RESUMEN
The 18067 C>T polymorphism of XRCC3 gene has been considered to be implicated in the development of cervical and ovarian cancers, but the results are inconsistent. Thus, we conducted a meta-analysis to assess the association of XRCC3 18067 C>T polymorphism with risk of cervical and ovarian cancers. All studies on the association of XRCC3 18067 C>T polymorphism with cervical and ovarian cancers risk were retrieved. Finally, a total of 17 studies including 10 studies with 5,637 cases and 10,057 controls on ovarian cancer and 7 studies with 1,112 cases and 1,233 controls on cervical cancer were selected. Overall, pooled results showed that the XRCC3 18067 C>T polymorphism was significantly associated with increased risk of ovarian cancer (TC vs. CC: OR = 0.904, 95% CI = 0.841-0.972, p = 0.006; TT + TC vs. CC: OR = 0.914, 95% CI = 0.853-0.979, p = 0.010) and cervical cancer (TC vs. CC: OR = 1.00, 95% CI = 1.066-1.585, p = 0.009). Further subgroup analysis by ethnicity revealed an increased risk of cervical and ovarian cancer in Asians and Caucasians, respectively. The present meta-analysis inconsistent with the previous meta-analysis suggests that the XRCC3 18067 C>T polymorphism might be implicated in the pathogenesis of cervical and ovarian cancers.
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Oral cancer is very common, occurring on head as well as neck region with poor prognosis. The X-ray repair cross-complementing group 3 (XRCC3) gene contained in DNA repairing pathway has been investigated for its functional role in oral cancer. Nevertheless, the corresponding results are inconclusive. This study investigated the association of XRCC3 Thr241Met polymorphism regarding oral cancer risk. Article and literature searches were performed using Embase, Medline, PubMed, Wanfang and China National Knowledge Infrastructure (CNKI) databases with a manual search. The keywords of 'XRCC3 or X-ray repair cross complementing protein 3', 'polymorphism or SNP', 'oral cancer or oral squamous cell carcinoma' and their combinations were used to search literature. In accordance with the criteria of inclusion, we focused on only case-and-control studies with the distribution of genotypes and alleles being available to be extracted. Systematic meta-analysis was conducted via the STATA software (version 11.0). After a comprehensive literature collection and review, 1,615 oral cancer cases and 1,897 matched controls extracted from 7 articles were included for this meta-analysis. Our results show that only Met/Met (TT) genotype with the recessive model was associated with high risk of oral cancer (CC + CT vs. TT, OR=1.81, P=0.001, 95% CI=1.28-2.567). A significant relationship was identified under both homozygous and recessive model in Asians (CC vs. TT: OR=2.15, 95% CI=1.107-4.170, P=0.024; CT + CC vs. TT: OR=2.140, 95% CI=1.105-4.144, P=0.024), but not among Caucasians (P>0.05). The results indicate that XRCC3 241Met allele might be a potential factor for oral cancer risk, particularly among Asian population. A further study using a larger population and more ethnicities should be performed to confirm the findings.
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Recent studies support the involvement of XRCC3 gene polymorphisms in carcinogenesis. Our study focuses on the identification of polymorphic variants of XRCC3 in hepatocellular carcinoma (HCC) and an analysis of the relationship between these polymorphic variants and clinicopathological (including the genotype specific risk) and survival characteristics. Fifty cases of HCC were genotyped using molecular biology techniques for Thr241Met, rs861539 (c.722C>T) and 5'-UTR, rs1799796 (c.562-14A>G) polymorphisms. Statistical analysis was based on ï£2, Fisher's, logistic regression (odd ratio - OR), and log-rank tests. Statistically significant differences were shown only for rs1799796 A>G and tumour grade, between wild type (AA) and heterozygote (AG) genotypes, and wild type (AA) and heterozygote & homozygote (AG & GG) genotypes. The logistic regression analysis found an OR of rs1799796 polymorphism occurrence in HCC related to tumour grade. The statistical analysis revealed, for the rs861539 C>T polymorphism, a better survival only for the homozygote genotype (TT) compared to the heterozygote (CT), and for rs1799796 A>G polymorphism, a longer survival for the wild type (AA) compared to heterozygote (AG) and to heterozygote & homozygote (AG & GG) genotypes, respectively. Our results suggest that XRCC3 gene SNPs could influence the tumour aggressiveness expressed by tumour grade.
