Several epidemiological studies have previously investigated the association between the TP53 codon 72 polymorphism and oral squamous cell carcinoma (OSCC) susceptibility; however, current results are inconsistent. We therefore performed this meta-analysis to thoroughly investigate any association among Asian patients.

A number of studies have investigated the association between human leukocyte antigen-G (HLA-G) 14-bp insertion/deletion polymorphism and cancer risk, but the results remain controversial. In this study we aimed to clarify whether this association really exists.

The association between Interleukin-17A (IL- 17A) G197A and IL-17F T7488C polymorphisms and risk for specific forms of cancer is inconclusive. We conducted a meta-analysis of all published studies to estimate the association of IL-17A G197A and IL-17F T7488C polymorphisms and cancer risk.

Previous case-control studies on the relation between angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and breast cancer did not reach the same conclusion. In the present study, we aimed to further evaluate the relationship between the ACE gene I/D polymorphism and breast cancer.

This meta-analysis aimed to comprehensively examine the relationship between the clinicopathological and demographical characteristics and ALK rearrangements in patients with non-small cell lung cancer (NSCLC).

Microarray technology shows great potential but previous studies were limited by small number of samples in the colorectal cancer (CRC) research. The aims of this study are to investigate gene expression profile of CRCs by pooling cDNA microarrays using PAM, ANN, and decision trees (CART and C5.0).

We performed meta-analysis to estimate pooled prevalence, risk factors, and outcomes of interval colorectal cancers (CRCs).

A number of studies have investigated the association between CRR9p polymorphism and risk of lung cancer (LC), yet the role in LC pathogenesis remains unclear owing to inconsistencies across studies. We searched PubMed, Embase, and Web of Science for all medical literature published until January 2014. Pooled odds ratios (ORs) and 95 % confidence intervals (CIs) were obtained by means of the fixed effects model. Data from eight studies satisfying the predesigned inclusion criteria were selected for this meta-analysis. We found a statistically significant evidence for a protective effect on the overall LC risk (TT vs. CC: OR = 0.78, 95 % CI = 0.70-0.87, P het = 0.299; TT vs. CT + CC: OR = 0.81, 95 % CI = 0.73-0.90, P het = 0.113; T vs. C: OR = 0.90, 95 % CI = 0.86-0.95, P het = 0.758; TT + CT vs. CC: OR = 0.92, 95 % CI = 0.87-0.98, P het = 0.892). Both Caucasian and Asian populations were suggested to have a reduced risk of developing such cancer. In the analysis of the association between rs401681 and non-small cell lung cancer (NSCLC) risks, all of the contrast models showed similar results except the CT vs. CC genetic model (OR = 0.93, 95 % CI = 0.84-1.02, P het = 0.568). Our meta-analysis provides supportive evidence that CRR9p polymorphism may influence a risk of LC and NSCLC in a protective model.

Numerous investigations have examined the association between MTR rs1805087 A> G polymorphism and non-Hodgkin lymphoma (NHL) susceptibility, yet have generated conflicting results. Therefore, the current meta-analysis was performed to comprehensively reevaluate this association. A systematic literature search of PubMed and Embase databases was conducted to seek eligible publications. The final analysis included 13 publications with a total of 4555 cases of NHL and 6931 controls. Overall, pooled analysis did not yield any statistically significant association between MTR rs1805087 A> G and NHL risk. Stratification analysis by source of controls showed a decreased risk of NHL with the polymorphism of interest in hospital-based studies, while no significant association was observed when data were stratified by ethnicity, sample size and NHL subtype. This meta-analysis does not indicate a major role of the MTR rs1805087 A> G polymorphism in modulating NHL risk. However, well-designed prospective studies with large sample sizes are encouraged to validate our findings.

