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BackgroundAldehyde dehydrogenase 2 (ALDH2), a critical enzyme for the detoxification of alcohol, is associated with many types of cancers. To verify the relationship of ALDH2 rs671 G>A polymorphism and esophageal cancer (EC), we performed a meta-analysis of a total of 31 published data including 8,510 patients and 16,197 controls.MethodsThe pooled odds ratio (OR) and the 95% confidence interval (CI) were calculated using a fixed or random-effects model. Heterogeneity (PH), publication bias, and sensitivity analysis were also determined.ResultsAlthough a protective effort was found in the rs671 homozygote comparison (AA/GG: OR=0.69; 95% CI=0.48–0.98), the heterozygote comparison was apparently associated with the risk of EC, particularly in the Chinese population (AG/GG: OR=1.39; 95% CI=1.03–1.87). Alcohol consumption remarkably increased this risk, especially in the AG genotype. Drinking men with the AG genotype appeared to show a higher risk (AG/GG: OR=4.39; 95% CI=1.24–6.55) than drinking women.ConclusionThe present meta-analysis provided advanced information regarding the association of the ALDH2 A>G polymorphism and EC. Taken together, insights from this study suggested an enhanced effect on the development of EC through a genetic–environmental interaction.

Background: Pre-treatment PLR (platelet-lymphocyte ratio) was reported to be associated with the prognosis in gastric cancer (GC), but the results remain inconclusive. This meta-analysis aimed to investigate the prognostic potential of the pre-treatment PLR in gastric cancer. Methods: We performed a systematic literature search in PubMed, Embase, and the Cochrane Library to identify eligible publications. The hazard ratio (HR)/odds ratio (OR) and its 95% confidence (CI) of survival outcomes and clinicopathological parameters were calculated. Results: A total of 49 studies (51 cohorts), collecting data from 28,929 GC patients, were included in the final analysis. The pooled results demonstrated that the elevated pre-treatment PLR was significantly associated with poor overall survival (OS) (HR 1.37, 95% CI 1.26-1.49, p < 0.001; I 2 = 79.90%, P h < 0.001) and disease-free survival (DFS) (HR 1.52, 95% CI 1.22-1.90, p < 0.001, I 2 = 88.6%, P h < 0.001). Furthermore, the patients with the elevated PLR had a higher risk of lymph node metastasis (OR = 1.17, 95% CI 1.02-1.33, p = 0.023), serosal invasion (T3+T4) (OR = 1.34, 95% CI 1.10-1.64, p = 0.003), and increased advanced stage (III+IV) (OR = 1.20, 95% CI 1.06-1.37, p = 0.004). Conclusions: An elevated pre-treatment PLR was a prognostic factor for poor OS and DFS and associated with poor clinicopathological parameters in GC patients.

Rho-associated coiled-coil-containing protein kinase 2 (ROCK2) has been known as an effector for the small GTPase Rho and plays an important role in tumor progression and metastasis. However, the effect of ROCK2 in gastric cancer (GC) has not been identified. This study showed that ROCK2 expression significantly increased in clinical GC tissues compared with adjacent non-cancer tissues. Immunohistochemistrical analysis showed that high expression of ROCK2 was correlated with tumor grade, tumor-node-metastasis stage, infiltration depth, lymph node invasion and Ki-67, and predicted poor prognosis in 135 gastric cancer specimens. In addition, we found that upregulated ROCK2 promoted proliferation, metastasis and invasion of GC cells, while ROCK2 knockdown led to the opposite results in vitro by Cell Counting Kit-8 (CCK-8) assay, colony formation assays, flow cytometric analysis and trans-well assays. Our findings supported that ROCK2 was a significant protein in the progress of GC and would provide a novel promising therapeutic strategy against human GC.