• Proceedings of the Zoological Society Korea Conference
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• 2003.08a
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• pp.211.4-211
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• 2003

No Abstract, See Full Text

• Proceedings of the Zoological Society Korea Conference
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• 1999.10b
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• pp.241.1-241
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• 1999

No Abstract, See Full Text

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.2
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• pp.665-669
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• 2012

Aim: The distribution of DNA repair gene XRCC1 and XRCC3 genotypes was used to assess the potential influence of genetic polymorphisms on risk of colorectal cancer, and interactions with other factors. Methods: a 1:2 matched case-control study was conducted with 485 cases and 970 controls. XRCC1 and XRCC2 genotype polymorphisms were based upon duplex polymerase-chain-reaction with the confronting-two-pairprimer (PCR-CTPP) method. Results:The XRCC1 399Cln allele polymorphism was found to be associated with an increased colorectal cancer risk, while an non-significant inversely association was noted for XRCC3 241Thr/Thr genotype. We also found that individuals with the XRCC1 399 Gln and XRCC3 241Met alleles had an elevated risk, while XRCC3241Thr/Thr was proctective. Conclusion: This study is the first to provide evidence of importance of XRCC1 and XRCC3 gene polymorphisms for risk of colorectal cancer in the Chinese population.

• Development and Reproduction
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• v.1 no.1
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• pp.37-43
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• 1997

DNA 회복효소인 MPG는 DNA의 퓨린기에 결합되어 있는 메틸기 등 이물질을 염기와 함께 제거하는 작용을 한다. 본 연구에서는 노던 블롯팅 방법을 이용하여 Balb/c mice의 각 조직별로 발생단계별 mRNA 발현 정도를 조사하였다. 뇌와 콩팥조직에서는 출생직후에 발현이 가장 활발하였으며, 성체시기까지 비교적 높은 활성도가 유지되었다. 위장 조직에서는 출생직후에서 일주일 후까지는 명확히 관찰되었으나, 그 이후는 발현이 약화되었다. 간장과 폐조직에서는 그 발현 정도가 매우 약했으며, 특히, 간조직의 경우 출생 직후보다 성체에서 그 발현이 현저히 감소되었다. 이들 조직에서의 활성도는 출생후 24시간 이내에서 1주일후까지 상대적으로 높게 유지되다가 점차 감소되었다. 즉, 수유기(출생직후부터 1주일후)에는 그 활성도가 성체시기(4주에서 6개월)보다 높게 유지되었다. 이러한 결과들로 미루어 보아 늙은 생쥐가 젊고 어린 생쥐보다 alkylating mutagen들에 노출되었을대 암에 걸릴 위험성이 높다고 생각된다.

• Journal of the Institute of Electronics Engineers of Korea SD
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• v.43 no.11 s.353
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• pp.69-76
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• 2006

This paper proposes a self-repair system which is able to self-repair in cell unit by imitating the structure of living beings. Because the data of artificial cells move even diagonally, our system can self-repair faults not in column unit, but in cell unit. It leads to design an efficient self-repair system for multiple faults. Moreover, in artificial cell design, the usage of logic-based design method has smaller system size than that of the previous register-based design method. Our experimental result for 2-bit up/down counter shows 40.3% reduction in hardware overhead, compared to the previous method [6].

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.6
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• pp.3809-3813
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• 2013

Background: X-ray repair cross-complementing group 1 (XRCC1) plays a key role in the base excision repair pathway, as a scaffold protein that brings together proteins of the DNA repair complex. XRCC1 is reported to be a candidate influence on cancer risk. The aim of our present study was to assess the association of rs1799782 (Arg194Trp) and rs25487 (Arg399Gln) XRCC1 gene polymorphisms with breast cancer in the Saudi population. Materials and Methods: The two SNP's were analyzed in breast cancer patients and healthy control subjects. Genotypes were determined by TaqMan SNP genotype analysis technique and data were analyzed using Chi-square or t test and logistic regression analysis by SPSS16.0 software. Results and Conclusions: Results showed that rs1799782 significantly increased susceptibility to breast cancer with Arg/Trp, Arg/Trp+Trp/Trp genotypes and at Trp allele overall study. It also increased risk of breast cancer in older age patients (above 48) and with the ER positive category. XRCC1rs25487 (Arg399Gln) did not showed any significant association. In conclusion the XRCC1rs1799782 polymorphism may be involved in the etiology of breast cancer in the Saudi population. Confirmation of our findings in larger populations of different ethnicities is warranted.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.8
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• pp.4177-4181
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• 2012

Cancer is a multi-factorial disease and variation in genetic susceptibility, due to inherited differences in the capacity to repair mismatches in the genome, is an important factor in the development of gastric cancer (GC), for example. Epigenetic changes, including aberrant methylation of 5/CpG islands in the promoter regions of mismatch repair (MMR) genes like hMLH1, have been implicated in the development of various types of GC. In the present study we evaluated the role of hMLH1 promoter hypermethylation in Kashmiri GC patients and controls, and assessed correlations with various dietary and lifestyle factors. The study included 70 GC patients (56 males and 14 females; age ($mean{\pm}S.D$) $50{\pm}11.4$ years). Distinction between methylated and unmethylated was achieved with MS-PCR and DNA band patterns. The Chi-square test was applied to assess the risk due to promoter hypermethylation. We found a strikingly high frequency of promoter hypermethylation in GC cases than in normal samples (72.9% (51/70) in GC cases vs 20% (14/70) in normal samples (p=0.0001).We also observed a statistically significant association between methylated hMLH1 gene promoter and smoking, consumption of sundried vegetables and hot salted tea with the risk of GC. This study revealed that hMLH1 hypermethylation is strongly associated with GC and suggested roles for epigenetic changes in stomach cancer causation in the Kashmir valley.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.10
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• pp.5839-5842
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• 2013

