The PI3K/AKT Pathway as a Target for Cancer Treatment

被引：635
作者：
Mayer, Ingrid A. [1 ,2 ,3 ]
Arteaga, Carlos L. [1 ,2 ,3 ]
机构：
[1] Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37232 USA
[2] Vanderbilt Univ, Sch Med, Dept Canc Biol, Nashville, TN 37232 USA
[3] Vanderbilt Univ, Sch Med, Breast Canc Program, Vanderbilt Ingram Canc Ctr, Nashville, TN 37232 USA
来源：
ANNUAL REVIEW OF MEDICINE, VOL 67 | 2016年 / 67卷
关键词：
phosphoinositide 3-kinase (PI3K)/AKT; mammalian target of rapamycin (mTOR); pathway inhibitors; breast cancer; lymphoproliferative disorders; mutation; CHRONIC LYMPHOCYTIC-LEUKEMIA; POSITIVE BREAST-CANCER; RENAL-CELL CARCINOMA; PIK3CA MUTATIONS; PHOSPHOINOSITIDE; 3-KINASE; PHOSPHATIDYLINOSITOL; ESTROGEN DEPRIVATION; TYROSINE KINASE; MAMMARY-TUMORS; UP-REGULATION;
D O I：
10.1146/annurev-med-062913-051343
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
Anticancer targeted therapies are designed to exploit a particular vulnerability in the tumor, which in most cases results from its dependence on an oncogene and/or loss of a tumor suppressor. Genes in the phosphoinositide 3-kinase (PI3K)/AKT pathway are the most frequently altered in human cancers. Aberrant activation of this pathway, as a result of these somatic alterations, is associated with cellular transformation, tumorigenesis, cancer progression, and drug resistance. Several drugs targeting PI3K/ATK are currently in clinical trials, alone or in combination, in both solid tumors and hematologic malignancies. These drugs are the focus of this review.
引用
收藏
页码：11 / 28
页数：18
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