The phosphoinositide 3-kinase pathway and therapy resistance in cancer.
The phosphoinositide 3-kinase pathway and therapy resistance in cancer.
复制标题
DOI：
10.12703/p7-13
复制
发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Toker A
中科院分区：
文献类型：
--
作者：
Brown KK;Toker A
磷脂酰肌醇3-激酶（PI 3 K）/Akt/雷帕霉素机制靶点（mTOR）信号传导网络是促成肿瘤发生和肿瘤维持的过程的主要调节剂。PI 3 K通路在驱动对多种抗癌疗法的抗性方面也起着关键作用。这篇综述文章重点介绍了PI 3 K通路导致癌症耐药的机制，并强调了潜在的联合治疗策略，以规避PI 3 K信号转导驱动的耐药。此外，耐药机制，限制了PI 3 K通路的小分子抑制剂的临床疗效进行了讨论。
The phosphoinositide 3-kinase (PI3K)/Akt/mechanistic target of rapamycin (mTOR) signaling network is a master regulator of processes that contribute to tumorigenesis and tumor maintenance. The PI3K pathway also plays a critical role in driving resistance to diverse anti-cancer therapies. This review article focuses on mechanisms by which the PI3K pathway contributes to therapy resistance in cancer, and highlights potential combination therapy strategies to circumvent resistance driven by PI3K signaling. In addition, resistance mechanisms that limit the clinical efficacy of small molecule inhibitors of the PI3K pathway are discussed.