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.
Keywords: EGFR; PI3K/Akt/mTOR pathway; glioblastoma; targeted therapy.
MeSH terms
- Animals
- Antineoplastic Agents / therapeutic use*
- Brain Neoplasms / drug therapy*
- Brain Neoplasms / enzymology
- Brain Neoplasms / mortality
- Brain Neoplasms / pathology
- ErbB Receptors / antagonists & inhibitors
- ErbB Receptors / metabolism
- Glioblastoma / drug therapy*
- Glioblastoma / enzymology
- Glioblastoma / mortality
- Glioblastoma / pathology
- Humans
- Molecular Targeted Therapy*
- Phosphatidylinositol 3-Kinase / metabolism
- Phosphoinositide-3 Kinase Inhibitors*
- Protein Kinase Inhibitors / therapeutic use*
- Proto-Oncogene Proteins c-akt / antagonists & inhibitors*
- Proto-Oncogene Proteins c-akt / metabolism
- Signal Transduction / drug effects
- TOR Serine-Threonine Kinases / antagonists & inhibitors*
- TOR Serine-Threonine Kinases / metabolism
- Treatment Outcome
Substances
- Antineoplastic Agents
- Phosphoinositide-3 Kinase Inhibitors
- Protein Kinase Inhibitors
- MTOR protein, human
- Phosphatidylinositol 3-Kinase
- EGFR protein, human
- ErbB Receptors
- Proto-Oncogene Proteins c-akt
- TOR Serine-Threonine Kinases