazhoohan ◽  
Azadeh Yazdani Cherati ◽  
Saghar Saber Amoli ◽  
Yousef Yahyapour ◽  
...  

Abstract Background: Epstein-Barr virus (EBV) is detected in epithelial tumors, such as nasopharyngeal carcinoma and gastric cancer (GC). EBV-associated gastric cancer is a distinct molecular subtype of gastrointestinal carcinomas as defined by Cancer Genome Atlas. This gamma-Herpes virus is present in approximately 10% of gastric carcinomas.Methods: The present study aimed to investigate the presence of EBV genome in gastric cancer and other gastroduodenal diseases either alone or together with Helicobacter pylori (HP). We examined 237 samples from Iranian patients diagnosed with GC and gastroduodenal disease for EBV infection by quantitative Real-Time PCR.Results: Of the 237 samples tested, EBV DNA was detected in 37 samples (15.6%), in 13 of the 81 GC cases (16%), and 24 of the 156 non-cancerous samples (15.4%). All samples containing EBV were gastric cancer of the intestinal type. Of 37 EBV-positive samples, 20 (54.1%) were over 55 years old and 20 (54.1%) were male. The EBV-EBER (EBV-encoded small RNA) DNA copy number in the gastric cancer group (mean = 2.14×10-1 copies/cell) was higher than that in the gastroduodenal disease group (mean = 1.39×10-2 copies/cell), and this difference was statistically significant (P> 0.001). Moreover, the concurrent infections with EBV and HP were detected in 17 out of 35 EBER-positive samples (48.6%), 6 (17/1%) cases were in the gastric cancer group and 11 (31/4%) cases were in the gastroduodenal disease group.Conclusions: In the present study, a high incidence (16%) of EBVaGC was observed in Babol city, Northern Iran. Also, the higher number of copies of EBV EBER DNA in the GC group than in the non-cancer group confirmed the possible role of EBV in inducing cancer. EBVaGC is not endemic in any region and varies in different nations. Therefore, further studies are needed to determine the role of this virus in the development of GC and other gastroduodenal diseases.


2021 ◽  
Author(s):  
Samia Alaoui Boukhris ◽  
Mounia El khadir ◽  
Safae Karim ◽  
Tiatou Souho ◽  
Dafr-Allah Benajah ◽  
...  

Abstract Purpose: Helicobacter pylori, Epstein-Barr virus and human papillomavirus are three pathogens associated with various human cancers. This study aimed to investigate the role of these pathogens in gastric cancer in Moroccan population Methods: For this, a retrospective study has been conducted on participants attending the gastroenterology department of Hassan II University Hospital of Fez. A total of 279 participants were enrolled. H. pylori, EBV and HPV were detected and genotyped by PCR.Results: A significant association has been established between H. pylori, EBV and gastric cancer. 93.4% and 43.3% of gastric cancer cases are related to H. pylori and EBV respectively (p≤0.01). H. pylori-EBV co-infection is responsible of 31.6% of gastric cancer cases (p<0.01). Correlation between pathogens genotypes and gastric cancer shows 55.6% of GC EBV positives are carrying the 30bp deletion in LMP1gene, while 16% of gastric cancers cases are carrying high-risk genotypes of HPV (p=0.21). Conclusion: The obtained results highlight the possible role of co-infection in gastric cancer development.


2020 ◽  
Vol 7 (3) ◽  
pp. 27-36
Author(s):  
E. O. Ignatova ◽  
D. A. Seryak ◽  
M. Yu. Fedyanin ◽  
A. A. Tryakin ◽  
I. A. Pokataev ◽  
...  

Epstein–Barr virus (EBV) associated gastric carcinoma is a special form of gastric adenocarcinoma that arises against the background of clonal growth of EBV-infected epithelial cells of the gastric mucosa. This subtype of tumors has unique genetic and epigenetic features that determine its characteristic phenotype. Determination of the molecular features of EBV-associated gastric cancer made it possible to identify potential targets for drug therapy of this subtype of tumors. The review presents modern data on the epidemiology and pathogenesis of EBVassociated gastric cancer, describes its unique pathomorphological and molecular features. Particular attention is paid to the prognostic role of EBV infection and drug therapy potentially applicable to the treatment of EBV-positive gastric cancer.


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.


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