| Literature DB >> 26233890 |
Huifang Guo1, Peter German2, Shanshan Bai2, Sean Barnes1, Wei Guo1, Xiangjie Qi3, Hongxiang Lou4, Jiyong Liang1, Eric Jonasch2, Gordon B Mills5, Zhiyong Ding6.
Abstract
The phosphatidylinositol 3 kinase (PI3K)/AKT pathway is genetically targeted in more pathway components and in more tumor types than any other growth factor signaling pathway, and thus is frequently activated as a cancer driver. More importantly, the PI3K/AKT pathway is composed of multiple bifurcating and converging kinase cascades, providing many potential targets for cancer therapy. Renal cell carcinoma (RCC) is a high-risk and high-mortality cancer that is notoriously resistant to traditional chemotherapies or radiotherapies. The PI3K/AKT pathway is modestly mutated but highly activated in RCC, representing a promising drug target. Indeed, PI3K pathway inhibitors of the rapalog family are approved for use in RCC. Recent large-scale integrated analyses of a large number of patients have provided a molecular basis for RCC, reiterating the critical role of the PI3K/AKT pathway in this cancer. In this review, we summarize the genetic alterations of the PI3K/AKT pathway in RCC as indicated in the latest large-scale genome sequencing data, as well as treatments for RCC that target the aberrant activated PI3K/AKT pathway.Entities:
Keywords: AKT; PI3K; Renal cell carcinoma; Targeted therapy; mTOR
Mesh：
Substances：
Year: 2015 PMID： 26233890 PMCID： PMC4624215 DOI： 10.1016/j.jgg.2015.03.003
Source DB: PubMed Journal: J Genet Genomics ISSN： 1673-8527 Impact factor: 4.275