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Genetic inactivation of Ikaros is a rare event in human T-ALL.
Marçais, Ambroise; Jeannet, Robin; Hernandez, Lucie; Soulier, Jean; Sigaux, François; Chan, Susan; Kastner, Philippe.
Afiliación
  • Marçais A; Department of Cancer Biology, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, France.
Leuk Res ; 34(4): 426-9, 2010 Apr.
Article en En | MEDLINE | ID: mdl-19796813
ABSTRACT
The Ikaros (Ikzf1) gene, encoding a transcription regulator, is a major tumor suppressor in B-cell acute lymphoblastic leukemia (B-ALL). In the mouse, however, loss of Ikaros is primarily associated with T-ALL development. Whether Ikaros is also implicated in human T-ALL remains unclear. We studied Ikaros in 25 human T-ALL samples from diverse molecular subtypes at the mRNA, protein, sequence and genomic copy number level. We found that Ikaros was abnormal in only one sample one allele was lost by genomic deletion, while proteins generated from the remaining allele were delocalized and concentrated at a single cytoplasmic structure. Thus, inactivation of Ikaros by deletion or mutation is rare in human T-ALL.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Silenciador del Gen / Factor de Transcripción Ikaros / Leucemia-Linfoma Linfoblástico de Células T Precursoras Tipo de estudio: Etiology_studies / Incidence_studies / Observational_studies / Risk_factors_studies Límite: Adolescent / Adult / Child / Child, preschool / Humans / Infant / Middle aged Idioma: En Revista: Leuk Res Año: 2010 Tipo del documento: Article País de afiliación: Francia

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Silenciador del Gen / Factor de Transcripción Ikaros / Leucemia-Linfoma Linfoblástico de Células T Precursoras Tipo de estudio: Etiology_studies / Incidence_studies / Observational_studies / Risk_factors_studies Límite: Adolescent / Adult / Child / Child, preschool / Humans / Infant / Middle aged Idioma: En Revista: Leuk Res Año: 2010 Tipo del documento: Article País de afiliación: Francia