Full metadata record
DC Field | Value | Language |
---|---|---|
dc.creator | Keersmaecker, K. (K.) de | |
dc.creator | Graux, C. (Carlos) | |
dc.creator | Odero, M.D. (Maria Dolores) | |
dc.creator | Mentens, N. (Nicole) | |
dc.creator | Somers, R. (Riet) | |
dc.creator | Maertens, J. (Johan) | |
dc.creator | Wlodarska, I. (Iwona) | |
dc.creator | Vandenberghe, P. (Peter) | |
dc.creator | Hagemeijer, A. (A.) | |
dc.creator | Marynen, P. (Peter) | |
dc.creator | Cools, J. (J.) | |
dc.date.accessioned | 2011-11-09T12:36:11Z | - |
dc.date.available | 2011-11-09T12:36:11Z | - |
dc.date.issued | 2005 | - |
dc.identifier.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 | es_ES |
dc.identifier.issn | 1528-0020 | - |
dc.identifier.uri | https://hdl.handle.net/10171/19475 | - |
dc.description.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. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | American Society of Hematology | es_ES |
dc.rights | info:eu-repo/semantics/openAccess | es_ES |
dc.subject | Chromosomes, Human, Pair 14 | es_ES |
dc.subject | Chromosomes, Human, Pair 9 | es_ES |
dc.subject | Leukemia, T-Cell/pathology | es_ES |
dc.subject | Oncogene Proteins, Fusion/genetics | es_ES |
dc.subject | Translocation, Genetic | es_ES |
dc.title | Fusion of EML1 to ABL1 in T-cell acute lymphoblastic leukemia with cryptic t(9;14)(q34;q32) | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.relation.publisherversion | http://bloodjournal.hematologylibrary.org/content/105/12/4849 | es_ES |
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