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This Article Full Text Full Text (PDF) 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 Laverdière, C. Articles by Krajinovic, M. Search for Related Content PubMed PubMed Citation Articles by Laverdière, C. Articles by Krajinovic, M. Related Collections Neoplasia Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 November 2002, Vol. 100, No. 10, pp. 3832-3834 BRIEF REPORT Polymorphism G80A in the reduced folate carrier gene and its relationship to methotrexate plasma levels and outcome of childhood acute lymphoblastic leukemia Caroline Laverdière, Sonia Chiasson, Irina Costea, Albert Moghrabi, and Maja Krajinovic From the Centre de Recherche, Hôpital Sainte-Justine, Montréal, QC, Canada. Methotrexate (MTX) is a key compound of chemotherapeutic regimens used in the treatment of childhood acute lymphoblastic leukemia (ALL). Resistance to this drug may arise by, among other factors, altered cellular uptake that may hamper the efficacy of the treatment. Recently, a G80A polymorphism has been described in the reduced folate carrier gene (RFC1), which encodes the major MTX transporter. Here, we assessed the association between the genetic polymorphisms G80A and both MTX plasma levels and childhood ALL outcome. Children with the A80 variant had worse prognoses than patients with the GG genotype (P = .04), as shown by event-free survival estimates. Patients homozygous for A80 had higher levels of MTX (P = .004) than the other genotype groups. Possible explanations for observed associations are discussed; however, additional experiments are required to achieve understanding of the underlying mechanism. © 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: B. Baslund, J. Gregers, and C. H. Nielsen Reduced folate carrier polymorphism determines methotrexate uptake by B cells and CD4+ T cells Rheumatology, April 1, 2008; 47(4): 451 - 453. [Abstract] [Full Text] [PDF] S. L. Hider, I. N. Bruce, and W. Thomson The pharmacogenetics of methotrexate Rheumatology, October 1, 2007; 46(10): 1520 - 1524. [Abstract] [Full Text] [PDF] S. Kishi, C. Cheng, D. French, D. Pei, S. Das, E. H. Cook, N. Hijiya, C. Rizzari, G. L. Rosner, T. Frudakis, et al. Ancestry and pharmacogenetics of antileukemic drug toxicity Blood, May 15, 2007; 109(10): 4151 - 4157. [Abstract] [Full Text] [PDF] C. M. Ulrich, K. Curtin, J. D. Potter, J. Bigler, B. Caan, and M. L. Slattery Polymorphisms in the Reduced Folate Carrier, Thymidylate Synthase, or Methionine Synthase and Risk of Colon Cancer Cancer Epidemiol. Biomarkers Prev., November 1, 2005; 14(11): 2509 - 2516. [Abstract] [Full Text] [PDF] K. Robien Folate During Antifolate Chemotherapy: What We Know... and Do Not Know Nutr Clin Pract, August 1, 2005; 20(4): 411 - 422. [Abstract] [Full Text] [PDF] S L Hider, C Morgan, E Bell, I N Bruce, P Ranganathan, and H L McLeod Will pharmacogenetics allow better prediction of methotrexate toxicity and efficacy in patients with RA? Ann Rheum Dis, June 1, 2003; 62(6): 591 - 591. [Full Text] [PDF]

	Copyright © 2002 by American Society of Hematology         Online ISSN: 1528-0020