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Blood, 1 February 2007, Vol. 109, No. 3, pp. 1233-1236. Prepublished online as a Blood First Edition Paper on October 5, 2006; DOI 10.1182/blood-2006-07-037853. This Article Full Text (PDF) All Versions of this Article: blood-2006-07-037853v1 109/3/1233    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 Smith, A. G Articles by Allan, J. M Search for Related Content PubMed PubMed Citation Articles by Smith, A. G Articles by Allan, J. M Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted July 26, 2006 Accepted September 17, 2006 A common genetic variant in XPD associates with risk of 5q and 7q deleted acute myeloid leukemia Alexandra G Smith, Lisa J Worrillow, and James M Allan* Epidemiology and Genetics Unit, Department of Health Sciences, University of York, Heslington, UK Epidemiology and Genetics Unit, Department of Biology, University of York, Heslington, UK * Corresponding author; email: jim.allan{at}egu.york.ac.uk. Numerous structural genetic abnormalities observed in acute myeloid leukemia (AML) illustrate the heterogeneity of this disease, which has likely contributed to the difficulty in identifying susceptibility alleles for AML. We previously reported that carriers of the glutamine-encoding allele at codon 751 of the xeroderma pigmentosum group D (XPD) DNA repair gene were significantly more likely to have a karyotype associated with a less favourable prognosis, and hypothesized that this observation was driven by an association between the codon 751 variant and risk of developing AML with specific structural abnormalities. Using a case series of 927 AML patients we show here that the XPD codon 751 glutamine-encoding variant significantly associates with risk of developing AML with a chromosome 5q deletion (odds ratio (OR) 2.09, 95% confidence interval (CI) 1.14-3.81, n=69, p=0.02) or a chromosome 7q deletion (OR 2.27, 95% CI 1.09-4.71, n=47, p=0.03), but not with any other commonly recurring cytogenetic lesion. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Czader and A. Orazi Therapy-Related Myeloid Neoplasms Am J Clin Pathol, September 1, 2009; 132(3): 410 - 425. [Abstract] [Full Text] [PDF] N. A. Ellis, D. Huo, O. Yildiz, L. J. Worrillow, M. Banerjee, M. M. Le Beau, R. A. Larson, J. M. Allan, and K. Onel MDM2 SNP309 and TP53 Arg72Pro interact to alter therapy-related acute myeloid leukemia susceptibility Blood, August 1, 2008; 112(3): 741 - 749. [Abstract] [Full Text] [PDF] 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]

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