FLT3 internal tandem duplication during myelodysplastic syndrome follow-up: a marker of transformation to acute myeloid leukemia

FLT3 internal tandem duplication during myelodysplastic syndrome follow-up: a marker of transformation to acute myeloid leukemia

Author Pinheiro, Ronald Feitosa Autor UNIFESP Google Scholar
Moreira, Eloisa de Sa Google Scholar
Regis Silva, Maria Regina Autor UNIFESP Google Scholar
Alberto, Fernando Lopes Google Scholar
Chauffaille, Maria de Lourdes L. F. Autor UNIFESP Google Scholar
Institution Universidade Federal de São Paulo (UNIFESP)
Fleury Inst
Abstract Myelodysplastic syndrome (MDS) is a clonal hematopoietic stem cell disorder characterized by ineffective hematopoiesis and risk for evolving to acute leukemia. Some molecular abnormalities related to acute myeloid leukemia (AML) transformation have been reported, such as FLT3 (FMS-like tyrosine kinase 3) mutations. FLT3, a member of the class 3 receptor tyrosine kinase family, mediates stem cell proliferation and differentiation, and its mutations, internal tandem duplication (ITD) and Asp835, have been reported in rare MDS patients. We studied FLT3 ITD, prospectively, in 50 MDS patients at diagnosis, at 6 and 12 months follow-up, and at any other time-point if AML transformation was detected. FLT3 ITD was not observed at diagnosis, but during follow-up the mutation was present in 2 of 50 patients (4%). of these, one case exhibited FLT3 ITD at the end of the 6 months of follow-up in similar to 8% of bone marrow cells; this case evolved into AML at 8 months, at which time FLT3 ITD was present in similar to 85% of bone marrow cells. the other case exhibited FLT3 ITD in 68% of bone marrow cells at 7 months, precisely at the time of AML transformation. Although rare in MDS, FLT3 ITD is associated with a high probability of evolution to AML. (C) 2008 Elsevier Inc. All rights reserved.
Language English
Date 2008-06-01
Published in Cancer Genetics and Cytogenetics. New York: Elsevier B.V., v. 183, n. 2, p. 89-93, 2008.
ISSN 0165-4608 (Sherpa/Romeo, impact factor)
Publisher Elsevier B.V.
Extent 89-93
Origin http://dx.doi.org/10.1016/j.cancergencyto.2008.02.006
Access rights Closed access
Type Article
Web of Science ID WOS:000256677900002
URI http://repositorio.unifesp.br/handle/11600/30698

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