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mTOR 信号通路在胶质母细胞瘤中的作用：从实验室到临床的经验教训。

mTOR signaling in glioblastoma: lessons learned from bench to bedside.

机构信息

The David Geffen UCLA School of Medicine, 10833 Le Conte Avenue, Los Angeles, CA 90095-1732, USA.

出版信息

Neuro Oncol. 2010 Aug;12(8):882-9. doi: 10.1093/neuonc/noq052. Epub 2010 May 14.

DOI:10.1093/neuonc/noq052
PMID:20472883
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2940679/
Abstract

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.

摘要

磷脂酰肌醇-3 激酶（PI3Ks）构成了一组细胞内脂质激酶，它们在神经胶质瘤中经常过度激活。PI3K 复合物将生长因子信号与细胞增殖、分化、代谢和存活联系起来。雷帕霉素（mTOR）的哺乳动物靶标既是 PI3K 的下游效应物，也是上游调节剂，因此突出了其在神经胶质瘤中的重要性。本综述强调了 mTOR 在神经胶质瘤中的作用的实验室和临床证据。还讨论了逃避 mTOR 抑制的机制以及 mTOR 抑制的未来临床策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0222/2940679/f6311f2e85ed/noq05201.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0222/2940679/f6311f2e85ed/noq05201.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0222/2940679/f6311f2e85ed/noq05201.jpg

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