Clinicopathological evidence of hepatitis B virus infection in the development of gastric adenocarcinoma

Cui, Hongxia; Jin, Yizi; Chen, Fang; Ni, Hengli; Hu, Caihong; Xu, Yudong; He, Xiangyi; Hu, Duanmin; Deng, Wei; Zhang, Yongsheng; Liu, Yao

doi:10.1002/jmv.25584

Cited by 23 publications

(26 citation statements)

References 17 publications

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“…As precancerosis to gastric cancer, gastric premalignant changes was found to be correlated with HBV infection 22 . Meta‐analyses also found the association between HBV infection and gastric cancer 43,44 . In our study, the seroprevalence of HBsAg was much higher in gastric cancer compared with matched controls ( p = 0.017).…”

Section: Discussionsupporting

confidence: 68%

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Associations between hepatitis B virus exposure and the risk of extrahepatic digestive system cancers: A hospital‐based, case–control study (SIGES)

et al. 2021

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ObjectivesThis case–control study was aimed to investigate associations between HBV infection and extrahepatic digestive system cancers.MethodsThe patients of gastric, small intestinal, colonic, rectal, anal, biliary tract, and pancreatic cancers were retrospectively collected between 2016.5 and 2017.12. Simultaneously, the healthy controls were collected from the health check‐up registry, and cancer‐free status was confirmed based on medical records. Propensity score matching was performed to reduce bias. Multinomial logit model and conditional logistic regression model were used to assess the risk of individual cancer according to HBV serological markers and classifications.ResultsTotally, 4748 patients involving seven cancers, and 57,499 controls were included. After matching, HBsAg was associated with increased risk of gastric cancer (aOR = 1.39, 95% CI: 1.05–1.85), and anti‐HBs served as a protective factor for gastric (aOR = 0.72, 95% CI: 0.61–0.85), colonic (aOR = 0.73, 95% CI: 0.60–0.89), rectal (aOR = 0.73, 95% CI: 0.63–0.85), and pancreatic (aOR = 0.58, 95% CI: 0.42–0.82) cancers. Compared to subgroups with non‐infection and vaccination status, inactive HBsAg carriers and active HBV infection subgroup were correlated with gastric carcinogenesis (aOR = 1.41, 95% CI: 1.03–1.93). However, no clear association was found between HBV infection and other cancers.ConclusionsHBV infection was potentially associated with an increased risk of gastric cancer. The development mechanism of HBV‐associated gastric cancer needs to investigate further.

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Section: Discussionsupporting

confidence: 68%

“…Chronic inflammation triggered by HBV caused immunosuppression which might play a role in gastric carcinogenesis. Cui et al found cellular atypia and lymphocytes’ infiltration induced by HBX in gastric epithelial cells 44 . As the oncogenic protein, HBX might also involve in the development of gastric cancer.…”

Section: Discussionmentioning

confidence: 99%

Associations between hepatitis B virus exposure and the risk of extrahepatic digestive system cancers: A hospital‐based, case–control study (SIGES)

et al. 2021

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“…As a causative pathogen for hepatocellular carcinoma, HBV infection was shown to be associated with the risk of GC in some sporadic studies ( 9 , 57 ). One meta‐analysis that included 3 case–control studies and 5 cohort studies also found that HBV infection is associated with a higher risk for GC (OR = 1.23, 95% CI 1.10–1.37) ( 58 ). As shown in this study, HBV DNA was investigated directly in gastric mucosa tissue by polymerase chain reaction method only in 2 studies with the low positive rate (0%–3.2% in GC), which was consistent with a previous study ( 59 ).…”

Section: Discussionmentioning

confidence: 99%

Associations Between Gastric Cancer Risk and Virus Infection Other Than Epstein-Barr Virus: A Systematic Review and Meta-analysis Based on Epidemiological Studies

