Lack of association of the cyclin D1 G870A variation with oral carcinoma risk: Evidence from 2,404 subjects.

Evidence implicates cyclin D1 (CCND1) G870A polymorphisms as risk factors for various cancers. An increasing number of investigations have been conducted on the association of CCND1 G870A polymorphisms with susceptibility to oral carcinoma, and have yielded inconclusive results. The aim of the present study was to derive a more precise estimation of the correlation. Meta-analyses examining the association between CCND1 G870A polymorphisms and oral carcinoma were performed. Separate analyses on ethnicity, smoking status and control sources were also implemented. Eligible studies were identified prior to February 2012. From the overall data from 1,128 cases and 1,276 controls, no associations of CCND1 G870A polymorphisms with oral carcinoma were observed [AA vs. GG: odds ratio (OR)=1.06; 95% confidence interval (CI), 0.62-1.82; dominant model: OR=1.04; 95% CI, 0.76-1.43; recessive model: OR=1.06; 95% CI, 0.70-1.59]. In the subgroup analysis by ethnicity, smoking status and control sources, no significant associations of CCND1 G870A polymorphisms and oral cancer were observed for the three genetic models. Collectively, the data failed to suggest CCND1 G870A polymorphism as a low-penetrant risk factor for developing oral carcinoma. Additional studies with large sample sizes concerning different ethnicities in different areas are required.

MTHFR C677T and A1298C polymorphisms and cervical carcinoma susceptibility: meta-analyses based on 4,421 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: OR = 1.07; 95 %CI = 0.73-1.58; dominant model: OR = 0.89; 95 %CI = 0.66-1.18; recessive model: OR = 1.13; 95 %CI = 0.84-1.52). In the subgroup analysis by ethnicity, MTHFR 677T allele was associated with decreased cervical cancer susceptibility among Caucasians (TT vs CC: OR = 0.65; 95 %CI = 0.45-0.93; dominant model: OR = 0.70; 95 %CI = 0.58-0.86) but not Asians. As for A1298C polymorphism, no marked associations of A1298C genetic variation with cervical cancer risk were observed (CC vs AA: OR = 1.01; 95 %CI = 0.60-1.73; dominant model: OR = 1.17; 95 %CI = 0.91-1.49; recessive model: OR = 0.99; 95 %CI = 0.60-1.63). 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.

NAT2 polymorphisms with oral carcinoma susceptibility: a meta-analysis.

Published data have implicated NAT2 polymorphisms as risk factors for various cancers. A number of studies have focused on the association of NAT2 polymorphisms with susceptibility to oral carcinoma and have yielded inconclusive results. The aim of the present study was to derive a more precise estimation of the relationship. We first carried out a deliberate search in the databases without a language limitation, covering all papers published up to Dec 2011. A total of seven case-control studies including 1,379 cases and 1,868 controls were selected and the relevant data were extracted for systematic meta-analyses. No significant association was found for the overall data (OR: 1.04, 95 % CI: 0.79-1.39). In subgroup analyses according to ethnicity, slow acetylators might increase oral cancer risk among Asians (OR: 1.38, 95 % CI: 1.04-1.82) but not Caucasians or Mixed races. The data suggested that NAT2 polymorphisms might be a low-penetrant risk factor for oral carcinoma in Asians.