ArticleProceedings of the National Academy of Sciences of the United States of America2012
Hepatocyte growth factor (HGF) autocrine activation predicts sensitivity to MET inhibition in glioblastoma.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
What it found
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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.
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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.
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Who cites it
75 citing papers in PubMed, 126 citations in OpenAlex.
- Phase II study of cetuximab in combination with cisplatin and radiation in unresectable, locally advanced head and neck squamous cell carcinoma: Eastern cooperative oncology group trial E3303.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Trial
- Targeting Kinase Signaling in Glioblastoma: Structural Optimization, Blood-Brain Barrier Dynamics and Combinatorial Translational Strategies.International journal of molecular sciences · 2026Review
- MET variants with activating N-lobe mutations identified in hereditary papillary renal cell carcinomas still require ligand stimulation.Molecular oncology · 2025Article
- Efficacy of MET-targeting CAR T cells against glioblastoma patient-derived xenograft models.Journal of translational medicine · 2025Article
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- Ribosome profiling: a powerful tool in oncological research.Biomarker research · 2024Review
- Inhibition of autocrine HGF maturation overcomes cetuximab resistance in colorectal cancer.Cellular and molecular life sciences : CMLS · 2024Article
- Targeted Glioma Therapy-Clinical Trials and Future Directions.Pharmaceutics · 2024Review
- Progress in Glioma Stem Cell Research.Cancers · 2023Review
- Tyrosine kinase signaling-independent MET-targeting with CAR-T cells.Journal of translational medicine · 2023Article
- Circular RNA encoded MET variant promotes glioblastoma tumorigenesis.Nature communications · 2023Article
- Role of Molecular Targeted Therapeutic Drugs in Treatment of Glioblastoma: A Review Article.Global medical genetics · 2023Review
- Translation of circHGF RNA encodes an HGF protein variant promoting glioblastoma growth through stimulation of c-MET.Journal of neuro-oncology · 2023Article
- Article
- Signaling pathways in brain tumors and therapeutic interventions.Signal transduction and targeted therapy · 2023Review
- Small Molecule Inhibitors for Hepatocellular Carcinoma: Advances and Challenges.Molecules (Basel, Switzerland) · 2022Review
- Therapeutic Strategies for Ovarian Cancer in Point of HGF/c-MET Targeting.Medicina (Kaunas, Lithuania) · 2022Review
- Immunotherapeutic Approaches for Glioblastoma Treatment.Biomedicines · 2022Review
- Glioma targeted therapy: insight into future of molecular approaches.Molecular cancer · 2022Review
- Looking Beyond the Glioblastoma Mask: Is Genomics the Right Path?Frontiers in oncology · 2022Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
Because oncogene MET and EGF receptor (EGFR) inhibitors are in clinical development against several types of cancer, including glioblastoma, it is important to identify predictive markers that indicate patient subgroups suitable for such therapies. We investigated in vivo glioblastoma models characterized by hepatocyte growth factor (HGF) autocrine or paracrine activation, or by MET or EGFR amplification, for their susceptibility to MET inhibitors. HGF autocrine expression correlated with high phospho-MET levels in HGF autocrine cell lines, and these lines showed high sensitivity to MET inhibition in vivo. An HGF paracrine environment may enhance glioblastoma growth in vivo but did not indicate sensitivity to MET inhibition. EGFRvIII amplification predicted sensitivity to EGFR inhibition, but in the same tumor, increased copies of MET from gains of chromosome 7 did not result in increased MET activity and did not predict sensitivity to MET inhibitors. Thus, HGF autocrine glioblastoma bears an activated MET signaling pathway that may predict sensitivity to MET inhibitors. Moreover, serum HGF levels may serve as a biomarker for the presence of autocrine tumors and their responsiveness to MET therapeutics.
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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.