Wang

Chen

et al. 2020

Clin Transl Gastroenterol

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INTRODUCTION: Besides Helicobacter pylori and Epstein-Barr virus, other viruses might play potential roles in gastric carcinogenesis. This systematic review and meta-analysis was conducted to compare the prevalence of the viruses between gastric cancer (GC) and any controls. METHODS: Comprehensive literature was searched up to January 25, 2019, and search was updated on April 6, 2020. The studies that compared the prevalence of viruses other than Epstein-Barr virus between GC and healthy or nonmalignant controls were eligible. Stata 12.0 software was used for heterogeneity tests and meta-analyses. Meanwhile, subgroup analysis, sensitivity analysis, and publication bias evaluation were performed where applicable. The power (1–β) was estimated by the PASS 11 software for each individual study. RESULTS: A total of 41 eligible studies were included, concerning 11 kinds of viruses. Prevalence were significantly higher in GC for hepatitis B virus (odds ratio [OR] = 1.39, 95% confidence interval [CI] 1.11–1.75), human cytomegalovirus (OR = 2.25, 95% CI 1.14–4.43), human papillomavirus (HPV) (OR = 1.63, 95% CI 1.05–2.54), and John Cunningham virus (OR = 2.52, 95% CI 1.26–5.04). In subgroup analyses, HPV-16 infection was significantly associated with GC (OR = 2.42, 95% CI 1.00–5.83). DISCUSSION: This study demonstrated that hepatitis B virus, human cytomegalovirus, HPV, and John Cunningham virus were more prevalent in GC. However, the causal relationship between their infection and risk of GC remains inconclusive, and further investigations are required.

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“…Clinical and epidemiological evidence supports the contribution of various viruses, including EBV, hepatitis virus, cytomegalovirus with gastritis and gastric cancer induced by H. pylori [67], and several studies have shown that gastric microbiota can regulate H. pylori infection and vice versa; this bacterium can modify the gastric microbiota composition [68][69][70]. On the other hand, the microbiota composition in several body niches exerts direct or indirect effects on virus infections, including EBV and human papilloma virus [71].…”

Section: Discussionmentioning

confidence: 98%

Epstein–Barr Virus and Helicobacter Pylori Co-Infection in Non-Malignant Gastroduodenal Disorders

Dávila-Collado¹,

Jarquín-Durán²,

Dong

et al. 2020

Pathogens

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Epstein–Barr virus (EBV) and Helicobacter pylori (H. pylori) are two pathogens associated with the development of various human cancers. The coexistence of both microorganisms in gastric cancer specimens has been increasingly reported, suggesting that crosstalk of both pathogens may be implicated in the carcinogenesis process. Considering that chronic inflammation is an initial step in the development of several cancers, including gastric cancer, we conducted a systematic review to comprehensively evaluate publications in which EBV and H. pylori co-infection has been documented in patients with non-malignant gastroduodenal disorders (NMGDs), including gastritis, peptic ulcer disease (PUD), and dyspepsia. We searched the PubMed database up to August 2019, as well as publication references and, among the nine studies that met the inclusion criteria, we identified six studies assessing EBV infection directly in gastric tissues (total 949 patients) and three studies in which EBV infection status was determined by serological methods (total 662 patients). Due to the substantial methodological and clinical heterogeneity among studies identified, we could not conduct a meta-analysis. The overall prevalence of EBV + H. pylori co-infection in NMGDs was 34% (range 1.8% to 60%). A higher co-infection rate (EBV + H. pylori) was reported in studies in which EBV was documented by serological methods in comparison with studies in which EBV infection was directly assessed in gastric specimens. The majority of these studies were conducted in Latin-America and India, with most of them comparing NMGDs with gastric cancer, but there were no studies comparing the co-infection rate in NMGDs with that in asymptomatic individuals. In comparison with gastritis caused by only one of these pathogens, EBV + H. pylori co-infection was associated with increased severity of gastric inflammation. In conclusion, only relatively small studies testing EBV and H. pylori co-infection in NMGDs have been published to date and the variable report results are likely influenced by geographic factors and detection methods.

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Clinicopathological evidence of hepatitis B virus infection in the development of gastric adenocarcinoma

Cited by 23 publications

References 17 publications

Associations between hepatitis B virus exposure and the risk of extrahepatic digestive system cancers: A hospital‐based, case–control study (SIGES)

Associations between hepatitis B virus exposure and the risk of extrahepatic digestive system cancers: A hospital‐based, case–control study (SIGES)

Associations Between Gastric Cancer Risk and Virus Infection Other Than Epstein-Barr Virus: A Systematic Review and Meta-analysis Based on Epidemiological Studies

Epstein–Barr Virus and Helicobacter Pylori Co-Infection in Non-Malignant Gastroduodenal Disorders

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