Hazlehurst Lori A, Bewry Nadine N, Nair Rajesh R, Pinilla-Ibarz Javier
Molecular Oncology Program, H. Lee Moffitt Cancer Center & Research Institute, Tampa, Florida 33612, USA.
Cancer Control. 2009 Apr;16(2):100-7. doi: 10.1177/107327480901600202.
The fusion protein BCR-ABL results in constitutive tyrosine kinase activity. It also affects downstream targets as well as the subcellular location of the normally tightly regulated Abl tyrosine kinase.
The authors review the current knowledge concerning the signaling networks associated with BCR-ABL-dependent transformation.
Although BCR-ABL is considered a single genetic change, the dysregulated tyrosine kinase activates a network of signals that contributes to cytokine-independent growth, resistance to apoptosis, and genetic instability.
The effectiveness of BCR-ABL-dependent transformation of hematopoietic stem cells is due not to a single pathway but rather to the culmination of a network of signaling pathways.
融合蛋白BCR-ABL可导致组成型酪氨酸激酶活性。它还会影响下游靶点以及通常受到严格调控的Abl酪氨酸激酶的亚细胞定位。
作者回顾了目前有关与BCR-ABL依赖性转化相关的信号网络的知识。
尽管BCR-ABL被认为是一种单一的基因改变，但失调的酪氨酸激酶会激活一个信号网络，该网络有助于细胞因子非依赖性生长、抗凋亡以及基因不稳定。
BCR-ABL依赖性造血干细胞转化的有效性并非归因于单一途径，而是多种信号通路网络共同作用的结果。
