Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.
Cancer Res. 2010 May 15;70(10):3857-60. doi: 10.1158/0008-5472.CAN-10-0163. Epub 2010 Apr 20.
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 modeling have been employed to predict integrated signaling 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.
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。最近对肿瘤的系统分析确定了受体酪氨酸激酶 (RTK) 共激活是癌细胞获得化疗耐药性的重要机制。这篇小型综述讨论了我们对 RTK 共激活这一复杂和动态过程的现有理解。我们强调了系统生物学和计算模型如何被用来预测 RTK 共激活下游的综合信号转导结果和癌症表型。最后,我们对靶向 RTK 网络克服癌症化疗耐药性的可行性进行了展望。