Effects of Xeroderma pigmentosum group C polymorphism on the likelihood of prostate cancer.

BACKGROUND: Numerous studies have assessed the association between xeroderma pigmentosum complementation group C (XPC) polymorphisms and susceptibility of prostate cancer (PCa); however, the findings remain inconsistent. METHODS: We performed an updated analysis utilizing data from electronic databases to obtain a more accurate estimation of the relationship between XPC rs2228001 A/C polymorphism and PCa risk. We further used in silico tools to investigate this correlation. RESULTS: Totally, 5,305 PCa cases and 6,499 control subjects were evaluated. When all studies pooled together, we detected no positive result (recessive genetic model: OR = 1.14, 95% CI = 0.93-1.40, Pheterogeneity  = 0.001, P = .212); nevertheless, the XPC rs2228001 A/C variant was associated with PCa risk in Asian descendants in the subgroup analysis (OR = 1.21, 95% CI = 1.01-1.43, Pheterogeneity  = 0.008, P = .034). In silico tools showed that more than 20 proteins can participate in the protein crosstalk with XPC. The expression of XPC was down-regulated in all Gleason scores of prostate cancer. CONCLUSIONS: The present study indicated that the XPC rs2228001 A/C variant may be associated with elevated PCa risk in Asian patients.

New insights into the association between AXIN2 148 C/T, 1365 C/T, and rs4791171 A/G variants and cancer risk.

BACKGROUND: Many epidemiological studies have investigated association of AXIN2 variants on overall cancer risks; however, the available results remain inconsistent. METHODS: An updated analysis was conducted to ascertain a more accurate estimation of the correlation between AXIN2 148 C/T, 1365 C/T, and rs4791171 A/G polymorphisms and cancer risk. We also used in silico tools to assess the effect of AXIN2 expression on cancer susceptibility and overall survival time. RESULTS: A total of 4281 cases and 3955 control participants were studied. The overall results indicated that AXIN2 148 C/T variant was associated with cancer risk (allelic contrast: OR = 0.88, 95% CI 0.77-0.99, P heterogeneity = 0.004; dominant model: OR = 0.82, 95% CI 0.69-0.96, P heterogeneity = 0.022), especially for lung and prostate adenocarcinoma. Similar results were observed in 1365 C/T polymorphism (OR = 0.71, 95% CI 0.61-0.98, P heterogeneity = 0.873; dominant model: OR = 0.66, 95% CI 0.47-0.94, P heterogeneity = 0.775). Moreover, in subgroup analysis by ethnicity, similar findings were obtained for Asian and Caucasian populations. Results from in silico tools suggested that AXIN2 expressions in lung adenocarcinoma were lower than that in normal group. CONCLUSIONS: Our findings indicated that AXIN2 148 C/T and 1365 C/T variants may be associated with decreased cancer susceptibility.

Rs4938723 Polymorphism Is Associated with Susceptibility to Hepatocellular Carcinoma Risk and Is a Protective Factor in Leukemia, Colorectal, and Esophageal Cancer.

BACKGROUND Growing evidence indicates that a non-coding RNA named miR-34b/c plays crucial roles in carcinogenesis, and its common polymorphism, pri-miR-34b/c rs4938723, also participates in this process and is associated with cancer susceptibility. However, this association was previously undefined and ambiguous. Therefore, we carried out an updated analysis to evaluate this relationship between rs4938723 polymorphism and cancer susceptibility. MATERIAL AND METHODS PubMed, EMbase, Web of Science and Chinese language (WanFang, CNKI and VIP) databases were searched for relevant studies until Sep 10, 2018. Odds ratios and 95% confidence interval were applied to assess this relationship. RESULTS Thirty case-control studies were retrieved. No positive association was found in either the overall study population or in the subgroups, based on ethnicity, source of group, sex, smoking, and drinking status. The main results were observed in the stratified analysis subgroups in cancer type subgroup: rs4938723 polymorphism may be a protective factor in leukemia, colorectal cancer, and esophageal cancer; however, C-allele was a risk factor in carriers for hepatocellular carcinoma. Last but not the least, poor positive results were discovered in the age subgroup. CONCLUSIONS Current meta-analysis suggested that rs4938723 polymorphism was potentially associated with hepatocellular carcinoma risk, but this polymorphism had a decreased association for susceptibility to esophageal cancer, leukemia, and colorectal cancer. Furthermore, studies with larger sample sizes and including gene-gene or gene-environment interactions should be carried out to elucidate the role of rs4938723 polymorphism in cancer risk.