{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,11]],"date-time":"2025-11-11T12:46:16Z","timestamp":1762865176449},"reference-count":23,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2006,7,24]],"date-time":"2006-07-24T00:00:00Z","timestamp":1153699200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Carcinogenesis"],"published-print":{"date-parts":[[2006,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The etiology of lung cancer in population with little or no tobacco exposure is not well understood. Individual genetic susceptibility factors have been suggested to contribute to lung cancer risk in this population. Mutations in the p53 tumor suppressor gene are implicated in the development of lung cancer as they are frequently found in lung tumors from both smokers and never\u2010smokers. In order to determine whether genetic polymorphisms affecting DNA repair capacity modulate p53 mutations in lung tumors from never\u2010smokers, we compared p53 mutations with genotypes of <jats:italic>XPD<\/jats:italic> 312, <jats:italic>XPD<\/jats:italic> 751, and <jats:italic>XRCC1<\/jats:italic> 399 in lung tumors from 43 lifetime never\u2010smokers. p53 mutations were identified in 10 (23%) cases and consisted mostly of G\/C to A\/T transitions. No statistically significant association was found between p53 mutations and genotypes of <jats:italic>XPD<\/jats:italic> 312 or <jats:italic>XPD<\/jats:italic> 751. However, patients with the <jats:italic>XRCC1<\/jats:italic> 399 Gln allele, that results in a lower base excision repair capacity, were more likely to have p53 mutations, compared with patients the wild\u2010type Arg allele (<jats:italic>P<\/jats:italic>\u2009=\u20090.03). In addition, the p53 mutation frequency increased with an increasing number of combined genotypes associated with a lower DNA repair capacity of <jats:italic>XPD<\/jats:italic> 312, <jats:italic>XPD<\/jats:italic> 751, and <jats:italic>XRCC1<\/jats:italic> 399 (<jats:italic>P<\/jats:italic>\u2009=\u20090.02). These results suggest that individuals who never smoked and had <jats:italic>XRCC1<\/jats:italic> 399 Gln allele may be at a greater risk of p53 mutations, especially if combined with the genotypes of <jats:italic>XPD<\/jats:italic> 312 and <jats:italic>XPD<\/jats:italic> 751 that may result in a lower DNA repair capacity. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/mc.20208","type":"journal-article","created":{"date-parts":[[2006,7,24]],"date-time":"2006-07-24T13:46:28Z","timestamp":1153748788000},"page":"828-832","source":"Crossref","is-referenced-by-count":13,"title":["Polymorphisms in DNA repair genes <i>XPD<\/i> and <i>XRCC1<\/i> and p53 mutations in lung carcinomas of never\u2010smokers"],"prefix":"10.1002","volume":"45","author":[{"given":"Wei\u2010Min","family":"Gao","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marjorie","family":"Romkes","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jill M.","family":"Siegfried","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James D.","family":"Luketich","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Phouthone","family":"Keohavong","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,7,24]]},"reference":[{"key":"e_1_2_6_2_2","unstructured":"ACS.Cancer facts and figures\u20102002. American Cancer Society;2002."},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/0169-5002(95)00566-8"},{"key":"e_1_2_6_4_2","first-page":"35","article-title":"Lung cancer in nonsmoking women: A multicenter case\u2010control study","volume":"1","author":"Fontham ET","year":"1991","journal-title":"Cancer Epidemiol Biomarkers Prev"},{"key":"e_1_2_6_5_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.3798109"},{"key":"e_1_2_6_6_2","doi-asserted-by":"publisher","DOI":"10.1093\/jnci\/86.11.869"},{"key":"e_1_2_6_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/1047-2797(94)90054-X"},{"key":"e_1_2_6_8_2","first-page":"4855","article-title":"Mutations in the p53 tumor suppressor gene: Clues to cancer etiology and molecular pathogenesis","volume":"54","author":"Greenblatt MS","year":"1994","journal-title":"Cancer Res"},{"key":"e_1_2_6_9_2","first-page":"297","article-title":"Comparison of mutations in the p53 and K\u2010ras genes in lung carcinomas from smoking and nonsmoking women","volume":"8","author":"Gealy R","year":"1999","journal-title":"Cancer Epidemiol Biomarkers Prev"},{"key":"e_1_2_6_10_2","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/22.3.367"},{"key":"e_1_2_6_11_2","doi-asserted-by":"publisher","DOI":"10.1289\/ehp.98106385"},{"key":"e_1_2_6_12_2","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/bgg115"},{"key":"e_1_2_6_13_2","first-page":"119","article-title":"Polymorphisms of the DNA repair gene XRCC1 and lung cancer risk","volume":"10","author":"Ratnasinghe D","year":"2001","journal-title":"Cancer Epidemiol Biomarkers Prev"},{"key":"e_1_2_6_14_2","first-page":"1354","article-title":"Modulation of nucleotide excision repair capacity by XPD polymorphisms in lung cancer patients","volume":"61","author":"Spitz MR","year":"2001","journal-title":"Cancer Res"},{"key":"e_1_2_6_15_2","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/22.4.593"},{"key":"e_1_2_6_16_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0921-8777(00)00059-8"},{"key":"e_1_2_6_17_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0169-5002(03)00035-7"},{"key":"e_1_2_6_18_2","first-page":"411","article-title":"Detection of K\u2010ras mutations in lung carcinomas: Relationship to prognosis","volume":"2","author":"Keohavong P","year":"1996","journal-title":"Clin Cancer Res"},{"key":"e_1_2_6_19_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1697983"},{"key":"e_1_2_6_20_2","first-page":"2906","article-title":"p53 mutations and exposure to environmental tobacco smoke in a multicenter study on lung cancer","volume":"60","author":"Husgafvel\u2010Pursiainen K","year":"2000","journal-title":"Cancer Res"},{"key":"e_1_2_6_21_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1383-5742(00)00032-6"},{"key":"e_1_2_6_22_2","doi-asserted-by":"publisher","DOI":"10.1038\/362709a0"},{"key":"e_1_2_6_23_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.24.12754"},{"key":"e_1_2_6_24_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.32.19633"}],"container-title":["Molecular Carcinogenesis"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1002%2Fmc.20208","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/pdf\/10.1002\/mc.20208","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,11,15]],"date-time":"2023-11-15T14:14:31Z","timestamp":1700057671000},"score":1,"resource":{"primary":{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/10.1002\/mc.20208"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2006,7,24]]},"references-count":23,"journal-issue":{"issue":"11","published-print":{"date-parts":[[2006,11]]}},"alternative-id":["10.1002\/mc.20208"],"URL":"https:\/\/doi.org\/10.1002\/mc.20208","archive":["Portico"],"relation":{},"ISSN":["0899-1987","1098-2744"],"issn-type":[{"value":"0899-1987","type":"print"},{"value":"1098-2744","type":"electronic"}],"subject":[],"published":{"date-parts":[[2006,7,24]]}}}