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Blood, 15 July 2004, Vol. 104, No. 2, pp. 558-560. Prepublished online as a Blood First Edition Paper on March 25, 2004; DOI 10.1182/blood-2004-01-0168. This Article Full Text (PDF) All Versions of this Article: 2004-01-0168v1 104/2/558    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 Paietta, E. Articles by Look, A T Search for Related Content PubMed PubMed Citation Articles by Paietta, E. Articles by Look, A T Related Collections Related Article in Blood Online Related Letter in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted January 14, 2004 Accepted March 1, 2004 Activating FLT3 Mutations in CD117/KIT PositiveT-Cell Acute Lymphoblastic Leukemias Elisabeth Paietta*, Adolfo A Ferrando, Donna Neuberg, John M Bennett, Janis Racevskis, Hillard Lazarus, Gordon Dewald, Jacob M Rowe, Peter H Wiernik, Martin S Tallman, and A T Look Cancer Center, Our Lady of Mercy Medical Center, Bronx, NY, USA Pediatric Oncology, Dana Farber Cancer Institute, Boston, MA, USA Biostatistics, Dana Farber Cancer Institute, Boston, MA, USA Medical Oncology, University of Rochester, Rochester, NY, USA Ireland Cancer Center, Case Western Reserve University, Cleveland, OH, USA Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA Hematology, Rambam Medical Center, Haifa, Israel Feinberg School of Medicine, Northwestern University, Chicago, IL, USA * Corresponding author; email: epaietta{at}earthlink.net. Activating FLT3 mutations are the most common genetic aberrations in acute myeloid leukemia (AML), resulting in the constitutive activation of this receptor tyrosine kinase (RTK), but such mutations are rarely found in acute lymphoblastic leukemia (ALL). Here we describe a unique subset of de novo adult T-cell ALL cases that coexpress CD117/KIT and cytoplasmic CD3 (CD117/KITpos ALL). Activating mutations in the FLT3 RTK gene were found in each of three CD117/KITpos cases that were analyzed, but not in 52 other adult T-ALL samples from the same series that lacked CD117/KIT expression. Our results indicate the need for clinical trials to test the efficacy of drugs that inhibit the FLT3 RTK in this subset of T-ALL patients. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: A "Ras-in-ALL" model of signaling? Mignon Loh and Kevin M. Shannon Blood 2004 104: 297-298. [Full Text] [PDF] Related Letter in Blood Online: Activating FLT3 mutations in CD4+/CD8- pediatric T-cell acute lymphoblastic leukemias Pieter Van Vlierberghe, Jules P. P. Meijerink, Ronald W. Stam, Wendy van der Smissen, Elisabeth R. van Wering, H. Berna Beverloo, and Rob Pieters Blood 2005 106: 4414-4415. [Full Text] [PDF] This article has been cited by other articles: D. Campana Molecular Determinants of Treatment Response in Acute Lymphoblastic Leukemia Hematology, January 1, 2008; 2008(1): 366 - 373. [Abstract] [Full Text] [PDF] P. Van Vlierberghe, J. P. P. Meijerink, R. W. Stam, W. van der Smissen, E. R. van Wering, H. B. Beverloo, and R. Pieters Activating FLT3 mutations in CD4+/CD8- pediatric T-cell acute lymphoblastic leukemias Blood, December 15, 2005; 106(13): 4414 - 4415. [Full Text] [PDF] R. Grundler, C. Miething, C. Thiede, C. Peschel, and J. Duyster FLT3-ITD and tyrosine kinase domain mutants induce 2 distinct phenotypes in a murine bone marrow transplantation model Blood, June 15, 2005; 105(12): 4792 - 4799. [Abstract] [Full Text] [PDF] K. De Keersmaecker, C. Graux, M. D. Odero, N. Mentens, R. Somers, J. Maertens, I. Wlodarska, P. Vandenberghe, A. Hagemeijer, P. Marynen, et al. Fusion of EML1 to ABL1 in T-cell acute lymphoblastic leukemia with cryptic t(9;14)(q34;q32) Blood, June 15, 2005; 105(12): 4849 - 4852. [Abstract] [Full Text] [PDF]

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