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Blood, 1 May 2004, Vol. 103, No. 9, pp. 3544-3546. Prepublished online as a Blood First Edition Paper on December 11, 2003; DOI 10.1182/blood-2003-07-2441. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-07-2441v1 103/9/3544    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 Armstrong, S. A. Articles by Korsmeyer, S. J. Search for Related Content PubMed PubMed Citation Articles by Armstrong, S. A. Articles by Korsmeyer, S. J. Related Collections Neoplasia Oncogenes and Tumor Suppressors Signal Transduction Gene Expression Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Brief report FLT3 mutations in childhood acute lymphoblastic leukemia Scott A. Armstrong, Meghann E. Mabon, Lewis B. Silverman, Aihong Li, John G. Gribben, Edward A. Fox, Stephen E. Sallan, and Stanley J. Korsmeyer From the Departments of Pediatric Oncology, Adult Oncology and Cancer Immunology and AIDS, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA; Division of Hematology/Oncology, Children's Hospital, Boston, MA; and the Howard Hughes Medical Institute, Boston, MA. Activating mutations of the FLT3 receptor tyrosine kinase are common in acute myelogenous leukemia (AML) but are rare in adult acute lymphoblastic leukemia (ALL). We have recently shown that FLT3 is highly expressed and often mutated in ALLs with rearrangement of the mixed lineage leukemia (MLL) gene on chromosome 11q23. Because hyperdiploid ALL samples also show high-level expression of FLT3, we searched for the presence of FLT3 mutations in leukemic blasts from 71 patients with ALL. The data show that approximately 25% (6 of 25) of hyperdiploid ALL samples possess FLT3 mutations, whereas only 1 of 29 TEL/AML1-rearranged samples harbored mutations (P = .04, Fisher exact test). Three mutations are novel in-frame deletions within a 7-amino acid region of the receptor juxtamembrane domain. Finally, 3 samples from patients whose disease would relapse harbored FLT3 mutations. These data suggest that patients with hyperdiploid or relapsed ALL might be considered candidates for therapy with newly described small-molecule FLT3 inhibitors. (Blood. 2004;103: 3544-3546) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. W. Tyner, M. W. Deininger, M. M. Loriaux, B. H. Chang, J. R. Gotlib, S. G. Willis, H. Erickson, T. Kovacsovics, T. O'Hare, M. C. Heinrich, et al. RNAi screen for rapid therapeutic target identification in leukemia patients PNAS, May 26, 2009; 106(21): 8695 - 8700. [Abstract] [Full Text] [PDF] L. Kearney, D. Gonzalez De Castro, J. Yeung, J. Procter, S. W. Horsley, M. Eguchi-Ishimae, C. M. Bateman, K. Anderson, T. Chaplin, B. D. Young, et al. Specific JAK2 mutation (JAK2R683) and multiple gene deletions in Down syndrome acute lymphoblastic leukemia Blood, January 15, 2009; 113(3): 646 - 648. [Abstract] [Full Text] [PDF] M. Case, E. Matheson, L. Minto, R. Hassan, C. J. Harrison, N. Bown, S. Bailey, J. Vormoor, A. G. Hall, and J. A.E. Irving Mutation of Genes Affecting the RAS Pathway Is Common in Childhood Acute Lymphoblastic Leukemia Cancer Res., August 15, 2008; 68(16): 6803 - 6809. [Abstract] [Full Text] [PDF] J. 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