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Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Oncología > Terapia celular > DA - CIMA - Oncología - Terapia celular - Artículos de Revista >

Coexistence of different clonal populations harboring the b3a2 (p210) and e1a2 (p190) BCR-ABL1 fusion transcripts in chronic myelogenous leukemia resistant to imatinib
Authors: Aguirre, X. (Xavier)
Roman-Gomez, J. (José)
Vazquez, I. (Iria)
Jimenez-Velasco, A. (A.)
Larrayoz, M.J. (María J.)
Lahortiga, I. (Idoya)
Andreu, E.J. (Enrique José)
Marquez, J. (José)
Beltran-de-Heredia, J. (J.M.)
Odero, M.D. (María D.)
Prosper, F. (Felipe)
Calasanz, M.J. (María José)
Keywords: Fusion Proteins, bcr-abl/genetics
Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy/genetics
Piperazines/therapeutic use
Pyrimidines/therapeutic use
RNA, Messenger/analysis
Issue Date: 2005
Publisher: Elsevier
Publisher version: http://dx.doi.org/10.1016/j.cancergencyto.2004.11.010
ISSN: 0165-4608
Citation: Agirre, X., Roman-Gomez, J., Vazquez, I., Jimenez-Velasco, A., Larrayoz, M. J., Lahortiga, I. et al. Coexistence of different clonal populations harboring the b3a2 (p210) and e1a2 (p190) BCR-ABL1 fusion transcripts in chronic myelogenous leukemia resistant to imatinib. Cancer genet. cytogenet. 2005; 160: 22–26
Abstract
In this study, we report the case of a Philadelphia (Ph) positive chronic myelogenous leukemia (CML) patient with the presence of p190 and p210 BCR-ABL1 mRNA fusion transcripts derived from e1a2 and b3a2 BCR-ABL1 genomic rearrangements, respectively. The presence of e1a2 BCRABL1 genomic rearrangement was seen in 2 different clones, one with the rearrangement and another one with the rearrangement and deletion of the BCR gene of the non-rearranged chromosome 22. After treatment with imatinib, the p210 transcript could not be detected, whereas p190 was still present 6 months after initiation of imatinib therapy and progression to blast phase. The absence of p210 transcript post treatment indicates that the clone with b3a2 responded to imatinib and that the observed resistance was associated to cells harboring the e1a2 genomic rearrangement. Despite resistance of this patient to imatinib, no evidence of mutations in the kinase domain of ABL1 was found. Loss of normal BCR in one cell clone may contribute to the resistance to imatinib due to the lack of BCR mediated inhibition of BCR-ABL1.
Permanent link: http://hdl.handle.net/10171/18561
Appears in Collections:DA - CIMA - Oncología - Síndromes mieloproliferativos - Artículos de Revista
DA - CIMA - Oncología - Terapia celular - Artículos de Revista
DA - CIMA - Oncología - Genética - Artículos de revista
DA - CUN - Área de Terapia Celular - Artículos de revista
DA - Medicina - Hematología - Artículos de revista
DA - Ciencias - Genética - Artículos de revista

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