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Prepublished online as a Blood First Edition Paper on July 18, 2002; DOI 10.1182/blood-2002-04-1152. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-04-1152v1 100/10/3761    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Seedhouse, C. Articles by Das-Gupta, E. Search for Related Content PubMed PubMed Citation Articles by Seedhouse, C. Articles by Das-Gupta, E. Related Collections Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 November 2002, Vol. 100, No. 10, pp. 3761-3766 NEOPLASIA The genotype distribution of the XRCC1 gene indicates a role for base excision repair in the development of therapy-related acute myeloblastic leukemia Claire Seedhouse, Rowena Bainton, Michael Lewis, Alexander Harding, Nigel Russell, and Emma Das-Gupta From the Division of Haematology, School of Clinical Laboratory Sciences, University of Nottingham, and Nottingham City Hospital, Nottingham, United Kingdom. Polymorphisms in several DNA repair genes have been described. These polymorphisms may affect DNA repair capacity and modulate cancer susceptibility by means of gene-environment interactions. We investigated DNA repair capacity and its association with acute myeloblastic leukemia (AML). We studied polymorphisms in 3 DNA repair genes: XRCC1, XRCC3, and XPD. We also assessed the incidence of a functional polymorphism in the NQO1 gene, which is involved in protection of cells from oxidative damage. We genotyped the polymorphisms by using polymerase chain reaction-restriction fragment-length polymorphism analysis in 134 patients with de novo AML, 34 with therapy-related AML (t-AML), and 178 controls. The distributions of the XRCC3 Thr241Met and NQO1 Pro187Ser genotypes were not significantly different in patients and controls. However, the distribution of the XRCC1 Arg399Gln genotypes was significantly different when comparing the t-AML and control groups (2, P = .03). The presence of at least one XRCC1 399Gln allele indicated a protective effect for the allele in controls compared with patients with t-AML (odds ratio 0.44; 95% confidence interval, 0.20-0.93). We found no interactions between the XRCC1 or XRCC3 and NQO1 genotypes. We also found no differences in the distribution of the XPD Lys751Gln or XRCC1 Arg194Trp genotypes. Our data provide evidence of a protective effect against AML in individuals with at least one copy of the variant XRCC1 399Gln allele compared with those homozygous for the common allele. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Voso, E Fabiani, F D'Alo', F Guidi, A Di Ruscio, S Sica, L Pagano, M Greco, S Hohaus, and G Leone Increased risk of acute myeloid leukaemia due to polymorphisms in detoxification and DNA repair enzymes Ann. Onc., September 1, 2007; 18(9): 1523 - 1528. [Abstract] [Full Text] [PDF] M Jawad, G Giotopoulos, C Cole, and M Plumb Target cell frequency is a genetically determined risk factor in radiation leukaemogenesis Br. J. Radiol., September 1, 2007; 80(Special_Issue_1): S56 - S62. [Abstract] [Full Text] [PDF] N. Kuptsova, K. J. Kopecky, J. Godwin, J. Anderson, A. Hoque, C. L. Willman, M. L. Slovak, and C. B. 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