What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis?

被引：0
|
作者：
S D Turner
D R Alexander
机构：
[1] The Babraham Institute,Laboratory of Lymphocyte Signalling and Development
[2] Babraham Research Campus,undefined
来源：
Leukemia | 2005年 / 19卷
关键词：
NPM-ALK; ALCL; oncogene; kinase;
D O I：
暂无
中图分类号：
学科分类号：
摘要：
The nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) is generated as a t(2;5) chromosomal breakpoint product, typically in CD30+ anaplastic large cell lymphomas. Activation of the NPM-ALK tyrosine kinase by NPM dimerisation causes autophosphorylation at multiple tyrosine residues and the consequent recruitment of a ‘signalosome’ that couples the fusion protein to pathways regulating mitogenesis and apoptosis. This review focuses on recent advances in our understanding of the transforming signals induced by this fusion protein in mouse models.
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页码：1128 / 1134
页数：6
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