PI3K/Akt/mTOR signaling pathway and targeted therapy for glioblastoma

TLDR: The reason why inhibition of the mTOR-complex pathway may serve as a compelling therapeutic target for the disease is explored, and update data of EFGR and PI3K/Akt/mTOR inhibitors in clinical trials is provided.

Abstract: // Xiaoman Li 1,* , Changjing Wu 1,* , Nianci Chen 2 , Huadi Gu 3 , Allen Yen 4 , Liu Cao 1 , Enhua Wang 3,5 and Liang Wang 3,5 1 Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang, China 2 Class 9 of the 97th Clinical Medicine of Seven-Year Program, China Medical University, Shenyang, China 3 Department of Pathology, The College of Basic Medical Sciences, China Medical University, Shenyang, China 4 School of Medicine, The University of Texas Southwestern Medical Center, Dallas, Texas, United States of America 5 Department of Pathology, The First Affiliated Hospital of China Medical University, Shenyang, China * These authors have contributed equally to this work Correspondence to: Liang Wang, email: // Keywords : glioblastoma, EGFR, PI3K/Akt/mTOR pathway, targeted therapy Received : December 05, 2015 Accepted : February 24, 2016 Published : March 07, 2016 Abstract Glioblastoma multiform (GBM) is the most common malignant glioma of all the brain tumors and currently effective treatment options are still lacking. GBM is frequently accompanied with overexpression and/or mutation of epidermal growth factor receptor (EGFR), which subsequently leads to activation of many downstream signal pathways such as phosphatidylinositol 3-kinase (PI3K)/Akt/rapamycin-sensitive mTOR-complex (mTOR) pathway. Here we explored the reason why inhibition of the pathway may serve as a compelling therapeutic target for the disease, and provided an update data of EFGR and PI3K/Akt/mTOR inhibitors in clinical trials.