Cadherin-1 (CHD1), as an invasion suppressor gene, could suppress tumor cell invasion and metastasis in various tumors, but reduced CHD1 levels, resulting from epigenetic silencing, are common in poorly differentiated, advanced stage carcinomas. This meta-analysis was performed to evaluate the relationships between promoter methylation of CHD1 and breast cancer. Relevant studies were retrieved from the Web of Science (1945 ~ 2013), the Cochrane Library (Issue 12, 2013), PubMed (1966 ~ 2013), EMBASE (1980 ~ 2013), CINAHL (1982 ~ 2013), and the Chinese Biomedical Database (CBM) (1982 ~ 2013) using a systematic literature search. Results were summarized by meta-analyses, conducted using the STATA software (version 12.0, Stata Corporation, College Station, TX, USA). Odds ratios (ORs) and 95 % confidence intervals (95 % CIs) were calculated. In the present meta-analysis, 9 cohort studies with a total of 425 patients with breast cancer were included. Our meta-analysis results demonstrated that the frequency of CHD1 promoter methylation in cancer tissues was significantly higher than that in normal tissues, adjacent tissues, and benign tissues (cancer tissue vs. normal tissue OR = 30.87, 95 % CI = 16.76 ~ 56.86, P < 0.001; cancer tissue vs. adjacent tissue OR = 23.30, 95 % CI = 12.85 ~ 42.26, P < 0.001; cancer tissue vs. benign tissue OR = 2.94, 95 % CI = 1.60 ~ 5.40, P < 0.001; respectively). Ethnicity-stratified analysis indicated that aberrant CHD1 promoter methylation was strongly correlated with breast cancer among both Asians and Caucasians in the majority of subgroups. Our results suggest that aberrant promoter methylation of the CHD1 gene may have a high frequency in breast cancer tissues. Thus, CHD1 methylation could be correlated with the pathogenesis of breast cancer.

Some publications have evaluated the correlation between KIF1B rs17401966 polymorphism and hepatocellular carcinoma (HCC) with conflicting results. We performed this meta-analysis to clarify the association of KIF1B rs17401966 polymorphism and HCC risk. We searched PubMed, ISI Web of Knowledge, ScienceDirect, and Google Scholar. The combined odds ratio (OR) with 95 % confidence interval (CI) was calculated to estimate the strength of the association. Heterogeneity and publication bias were also assessed. In total, 15 case-control studies with 7,596 HCC cases and 9,614 controls were included in the meta-analysis. A significant association between KIF1B rs17401966 polymorphism and HCC risk was detected (OR = 0.81, 95 % CI 0.72-0.91, P < 0.001). We also found a significant association between KIF1B rs17401966 polymorphism and HCC risk in Chinese (OR = 0.77, 95 % CI 0.67-0.89, P < 0.001). In the subgroup analysis by gender, KIF1B rs17401966 polymorphism was significantly associated with HCC risk in man (OR = 0.57, 95 % CI 0.51-0.64, P < 0.001). In the subgroup analyses of age, the similar associations were also observed in young patients (OR = 0.50, 95 % CI 0.39-0.66, P < 0.001) and old patients (OR = 0.66, 95 % CI 0.57-0.77, P < 0.001). However, no association was observed in women subgroup (OR = 0.79, 95 % CI 0.59-1.06, P = 0.11). This meta-analysis showed a significant association between KIF1B rs17401966 polymorphism and HCC.

Human leukocyte antigen-G (HLA-G) is involved in the development and progression of human cancers, and numerous molecular epidemiological studies have been conducted to explore the potential relationship of HLA-G 14-bp insertion/deletion (ins/del) polymorphism with cancer risk. However, results from published studies were inconclusive.

TAZ, also known as WWTR1, has recently been suggested as an oncogene in non-small cell lung cancer (NSCLC). We investigated the clinical relevance of TAZ expression and its functional role in NSCLC tumorigenesis.

It has been proven that epidermal growth factor receptor (EGFR) mutation is the most important predictive factor for determining the effect of EGFR tyrosine kinase inhibitors (TKIs) applied to non-small cell lung cancer (NSCLC) patients. The patients with EGFR mutations response better to TKIs. To detect EGFR mutation has been particularly essential to select first-line treatment for lung cancer patients. To research and analyze the sensitivity and specificity of immunohistochemistry (IHC) using mutation specific antibodies in detecting EGFR mutations compared with DNA sequencing, and further evaluate the accuracy and clinical application value of IHC.

In recent years, high throughput technologies such as microarray platform have provided a new avenue for hepatocellular carcinoma (HCC) investigation. Traditionally, gene sets enrichment analysis of survival related genes is commonly used to reveal the underlying functional mechanisms. However, this approach usually produces too many candidate genes and cannot discover detailed signaling transduction cascades, which greatly limits their clinical application such as biomarker development. In this study, we have proposed a network biology approach to discover novel biomarkers from multidimensional omics data. This approach effectively combines clinical survival data with topological characteristics of human protein interaction networks and patients expression profiling data. It can produce novel network based biomarkers together with biological understanding of molecular mechanism. We have analyzed eighty HCC expression profiling arrays and identified that extracellular matrix and programmed cell death are the main themes related to HCC progression. Compared with traditional enrichment analysis, this approach can provide concrete and testable hypothesis on functional mechanism. Furthermore, the identified subnetworks can potentially be used as suitable targets for therapeutic intervention in HCC.

