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Blood, 15 May 2006, Vol. 107, No. 10, pp. 3847-3853. Prepublished online as a Blood First Edition Paper on January 24, 2006; DOI 10.1182/blood-2005-08-3522. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-08-3522v1 107/10/3847    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 Bacher, U. Articles by Schnittger, S. Search for Related Content PubMed PubMed Citation Articles by Bacher, U. Articles by Schnittger, S. Related Collections Neoplasia Oncogenes and Tumor Suppressors Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CLINICAL TRIALS AND OBSERVATIONS Implications of NRAS mutations in AML: a study of 2502 patients Ulrike Bacher, Torsten Haferlach, Claudia Schoch, Wolfgang Kern, and Susanne Schnittger From the Laboratory for Leukemia Diagnostics, Department of Internal Medicine III and the Department of Clinical Chemistry, University Hospital Munich, Ludwig-Maximilians University, Munich; and the MLL-Munich Leukemia Laboratory, Munich, Germany. We analyzed 2502 patients with acute myeloid leukemia at diagnosis for NRAS mutations around the hot spots at codons 12, 13, and 61 and correlated the results to cytomorphology, cytogenetics, other molecular markers, and prognostic relevance of these mutations. Two hundred fifty-seven (10.3%) of 2502 patients had NRAS mutations (NRASmut). Most mutations (112 of 257; 43.6%) were found at codon 12, mostly resulting in changes from glycine to asparagine. The history of AML did not differ significantly in association with NRAS mutations. The subgroups with inv(16)/t(16;16) and inv(3)/t(3;3) showed a significantly higher frequency of NRASmut (50 of 133, 37.6% [P < .001], and 11 of 41, 26.8% [P = .004], respectively) than the total cohort. In addition, in these 2 subgroups, mutations of codon 61 were significantly overrepresented (both P < .001). In contrast, NRAS mutations were significantly underrepresented in t(15;17) (2 of 102; 2%; P = .005) in the subgroup with MLL/11q23 rearrangements (3 of 77; 3.9%; P = .061) and in the complex aberrant karyotype (4 of 258; 1.6%; P < .001). Overall, we did not find a significant prognostic impact of NRASmut for overall survival, event-free survival, and disease-free survival. However, there was a trend to better survival in most subgroups, especially when other molecular markers (FLT3-LM, MLL-PTD, and NPM) were taken into account. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. Slape, L. Y. Liu, S. Beachy, and P. D. Aplan Leukemic transformation in mice expressing a NUP98-HOXD13 transgene is accompanied by spontaneous mutations in Nras, Kras, and Cbl Blood, September 1, 2008; 112(5): 2017 - 2019. [Abstract] [Full Text] [PDF] M. Jongen-Lavrencic, S. M. Sun, M. K. Dijkstra, P. J. M. Valk, and B. Lowenberg MicroRNA expression profiling in relation to the genetic heterogeneity of acute myeloid leukemia Blood, May 15, 2008; 111(10): 5078 - 5085. [Abstract] [Full Text] [PDF] U. Bacher, C. Haferlach, W. Kern, T. Haferlach, and S. 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