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Title: Fusion of EML1 to ABL1 in T-cell acute lymphoblastic leukemia with cryptic t(9;14)(q34;q32)
Authors: De Keersmaecker, Kim
Graux, Carlos
Odero, Maria D
Mentens, Nicole
Somers, Riet
Maertens, Johan
Wlodarska, Iwona
Vandenberghe, Peter
Hagemeijer-Hausman, Anne
Marynen, Peter
Cools, Jan # ×
Issue Date: Jun-2005
Publisher: W.B. Saunders
Series Title: Blood vol:105 issue:12 pages:4849-4852
Abstract: 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.
URI: 
ISSN: 0006-4971
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Clinical Genetics Section (-)
Molecular Genetics Section (-)
Human Genome Laboratory
Laboratory of Molecular Biology of Leukemia
Laboratory for Genetics of Malignant Disorders
Department of Human Genetics - miscellaneous
× corresponding author
# (joint) last author

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