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Blood, 15 June 2005, Vol. 105, No. 12, pp. 4849-4852.
Prepublished online as a Blood First Edition Paper on February 15, 2005; DOI 10.1182/blood-2004-12-4897.
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NEOPLASIA
Brief report
Fusion of EML1 to ABL1 in T-cell acute lymphoblastic leukemia with cryptic t(9;14)(q34;q32)
Kim De Keersmaecker,
Carlos Graux,
Maria D. Odero,
Nicole Mentens,
Riet Somers,
Johan Maertens,
Iwona Wlodarska,
Peter Vandenberghe,
Anne Hagemeijer,
Peter Marynen, and
Jan Cools
From the Department of Human Genetics, Flanders Interuniversity Institute for Biotechnology (VIB), Leuven, Belgium; Departments of Human Genetics and Hematology, University of Leuven, Leuven, Belgium; and Department of Genetics, University of Navarra, Pamplona, Spain.
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. (Blood. 2005;105:4849-4852)
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