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

Autor 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
Instituição Universidade Federal de São Paulo (UNIFESP)
Fleury Inst
Resumo 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.
Idioma Inglês
Data 2008-06-01
Publicado em Cancer Genetics and Cytogenetics. New York: Elsevier B.V., v. 183, n. 2, p. 89-93, 2008.
ISSN 0165-4608 (Sherpa/Romeo, fator de impacto)
Editor Elsevier B.V.
Extensão 89-93
Fonte http://dx.doi.org/10.1016/j.cancergencyto.2008.02.006
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000256677900002
URI http://repositorio.unifesp.br/handle/11600/30698

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