• Korean Journal of Head & Neck Oncology
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• v.22 no.2
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• pp.117-122
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• 2006

Background and Objectives : Thyroid carcinoma is the sixth commonest cancer in Korea and the papillary carcinoma is the most common type(88%) of the malignant thyroid tumors. Bulky DNA adducts formed by the carcinogens are repaired by DNA repair process, but failure to repair this DNA damage can cause mutations in oncogenes and tumor suppressor genes resulting in tumor formation. The xeroderma pigmentosum group C(XPC) gene is essential for this repair procedure and the XPC-PolyAT(PAT) polymorphisms may alter DNA repair capacity(DRC) and genetic susceptibility to cancer. Subjects and Methods : In a case-control study of 113 Korean patients with pathologically diagnosed thyroid papillary carcinoma and 65 control subjects, we investigated the association between the three XPC-PAT gene polymorphisms and thyroid papillary cancer susceptibility. Results : The frequency of the variant XPC-PAT allele was lower in the cases(0.349) than in the controls (0.423), but the difference was not significant(p=0.140). Using logistic regression adjusting for age and sex, risk for thyroid papillary cancer was not increased in the XPC-PAT-/+ and XPC-PAT+/+ compared to XPCPAT-/-(adjusted overall odds ratio[95% confidence intervals;95%CI]=0.52[0.26-1.03] and 0.62 [0.22-1.75], respectively; trend test, p=0.167). Conclusion : There are no relationship between the XPC-PAT polymorphism and the risk of thyroid papillary carcinoma in Korean population. Based on our results, XPC-PAT polymorphism do not modulate genetic susceptibility to thyroid papillary cancer.

• BMB Reports
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• v.34 no.6
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• pp.489-495
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• 2001

DNA damage by UV and environmental agents are the major cause of genomic instability that needs to be repaired, otherwise it give rise to cancer. Accordingly, mammalian cells operate several DNA repair pathways that are not only responsible for identifying various types of DNA damage but also involved in removing DNA damage. In mammals, nucleotide excision repair (NER) machinery is responsible for most, if not all, of the bulky adducts caused by UV and chemical agents. Although most of the proteins involved in NER pathway have been identified, only recently have we begun to gain some insight into the mechanism by which proteins recognize damaged DNA. Binding of Xeroderma pigmentosum group C protein (XPC)-hHR23B complex to damaged DNA is the initial damage recognition step in NER, which leads to the recruitment of XPA and RPA to form a damage recognition complex. Formation of damage recognition complex not only stabilizes low affinity binding of XPA to the damaged DNA, but also induces structural distortion, both of which are likely necessary for the recruitment of TFIIH and two structure-specific endonucleases for dual incision.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.10
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• pp.4983-4988
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• 2012

The xeroderma pigmentosum complementation group C gene (XPC) has been identified as important for repairing UV-related DNA damage. Some subtle changes in this gene may impair repair efficiency and influence susceptibility to human cancers, including skin cancer. Two polymorphisms in XPC, 939A>C (rs2228001) and 499C>T (rs2228000), are considered to have possible associations with the risk of skin cancer, but the reported results have been inconsistent. Here we performed a meta-analysis of the available evidence regarding the relationship between these two polymorphisms and the risk of skin cancer. All relevant studies were searched using PubMed, Embase and Web of Science before February 2012. A total of 8 case-control studies were included in this analysis, and no convincing associations between the two polymorphisms and risk of skin cancer were observed in any of the genetic models. Stratified analyses by skin cancer type also did not detect significant associations in any subgroup. This meta-analysis suggested that the XPC 939A>C and 499C>T polymorphisms may have little involvement in susceptibility to skin cancer.