Background: Statin may confer anticancer effect. However, the association between statin and risk of hepatocellular carcinoma (HCC) in patients with hepatitis B virus (HBV) or hepatitis C (HCV) virus infection remains inconsistent according to results of previous studies. A meta-analysis was performed to summarize current evidence. Methods: Related follow-up studies were obtained by systematic search of PubMed, Cochrane's Library, and Embase databases. A random-effect model was used to for the meta-analysis. Stratified analyses were performed to evaluate the influences of study characteristics on the outcome. Results: Thirteen studies with 519,707 patients were included. Statin use was associated with reduced risk of HCC in these patients (risk ratio [RR]: 0.54, 95% CI: 0.44 to 0.66, p < 0.001; I 2 = 86%). Stratified analyses showed that the association between statin use and reduced HCC risk was consistent in patients with HBV or HCV infection, in elder (≥ 50 years) or younger (< 50 years) patients, in males or females, in diabetic or non-diabetic, and in those with or without cirrhosis (all p < 0.05). Moreover, lipophilic statins was associated with a reduced HCC risk (RR: 0.52, p < 0.001), but not for hydrophilic statins (RR: 0.89, p = 0.21). The association was more remarkable in patients with highest statin accumulative dose compared to those with lowest accumulative dose (p = 0.002). Conclusions: Satin use was independently associated with a reduced risk of HCC in patients with HBV or HCV infection.

Background: Association between statin use and prognosis in patients with hepatocellular carcinoma (HCC) remains unknown. We performed a meta-analysis of follow-up studies to systematically evaluate the influence of statin use on clinical outcome in HCC patients. Methods: Studies were obtained via systematic search of PubMed, Cochrane’s Library, and Embase databases. A randomized-effect model was used to pool the results. Subgroup analyses were performed to evaluate the influence of study characteristics on the association. Results: Nine retrospective cohort studies were included. Overall, statin use was associated with a reduced all-cause mortality in HCC patients (risk ratio [RR]: 0.81, 95% CI: 0.74–0.88, P &lt; 0.001; I2 = 63%). Subgroup analyses showed similar results for patients with stage I-III HCC (RR: 0.83, 0.79, and 0.90 respectively, P all &lt; 0.01) and patients after palliative therapy for HCC (RR: 0.80, P &lt; 0.001), but not for patents with stage IV HCC (RR: 0.91, P = 0.28) or those after curative therapy (RR: 0.92, P = 0.20). However, the different between subgroups were not significant (both P &gt; 0.05). Moreover, statin use was associated with reduced HCC-related mortality (RR: 0.78, P = 0.001) in overall patient population and HCC recurrence in patients after curative therapies (RR: 0.55, P &lt; 0.001). Conclusions: Satin use is associated with reduced mortality and recurrence of HCC. These results should be validated in prospective cohort studies and randomized controlled trials.

Our aim was to investigate whether genetic polymorphism of IL-1Beta-511, IL-1RN, TNF-A-308 are involved in the susceptibility to duodenal ulcer (DU). 437 unrelated Chinese Han patients with DU and 148 healthy controls were genotyped by the polymerase chain reaction-restriction fragment length polymorphism method for the IL-1B-511, TNF-A-308 gene polymorphisms and the VNTR polymorphism in intron 2 of the IL-1RN gene polymorphisms. There was no difference in the genetic polymorphism of IL-1Beta-511, IL-1RN and TNF-A-308 in the patients with DU compared with control. After stratified by Helicobacter pylori infection, they also could not reach significant differences in this study. No statistically significant differences were observed in DU group compared with control according to combination of the IL-1Beta-511 and IL-1RN genotypes regardless of H. pylori positivity. These findings show that no evidence for the involvement of a proinflammatory polymorphism in the IL-1Beta-511, IL-1RN and TNF-A-308 in the susceptibility to DU in China.

AimsConcerns have increased about the risk of fatal adverse events (FAEs) associated with molecular targeted agents (MTAs) in the treatment of advanced hepatocellular carcinoma (HCC). The purpose of this study is to investigate the overall incidence and risk of FAEs in advanced HCC with administration of MTAs by using a meta-analysis of available clinical trials.Materials and methodsElectronic databases were searched for relevant articles before March 2017. Eligible studies were selected according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement. Pooled incidence, Peto ORs and 95% CIs were calculated according to the heterogeneity of selected studies.ResultsA total of 4,716 HCC participants from 10 randomized controlled trials (RCTs) were finally considered for this meta-analysis. The pooled incidence of death due to MTAs was 2.1% (95% CI 1.6%–2.8%) with a Peto OR of 1.79 (95% CI 1.07–3.01; p=0.027) in comparison with controlled groups. Subgroup analysis according to biological agents showed that brivanib treatment in HCC patients significantly increased the risk of developing FAEs (Peto OR 3.97; 95% CI 1.17–13.51; p=0.028) but not for sorafenib (Peto OR 1.78; 95% CI 0.54–5.89; p=0.34) and other MTAs (Peto OR 1.43; 95% CI 0.75–2.76; p=0.28). Sensitive analysis showed that the pooled results were influenced by removing each single trial. The most common causes of FAEs were hepatic failure (22.2%) and hemorrhage (13.3%), respectively.ConclusionClinicians should be aware of the risks of FAEs during the administration of MTAs in advanced HCC patients, especially for patients with abnormal liver function. However, the use of sorafenib remains justified in its approved indications due to their potential survival benefits and limited toxicities.

Our study intended to investigate five cytokine gene single nucleotide polymorphisms (SNPs) and their associations with prostate cancer risk. Genotypes of five cytokine gene SNPs were detected by MassARRAY for blood samples from a group of patients with prostate cancer (n = 90) and a control group (n = 140) in central China. The differences in tumor clinical stages, Gleason scores, and PSA values in patients with prostate cancer were also investigated. The frequencies of the five cytokine gene SNPs (L-1β rs16944, IL-4 rs2070874, IL-4rs2227284, IL-16 rs7175701, and IL-16 rs11556218) genotypes were not found to be significantly mutated in prostate cancer patients compared with the control group. In addition, for five cytokine gene SNPs genotypic comparisons, patients with different Gleason scores, clinical stages, and PSA values were grouped into two subgroups. There was also no statistically significant association in all these subgroups. Our study suggests that cytokine gene polymorphisms may not be a risk factor for prostate cancer in a central Chinese population. Nevertheless, more large-scale studies on the Chinese population are necessary to examine our conclusions. The discovery of cytokine gene polymorphisms related to prostate cancer could update our understanding of the etiology and improve our knowledge of the early detection, diagnosis, and treatment of prostate cancer.