Related Experiment Video
Updated: Apr 20, 2026
Preparation Of Neovascular Tissues from Human Glioma Tissues for Quantitative Proteomics Analysis of Tumor Angiogenesis
Published on: March 20, 2026
Targeting MET for glioma therapy
Ahmed J Awad1, Terry C Burns, Ying Zhang
1Departments of Neurosurgery and.
Abstract:
Glioblastoma multiforme is the most common and most lethal of all primary brain tumors. Even with the standard therapy, life expectancy is still poor, with an average survival of approximately 14 months following initial diagnosis. Hence, there is an urgent need for novel treatment strategies that inhibit proliferation and angiogenesis in high-grade gliomas. One such strategy consists of inhibiting receptor tyrosine kinases, including MET and/or its ligand hepatocyte growth factor (HGF). Because of their widespread involvement in human cancer, HGF and MET have emerged as promising therapeutic targets, and some inhibitory agents that target them have already entered clinical trials. In this paper, the authors highlight recent evidence implicating HGF/MET pathway deregulation in glioblastoma multiforme, discuss therapeutic approaches to inhibit HGF/MET signaling, and summarize ongoing clinical trials targeting this pathway.
Insights
Glioblastoma multiforme, a lethal brain cancer, has poor survival rates. Targeting the HGF/MET pathway offers a promising new strategy to inhibit tumor growth and angiogenesis, with agents in clinical trials.
Area of Science:
- Neuro-oncology
- Molecular biology
- Cancer research
Background:
- Glioblastoma multiforme is the most aggressive primary brain tumor, with limited treatment options and poor prognosis.
- Current standard therapies offer minimal survival benefits, necessitating novel therapeutic strategies.
- The hepatocyte growth factor (HGF)/MET pathway is implicated in various cancers, including glioblastoma.
Purpose of the Study:
- To review the role of HGF/MET pathway deregulation in glioblastoma multiforme.
- To discuss therapeutic strategies targeting HGF/MET signaling in high-grade gliomas.
- To summarize current clinical trials investigating HGF/MET inhibitors for glioblastoma.
Main Methods:
- Literature review of recent evidence on HGF/MET pathway in glioblastoma.
- Analysis of therapeutic approaches targeting HGF/MET signaling.
- Summary of ongoing clinical trials for HGF/MET inhibitors.
Main Results:
- HGF/MET pathway deregulation is implicated in glioblastoma progression, proliferation, and angiogenesis.
- Inhibiting HGF/MET signaling presents a viable therapeutic strategy for glioblastoma.
- Several agents targeting HGF/MET are in various phases of clinical trials.
Conclusions:
- The HGF/MET pathway is a critical target for glioblastoma treatment.
- Targeted inhibition of HGF/MET signaling holds promise for improving patient outcomes.
- Further research and clinical trials are essential to validate HGF/MET inhibitors for glioblastoma therapy.