Asunto(s)
Biomarcadores de Tumor/genética , Carcinoma Hepatocelular/genética , Proteínas de Unión al ADN/genética , Neoplasias Hepáticas/genética , Polimorfismo de Nucleótido Simple , Anciano , Carcinoma Hepatocelular/mortalidad , Carcinoma Hepatocelular/patología , Carcinoma Hepatocelular/terapia , Distribución de Chi-Cuadrado , Femenino , Frecuencia de los Genes , Predisposición Genética a la Enfermedad , Heterocigoto , Homocigoto , Humanos , Estimación de Kaplan-Meier , Neoplasias Hepáticas/mortalidad , Neoplasias Hepáticas/patología , Neoplasias Hepáticas/terapia , Modelos Logísticos , Masculino , Persona de Mediana Edad , Clasificación del Tumor , Estadificación de Neoplasias , Oportunidad Relativa , Fenotipo , Factores de Riesgo , Factores de Tiempo , Resultado del TratamientoRESUMEN
BACKGROUND AND AIMS: Deoxyribonucleic Acid (DNA) repair mechanisms play a critical role in protecting the cellular genome against carcinogens. X-ray cross-complementing gene 3 (XRCC3) is involved in DNA repair and therefore certain genetic polymorphisms that occur in DNA repair genes may affect the ability to repair DNA defects and may represent a risk factor in carcinogenesis. The purpose of our study was to investigate the association between XRCC3 gene substitution of Threonine with Methionine in codon 241 of XRCC3 gene (Thr241Met) polymorphism and the risk of lung cancer, in a Romanian population. METHODS: We recruited 93 healthy controls and 85 patients with lung cancer, all smokers. Thr241Met, XRCC3 gene genotyping was determined by multiplex Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP). RESULTS: Statistical analysis (OR, recessive model), did not revealed an increased risk for lung cancer, for the variant 241Met allele and Thr241Met genotypes (p=0.138, OR=0.634, CI=0.348-1.157; p=0.023, OR=0.257, CI=0.085-6.824). Also, there were no positive statistical associations between Thr241Met polymorphism of XRCC3 gene, gender, tobacco and various histopathological tumor type of lung cancer. CONCLUSION: In conclusion, the results of the study suggest that the XRCC3 gene Thr241Met polymorphism is not associated with an increased risk for the development of lung cancer in this Romanian group.
RESUMEN
BACKGROUND: Previous studies suggest that the X-ray repair cross-complementing group 3 gene (XRCC3) Thr241Met genetic variant could be potentially associated with the risk of prostate cancer. However, results from these published studies were conflicting rather than conclusive. OBJECTIVES: his meta-analysis aimed to conduct a better understanding of the effects of XRCC3 Thr241Met genetic variant on prostate cancer risk. METHODS: We identified three eligible studies, 499 prostate cancer cases and 571 controls. RESULTS: Overall, significant associations were detected in the heterozygote comparison genetic model (CT versus (vs.) CC: OR = 0.71, 95% CI 0.53-0.94, Z =2.38, p= 0.017), and the dominant genetic model (TT/CT vs. CC: OR = 0.74, 95% CI 0.57-0.98, Z = 2.11, p =0.035). In the subgroup analysis by ethnicities, we found that this genetic variant was significantly associated with the decrease risk of prostate cancer in Caucasians for heterozygote comparison genetic model (CT vs. CC: OR = 0.66, 95% CI 0.44-0.98, Z = 2.04, p = 0.042). No publication bias was found in this study. CONCLUSIONS: Results from this meta-analysis indicate that the XRCC3 Thr241Met genetic variant is associated with prostate cancer risk.