Human papillomavirus as a potential risk factor for gastric cancer: a meta-analysis of 1,917 cases

BACKGROUND: Human papillomaviruses (HPVs) are causally associated with the tumorigenesis of several classes of cancers. However, the prevalence of HPV in gastric cancer (GC) has not yet been systematically reviewed. Hence, a meta-analysis was conducted to estimate the HPV prevalence in patients with GC, and its potential etiologic significance was assessed. METHODS: The pooled HPV prevalence and 95% confidence intervals (CIs) were estimated among all GC patients. Heterogeneity was described by using the I(2) statistic. Sources of heterogeneity were explored by meta-regression and stratified analyses. The meta-influence was applied to evaluate the influence of a single study on the pooled estimates. Odds ratios (ORs) and 95% CIs were computed for case–control studies. For research providing clinicopathological parameters of age, sex, pathological, differentiated, and clinical stages, and HPV subtypes, the corresponding pooled ORs and 95% CIs were also calculated. RESULTS: Thirty studies were included in the current meta-analysis, involving 1,917 patients with GC and 576 controls. The pooled HPV prevalence was 28.0% (95% CI: 23.2%, 32.7%) among all the patients with GC, and the I(2) was 96.9% (P<0.001). A pooled OR of 7.388 (95% CI: 3.876, 14.082) was achieved based on 15 case–control studies (I(2)=56.7%, P=0.004). Moreover, the HPV prevalence was significantly higher in patients from China than in those from non-Chinese regions (31% vs 9%, I(2)=95.0%, P<0.001). The pooled prevalence of HPV16 was 21% in GC tissues, and the pooled prevalence of HPV18 was 7% with an OR of 3.314 (95% CI =1.617, 6.792). HPV16 was 3 times more frequently detected than HPV18. CONCLUSION: HPV could play a potential role in the pathogenesis of GC. A causal relationship can be confirmed only by detecting HPV in the cells of GC precursor lesions (gastric dysplasia or adenoma). In addition, this study might be beneficial for expounding the potential etiologic significance of molecular mechanism of gastric tumorigenesis and providing opinions regarding precautionary measures.