Activating Notch1 mutations are an early event in T-cell malignancy of Ikaros point mutant Plastic/+ mice

被引:17
作者
Mantha, Simon
Ward, Maureen
McCafferty, Jonathan
Herron, Alan
Palomero, Teresa
Ferrando, Adolfo
Bank, Arthur
Richardson, Christine
机构
[1] Columbia Univ, Dept Med, New York, NY 10032 USA
[2] Columbia Univ, Dept Genet & Dev, New York, NY 10032 USA
[3] Columbia Univ, Inst Canc Genet, New York, NY 10032 USA
[4] Columbia Univ, Dept Comparat Med, New York, NY 10032 USA
关键词
T-cell lymphoma; plastic; Ikaros; Notch; hematopoiesis; chromatin remodeling; genome instability;
D O I
10.1016/j.leukres.2006.06.009
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Ikaros and Notch1 genes are critical to T-cell differentiation through transcriptional activation of target genes and interaction with chromatin remodeling complexes. An Ikaros (Plastic) point mutation inhibits activity of normal Ikaros and Ikaros family members, and leads to T-cell lymphoma in heterozygotes (Plstc/+). Analysis revealed Notch1 activating mutations in 12 of 17 Plstc/+ lymphomas (70%), analogous to those in human T-ALL. Mice acquired Notch1 mutations in lymph nodes as early as 7 weeks. Thus, combined Notch1 and Ikaros dysfunction can be a significant early event in T-cell proliferation and tumorigenesis. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:321 / 327
页数:7
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