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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.

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NEOPLASIA
Brief report

Activating FLT3 mutations in CD117/KIT+ T-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. Thomas Look

From Our Lady of Mercy Cancer Center, New York Medical College, Bronx, NY; Department of Pediatric Oncology and Eastern Cooperative Oncology Group (ECOG) Statistical Center, Dana-Farber Cancer Institute, Boston, MA; University of Rochester, NY; Ireland Cancer Center, Case Western Reserve University, Cleveland, OH; Mayo Clinic, Rochester, MN; Rambam Medical Center, Haifa, Israel; Northwestern University Feinberg School of Medicine, Chicago, IL; and the Eastern Cooperative Oncology Group, Boston, MA.

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 (T-ALL) cases that coexpress CD117/KIT and cytoplasmic CD3 (CD117/KIT+ ALL). Activating mutations in the FLT3 RTK gene were found in each of 3 CD117/KIT+ 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 patients with T-ALL. (Blood. 2004;104:558-560)


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