hOGG1 encodes a DNA repair enzyme responsible for the excision of reactive oxygen species (ROS) in damaged DNA. Previous studies have obtained inconsistent results. To validate the association between the hOGG1Ser326Cys polymorphism and lung cancer risk, we performed an updated meta-analysis of 20 studies (8739 cases and 10385 controls) using STATA version 11.1. With this approach, we tested the overall and subgroup association between the SNP and lung cancer susceptibility stratified by ethnicity, control sources, cell histotypes, and smoking status. We demonstrated a novel, significant correlation between the hOGG1 Ser326Cys polymorphism and increased lung cancer susceptibility in Caucasians. Our findings indicate a need for larger-scale studies to verify the association of this SNP with lung cancer risk in Caucasians.

The association of VEGF+405G/C (where VEGF is vascular endothelial growth factor) polymorphism and malignancy susceptibility attracts considerable attention because VEGF is one of the most potent angiogenic factors and plays a critical role in the onset and development of malignancy. However, the published findings remain inconclusive. In order to derive a more precise assessment of the association, we performed a meta-analysis including 30 published case-control studies from PubMed, Embase, and Ovid databases. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of the association. In the pooled analyses, no significant association was found between VEGF+405G/C polymorphism and malignancy susceptibility in different genetic models (G-allele vs. C-allele: OR=1.00, 95% CI: 0.93-1.07; CC vs. GG: OR=1.01, 95% CI: 0.88-1.15; GC+CC vs. GG: OR=1.00, 95% CI: 0.91-1.10; CC vs. GC+GG: OR=1.01, 95% CI: 0.90-1.13). When stratified by ethnicity, a weak association between this polymorphism and malignancy susceptibility was found in African under allelic frequency comparison (OR=0.65, 95% CI: 0.43-0.98) and dominant genetic model comparison (OR=1.95, 95% CI: 1.09-3.50). In summary, although our meta-analysis indicated a weak association of VEGF+405G/C polymorphism with malignancy susceptibility in African, no persuasive evidence of association between the polymorphism and malignancy susceptibility was detected in the pooled analyses. Therefore, more studies with larger scale of participants, especially Africans, are required to further evaluate gene-environment interaction on this polymorphism and malignancy susceptibility.

The association between hepatocellular carcinoma (HCC) and the 61A>G polymorphism in the epidermal growth factor (EGF) gene has been analyzed in several studies, but results have been inconsistent. The aim of this study was to integrate previous findings and explore whether this polymorphism is associated with susceptibility to HCC. A meta-analysis was performed by searching PubMed, Web of Science, and Cochrane Library databases. Data were extracted using predefined form and pooled odds ratios (OR) with 95% confidence intervals (CI) and were calculated to evaluate the strength of this association. Five studies involving 690 cases, 514 healthy controls, and 1419 controls with cancer-free liver diseases were identified. On the basis of healthy controls, the significant main effects on HCC risk were observed in a heterozygote comparison (OR=1.76, 95% CI 1.07-2.90, p=0.02) and a dominant genetic model (OR=1.65, 95% CI 1.03-2.66, p=0.04). On the basis of the controls with cancer-free liver diseases, a significantly increased risk of HCC was found in all the genetic models. Subgroup analyses stratified by ethnicity and etiology of HCC also showed positive associations. The EGF 61G allele is a risk factor for developing HCC without the influence of ethnic and etiological diversity.

Evidence indicates that CYP1A1 MspI polymorphism might be a possible risk factor for several malignancies. A growing body of literature has been devoted to the association of CYP1A1 MspI polymorphism with acute myeloid leukemia (AML). However, the results remain conflicting. The aim of the present study was to derive a more precise estimation of the relationship.

Evidence suggests that MDM2 T309G polymorphism may be a risk factor for several cancers. Increasing investigations have been conducted on the association of MDM2 T309G polymorphisms with lung cancer risk and have yielded conflicting results. Previous meta-analyses on this issue have reported inconclusive data. The aim of the present study was to derive a more precise estimation of the relationship.

Many microRNAs (miRNAs) exhibit altered expression levels in cancers, and they may be considered as valuable prognostic biomarkers for cancers. Here we aimed to summarize the recent advances in miR-210 involvement in human breast cancer and analyze the predicting role of miR-210 for survival.

The aim of this meta-analysis was to explore the association between the manganese superoxide dismutase (MnSOD) gene polymorphism and breast cancer risk, and to investigate the interaction of this gene polymorphism with known risk factors for breast cancer. Crude odds ratios (ORs) with 95% confidence intervals (CIs) for breast cancer risk associated with co-dominant models [valine/alanine (Val/Ala) vs. Val/Val, Ala/Ala vs. Val/Val], a dominant model (Val/Ala + Ala/Ala vs. Val/Val) and a recessive model (Ala/Ala vs. Val/Ala + Val/Val) were statistically estimated. This meta‑analysis included 8,102 breast cancer cases and 9,740 controls from 14 published case-control studies. The data revealed no significant association between the MnSOD polymorphism and the risk of developing breast cancer. However, upon subgroup analyses, the risk was significantly increased in premenopausal women with the dominant model of the MnSOD gene polymorphism (OR, 1.15; 95% CI, 1.01-1.31). Statistically significant increased risks were also identified in women with the MnSOD genotypes containing the Ala allele who had a tobacco smoking history (OR, 1.17; 95% CI, 1.02-1.34), a higher body mass index (OR, 1.26; 95% CI, 1.02-1.56) or who used oral contraceptives (OR, 1.98; 95% CI, 1.34-2.93). By contrast, there was no significant association between breast cancer risk and alcohol consumption and ethnicity. This meta‑analysis demonstrated no statistically significant association between the MnSOD gene polymorphism and breast cancer susceptibility, except in premenopausal women with certain unhealthy lifestyle habbits.

