{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,28]],"date-time":"2026-07-28T12:57:05Z","timestamp":1785243425492,"version":"3.55.0"},"reference-count":31,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[2014,12,10]],"date-time":"2014-12-10T00:00:00Z","timestamp":1418169600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Genetic Testing and Molecular Biomarkers"],"published-print":{"date-parts":[[2015,1,1]]},"abstract":"\n DNA repair genes are involved in several diseases such as cancers and autoimmune diseases. Previous studies indicated that a DNA repair system was involved in the development of rheumatoid arthritis (RA). In this study, we aimed to examine whether four polymorphisms in the DNA repair genes (xeroderma pigmentosum complementation group D [\n XPD<\/jats:italic>\n ], X-ray repair cross-complementing group 1 [\n XRCC1<\/jats:italic>\n ], and X-ray repair cross-complementing group 4 [\n XRCC4<\/jats:italic>\n ]) were associated with RA. Sixty-five patients with RA and 70 healthy controls (HCs) were examined for\n XPD<\/jats:italic>\n (A-751G),\n XRCC1<\/jats:italic>\n (A399G), and\n XRCC4<\/jats:italic>\n (intron 3 VNTR and G-1394T) polymorphisms. All polymorphisms were genotyped by PCR and\/or PCR-RFLP. The association between the polymorphisms and RA was analyzed using the chi-square test and de Finetti program. The intron 3 VNTR polymorphism in the\n XRCC4<\/jats:italic>\n gene showed an association with RA patients. The DI genotype was found lower in RA patients (\n \u03c7<\/jats:italic>\n 2<\/jats:sup>\n =8.227;\n p<\/jats:italic>\n =0.0021), while the II genotype was higher in RA patients (\n \u03c7<\/jats:italic>\n 2<\/jats:sup>\n =5.285;\n p<\/jats:italic>\n =0.010). There were deviations from the Hardy-Weinberg Equilibrium (HWE) in both intron 3 VNTR and G-1394T polymorphisms in the\n XRCC4<\/jats:italic>\n gene and in the polymorphism in the\n XRCC1<\/jats:italic>\n gene, and the observed genotype counts deviated from those expected according to the HWE (\n p<\/jats:italic>\n =0.027, 0.004, and 0.002, respectively); however, there was no deviation in the other gene polymorphisms. There is no statistical difference between the RA patients and HCs for\n XPD<\/jats:italic>\n (A-751G),\n XRCC1<\/jats:italic>\n (A399G), and\n XRCC4<\/jats:italic>\n (G-1394T) gene polymorphisms (\n p<\/jats:italic>\n >0.05). Although\n XPD<\/jats:italic>\n (A-751G),\n XRCC1<\/jats:italic>\n (A399G), and\n XRCC4<\/jats:italic>\n (G-1394T) gene polymorphisms have been extensively investigated in different clinical pictures, this is the first study to evaluate the role of these polymorphisms in the genetic etiopathogenesis of RA in Turkish patients. In conclusion, we suggested that the intron 3 VNTR polymorphism in the\n XRCC4<\/jats:italic>\n gene may be associated with the etiopathogenesis of RA as a marker of immune aging.\n <\/jats:p>","DOI":"10.1089\/gtmb.2014.0230","type":"journal-article","created":{"date-parts":[[2014,12,10]],"date-time":"2014-12-10T15:17:43Z","timestamp":1418224663000},"page":"48-51","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":4,"title":["Might There Be a Link Between Intron 3 VNTR Polymorphism in the\n XRCC4<\/i>\n DNA Repair Gene and the Etiopathogenesis of Rheumatoid Arthritis?"],"prefix":"10.1177","volume":"19","author":[{"given":"Sacide","family":"Pehlivan","sequence":"first","affiliation":[{"name":"Istanbul University","place":["Turkey"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sibel Oguzkan","family":"Balci","sequence":"additional","affiliation":[{"name":"Gaziantep University","place":["Turkey"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ali","family":"Aydeniz","sequence":"additional","affiliation":[{"name":"Gaziantep University","place":["Turkey"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mustafa","family":"Pehlivan","sequence":"additional","affiliation":[{"name":"Gaziantep University","place":["Turkey"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tugce","family":"Sever","sequence":"additional","affiliation":[{"name":"Gaziantep University","place":["Turkey"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Savas","family":"Gursoy","sequence":"additional","affiliation":[{"name":"Gaziantep University","place":["Turkey"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2014,12,10]]},"reference":[{"key":"e_1_3_2_2_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0908492106"},{"key":"e_1_3_2_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2005.12.031"},{"key":"e_1_3_2_4_1","doi-asserted-by":"publisher","DOI":"10.1007\/s12094-013-1055-8"},{"key":"e_1_3_2_5_1","first-page":"1","article-title":"DNA damage and innate immunity: links and trade-offs","author":"Chatzinikolaou G","year":"2014","unstructured":"Chatzinikolaou G, , Karakasilioti I, , Garinis GA (2014) DNA damage and innate immunity: links and trade-offs. 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