Artigo Revisado por pares

FLT3 mutations are associated with other molecular lesions in AML

2003; Elsevier BV; Volume: 28; Issue: 1 Linguagem: Inglês

10.1016/s0145-2126(03)00125-5

ISSN

1873-5835

Autores

Maria J. Carnicer, Josep Nomdedéu, Adriana Lasa, Camino Estivill, Salut Brunet, Anna Aventı x n, Jorge Sierra,

Tópico(s)

Retinoids in leukemia and cellular processes

Resumo

The basic molecular defects underlying acute myeloid leukemias (AML) seem to be caused by inactivating mutations in transcription factors which control normal myeloid differentiation (Class II mutations) and genetic lesions in tyrosine kinases resulting in constitutive activation (Class I mutations). We sought to determine the frequency of associated mutations (Class I + Class II) in a consecutive series of adult de novo AML (353 patients) in order to stress the validity of this model. Mutations and rearrangements at the FLT3, AML1/ETO, CBFβ/MYH11, AML1, CEBPα and MLL genes were investigated using standard molecular methods. Despite the limitations of the study (DNA availability hampered c-kit and ras mutational analysis), 3.4% of patients showed Class I + Class II mutations. Our findings could be consistent with the cooperative model. The search for new tyrosine kinases which can be the target of molecular lesions in AML warrants further investigation.

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