mTOR signaling in glioblastoma: lessons learned from bench to bedside

被引:156
作者
Akhavan, David [1 ,2 ,3 ,4 ]
Cloughesy, Timothy F. [5 ,6 ,7 ]
Mischel, Paul S. [1 ,2 ,3 ,5 ,6 ]
机构
[1] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol, Los Angeles, CA 90095 USA
[2] Univ Calif Los Angeles, David Geffen Sch Med, Dept Lab Med, Los Angeles, CA 90095 USA
[3] Univ Calif Los Angeles, David Geffen Sch Med, Dept Mol & Med Pharmacol, Los Angeles, CA 90095 USA
[4] Univ Calif Los Angeles, David Geffen Sch Med, UCLA Med Scientist Training Program, Los Angeles, CA 90095 USA
[5] Univ Calif Los Angeles, David Geffen Sch Med, Henry Singelton Brain Tumor Program, Los Angeles, CA 90095 USA
[6] Univ Calif Los Angeles, David Geffen Sch Med, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90095 USA
[7] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA
关键词
glioblastoma; mTOR; PI3K; GROWTH-FACTOR RECEPTOR; PROTEIN-KINASE-B; RECURRENT GLIOBLASTOMA; CANCER-THERAPY; PTEN-DEFICIENT; IN-VIVO; ENHANCED SENSITIVITY; PATHWAY ACTIVATION; ASTROCYTOMA MODEL; MAMMALIAN TARGET;
D O I
10.1093/neuonc/noq052
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Phosphatidyl-inositol-3 kinases (PI3Ks) constitute a family of intracellular lipid kinases that are frequently hyperactivated in glioblastoma. The PI3K complex links growth factor signaling with cellular proliferation, differentiation, metabolism, and survival. Mammalian target of rapamycin (mTOR) acts both as a downstream effector and upstream regulator of PI3K, thus highlighting its importance in glioblastoma. This review highlights laboratory and clinical evidence of mTOR's role in glioblastoma. Mechanisms of escape from mTOR inhibition are also discussed, as well as future clinical strategies of mTOR inhibition.
引用
收藏
页码:882 / 889
页数:8
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