Epstein-Barr virus-associated gastric carcinoma in Cali, Colombia

Carrascal, Edwin; Koriyama, Chihaya; Akiba, Suminori; Tamayo, Oscar; Itoh, Tetsuhiko; Eizuru, Yoshito; Garcia, Felipe; Sera, Mauricio; Carrasquilla, Gabriel; Piazuelo, M. Blanca; Florez, Luisa; Bravo, Juan Carlos

doi:10.3892/or.10.4.1059

Cited by 18 publications

(32 citation statements)

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“…The presence of EBV in GC tissues has been previously documented [7,8,14,15,16,17,18,19,20], and as such, of four EBV positive GC tissues tested, all four showed a positive signal in most or all of the gastric tumor cells (Figure 5a). EBV infection in NAG samples have been poorly explored, and since it is uncertain whether infected/damaged cells are already undergoing limited rounds of clonal expansion, and since a more sensitive PCR was used as criteria for positivity, it is unclear whether in GC precursor lesions there are already infected epithelial cells.…”

Section: Resultssupporting

confidence: 64%

Evidence of Epstein-Barr Virus Association with Gastric Cancer and Non-Atrophic Gastritis

Martínez-López

Torres

Camorlinga‐Ponce

et al. 2014

Viruses

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Different lines of evidence support an association between Epstein-Barr virus (EBV) and gastric cancer (GC). The main understood risk factor to develop GC is infection by Helicobacter pylori (H. pylori), which triggers a local inflammatory response critical for progression from gastritis to GC. The role of EBV in early inflammatory gastric lesions has been poorly studied. A recent study proposed a cutoff value of 2000 EBV particles to identify patients with increased chances of infection of the gastric epithelium, which may favor the inflammatory process. To better understand the role of EBV in cancer progression, we analyzed 75 samples of GC, 147 control samples of non-tumor gastric tissue derived from GC patients and 75 biopsies from patients with non-atrophic gastritis (NAG). A first-round PCR was used for EBV detection in tumor and non-tumor controls and a more sensitive nested PCR for gastritis samples; both PCRs had lower detection limits above the proposed cutoff value. With this strategy 10.67% of GC, 1.3% of non-tumor controls and 8% of gastritis samples were found positive. An EBER1 in situ hybridization showed EBV infection of epithelial cells in GC and in a third of NAG samples, while in the other NAGs infection was restricted to the mononuclear cell infiltrate. EBV-positive GCs were enriched in lace and cribriform patterns, while these rare patterns were not observed in EBV negative samples. Our results support a role for EBV in GC and early precursor lesions, either as directly oncogenic infecting epithelial cells or indirectly as an inflammatory trigger.

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Section: Resultssupporting

confidence: 64%

Evidence of Epstein-Barr Virus Association with Gastric Cancer and Non-Atrophic Gastritis

Martínez-López

Torres

Camorlinga‐Ponce

et al. 2014

Viruses

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“…Almost all of the studies so far showed a male predominance of EBVaGC. 5,6,18,19,22,23,25,26,[28][29][30][31][32]34,[36][37][38] In the recent meta-analysis, the prevalence of EBVaGC in males is 2-fold higher than that in females. 42 The male predominance suggests that lifestyles and occupational factors that are common among males may contribute to the development of EBVaGC.…”

Section: Age and Sex Distributionmentioning

confidence: 99%

Epstein-Barr Virus-associated Gastric Carcinoma

Chen

Tang

et al. 2012

Journal of Clinical Gastroenterology

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Epstein-Barr virus (EBV)-associated gastric carcinoma (EBVaGC) is a recently recognized entity, which is defined by the presence of EBV in the gastric carcinoma cells. EBVaGC represents about 10% of gastric carcinoma worldwide, and >80,000 patients are estimated to develop EBVaGC annually. EBVaGC shows some distinct clinicopathologic characteristics, such as male predominance, predisposition to the proximal stomach, and a high proportion in diffuse-type gastric carcinomas. Besides, EBVaGC also shows characteristic molecular abnormality, that is, global and nonrandom CpG-island methylation of the promoter region of many cancer-related genes, which causes downregulation of their expression. Moreover, EBVaGC has a relative favorable prognosis. The uniform presence of EBV-encoded small RNA in tumor cells but not in the surrounding normal epithelial cells, and the detection of monoclonal EBV episomes in EBVaGC, strongly suggests that EBV play an etiological role in gastric carcinogenesis. Therefore, EBVaGC should be regarded as a distinct entity of gastric carcinoma, although it only accounts for a relatively small fraction of total gastric carcinomas. In this review, the epidemiological and clinicopathologic features of EBVaGC and the genetic abnormalities of EBVaGC cell including chromosomal and epigenetic abnormalities are described. The roles of EBV in gastric carcinogenesis are discussed. We make an emphasis on the EBV latency pattern and genome polymorphisms as well as local immunity in EBVaGC. In addition, the treatment of EBVaGC is also briefly discussed. Taken together, this review aims to give the reader a full understanding of a newly defined entity of gastric carcinoma, EBVaGC.

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“…EBV-GC shows some constant characteristic clinicopathologic features such as predisposition to upper two-third of the stomach [15-17,19-31]; a moderately differentiated tubular to poorly differentiated solid type of histology [16-22,32,33]; having no effect in stromal invasion and survival [15,16]; and male predominance in most of the studies. However, the last one is not seen in some exceptional studies which are performed in Mexico [32,37], Chile [16] and China [38].…”

Section: Introductionmentioning

confidence: 99%