Yin, Q. H., Liu, C., Li, L., Zu, X. Y. & Wang, Y. J. Association between the XRCC3 T241M polymorphism and head and neck cancer susceptibility: a meta-analysis of case-control studies. Asian. Pac. J. Cancer Prev. 13, 5201-5205
To evaluate the role of the X-ray repair cross complementing group 3 (XRCC3) T241M polymorphism in head and neck cancer susceptibility.
Materials and methods:
We performed a meta-analysis of all available studies, which included 3,191 cases and 5,090 controls.
Overall, a significant risk effect of the T241M polymorphism was not found under homologous contrast (MM vs TT: OR=1.293, 95% CI=0.926-1.805; TM vs TT: OR=1.148 95% CI=0.930-1.418) and recessive models (MM vs TT+TM): OR=1.170, 95% CI=0.905- 1.512, but a significantly increased risk was observed under a dominant model (MM+TM vs TT): OR=1.243, 95% CI=1.001-1.544. In stratified analyses, there were no significant associations for Asians or Caucasians.
Our meta-analysis suggested the XRCC3 241M allele (MM+TM) might act as a head and neck cancer risk factor among all subjects, and the effect of T241M polymorphism on head and neck susceptibility should be studied with a larger, stratified population.
"Since the identification of XRCC3 Thr241Met polymorphism, a growing number of studies suggested that XRCC3 Thr241Met polymorphism plays an important role in the development of cancers, such as glioma , hepatocellular carcinoma , head and neck cancer , lung cancer , and so on. Many published studies that aim at the role of XRCC3 Thr241Met polymorphism in ovarian cancer risk have been performed, but the results are controversial. "
[Show abstract][Hide abstract] ABSTRACT: Genetic polymorphism of X-ray repair crosscomplementing group 3 (XRCC3) Thr241Met has been implicated to alter the risk of ovarian cancer, but the results are controversial. In order to get a more precise result, a meta-analysis was performed. All eligible studies were identified through an extensive search in PubMed, Excerpta Medica Database (Embase), Chinese National Knowledge Infrastructure database, and Chinese Biomedical Literature Database before August 2013. The association between the XRCC3 Thr241Met polymorphism and ovarian cancer risk was conducted by odds ratios (ORs) and 95 % confidence intervals (95 % CIs). Finally, a total of four publications including seven studies with 3,635 cases and 5,473 controls were included in our meta-analysis. Overall, there was no association between XRCC3 Thr241Met polymorphism and risk of ovarian cancer under all five genetic models in overall population (T vs. C: OR = 0.99, 95 % CI = 0.960-1.03, P = 0.752; TT vs. CC: OR = 1.00, 95 % CI = 0.91-1.10, P = 0.943; TC vs. TT: OR = 0.97, 95 % CI = 0.92-1.04, P = 0.396, Fig. 1; TT vs.
OR = 1.00, 95 % CI = 0.91-1.12, P = 0.874; TT/TC vs. CC: OR = 0.98, 95 % CI = 0.94-1.03, P = 0.486). In the subgroup analysis according to ethnicity, the results suggested that XRCC3 Thr241Met polymorphism was not associated with the risk of ovarian cancer in Caucasians population. No significant association was found between the XRCC3 Thr241 Met polymorphism and the risk of ovarian cancer. Given the limited sample size and ethnicities included in the meta-analysis, further large scaled and well-designed studies are needed to confirm our results.
"ncbi.nlm.nih.gov/projects/SNP/), the main Thr241Met (rs861539) SNP in XRCC3 leads to an amino acid substitution at codon 241, which has been reported to be associated with slightly but not significantly decreased DNA repair capacity  . Recently, a metaanalysis of 15 eligible studies with 3,191 cases and 5,090 controls found some evidence for an association between the Thr241Met SNP and HNC risk  . However , another meta-analysis by Flores-Obando et al. revealed that the SNP did not contribute to the risk of HNC  . "
[Show abstract][Hide abstract] ABSTRACT: Although tobacco and alcohol consumption are two common risk factors of head and neck cancer (HNC), other specific etiologic causes, such as viral infection and genetic susceptibility factors, remain to be understood. Human DNA is often damaged by numerous endogenous and exogenous mutagens or carcinogens, and genetic variants in interaction with environmental exposure to these agents may explain interindividual differences in HNC risk. Single nucleotide polymorphisms (SNPs) in genes involved in the DNA damage-repair response are reported to be risk factors for various cancer types, including HNC. Here, we reviewed epidemiological studies that have assessed the associations between HNC risk and SNPs in DNA repair genes involved in base-excision repair, nucleotide-excision repair, mismatch repair, double-strand break repair and direct reversion repair pathways. We found, however, that only a few SNPs in DNA repair genes were found to be associated with significantly increased or decreased risk of HNC, and, in most cases, the effects were moderate, depending upon locus-locus interactions among the risk SNPs in the pathways. We believe that, in the presence of exposure, additional pathway-based analyses of DNA repair genes derived from genome-wide association studies (GWASs) in HNC are needed.
[Show abstract][Hide abstract] ABSTRACT: The polymorphism of XRCC3 Thr241Met has been indicated to be correlated with glioma susceptibility, but study results are still debatable. The present meta-analysis was performed to investigate the association between XRCC3 Thr241Met polymorphism and glioma.
A total of 3754 glioma patients and 4849 controls from nine separate studies were involved. The pooled odds ratio (OR) and its corresponding 95% confidence interval (CI) was assessed by the random-effects model.
The association between XRCC3 Thr241Met polymorphism and glioma was significant in the recessive model (OR = 1.36; 95% CI, 1.02 - 1.82; P = 0.03). In a stratified analysis by the ethnicity, significantly increased risk was detected in Asians (OR = 1.93; 95% CI, 1.18 - 3.17; P = 0.009).
In conclusion, XRCC3 Thr241Met polymorphism was implied to be associated with increased glioma risk. More studies are needed to validate this result.
International Journal of Clinical and Experimental Medicine 07/2013; 6(6):438-443. · 1.28 Impact Factor
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