Mutation of FLT3 is not a general phenomenon in CD117-positive T-ALL

V. Scharnhorst, J. Wals, H.B. Beverloo, A.W. Langerak, V.H.J. Velden, van der

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CD117 is considered to be a marker of leukemic cells committed to the myeloid lineage, however up to 11% of T-ALLs have been found to express CD117 [1]. Activating mutations in the FLT3 gene are common in acute myeloid leukemia (AML) but are rarely found in acute lymphoblastic leukemia (ALL) [2]. Recently, a subset (3 out of 55) of adult T-ALLs characterized by expression of CD117 (in >90% of T-lymphoblasts) and FLT3 mutations (either internal tandem duplications (ITD) in the juxtamembrane region or mutations in the activation-loop coding region) was described [3]. These data suggested that CD117 expression in T-ALL lymphoblasts might identify a subset of T-ALLs in which activating FLT3 mutations are essential in oncogenesis. If FLT3 mutations would be present in all CD117-positive T-ALLs, up to 11% of all T-ALL patients could potentially benefit from therapy with FLT3 inhibitors, which are currently under investigation for AML treatment [2] and [4]. We report here on the FLT3 mutation status of a 75-year-old man diagnosed with CD117-positive T-ALL. The patient presented with pancytopenia and anemia. Bone marrow analysis revealed 70% blasts with an L1 ALL morphology according to the French–American–British classification. There was no cytochemical evidence of myeloid differentiation, i.e. Sudan black B, specific and non-specific esterase stains were negative. Flowcytometry demonstrated 85% blasts, 9% T-lymphocytes, 1% B-lymphocytes, 2% granulocytes, and 90% of the blast cells were positive for CD117, CD2, CD7, CD13, CD45, and CD56, whereas CD34, CD33, CD5, and CD19 were expressed on a subset of blast cells only (about 75, 30, 30 and 40% of blasts, respectively). Blast cells did not significantly express TdT, MPO, CD1a, CD4, CD8, CD10, CD14, CD15, CD22, CD65, CD133 and SmCD3 (all
Original languageEnglish
Pages (from-to)245-246
JournalLeukemia Research
Issue number2
Publication statusPublished - 2005


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