Receptor tyrosine kinase coactivation networks in cancer.
Receptor tyrosine kinase coactivation networks in cancer.
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DOI：
10.1158/0008-5472.can-10-0163
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发表时间：
2010-05-15
期刊：
影响因子：
11.2
通讯作者：
Huang PH
中科院分区：
文献类型：
--
作者：
Xu AM;Huang PH
癌细胞采用多种机制来逃避严格调控的细胞过程，如增殖、凋亡和衰老。肿瘤的全系统分析最近已经确定受体酪氨酸激酶（RTK）共激活是癌细胞实现化学抗性的重要机制。这篇简短的评论讨论了我们目前对RTK共激活的复杂和动态过程的理解。我们强调如何系统生物学和计算建模已被用于预测集成的信号转导结果和癌症表型下游的RTK共激活。最后，我们提供了一个前景的可行性，有针对性的RTK网络，以克服癌症的耐药性。
Cancer cells employ multiple mechanisms to evade tightly regulated cellular processes such as proliferation, apoptosis and senescence. Systems-wide analyses of tumors have recently identified receptor tyrosine kinase (RTK) coactivation as an important mechanism by which cancer cells achieve chemoresistance. This mini-review discusses our current understanding of the complex and dynamic process of RTK coactivation. We highlight how systems biology and computational modelling have been employed to predict integrated signalling outcomes and cancer phenotypes downstream of RTK coactivation. We conclude by providing an outlook on the feasibility of targeting RTK networks to overcome chemoresistance in cancer.