Glutathione S-transferases (GSTs) have proved to be involved in the detoxifying several carcinogens and may play an important role in carcinogenesis of cancer. Previous studies on the association between Glutathione S-transferase M1 (GSTM1) polymorphism and gastric cancer (GC) risk reported inconclusive results. To get a precise result, we conducted this present meta-analysis through pooling all eligible studies.

Published studies investigating the association between XPC Lys939Gln polymorphism and colorectal cancer (CRC) risk reported inconclusive results. We performed a meta-analysis to derive a precise estimation of the relationship.

The 677 C>T and 1298 A>C polymorphisms of methylenetetrahydrofolate reductase (MTHFR) gene have been widely reported and considered to have a significant effect on breast cancer risk, but the results are inconsistent. A meta-analysis based on 57 eligible studies was carried out to clarify the role of MTHFR gene polymorphisms in breast cancer.

Many studies have suggested that microRNAs (miRNAs) might serve as novel diagnostic indicators of thyroid cancer (TC). However, inconsistent results have also been reported. This meta-analysis was conducted to assess the diagnostic value of miRNAs in discriminating malignant thyroid nodules from benign ones on fine-needle aspiration samples. A systematic literature search for relevant literature published up to April 5, 2014 was conducted in PubMed, Embase, Chinese National Knowledge Infrastructure (CNKI), and Chinese Biological Medicine (CBM) databases. Data from different studies were pooled to estimate the summary sensitivity (SEN), specificity (SPE), positive likelihood ratios (PLR), negative likelihood ratios (NLR), diagnostic odds ratio (DOR), using the random-effect model. Summary receiver operator characteristic curves (SROCs) were plotted and areas under the SROC curve (AUC) were calculated to evaluate the overall test performance. Between-study heterogeneity was tested using the Q tests and the I (2) statistics. Potential sources of heterogeneity were analyzed through subgroup analyses and meta-regression. Deeks' funnel plot asymmetry test was performed to evaluate publication bias. All analyses were performed using STATA 12.0 software. Eighteen studies from 7 articles, including 543 patients with malignant thyroid nodules (n = 266) and benign ones (n = 277), were included in this meta-analysis. The pooled SEN was 0.77 (95 % CI: 0.70-0.83), SPN was 0.75 (95 % CI: 0.68-0.81), PLR was 3.1 (95 % CI: 2.4-4.0), NLR was 0.30 (95 % CI: 0.23-0.39), DOR was 10 (95 % CI: 7-16), and AUC was 0.83 (95 %CI: 0.79-0.86). Subgroup analyses indicated that multiple miRNAs assays showed a higher diagnostic accuracy than single miRNA assays. In conclusion, this meta-analysis suggests that miRNAs analysis can significantly improve diagnostic accuracy for differentiating malignant thyroid nodules from benign indeterminate ones on fine-needle aspiration (FNA) samples. With further confirmation, multiple miRNAs assays may play a critical role as a complement to fine-needle aspiration biopsy (FNAB).

Conflicting results were implicated in both single case-control studies and meta-analyses of the correlation between p73 G4C14-to-A4T14 polymorphism and lung cancer risk. We designed this study to further assess the association by meta-analysis. A meta-analysis was performed based on five case-control studies (5,467 subjects) retrieved from PubMed and Embase. Odds ratios (ORs) with 95 % confidence intervals (CIs) were measured for the association using the models of random effects and fixed effects. The results showed no evidence between p73 G4C14-to-A4T14 polymorphism and lung cancer risk in any genetic model (allele model: OR, 1.06, 95 % CI, 0.89-1.26; homozygote genotypes: OR, 1.18, 95 % CI, 0.80-1.73; heterozygote genotypes: OR, 1.04, 95 % CI, 0.89-1.23; dominant model: OR, 1.05, 95 % CI, 0.89-1.24; recessive model: OR, 1.17, 95 % CI, 0.93-1.47). Subgroup analyses according to ethnicity, however, detected significant association in Caucasian population. Our study provides evidence that p73 G4C14-to-A4T14 polymorphism may play a major role in susceptibility to lung cancer in Caucasians.