Current clinical development of PI3K pathway inhibitors in glioblastoma

被引：117

作者：

Wen, Patrick Y. ^{[1
,2
,6
]}

Lee, Eudocia Q. ^{[1
,2
,6
]}

Reardon, David A. ^{[1
,6
]}

Ligon, Keith L. ^{[3
,4
,5
,6
]}

Yung, W. K. Alfred ^{[7
]}

机构：

[1] Dana Farber Brigham & Womens Canc Ctr, Ctr Neurooncol, Boston, MA USA

[2] Brigham & Womens Hosp, Dept Neurol, Div Neurooncol, Boston, MA 02115 USA

[3] Dana Farber Canc Inst, Ctr Mol Oncol Pathol, Boston, MA 02215 USA

[4] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA

[5] Childrens Hosp Boston, Boston, MA USA

[6] Harvard Univ, Sch Med, Boston, MA USA

[7] Univ Texas MD Anderson Canc Ctr, Div Neurooncol, Houston, TX 77030 USA

来源：

NEURO-ONCOLOGY | 2012年 / 14卷 / 07期

关键词：

AKT; glioblastoma; GBM; mTOR; PI3K; PHASE-II TRIAL; PHOSPHATIDYLINOSITOL 3-KINASE/MAMMALIAN TARGET; DUAL PI3K/MTOR INHIBITOR; FACTOR RECEPTOR GENE; RAPAMYCIN INHIBITOR; SIGNALING PATHWAYS; ANTITUMOR-ACTIVITY; MAMMALIAN TARGET; CANCER-CELLS; EVEROLIMUS;

D O I：

10.1093/neuonc/nos117

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Glioblastoma (GBM) is the most common and lethal primary malignant tumor of the central nervous system, and effective therapeutic options are lacking. The phosphatidylinositol 3-kinase (PI3K) pathway is frequently dysregulated in many human cancers, including GBM. Agents inhibiting PI3K and its effectors have demonstrated preliminary activity in various tumor types and have the potential to change the clinical treatment landscape of patients with solid tumors. In this review, we describe the activation of the PI3K pathway in GBM, explore why inhibition of this pathway may be a compelling therapeutic target for this disease, and provide an update of the data on PI3K inhibitors in clinical trials and from earlier investigation.

引用

页码：819 / 829

页数：11

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