ReviewCancers2017
Role and Therapeutic Targeting of the HGF/MET Pathway in Glioblastoma.
Review in Cancers, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Overexpression of c-Met is Associated with Poor Prognosis in Glioblastoma Multiforme: A Systematic Review and Meta-Analyses.Asian Pacific journal of cancer prevention : APJCP · 2021Pooled it
- Targeting MET and mTOR Synergistically Overcomes Adaptive Resistance in Glioblastoma.International journal of molecular sciences · 2026Article
- Integrating Molecular Pathology, Tumor Microenvironment, and Novel Therapies to Overcome Resistance in Glioblastoma.Journal of molecular neuroscience : MN · 2026Review
- Redundancy in Growth Factor Receptor Signaling in Adult Astrocytoma Resistance to Small-Molecule Tyrosine Kinase Inhibitors.International journal of molecular sciences · 2026Review
- FOLR1 Regulates the Malignant Progression of Glioblastoma through the SRC/ERK1/2 Axis.Combinatorial chemistry & high throughput screening · 2026Article
- BNIP3-mTOR Signaling Mediates Resistance to MET Inhibition in Glioblastoma.bioRxiv : the preprint server for biology · 2025Article
- Targeting CAFs-Mediated Stromal Signaling in a Patient-Derived Organotypic Colorectal Tumor Model.Molecular cancer therapeutics · 2025Article
- Current Research Trends in Glioblastoma: Focus on Receptor Tyrosine Kinases.International journal of molecular sciences · 2025Review
- Analysis of transcription profiles for the identification of master regulators as the key players in glioblastoma.Computational and structural biotechnology journal · 2024Article
- Non-Immune-Mediated, p27-Associated, Growth Inhibition of Glioblastoma by Class-II-Transactivator (CIITA).Cells · 2024Article
- Interleukin 6 and cancer resistance in glioblastoma multiforme.Neurosurgical review · 2024Review
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- A Synopsis of Biomarkers in Glioblastoma: Past and Present.Current issues in molecular biology · 2024Review
- A first comprehensive analysis of Transcribed Ultra Conserved Regions uncovers important regulatory functions of novel non-coding transcripts in gliomas.Research square · 2024Article
- AberrantCells · 2024Review
- Crebanine, an aporphine alkaloid, induces cancer cell apoptosis through PI3K-Akt pathway in glioblastoma multiforme.Frontiers in pharmacology · 2024Article
- Tumor Niches: Perspectives for Targeted Therapies in Glioblastoma.Antioxidants & redox signaling · 2023Review
- Discovery and Optimization of the First ATP Competitive Type-III c-MET Inhibitor.Journal of medicinal chemistry · 2023Article
- Evaluating glioblastoma tumour sphere growth and migration in interaction with astrocytes using 3D collagen-hyaluronic acid hydrogels.Journal of materials chemistry. B · 2023Article
- A receptor-mediated landscape of druggable and targeted nanomaterials for gliomas.Materials today. Bio · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Glioblastoma (GBM) is a lethal brain tumor with dismal prognosis. Current therapeutic options, consisting of surgery, chemotherapy and radiation, have only served to marginally increase patient survival. Receptor tyrosine kinases (RTKs) are dysregulated in approximately 90% of GBM; attributed to this, research has focused on inhibiting RTKs as a novel and effective therapy for GBM. Overexpression of RTK mesenchymal epithelial transition (MET), and its ligand, hepatocyte growth factor (HGF), in GBM highlights a promising new therapeutic target. This review will discuss the role of MET in cell cycle regulation, cell proliferation, evasion of apoptosis, cell migration and invasion, angiogenesis and therapeutic resistance in GBM. It will also discuss the modes of deregulation of HGF/MET and their regulation by microRNAs. As the HGF/MET pathway is a vital regulator of multiple pro-survival pathways, efforts and strategies for its exploitation for GBM therapy are also described.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.