title: PI3K/Akt/mTOR signaling pathway and targeted therapy for glioblastoma.
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.
authors.affiliation: Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang, China.
authors.forename: Xiaoman
authors.initials: X
authors.lastname: Li
authors.affiliation: Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang, China.
authors.forename: Changjing
authors.initials: C
authors.lastname: Wu
authors.affiliation: Class 9 of The 97th Clinical Medicine of Seven-Year Program, China Medical University, Shenyang, China.
authors.forename: Nianci
authors.initials: N
authors.lastname: Chen
authors.affiliation: Department of Pathology, The College of Basic Medical Sciences, China Medical University, Shenyang, China.
authors.forename: Huadi
authors.initials: H
authors.lastname: Gu
authors.affiliation: School of Medicine, The University of Texas Southwestern Medical Center, Dallas, Texas, United States of America.
authors.forename: Allen
authors.initials: A
authors.lastname: Yen
authors.affiliation: Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang, China.
authors.forename: Liu
authors.initials: L
authors.lastname: Cao
authors.affiliation: Department of Pathology, The College of Basic Medical Sciences, China Medical University, Shenyang, China.|Department of Pathology, The First Affiliated Hospital of China Medical University, Shenyang, China.
authors.forename: Enhua
authors.initials: E
authors.lastname: Wang
authors.affiliation: Department of Pathology, The College of Basic Medical Sciences, China Medical University, Shenyang, China.|Department of Pathology, The First Affiliated Hospital of China Medical University, Shenyang, China.
authors.forename: Liang
authors.initials: L
authors.lastname: Wang
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001932:Brain Neoplasms / Q000188:drug therapy* / Q000201:enzymology / Q000401:mortality / Q000473:pathology; D066246:ErbB Receptors / Q000037:antagonists & inhibitors / Q000378:metabolism; D005909:Glioblastoma / Q000188:drug therapy* / Q000201:enzymology / Q000401:mortality / Q000473:pathology; D006801:Humans; D058990:Molecular Targeted Therapy; D058539:Phosphatidylinositol 3-Kinase / Q000378:metabolism; D000081082:Phosphoinositide-3 Kinase Inhibitors; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*; D051057:Proto-Oncogene Proteins c-akt / Q000037:antagonists & inhibitors* / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D058570:TOR Serine-Threonine Kinases / Q000037:antagonists & inhibitors* / Q000378:metabolism; D016896:Treatment Outcome
chemical_list: D000970:Antineoplastic Agents; D000081082:Phosphoinositide-3 Kinase Inhibitors; D047428:Protein Kinase Inhibitors; C546842:MTOR protein, human; D058539:Phosphatidylinositol 3-Kinase; C512478:EGFR protein, human; D066246:ErbB Receptors; D051057:Proto-Oncogene Proteins c-akt; D058570:TOR Serine-Threonine Kinases
keywords: EGFR; PI3K/Akt/mTOR pathway; glioblastoma; targeted therapy