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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 (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 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. H Articles by Das-Gupta, E. Search for Related Content PubMed PubMed Citation Articles by Seedhouse, C. H Articles by Das-Gupta, E. Social Bookmarking                   What's this? Submitted April 16, 2002 Accepted July 1, 2002 The genotype distribution of the XRCC1 gene indicates a role for base excision repair in the development of therapy-related AML Claire H Seedhouse*, Rowena Bainton, Michael Lewis, Alexander Harding, Nigel Russell, and Emma Das-Gupta Academic Haematology, University Of Nottingham, Nottingham, United Kingdom * Corresponding author; email: claire.seedhouse{at}nottingham.ac.uk. Recently polymorphisms in several DNA repair genes have been described. These polymorphisms may affect DNA repair capacity and modulate cancer susceptibility via gene-environment interactions. We have investigated DNA repair capacity and its association with acute myeloblastic leukaemia (AML). We have studied polymorphisms in three DNA repair genes, XRCC1, XRCC3 and XPD. In addition, we have looked at the incidence of a functional polymorphism in the NQO1 gene, which is involved in the protection of cells from oxidative damage. We have genotyped the above polymorphisms by PCR-RFLP in 134 de novo AML and 34 therapy-related AML (t-AML) cases and 178 controls. The distributions of the XRCC3 Thr241Met and NQO1 Pro187Ser genotypes were not significantly different among patients and controls. However the distribution of the XRCC1 Arg399Gln genotypes was significantly different when comparing the t-AML and control groups (2, p = 0.03). The presence of at least one XRCC1 399Gln allele indicates a protective effect for the allele in controls compared to t-AML cases, odds ratio 0.44 (95% CI 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 provides evidence of a protective effect against AML in individuals who carry at least one copy of the variant XRCC1 399Gln allele compared to those homozygous for the common allele. 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