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Blood, 1 January 2006, Vol. 107, No. 1, pp. 39-45. Prepublished online as a Blood First Edition Paper on September 8, 2005; DOI 10.1182/blood-2005-06-2305. This Article Full Text (PDF) All Versions of this Article: 2005-06-2305v1 107/1/39    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 Mehta, P. A Articles by Davies, S. M Search for Related Content PubMed PubMed Citation Articles by Mehta, P. A Articles by Davies, S. M Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted June 9, 2005 Accepted August 4, 2005 XPD Lys751gln polymorphism: Etiology and outcome of childhood acute myeloid leukemia. A children's oncology group report Parinda A Mehta*, Todd A Alonzo, Robert B Gerbing, James S Elliott, Tiffany A Wilke, Rebekah J Kennedy, Julie A Ross, John P Perentesis, Beverly J Lange, and Stella M Davies Division of Hematology/Oncology, Department of Pediatrics, University of Cincinnati College of Medicine, and Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA University of Southern California Keck School of Medicine, Los Angeles, CA, USA Children's Oncology Group, Arcadia, CA, USA Department of Pediatrics, University of Minnesota Cancer Center, Minneapolis, MN, USA Department of Pediatrics, The Children's Hospital of Philadelphia, Philadelphia, PA, USA * Corresponding author; email: parinda.mehta{at}cchmc.org. Genetic polymorphisms result in inter-individual variation in DNA repair capacity, and may in part, account for susceptibility of a cell to genotoxic agents, and to malignancy. Polymorphisms in XPD, a member of the nucleotide excision repair pathway, have been associated with development of treatment-related AML and with poor outcome of AML in elderly patients. We hypothesized that XPD Lys751Gln polymorphism may play a role in causation of AML in children and, as shown in adults, may affect the outcome of childhood AML therapy. 456 children treated for de novo AML were genotyped at XPD exon 23. Genotype frequencies in cases were compared with normal control frequencies and patient outcomes were analyzed according to genotype. Gene frequencies in AML patients and normal controls were similar. There were no significant differences in overall survival (p= 0.82), event-free survival (p= 0.78), treatment-related mortality, (p= 0.43) or relapse rate (RR) (p= 0.92) between patients with XPD751AA vs. 751AC vs. 751CC genotypes, in contrast to reports in adult AML. These data, representing the only data in pediatric AML, suggest that XPD genotype does not affect the etiology or outcome of childhood AML. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: F. Wang, D. Chang, F.-l. Hu, H. Sui, B. Han, D.-d. li, and Y.-s. Zhao DNA Repair Gene XPD Polymorphisms and Cancer Risk: A Meta-analysis Based on 56 Case-Control Studies Cancer Epidemiol. Biomarkers Prev., March 1, 2008; 17(3): 507 - 517. [Abstract] [Full Text] [PDF] G. J.L. Kaspers and C. M. Zwaan Pediatric acute myeloid leukemia: towards high-quality cure of all patients Haematologica, November 1, 2007; 92(11): 1519 - 1532. [Abstract] [Full Text] [PDF] N. Kuptsova, K. J. Kopecky, J. Godwin, J. Anderson, A. Hoque, C. L. Willman, M. L. Slovak, and C. B. Ambrosone Polymorphisms in DNA repair genes and therapeutic outcomes of AML patients from SWOG clinical trials Blood, May 1, 2007; 109(9): 3936 - 3944. [Abstract] [Full Text] [PDF]

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