Epstein-Barr Virus-associated Gastric Carcinoma

Chen, Jianning; He, Dan; Tang, Fang; Shao, Chun-Kui

doi:10.1097/mcg.0b013e318249c4b8

Cited by 86 publications

(81 citation statements)

References 113 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In recent years, reports have been published suggesting a relationship between EBV and gastric cancer [19][20][21][22]. It has been reported that EBV is associated with 10% of gastric carcinomas and that in most cases positive EBV is diagnosed in poorly differentiated or moderately differentiated grades [23,24].…”

Section: Discussionmentioning

confidence: 99%

Original paper Epstein-Barr virus DNA in colorectal carcinoma in Iranian patients

Tafvizi¹,

Fard²,

Assareh³

2015

pjp

View full text Add to dashboard Cite

Colorectal cancer is an often fatal cancer with a rapidly increasing incidence. Current mortality is estimated to be approximately 600,000 per year, and both environmental and genetic factors are involved in its etiology. Viral and bacterial factors have a proven role in the incidence of approximately 20% of cancers. In the present study, the Epstein-Barr virus (EBV) was detected in 50 colorectal adenocarcinomas, 12 colon adenomas, and 38 control tissue samples using polymerase chain reaction (PCR). Epstein-Barr virus DNA was identified in 19 of the adenocarcinoma tissues, 1 adenoma tissue and 24 control specimens. In total, 15.8% (3/18) of the colorectal samples in the well-differentiated grade, 79% (15/30) in the moderately differentiated, and 5.2% (1/2) in the poorly differentiated grade tested positive for viral infection. Epstein-Barr virus was more prevalent in the moderately differentiated grade. Statistical analysis did not suggest a significant association between EBV and the incidence of colorectal cancer. However, it appears that the virus stimulates progression of the malignancy.

show abstract

Section: Discussionmentioning

confidence: 99%

Original paper Epstein-Barr virus DNA in colorectal carcinoma in Iranian patients

Tafvizi¹,

Fard²,

Assareh³

2015

pjp

View full text Add to dashboard Cite

show abstract

“…Under normal conditions, DNA methylation is a basic physiological process in biological organisms, which transforms cytosine into 5'-methylcytosine using DNA methyltransferases (DNMTs). Therefore, DNA methylation serves an important role in maintaining chromatin structures, DNA conformation, DNA stability and DNA-protein interactions (5). However, abnormal methylation of DNA in certain pathological conditions may deactivate tumor suppressor genes and activate oncogenes (6,7).…”

Section: Introductionmentioning

confidence: 99%

Casticin inhibits the activity of transcription factor Sp1 and the methylation of RECK in MGC803 gastric cancer cells

Yang

Huang

et al. 2016

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

Abstract. The present study investigated the effect of casticin on reversion-inducing-cysteine-rich protein with kazal motifs (RECK) gene expression and intracellular methylation levels in MGC803 gastric cancer cells. Cells were treated with 1, 10 and 30 µmol/l casticin. Western blotting and reverse transcription-quantitative polymerase chain reaction assays were performed to determine the protein expression and mRNA levels of RECK and DNA methyltransferase 1 (DNMT1), respectively. High-performance liquid chromatography coupled to electrospray ionization tandem mass spectrometry was used to detect RECK methylation. In addition, MGC803 cell proliferation was measured by an MTT assay and the DNA-binding activity of transcription factor Sp1 was determined using an enzyme-linked immunosorbent assay. The results demonstrated that treatment with 1, 10 and 30 µmol/l casticin significantly increased RECK protein expression and mRNA levels. In addition, casticin (30 µmol/l) decreased RECK promoter methylation levels by 31%, global DNA methylation levels by 39% and nuclear methylation activity by 71.6%. Furthermore, casticin downregulated the mRNA levels and protein expression of DNMT1. The MTT assay demonstrated that MGC803 cell proliferation was inhibited by casticin treatment and DNA binding assays indicated that casticin reduced the DNA-binding activity of Sp1. The present study therefore indicated that casticin inhibits the proliferation of gastric cancer MGC803 cells by upregulating RECK gene expression and reducing intracellular methylation levels.

show abstract

“…The GAC-EBV is a unique clinicopathological entity: it appears to be more prevalent in men, is usually found in the proximal region of the stomach and is frequently present in younger subjects [35,36]. A recent publication found PIK3CA mutations in about 80% of GAC-EBV [20], and papers have reported that GAC-EBV patients usually have less lymph node disease but with contradictory prognosis reports [35][36][37][38].…”

Section: The Investigation Of Exogenous Elementsmentioning

confidence: 99%

Genomics and epidemiology for gastric adenocarcinomas

2017

Appl Cancer Res

View full text Add to dashboard Cite

Whereas the pathological aspects of Gastric Adenocarcinomas (GACs) have been well defined, the actual knowledge of its genesis and evolution remains to be translated to better diagnosis and to more effective therapeutics. As a consequence, the current treatment modalities are not yet able to modify the natural history of the disease, which still presents high mortality-rates worldwide. In this review we highlight the current status of relevant epidemiologic, therapeutic and genomics aspects of GACs and point to some of the current knowledge gaps that, if fully addressed, could contribute to a more effective treatment and better management of the patients that suffer from this often-lethal disease.

show abstract

Epstein-Barr Virus-associated Gastric Carcinoma

Cited by 86 publications

References 113 publications

Original paper Epstein-Barr virus DNA in colorectal carcinoma in Iranian patients

Original paper Epstein-Barr virus DNA in colorectal carcinoma in Iranian patients

Casticin inhibits the activity of transcription factor Sp1 and the methylation of RECK in MGC803 gastric cancer cells

Genomics and epidemiology for gastric adenocarcinomas

Contact Info

Product

Resources

About