Abstract
BackgroundPrevious studies reported that Epstein–Barr virus (EBV) may play a causal role in the pathogenesis of gastric remnant carcinoma (GRC). However, there was still some controversy.MethodsArticles published until July 15, 2020, in PubMed, MEDLINE, Embase and CNKI databases were selected. According to the inclusion criteria, corresponding data of included articles were abstracted and used for statistical analysis.ResultsThirteen papers were finally enrolled, nine of which showed the result that the risk of EBV infection rate in the GRC was higher than conventional gastric carcinoma (OR = 5.22, 95% CI 3.89–7.00). In addition, we found that EBV associated GRC (EBVaGRC) had higher rate of Billroth-II (OR = 3.80, 95% CI 1.90–7.57), carcinoma in anastomotic site (OR = 2.41, 95% CI 1.27–4.56) and diffuse type (Lauren classification) (OR = 1.97, 95% CI 1.04–3.73),while sex, initial diagnosis and lymphocytic infiltration were calculated no statistical difference. By genetic polymorphism analysis, “V-val” subtype of EBNA1 (OR = 21.84, 95% CI 11.92–31.76) and “C” subtype of BamHI-W1/I1 (OR = 7.07, 95% CI 1.47–34.03) were observed to be highly expressed in EBVaGRC.ConclusionEBV infection rate in the GRC was higher. Further analysis showed that Billroth-II, carcinoma in anastomotic site and diffuse type (Lauren classification) were associated to EBVaGRC. Through analysis of EBV genome polymorphisms, we thought that “V-val” subtype of EBNA1 and “C” subtype of BamHI-W1/I1 may become predictor of EBVaGRC.
Highlights
Previous studies reported that Epstein–Barr virus (EBV) may play a causal role in the pathogenesis of gastric remnant carcinoma (GRC)
According to the limited information provided in the articles, we analyzed clinicopathologic characteristics on reconstruction style after surgery (6 studies), initial diagnosis (3 studies), location of GRC (6 studies), Lauren classification (6 studies), sex of patients (5 studies), lymphocytic infiltration (3 studies)
The amount of Billroth-II was 3.8 times in EBV-associated-gastric remnant carcinoma (EBVaGRC) that of EBV-negative-gastric remnant carcinoma (EBVnGRC) (OR = 3.80, 95% confidence intervals (CIs) 1.90–7.57, I2 = 0, P = 0.463) (Fig. 3a)
Summary
Previous studies reported that Epstein–Barr virus (EBV) may play a causal role in the pathogenesis of gastric remnant carcinoma (GRC). An oncogenic association between gastric carcinoma (GC) and Epstein–Barr virus (EBV) is well known [3]. EBV-associated-gastric carcinoma (EBVaGC) prevalence varied from 2 to 18% in different countries [4]. Lee et al have reported a meta-analysis indicating that the clinicopathological and molecular characteristics of EBVaGC were quite different from those of conventional gastric adenocarcinoma [5]. The exact role of EBV in the pathogenesis of EBV-associated-gastric remnant carcinoma (EBVaGRC) remains to be determined. Previous study has reported that different genotype EBV expressed in GRC, which may play a key role in the pathogenesis of EBVaGRC [11].
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