It's T-ALL about Notch

被引:0
作者
R M Demarest
F Ratti
A J Capobianco
机构
[1] Molecular and Cellular Oncogenesis,
[2] The Wistar Institute,undefined
来源
Oncogene | 2008年 / 27卷
关键词
p53; Ikaros; PTEN; Fbw7; C-myc; CSL;
D O I
暂无
中图分类号
学科分类号
摘要
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive subset of ALL with poor clinical outcome compared to B-ALL. Therefore, to improve treatment, it is imperative to delineate the molecular blueprint of this disease. This review describes the central role that the Notch pathway plays in T-ALL development. We also discuss the interactions between Notch and the tumor suppressors Ikaros and p53. Loss of Ikaros, a direct repressor of Notch target genes, and suppression of p53-mediated apoptosis are essential for development of this neoplasm. In addition to the activating mutations of Notch previously described, this review will outline combinations of mutations in pathways that contribute to Notch signaling and appear to drive T-ALL development by ‘mimicking’ Notch effects on cell cycle and apoptosis.
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收藏
页码:5082 / 5091
页数:9
相关论文
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