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Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Oncología > Genética > DA - CIMA - Oncología - Genética - Artículos de revista >

Fusion of EML1 to ABL1 in T-cell acute lymphoblastic leukemia with cryptic t(9;14)(q34;q32)
Authors: Keersmaecker, K. (K.) de
Graux, C. (Carlos)
Odero, M.D. (Maria Dolores)
Mentens, N. (Nicole)
Somers, R. (Riet)
Maertens, J. (Johan)
Wlodarska, I. (Iwona)
Vandenberghe, P. (Peter)
Hagemeijer, A. (A.)
Marynen, P. (Peter)
Cools, J. (J.)
Keywords: Chromosomes, Human, Pair 14
Chromosomes, Human, Pair 9
Leukemia, T-Cell/pathology
Oncogene Proteins, Fusion/genetics
Translocation, Genetic
Issue Date: 2005
Publisher: American Society of Hematology
Publisher version:
ISSN: 1528-0020
Citation: De Keersmaecker K, Graux C, Odero MD, Mentens N, Somers R, Maertens J, et al. Fusion of EML1 to ABL1 in T-cell acute lymphoblastic leukemia with cryptic t(9;14)(q34;q32). Blood 2005 Jun 15;105(12):4849-4852
The BCR-ABL1 fusion kinase is frequently associated with chronic myeloid leukemia and B-cell acute lymphoblastic leukemia but is rare in T-cell acute lymphoblastic leukemia (T-ALL). We recently identified NUP214-ABL1 as a variant ABL1 fusion gene in 6% of T-ALL patients. Here we describe the identification of another ABL1 fusion, EML1-ABL1, in a T-ALL patient with a cryptic t(9;14)(q34;q32) associated with deletion of CDKN2A (p16) and expression of TLX1 (HOX11). Echinoderm microtubule-associated protein-like 1-Abelson 1 (EML1-ABL1) is a constitutively phosphorylated tyrosine kinase that transforms Ba/F3 cells to growth factor-independent growth through activation of survival and proliferation pathways, including extracellular signal-related kinase 1/2 (Erk1/2), signal transducers and activators of transcription 5 (Stat5), and Lyn kinase. Deletion of the coiled-coil domain of EML1 abrogated the transforming properties of the fusion kinase. EML1-ABL1 and breakpoint cluster region (BCR)-ABL1 were equally sensitive to the tyrosine kinase inhibitor imatinib. These data further demonstrate the involvement of ABL1 fusions in the pathogenesis of T-ALL and identify EML1-ABL1 as a novel therapeutic target of imatinib.
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DA - Ciencias - Genética - Artículos de revista

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