The current study aimed to investigate the effects of p16 hypermethylation on breast cancer quantitatively through a meta-analysis of available case-control studies (including malignant, benign and normal breast cancer tissues). The PubMed, Web of Science and EBSCO databases were searched from their inceptions to February 1, 2012. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were extracted and pooled to assess the strength of the association between p16 hypermethylation and breast cancer risk. A total of eight studies, including 691 breast cancer cases and 525 control cases, were identified for meta-analysis. Statistically significant ORs of p16 hypermethylation were obtained from the breast cancer and control groups (OR, 6.58; 95% CI, 1.15-37.75; P=0.03). However, no significant associations between the methylation and ER and PR status in breast cancer were detected (OR, 1.24; 95% CI, 0.64-2.41; P=0.52; OR, 1.49; 95% CI, 0.81-2.75; P=0.20, respectively). The meta-analysis indicated that p16 hypermethylation significantly increases breast cancer risk. However, no significant associations between the methylation and ER and PR status in breast cancer were detected.

Relationship between the p27Kip1 (here after referred to as p27) V109G polymorphism and cancer risk has been extensively studied; however, results from different studies were not fully consistent. Therefore, we carried out a meta-analysis to comprehensively assess the correlation between the p27V109G polymorphism and the cancer risk. Articles on the relationship of the p27V109G polymorphism with cancer risk were searched from Medline, Pub Med, and Web of science databases. A total of eight eligible studies with 3591 cases and 3799 controls were included in this meta-analysis. Overall, it seemed that the G allele was not associated with the elevated cancer risk (pooled odds ratio [OR]=0.98, 95% confidence interval [CI]: 0.88-1.09, p=0.68, fixed effects). Analyses in different populations revealed that no statistically significant associations between the G allele and cancer risk were demonstrated in Caucasians or Asians. When analyzed in different types of cancer that, from two studies, the G allele was found to be associated with a decreased risk of prostate cancer in a dominant genetic model (pooled OR=0.60, 95% CI=0.36-0.98, p=0.04, fixed effects), but did not alter the breast cancer risk from four studies. In conclusion, this meta-analysis indicated that the p27V109G polymorphism did not correlate with the overall cancer risk in the general population.

Excision repair cross complementing group 5 (ERCC5 or XPG) plays an important role in regulating DNA excision repair, removal of bulky lesions caused by environmental chemicals or UV light. Mutations in this gene cause a rare autosomal recessive syndrome, and its functional single nucleotide polymorphisms (SNPs) may alter DNA repair capacity phenotype and cancer risk. However, a series of epidemiological studies on the association between the ERCC5 Asp1104His polymorphism (rs17655, G>C) and cancer susceptibility generated conflicting results.

Non-small cell lung cancer (NSCLC) is one of the most common malignant tumors; however, its causes are still not completely understood. This study was designed to screen the key genes and pathways related to NSCLC occurrence and development and to establish the scientific foundation for the genetic mechanisms and targeted therapy of NSCLC.

The C677T and A1298C polymorphisms of methylenetetrahydrofolate reductase (MTHFR) have been reported to alter the risk of ovarian cancer. However, the results are still inconclusive. For better understanding of the effect of these two polymorphisms on ovarian cancer risk, a meta-analysis was performed. An extensive search was performed to identify all case-control studies investigating such association. The strength of association between these two polymorphisms and ovarian cancer risk was assessed by odds ratio (OR) with the corresponding 95 % confidence interval (95 % CI). 3,496 cases and 3,631 controls for C677T polymorphism and 3,280 cases and 3,346 controls for A1298C polymorphism were included in this meta-analysis. The results suggested that there were no significant associations between C677T and A1298C polymorphisms and ovarian cancer risk in overall comparisons in all genetic models (For C677T: TT vs. CC: OR = 0.94, 95 % CI = 0.71-1.24, P = 0.65; CT vs. CC: OR = 1.03, 95 % CI = 0.93-1.14, P = 0.57; TT/CT vs. CC: OR = 1.01, 95 % CI = 0.88-1.16, P = 0.87; TT vs.

: The K-ras gene is one of the commonly mutated oncogenes associated with colorectal cancer. However, its prognostic significance for patients with colorectal cancer remains inconclusive.

Lymph node invasion is one of the most powerful clinical factors in cancer prognosis. However, molecular level signatures of their correlation are remaining poorly understood. Here, we propose a new approach, monotonically expressed gene analysis (MEGA), to correlate transcriptional patterns of lymph node invasion related genes with clinical outcome of breast cancer patients.

FTO gene single nucleotide polymorphisms (SNPs) have been shown to be associated with obesity-related traits and type 2 diabetes. Several small studies have suggested a greater than expected effect of the FTO rs9939609 SNP on weight in polycystic ovary syndrome (PCOS). We therefore aimed to examine the impact of FTO genotype on BMI and weight in PCOS.

The cell cycle checkpoint kinase 2 (CHEK2) gene I157T variant may be associated with an increased risk of breast cancer, but it is unclear whether the evidence is sufficient to recommend testing for the mutation in clinical practice.

Previous studies concerning the association between methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism and colorectal cancer risk in Asian populations generated conflicting results. A meta-analysis was therefore performed to allow a more reliable estimate of any link.

To clarify any association between the hOGG1 Ser326Cys polymorphism and susceptibility to gastric cancer.

The -160C/A polymorphism (rs16260) of E-cadherin, a tumor repressor gene, has been shown to be a tumor susceptibility allele for various types of cancers. Because the significance of this polymorphism to cancer risk has been recognized, there are increasing studies investigating -160C/A in different types of cancers and ethnic populations. However, there is still uncertainty about the level of risk for a variety of cancers.