Yi Zhu

MTHFR C677T and A1298C polymorphisms and cervical carcinoma susceptibility: meta-analyses based on 4421 individuals

MTHFR polymorphisms have been implicated as risk factors for several cancers. Studies have conducted on the associations of MTHFR polymorphisms with cervical carcinoma risk and have generated inconclusive results. The aim of the present study was to increase power demonstrating the possible relations. Meta-analyses examining the association between MTHFR C677T and A1298C polymorphisms and cervical carcinoma risk were performed. Separate analyses on ethnicity and source of controls were also implemented. Eligible studies were identified for the period up to Dec 2011. Eleven case–control studies containing 1859 cases and 2562 controls regarding MTHFR C677T polymorphisms were selected, of which four studies containing 461 cases and 832 controls described A1298C polymorphisms. For the overall data, no associations of MTHFR C677T polymorphisms with cervical carcinoma were observed (TT vs CC: ORxa0=xa01.07; 95xa0%CIxa0=xa00.73–1.58; dominant model: ORxa0=xa00.89; 95xa0%CIxa0=xa00.66–1.18; recessive model: ORxa0=xa01.13; 95xa0%CIxa0=xa00.84–1.52). In the subgroup analysis by ethnicity, MTHFR 677T allele was associated with decreased cervical cancer susceptibility among Caucasians (TT vs CC: ORxa0=xa00.65; 95xa0%CIxa0=xa00.45–0.93; dominant model: ORxa0=xa00.70; 95xa0%CIxa0=xa00.58–0.86) but not Asians. As for A1298C polymorphism, no marked associations of A1298C genetic variation with cervical cancer risk were observed (CC vs AA: ORxa0=xa01.01; 95xa0%CIxa0=xa00.60–1.73; dominant model: ORxa0=xa01.17; 95xa0%CIxa0=xa00.91–1.49; recessive model: ORxa0=xa00.99; 95xa0%CIxa0=xa00.60–1.63). Collectively, the results of the present study suggest that MTHFR 677T allele might play a preventive role for cervical carcinoma among Caucasians. A1298C polymorphisms might exert little effect on cervical cancerigenesis.

Cadmium Levels in Tissue and Plasma as a Risk Factor for Prostate Carcinoma: a Meta-Analysis

Cadmium is a heavy metal that has been suggested to be a carcinogen by evidence. A number of published studies have investigated the association between cadmium levels and prostate cancer, but the results were inconsistent. Thus, we conducted a meta-analysis to get a precise estimate of this subject. After a careful searching and screening, a total of 11 publications containing 14 separated studies were included. Based on a random-effect model, the pooled data showed that cadmium levels of prostate tissues (standard mean difference (SMD)u2009=u20093.17, 95xa0% confidence interval (CI)u2009=u20090.60–5.74, Pu2009<u20090.05) and plasma (SMDu2009=u20094.07, 95xa0% CIu2009=u20092.01–6.13, Pu2009<u20090.05) were significantly higher in prostate cancer patients than those in the healthy controls. No difference of hair and nail cadmium levels between the prostate cancer cases and the controls was found. The data suggested that cadmium exposure might exert an influence on the tumorigenesis of prostate tissues. Future investigations with large sample sizes are needed to verify the results.

Overexpression of SLC7A11: a novel oncogene and an indicator of unfavorable prognosis for liver carcinoma

AIMnSLC7A11 is a gene that encodes a cystine-glutamate antiporter, which has been detected to be overexpressed in various cancers. Thus, we aimed to validate its expression and clinical significance in liver cancer.nnnMETHODSnBioinformatic analysis was conducted and a tissue microarray was utilized for detecting SLC7A11 expression in liver cancer tissues by immunohistochemistry assay.nnnRESULTSnHigh expressions of SLC7A11 have no association with clinical parameters such as age, sex and clinical stages, except for advanced pathological stages. Cox regression analysis revealed that SLC7A11 might be an independent prognostic factor for liver cancer patients.nnnCONCLUSIONnSLC7A11 overexpression might be a novel biomarker and a potential unfavorable prognostic factor as well as a potential therapeutic target for liver carcinoma.

The health hazards of potentially toxic metals in the daily diets of adults and children from a mining and smelting region (Hezhang County) in southwestern China

Toxic metals accumulated in the human body are predominantly absorbed by the digestive tract in non-occupationally exposed populations. In the current study, we collected plowed soil samples, and investigated the varied food compositions in a mining and smelting area in southwestern China, to measure the concentrations of ten potentially toxic metals—As, Ba, Cd, Cr, Cu, Mn, Ni, Pb, Sr, and Zn. We collected information on the daily intakes of these metals to assess the health risks associated with their exposure among children and adults. The urine concentrations of the metals were also measured to obtain data on the amounts present in the body. The results showed that the hazard indexes (HIs) of As, Ba, Cd, Cr, Ni, Pb, and Sr were all larger than 1, for both adults and children; the Zn and Cu values were comparatively higher in children. The intake of staple foods of the region posed the greatest health risk, while drinking water only posed risks clearly associated with As exposure. The urine samples of local residents contained larger amounts of As, Cd, Cr, Cu, Mn, Ni, Pb, and Zn, confirming the hazards in the health risk assessment. Obvious differences in the urine metal concentrations between men and women were confirmed. In conclusion, higher concentrations of metals in the surface soil and rain water were the predominant cause of elevated exposure through home-grown crops and produce to accumulate in local residents’ bodies.

