{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,25]],"date-time":"2025-09-25T16:02:34Z","timestamp":1758816154923},"reference-count":34,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2007,2,8]],"date-time":"2007-02-08T00:00:00Z","timestamp":1170892800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[2007,5,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Polymorphisms at <jats:italic>N<\/jats:italic>\u2010acetyl transferase 2 locus (<jats:italic>NAT2<\/jats:italic>) lead to slow, intermediate and rapid acetylation properties of the enzyme. Improper acetylation of heterocyclic and aromatic amines, present in tobacco, might cause DNA adduct formation. Generally, DNA repair enzymes remove these adduct to escape malignancy. But, tobacco users carrying susceptible <jats:italic>NAT<\/jats:italic>2 and DNA repair loci might be at risk of oral leukoplakia and cancer. In this study, 389 controls, 224 leukoplakia and 310 cancer patients were genotyped at 5 polymorphic sites on <jats:italic>NAT2<\/jats:italic> and 3 polymorphic sites on each of <jats:italic>XRCC1<\/jats:italic> and <jats:italic>XPD<\/jats:italic> loci by PCR\u2010RFLP method to determine the risk of the diseases. None of the SNPs on these loci independently could modify the risk of the diseases in overall population but variant genotype (<jats:italic>Gln\/Gln<\/jats:italic>) at codon 399 on <jats:italic>XRCC1<\/jats:italic> and major genotype (<jats:italic>Lys\/Lys<\/jats:italic>) at codon 751 on <jats:italic>XPD<\/jats:italic> were associated with increased risk of leukoplakia and cancer among slow acetylators, respectively (OR = 4.2, 95% CI = 1.2\u201315.0; OR = 1.6, 95% CI = 1.1\u20132.3, respectively). Variant genotype (<jats:italic>Asn\/Asn<\/jats:italic>) at codon 312 on <jats:italic>XPD<\/jats:italic> was also associated with increased risk of cancer among rapid and intermediate acetylators (OR = 1.9, 95% CI = 1.2\u20132.9). Variant <jats:italic>C\u2010G\u2010A<\/jats:italic> haplotype at <jats:italic>XRCC1<\/jats:italic> was associated with increased risk of leukoplakia (OR = 1.7, 95% CI = 1.2\u20132.4) but leukoplakia and cancer in mixed tobacco users (OR = 3.1, 95% CI = 1.4\u20137.1, OR = 2.4, 95% CI = 1.1\u20135.4, respectively) among slow acetylators. Although none of the 3 loci could modulate the risk of the diseases independently but 2 loci in combination, working in 2 different biochemical pathways, could do so in these patient populations. \u00a9 2007 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ijc.22547","type":"journal-article","created":{"date-parts":[[2007,2,8]],"date-time":"2007-02-08T17:46:40Z","timestamp":1170956800000},"page":"2148-2156","source":"Crossref","is-referenced-by-count":59,"title":["Polymorphisms at <i>XPD<\/i> and <i>XRCC1<\/i> DNA repair loci and increased risk of oral leukoplakia and cancer among <i>NAT2<\/i> slow acetylators"],"prefix":"10.1002","volume":"120","author":[{"given":"Mousumi","family":"Majumder","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nilabja","family":"Sikdar","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Saurabh","family":"Ghosh","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bidyut","family":"Roy","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2007,3,23]]},"reference":[{"key":"e_1_2_6_2_2","first-page":"517","article-title":"Definition of leukoplakia and related lesions: an aid to studies to precancer","volume":"46","author":"World Health Organization","year":"1978","journal-title":"Oral Surg Oral Med Oral Pathol"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0528.1980.tb01302.x"},{"key":"e_1_2_6_4_2","doi-asserted-by":"crossref","first-page":"203","DOI":"10.1289\/ehp.9298203","article-title":"Role of lime in the generation of reactive oxygen species from betel quid ingredients","volume":"98","author":"Nair UJ","year":"1997","journal-title":"Environ Health Prespect"},{"key":"e_1_2_6_5_2","volume-title":"GLOBOCAN 2002: cancer incidence, mortality and prevalence (Worldwide IARC Cancer Base No. 5, Version 2.0)","author":"Ferlay J","year":"2004"},{"key":"e_1_2_6_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.tpj.6500053"},{"key":"e_1_2_6_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0027-5107(02)00153-7"},{"key":"e_1_2_6_8_2","doi-asserted-by":"publisher","DOI":"10.1002\/hed.20284"},{"key":"e_1_2_6_9_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1209374"},{"key":"e_1_2_6_10_2","first-page":"533","article-title":"Role of arylamine N\u2010acetyltransferase 1 and 2 (NAT1 and NAT2) genotypes in susceptibility to oral\/pharyngeal and laryngeal cancers","volume":"9","author":"Jourenkova\u2010Mironova N","year":"1999","journal-title":"Pharmacogenetics"},{"key":"e_1_2_6_11_2","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/19.10.1803"},{"key":"e_1_2_6_12_2","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/22.12.1993"},{"key":"e_1_2_6_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.oraloncology.2005.11.003"},{"key":"e_1_2_6_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.mrfmmm.2005.01.027"},{"key":"e_1_2_6_15_2","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/21.12.2219"},{"key":"e_1_2_6_16_2","first-page":"8654","article-title":"A Xeroderma Pigmentosum Group D gene polymorphism predicts clinical outcome to platinum\u2010based chemotherapy in patients with advanced colorectal cancer","volume":"61","author":"Park DJ","year":"2001","journal-title":"Cancer Res"},{"key":"e_1_2_6_17_2","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/20.11.2125"},{"key":"e_1_2_6_18_2","first-page":"1513","article-title":"Polymorphisms in DNA repair genes and associations with cancer risk","volume":"11","author":"Goode EL","year":"2002","journal-title":"Cancer Epidemiol Biomarkers Prev"},{"key":"e_1_2_6_19_2","doi-asserted-by":"publisher","DOI":"10.1002\/ijc.20338"},{"key":"e_1_2_6_20_2","doi-asserted-by":"publisher","DOI":"10.1158\/1055-9965.EPI-05-0108"},{"key":"e_1_2_6_21_2","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/16.3.1215"},{"key":"e_1_2_6_22_2","doi-asserted-by":"publisher","DOI":"10.1093\/carcin\/22.8.1185"},{"key":"e_1_2_6_23_2","first-page":"3961","article-title":"Homozygous rapid arylamine N\u2010acetyltransferase (NAT2) genotype as susceptibility factor for lung cancer","volume":"56","author":"Cascorbi I","year":"1996","journal-title":"Cancer Res"},{"key":"e_1_2_6_24_2","unstructured":"http:\/\/www.louisville.edu\/medschool\/pharmacology\/nat.html"},{"key":"e_1_2_6_25_2","unstructured":"MajumdarP MajumderPP. 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