Association of MTHFR C677T and A1298C polymorphisms with oral cancer susceptibility: evidence from a meta-analysis.

Methylenetetrahydrofolate reductase (MTHFR) is a central enzyme involved in folate metabolism and plays an important role in DNA synthesis and methylation. Several studies have been conducted to illustrate the associations between MTHFR C677T and A1298C polymorphisms with oral cancer susceptibility; however, the results are inconsistent. Therefore, we conducted an updated meta-analysis to obtain a more reliable estimation of the associations. We retrieved eligible studies from PubMed, EMBASE, and CBM databases through September 2016. Ultimately, pooled analyses involved 10 studies with 1443 cases and 1640 controls for the C677T polymorphism, as well as five studies with 973 cases and 1024 controls for the A1298C polymorphism. Risk estimates were presented as odds ratios (ORs) and 95% confidence intervals (95% CIs). Pooled results indicated that neither C677T nor A1298C polymorphism was associated with oral cancer susceptibility. However, a borderline significant association was detected between MTHFR C677T polymorphism and a decreased oral cancer risk (homozygous model: OR=0.71, 95% CI=0.50-1.00) in hospital-based studies. Our results suggested that MTHFR C677T and A1298C polymorphisms might not be associated with oral cancer risk. However, more evidence is needed to further confirm these findings in the future.

Smoking and hOGG1 Ser326Cys polymorphism contribute to lung cancer risk: evidence from a meta-analysis.

The human 8-oxoguanine DNA glycosylase (hOGG1) gene plays an important role in the repair of oxidatively damaged DNA base lesions and its functional single nucleotide polymorphisms (SNPs) may alter DNA repair capacity and thus contributes to cancer susceptibility. Numerous studies have investigated the association between hOGG1 Ser326Cys polymorphism and lung cancer susceptibility; however, the conclusions are still inconclusive. We searched eligible publications from MEDLINE, EMBASE, and CBM and performed a meta-analysis to assess the associations between hOGG1 Ser326Cys polymorphism and lung cancer risk. Pooled odds ratios (ORs) and 95 % confidence intervals (CIs) were calculated to estimate risk associations, and false-positive report probability (FPRP) analysis was also carried out to evaluate significant findings. A total of 31 investigations with 10,220 cases and 12,284 controls were identified. When all studies were pooled, a significantly increased overall lung cancer risk was found (Cys/Cys vs. Ser/Ser: OR = 1.24, 95 % CI = 1.05-1.47, P = 0.013; recessive model: OR = 1.22, 95 % CI = 1.05-1.41, P = 0.008, and Cys vs. Ser: OR = 1.11, 95 % CI = 1.02-1.21, P = 0.022), and further stratification analysis showed that the association was stronger in Asians, never smokers, and more-cigarette takers. These results were confirmed by FPRP analysis. Despite some limitations, this meta-analysis provides solid evidence that hOGG1 Ser326Cys polymorphism may contribute to lung cancer risk, particularly for Asian populations, never smokers, and more-cigarette takers. Nevertheless, these findings warrant further validation in single large investigations.

Poly (AT) deletion/insertion polymorphism of the XPC gene contributes to urinary system cancer susceptibility: a meta-analysis.

Numerous studies have investigated the association between xeroderma pigmentosum complementation group C (XPC) poly (AT) deletion/insertion (PAT -/+) polymorphism and cancer susceptibility; however, the findings are inconsistent. Therefore, we performed a meta-analysis based on 32 publications including 10,214 cases and 11,302 controls to acquire a more robust estimation of the relationship. We searched publications from MEDLINE, EMBASE and CBM which assessed the associations between XPC PAT -/+ polymorphism and cancer risk. We calculated pooled odds ratio (OR) and 95% confidence interval (CI) by using either fixed-effects or random-effects model. We found that individuals carrying the PAT +/+ genotype have significantly increased cancer risk (PAT +/+ vs. PAT -/-: OR=1.18, 95% CI=1.03-1.35 and recessive model: OR=1.19, 95% CI=1.06-1.33). Further stratification analysis showed a significantly increased risk for prostate cancer (PAT +/+ vs. PAT -/-: OR=2.20, 95% CI=1.39-3.48, recessive model: OR=2.07, 95% CI=1.33-3.23 and PAT + vs. PAT -: OR=1.39, 95% CI=1.12-1.71), bladder cancer (recessive model: OR=1.33, 95% CI=1.03-1.72), Caucasian ethnicity (recessive model: OR=1.21, 95% CI=1.02-1.43), population-based studies (recessive model: OR=1.23, 95% CI=1.05-1.43) and studies with relatively large sample size (PAT +/+ vs. PAT -/-: OR=1.18, 95% CI=1.04-1.35 and recessive model: OR=1.20, 95% CI=1.08-1.33). Despite some limitations, this meta-analysis established solid statistical evidence for the association between the XPC PAT +/+ genotype and cancer risk, especially for urinary system cancer, but this association warrants further validation in single large studies.

[Relation of nerve growth factor expression with perineural invasion and pain in pancreatic cancer].

OBJECTIVE: To investigate the association of nerve growth factor (NGF) expression with perineural invasion and pain in pancreatic cancer. METHODS: NGF expression was detected by Northern blotting and immunohistochemistry in 28 pancreatic cancer and 20 normal pancreatic tissue samples. Correlation analysis of the results with the extent of perineural invasion, pain and histopathologic characteristics of the tumor was performed. RESULTS: Northern blot analysis revealed that NGF levels in pancreatic cancer tissues increased by 3.1 folds in comparison with normal pancreas tissue (P<0.05), and immunohistochemistry detected the presence of obvious NGF expression in the cytoplasm of pancreatic cancer cells. Tumors with high NGF expression were associated with more frequent perineural invasion (P<0.01), and increased NGF expression was related to more intense pain (P<0.01). CONCLUSION: Increased NGF expression may contribute to perineural invasion and pain in pancreatic cancer.