除PTEN突变外：PI3K通路在肿瘤发生过程中作为多种输入信号的整合者
Beyond PTEN mutations: the PI3K pathway as an integrator of multiple inputs during tumorigenesis.
作者信息
Cully Megan, You Han, Levine Arnold J, Mak Tak W
机构信息
The Campbell Family Institute for Breast Cancer Research, University Health Network, University of Toronto, Toronto, Ontario M5G 2C1, Canada.
出版信息
Nat Rev Cancer. 2006 Mar;6(3):184-92. doi: 10.1038/nrc1819.
The tumour-suppressor phosphatase with tensin homology (PTEN) is the most important negative regulator of the cell-survival signalling pathway initiated by phosphatidylinositol 3-kinase (PI3K). Although PTEN is mutated or deleted in many tumours, deregulation of the PI3K-PTEN network also occurs through other mechanisms. Crosstalk between the PI3K pathways and other tumorigenic signalling pathways, such as those that involve Ras, p53, TOR (target of rapamycin) or DJ1, can contribute to this deregulation. How does the PI3K pathway integrate signals from numerous sources, and how can this information be used in the rational design of cancer therapies?
具有张力蛋白同源性的肿瘤抑制磷酸酶（PTEN）是由磷脂酰肌醇3-激酶（PI3K）启动的细胞存活信号通路中最重要的负调节因子。尽管PTEN在许多肿瘤中发生突变或缺失，但PI3K-PTEN网络的失调也通过其他机制发生。PI3K通路与其他致癌信号通路（如涉及Ras、p53、雷帕霉素靶蛋白（TOR）或DJ1的信号通路）之间的相互作用可导致这种失调。PI3K通路如何整合来自众多来源的信号，以及如何将这些信息用于癌症治疗的合理设计？
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