Effects of TiO 2 , SiO 2 , Ag and CdTe/CdS quantum dots nanoparticles on toxicity of cadmium towards Chlamydomonas reinhardtii

Nanoparticles (NPs) are inevitably released into the aquatic environment for being widely used and may affect the toxicity of other contaminants already present in the environment, such as trace metals. However, the effects of NPs on the ecotoxicity of cadmium (Cd), a common environmental trace metal pollutant, are not well explored. In this study, effects of four widely used NPs TiO2 (n-TiO2), SiO2 (n-SiO2), Ag (n-Ag) and CdTe/CdS core/shell quantum dots (QD) on the toxicity of Cd to the freshwater algae Chlamydomonas reinhardtii were assessed respectively. Cd reduced the algae biomass, impaired the photosynthetic activities, and led to intracellular oxidative stress of algae. At non-toxic concentrations, both n-TiO2 (100u202fmgu202fL-1) and n-SiO2 (400u202fmgu202fL-1) attenuated the toxicity of Cd towards the algae for reducing the intracellular Cd contents, and the former was more pronounced. QD (0.5u202fmgu202fL-1) increased the toxicity of Cd to algae, but n-Ag (0.2u202fmgu202fL-1) had no significant influence on the Cd toxicity to algae. The microscopic observations on the ultrastructure of algae cells presented the same phenomena and n-TiO2, n-SiO2 aggregations were clearly observed outside the cell wall. Furthermore, the regulation of NPs to the Cd toxicity towards algae was related to the intracellular nitric oxide (NO), an important signaling molecule, rather than the phototaxis of algae. Above all, this study provided a basic understanding about the difference in joint toxicity of different kinds of NPs and Cd to aquatic organisms.

Identification and Characterization of Cadmium-Related Genes in Liver Carcinoma

Evidence indicates that exposure to heavy trace element might be a risk factor for liver carcinoma. Cadmium has been supposed to be a carcinogen that has a correlation with the risk of a number of cancers, including liver cancer. However, the mechanisms underlying Cadmium-induced malignant transformation in liver cells are not fully understood. In the present study, we aimed to screen the differentially expressed genes (DEGs) that might play a role in both the Cadmium-related liver cell transformation and the development of liver cancer. Microarray-based gene expression profiles concerning liver carcinoma vs non-cancerous tissue (GSE64041) and Cadmium-treated liver cells vs controls (GSE8865 and GSE31286), respectively, were retrieved from Gene Expression Omnibus (GEO) database. Then, DEGs of each profile were calculated and screened. The intersection of each DEGs was obtained by Venn analysis. Afterwards, the possible roles of the selected genes in cancer development were evaluated by using Oncomine database and TCGA cohort analysis. Consequently, three DEGs, LRAT, SLC7A11, and ITGA2, were selected for further analysis. SLC7A11 and ITGA2, but not LRAT, were upregulated in liver cancer compared with those in normal tissues, respectively. After using a TCGA cohort analysis, results failed to show a significant correlation between SLC7A11 or ITGA2 expression and clinical parameters. However, the survival analysis showed that patients with high expression levels of SLC7A11 had a shorter overall survival time relative to those of the patients with low levels. In conclusion, SLC7A11 and ITGA2 might play a role in the Cadmium-induced liver cell damage or transformation, and the development of liver carcinoma. SLC7A11 might be a prognostic factor for patients with liver carcinoma. Future validation experiments are needed to verify the results.

N-acetyltransferase 2 genetic variants confer the susceptibility to head and neck carcinoma: evidence from 23 case-control studies

Previous evidence indicated that N-acetyltransferase 2 (NAT2) polymorphisms might be a risk factor for several cancers. A number of studies have been conducted on the association between NAT2 polymorphisms and head and neck cancer (HNC) risk. Nevertheless, the results were conflicting. Published meta-analysis on this issue has generated inconclusive results. Thus, we aimed to derive a more precise estimation of the relationship by conducting an updated meta-analysis. Published data prior to August 2013 have been searched and screened. Subgroup analysis on ethnicity, source of controls, sample size, and genotyping method were also performed. As a result, a total of 23 case–control studies including 4,028 cases and 4,872 controls were selected for analysis. Interestingly, the results showed that NAT2 polymorphisms might increase HNC risk for the overall data (OR 1.23, 95xa0% CI 1.01–1.49). Moreover, in subgroup analyses according to ethnicity, data showed that slow acetylators might increase HNC susceptibility among Asians (OR 1.78, 95xa0% CI 1.27–2.49), but not among Caucasians or mixed ethnicities. In conclusion, NAT2 polymorphism might be a low-penetrant risk factor for HNC among Asians.

Identification of key genes and pathways and therapeutic agents in cadmium-treated liver cells: A bioinformatics study.

Evidence indicates that Cadmium (Cd) can accumulate in liver, which results in acute or chronic cell damage with unclear complex mechanisms. Thus, we aimed to explore the possible molecules and pathways by using bioinformatics methods Consequently, two datasets (GSE8865 and GSE31286) were retrieved and the differentially expressed genes (DEGs) were screened out. The intersection of the DEGs included seven up-regulated and forty-three down-regulated genes, which were mainly enriched in biological cell proliferation items, and were enriched in several metabolism-related pathways. Among the DEGs, several hub genes such as EGR1, FOSL1, ITGA2, EDN1, and IER3 were screened out through protein-protein interaction analysis. Interestingly, BW-B70C was predicted to be a potential agent for attenuating Cd-induced liver cell damage. The present study gave a novel insight into the mechanisms of Cd-induced liver cell damage or malignant transformation and identified several small agents that might be critical for Cd toxicity prevention and treatment.