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Garcia-Quispes W.A.,Autonomous University of Barcelona | Pastor S.,Autonomous University of Barcelona | Pastor S.,CIBER ISCIII | Galofre P.,Hospitals Universitaris Vall dHebron | And 6 more authors.
PLoS ONE | Year: 2012

The role of the WDR3 gene on genomic instability has been evaluated in a group of 115 differentiated thyroid cancer (DTC) patients. Genomic instability has been measured according to the response of peripheral blood lymphocytes to ionizing radiation (0.5 Gy). The response has been measured with the micronucleus (MN) test evaluating the frequency of binucleated cells with MN (BNMN), both before and after the irradiation. No differences between genotypes, for the BNMN frequencies previous the irradiation, were observed. Nevertheless significant decreases in DNA damage after irradiation were observed in individuals carrying the variant alleles for each of the three genotyped SNPs: rs3754127 [-8.85 (-15.01 to -2.70), P<0.01]; rs3765501 [-8.98 (-15.61 to -2.36), P<0.01]; rs4658973 [-8.70 (-14.94 to -2.46), P<0.01]. These values correspond to those obtained assuming a dominant model. This study shows for the first time that WDR3 can modulate genome stability. © 2012 García-Quispes et al. Source


Garcia-Quispes W.A.,Autonomous University of Barcelona | Pastor S.,Autonomous University of Barcelona | Pastor S.,CIBER ISCIII | Galofre P.,Hospitals Universitaris Vall dHebron | And 6 more authors.
Mutation Research - Genetic Toxicology and Environmental Mutagenesis | Year: 2013

The role of different DNA-repair genes (OGG1, XRCC1, XRCC2 and XRCC3) on both the spontaneous and the induced frequency of micronuclei (MN) has been studied in the lymphocytes of a group of 114 patients with differentiated thyroid cancer (DTC). Induction of MN was achieved by treatment of the lymphocytes with 0.5. Gy of gamma-radiation.The selected genes are involved in base-excision repair (BER) (OGG1, Ser326Cys; XRCC1, Arg280His and Arg399Gln), and in homologous recombination repair (HRR) (XRCC2, Arg188His and XRCC3, IVS5-14G). Genotyping was carried out by use of the iPLEX (Sequenom) technique.Results indicate that only the OGG1-Ser326Cys polymorphism was able to modulate the MN frequency. This effect was only observed in the spontaneous MN frequency (P=0.016), but not in the MN frequency induced after irradiation. In addition, a strong correlation was observed between spontaneous and induced MN frequency, which would suggest an underlying genetic background. © 2012 Elsevier B.V. Source


Garcia-Quispes W.-A.,Autonomous University of Barcelona | Perez-Machado G.,Autonomous University of Barcelona | Perez-Machado G.,Santa Clara University | Akdi A.,Autonomous University of Barcelona | And 9 more authors.
Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis | Year: 2011

The role of the DNA repair genes OGG1, XRCC1, XRCC2 and XRCC3 on differentiated thyroid cancer (DTC) susceptibility was examined in 881 individuals (402 DTC and 479 controls). DNA repair genes were proposed as candidate genes, since the current data indicate that exposure to ionizing radiation is the only established factor in the development of thyroid cancer, especially when it occurs in early stages of life. We have genotyped DNA repair genes involved in base excision repair (BER) (OGG1, Ser326Cys; XRCC1, Arg280His and Arg399Gln), and homologous recombination repair (HRR) (XRCC2, Arg188His and XRCC3, ISV-14G). Genotyping was carried out using the iPLEX (Sequenom) technique. Multivariate logistic regression analyses were performed in a case-control study design. From all the studied polymorphism, only a positive association (OR = 1.58, 95% CI 1.05-2.46, P= 0.027) was obtained for XRCC1 (Arg280His). No associations were observed for the other polymorphisms. No effects of the histopathological type of tumor were found when the DTC patients were stratified according to the type of tumor. It must be emphasized that this study include the greater patients group, among the few studies carried out until now determining the role of DNA repair genes in thyroid cancer susceptibility. © 2011 Elsevier B.V. Source

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