Aim: We assessed the association between genetic variants of XPG, XPA, XPD, CSB, XPC and CCNH in the nucleotide excision repair (NER) pathway and risk of prostate cancer. Methods: We genotyped the XPG, XPA, XPD, CSB, XPC and CCNH polymorphisms by a 384-well plate format on the MassARRAY(R) platform. Multivariate logistical regression analysis was used to assess the associations between the six gene polymorphisms and risk of prostate cancer. Results: Individuals carrying the XPG rs229614 TT (OR=2.01, 95%CI=1.35-3.27) genotype and T allele (OR=1.73, 95%CI=1.37-2.57) were moderately significantly associated with a higher risk of prostate cancer. Subjects with XPD rs13181 G allele had a marginally increased risk of prostate cancer, with adjusted OR(95%CI) of 1.53 (1.04-2.37). Moreover, individuals carrying with CSB rs2228526 GG genotype (OR=2.05, 95% CI=1.23-3.52) and G allele (OR=1.56, 95%CI=1.17-2.05) were associated with a higher increased risk of prostate cancer. The combination genotype of XPG rs2296147 T and CSB rs2228526 G allele had accumulative effect on the risk of this cancer, with an OR (95% CI) of 2.23(1.37-3.59). Conclusions: Our study indicates that XPG rs2296147 and CSB rs2228526 polymorphisms are significantly associated with increased risk of prostate cancer, and that combination of XPG rs2296147 T allele and CSB rs2228526 G allele is strongly associated with an increased risk.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.12
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• pp.6121-6128
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• 2012

Radiation-induced side effects on normal tissue are determined largely by the capacity of cells to repair radiation-induced DNA damage. X-ray repair cross-complementing group 1 (XRCC1) plays an important role in the repair of DNA single-strand breaks. Studies have shown conflicting results regarding the association between XRCC1 gene polymorphisms (Arg399Gln, Arg194Trp, -77T>C and Arg280His) and radiation-induced side effects in patients undergoing whole breast radiotherapy. Therefore, we conducted a meta-analysis to determine the predictive value of XRCC1 gene polymorphisms in this regard. Analysis of the 11 eligible studies comprising 2,199 cases showed that carriers of the XRCC1 399 Gln allele had a higher risk of radiation-induced toxicity than those with the 399 ArgArg genotype in studies based on high-quality genotyping methods [Gln vs. ArgArg: OR, 1.85; 95% CI, 1.20-2.86] or in studies with mixed treatment regimens of radiotherapy alone and in combination with chemotherapy [Gln vs. ArgArg: OR, 1.60; 95% CI, 1.09-2.23]. The XRCC1 Arg399Gln variant allele was associated with mixed acute and late adverse reactions when studies on late toxicity only were excluded [Gln allele vs. Arg allele: OR, 1.22; 95% CI, 1.00-1.49]. In contrast, the XRCC1 Arg280His variant allele was protective against radiation-induced toxicity in studies including patients treated by radiotherapy alone [His allele vs. Arg allele: OR, 0.58; 95% CI, 0.35-0.96]. Our results suggest that XRCC1 399Gln and XRCC1 280Arg may be independent predictors of radiation-induced toxicity in post-surgical breast cancer patients, and the selection of genotyping method is an important factor in determining risk factors. No evidence for any predictive value of XRCC1 Arg194Trp and XRCC1 -77T>C was found. So, larger and well-designed studies might be required to further evaluate the predictive value of XRCC1 gene variation on radiation-induced side effects in patients undergoing whole breast radiotherapy.

• BMB Reports
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• v.28 no.6
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• pp.484-489
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• 1995

The product of bacteriophage T7 gene 2.5 is a single-stranded DNA binding protein and plays an important role in T7 DNA replication, recombination, and repair. Genetic analysis of T7 phage defective in gene 2.5 shows that the gene 2.5 protein is essential for T7 DNA replication and growth (Kim and Richardson, 1993). The C-terminal truncated gene 2.5 protein ($GP2.5-{\Delta}21C$) cannot substitute for wild-type gene 2.5 protein in vivo; suggesting that the C-terminal domain of gene 2.5 protein is essential for protein-protein interactions (Kim and Richardson, 1994; J. Biol. Chem. 269, 5070-5078). Truncated gene 2.5 proteins lacking 19 residues ($GP2.5-{\Delta}19N$) and 39 residues ($GP2.5-{\Delta}39N$) from the amino-terminal domain were constructed by in vitro mutagenesis. $GP2.5-{\Delta}19N$ can support the growth of T7 phage lacking gene 2.5 while $GP2.5-{\Delta}39N$ cannot substitute for wild-type gene 2.5 protein in vivo; however, its ability to bind to single-stranded DNA is not affected. These results clearly demonstrate that the 20~39 amino-terminal region of gene 2.5 protein is required for T7 growth in vivo but may not be involved in DNA binding activity.