A new X-ray sensitive CHO cell mutant of ionizing radiation group 7, XR-C2, that is defective in DSB repair but has only a mild defect in V(D)J recombination

Errami, Abdellatif; Overkamp, Wilhelmina J. I.; He, Dong Ming; Friedl, Anna A.; Gell, David A.; Eckardt‐Schupp, Friederike; Jackson, Stephen; Hendrickson, Eric A.; Lohman, P.H.M.; Zdzienicka, M. Z.

doi:10.1016/s0921-8777(00)00038-0

Cited by 17 publications

(13 citation statements)

References 48 publications

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“…it is radiosensitive, but shows only a minor defect in V(D)J recombination [30]. Interestingly, this cell line showed an intermediate level of microhomology use (32%).…”

Section: Mutants In Dna-pk Componentsmentioning

confidence: 91%

Different types of V(D)J recombination and end-joining defects in DNA double-strand break repair mutant mammalian cells

et al. 2002

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“…it is radiosensitive, but shows only a minor defect in V(D)J recombination [30]. Interestingly, this cell line showed an intermediate level of microhomology use (32%).…”

Section: Mutants In Dna-pk Componentsmentioning

confidence: 91%

Different types of V(D)J recombination and end-joining defects in DNA double-strand break repair mutant mammalian cells

et al. 2002

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“…Each KU and DNA‐PKcs can bind to one end of DNA independently, and KU can improve the affinity of DNA‐PKcs for DNA ends by 100‐fold 19 . Murine mutants defective in the gene have non‐detectable DNA‐PK activity and share similar phenotypes to those of KU70 deficiency, except for growth retardation 20 …”

Section: Introductionmentioning

confidence: 99%

“…19 Murine mutants defective in the XRCC7 gene have non-detectable DNA-PK activity and share similar phenotypes to those of KU70 deficiency, except for growth retardation. 20 Genetic variants of KU70 -61C > G (rs2267437) and XRCC76721G > T (rs7003908) are located in the promoter region of the KU70 gene and the intron 8 of the XRCC7 gene, respectively. Although the functional relevance of these two polymorphisms is unknown, bioinformatics analysis (http://www.gene-regulation.com/ pub/programs/alibaba2/index.html) suggests that DNA sequence containing KU70-61G has more recognition elements (i.e.…”

Section: Introductionmentioning

confidence: 99%

Genetic variants of the XRCC7 gene involved in DNA repair and risk of human bladder cancer

Wang

Peng

et al. 2008

Int J of Urology

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Objective: To investigate the association between the polymorphisms of the KU70 and X-ray repair cross complementing group 7 (XRCC7) genes and the risk of bladder cancer. Methods: This hospital-based case-control study included 213 patients with newly diagnosed bladder transitional cell carcinoma and 235 cancer-free controls frequency-matched by age and sex. Two polymorphisms, KU70 and XRCC7, using a method involving polymerase chain reaction-restriction fragment length polymorphism were genotyped. Results: The risk of bladder cancer decreased in a dose-response manner as the number of XRCC76721G alleles increased (adjusted odds ratio [OR] = 0.70, 95% confident interval [CI] = 0.47-1.03 for 6721GT and OR = 0.31, 95% CI = 0.10-0.99 for 6721GG; Ptrend = 0.013). However, when we used 6721 (GT + GG) as the reference, we found a statistically significant increased risk of bladder cancer associated with the 6721TT genotype (OR = 1.53, 95% CI = 1.04-2.25). In the stratification analysis, this increased risk was more pronounced among subgroups of patients aged >65 years (OR = 2.27; 95% CI = 1.25-4.10) and ever smokers (OR = 2.06, 95% CI = 1.15-3.68). Furthermore, we observed a 3.24-fold increased risk (95% CI = 1.35-7.78) for smokers aged >65 years carrying 6721TT genotype compared with those carrying the 6721 (GG + GT) genotype. However, the KU70 -61C > G polymorphism was not associated with a significantly increased risk of bladder cancer. Conclusions:The XRCC7 but not the KU70 polymorphism appears to be involved in the etiology of human bladder cancer. Larger studies with more detailed data on environmental exposure are needed to verify these initial findings.

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“…Defects in the XRCC7 gene make the DNA-activated protein kinase activity undetectable in murine mutants and these cells sensitive to ionizing radiation (23). Furthermore, the XRCC7 gene is a strong candidate gene involved in severe combined immunodeficiency (23,24).…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms of DNA Repair Genes and Risk of Glioma

Wang¹,

Bondy²,

Shen³

et al. 2004

Cancer Research

149

105

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DNA repair genes play a major role in maintaining genomic stability through different repair pathways that are mediated by cell cycle control genes such as p53. We found previously that glioma patients were susceptible to ␥-ray-induced chromosomal breaks, which may be influenced by genetic variation in genes involved in DNA strand breaks, such as XRCC1 in single-strand break repair, XRCC3 and RAD51 in homologous recombination repair, and XRCC7 in nonhomologous end joining double-strand break repair. Therefore, we tested the hypothesis that genetic polymorphisms in XRCC1, XRCC3, RAD51, XRCC7, and p53 were associated with risk of glioma in 309 patients with newly diagnosed glioma and 342 cancer-free control participants frequency matched on age (؎5 years), sex, and self-reported ethnicity. We did not find any statistically significant differences in the distributions of XRCC1 Arg399Gln, XRCC3 Thr241Met, RAD51 G135C, and P53 Arg72Pro polymorphisms between the cases and the controls. However, the XRCC7 G6721T variant T allele and TT genotype were more common in the cases (0.668 and 43.4%, respectively) than in the controls (0.613 and 38.9%, respectively), and the differences were statistically significant (P ‫؍‬ 0.045 and 0.040, respectively). The adjusted odds ratios were 1.78 (95% confidence interval, 1.08 -2.94) and 1.86 (95% confidence interval, 1.12-3.09) for the GT heterozygotes and TT homozygotes, respectively. The combined T variant genotype (GT؉TT) was associated with a 1.82-fold increased risk of glioma (95% confidence interval, 1.13-2.93). These results suggest that the T allele may be a risk allele, and this XRCC7 polymorphism may be a marker for the susceptibility to glioma. Larger studies are needed to confirm our findings and unravel the underlying mechanisms.

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A new X-ray sensitive CHO cell mutant of ionizing radiation group 7, XR-C2, that is defective in DSB repair but has only a mild defect in V(D)J recombination

Cited by 17 publications

References 48 publications

Different types of V(D)J recombination and end-joining defects in DNA double-strand break repair mutant mammalian cells

Different types of V(D)J recombination and end-joining defects in DNA double-strand break repair mutant mammalian cells

Genetic variants of the XRCC7 gene involved in DNA repair and risk of human bladder cancer

Polymorphisms of DNA Repair Genes and Risk of Glioma

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