ArticleCancer research2009
The MET receptor tyrosine kinase is a potential novel therapeutic target for head and neck squamous cell carcinoma.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers.
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Who cites it
133 citing papers in PubMed, 264 citations in OpenAlex.
- Near-infrared fluorescence imaging with an MET-targeting probe for biopsy site selection in patients with oral potentially malignant disorders.Cell reports. Medicine · 2025Trial
- A Phase I Trial of the MET/OncoTargets and therapy · 2021Trial
- Trial
- Met Receptor Tyrosine Kinase and Chemoprevention of Oral Cancer.Journal of the National Cancer Institute · 2018Trial
- Trial
- Prognostic biomarkers in phase II trial of cetuximab-containing induction and chemoradiation in resectable HNSCC: Eastern cooperative oncology group E2303.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Trial
- Phase III randomized, placebo-controlled trial of docetaxel with or without gefitinib in recurrent or metastatic head and neck cancer: an eastern cooperative oncology group trial.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2013Trial
- Phase II trial of single-agent foretinib (GSK1363089) in patients with recurrent or metastatic squamous cell carcinoma of the head and neck.Investigational new drugs · 2013Trial
- Prognostic and predictive significance of plasma HGF and IL-8 in a phase III trial of chemoradiation with or without tirapazamine in locoregionally advanced head and neck cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012Trial
- HGF/c-MET signaling induces glutamine metabolism in MET-amplified head and neck squamous cell carcinoma via MAPK/ERK-dependent induction of GLS-1.Medical oncology (Northwood, London, England) · 2026Article
- PPIB interacts with MET to activate the PI3K-AKT pathway and promote head and neck squamous cell carcinoma pathogenesis.Molecular biology reports · 2026Article
- Identification of novel biomarkers involved in oral squamous cell carcinoma by whole transcriptome sequencing and bioinformatics analysis.Cancer cell international · 2025Article
- The MET Oncogene Network of Interacting Cell Surface Proteins.International journal of molecular sciences · 2024Review
- Evaluation of a Novel MET-Targeting Camelid-Derived Antibody in Head and Neck Cancer.Molecular pharmaceutics · 2024Article
- Review
- Nanomedicine in HNSCC therapy-a challenge to conventional therapy.Frontiers in pharmacology · 2024Review
- New insights into RAS in head and neck cancer.Biochimica et biophysica acta. Reviews on cancer · 2023Review
- Oral squamous cell carcinomas: state of the field and emerging directions.International journal of oral science · 2023Review
- An oncogene addiction phosphorylation signature and its derived scores inform tumor responsiveness to targeted therapies.Cellular and molecular life sciences : CMLS · 2022Article
- Aptamer-Modified Erythrocyte Membrane-Coated pH-Sensitive Nanoparticles for c-Met-Targeted Therapy of Glioblastoma Multiforme.Membranes · 2022Article
73 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
Abstract
Recurrent/metastatic head and neck cancer remains a devastating disease with insufficient treatment options. We investigated the MET receptor tyrosine kinase as a novel target for the treatment of head and neck squamous cell carcinoma (HNSCC). MET/phosphorylated MET and HGF expression was analyzed in 121 tissues (HNSCC/normal) by immunohistochemistry, and in 20 HNSCC cell lines by immunoblotting. The effects of MET inhibition using small interfering RNA/two small-molecule inhibitors (SU11274/PF-2341066) on signaling, migration, viability, and angiogenesis were determined. The complete MET gene was sequenced in 66 head and neck cancer tissue samples and eight cell lines. MET gene copy number was determined in 14 cell lines and 23 tumor tissues. Drug combinations of SU11274 with cisplatin or erlotinib were tested in SCC35/HN5 cell lines. Eighty-four percent of the HNSCC samples showed MET overexpression, whereas 18 of 20 HNSCC cell lines (90%) expressed MET. HGF overexpression was present in 45% of HNSCC. MET inhibition with SU11274/PF-2341066 abrogated MET signaling, cell viability, motility/migration in vitro, and tumor angiogenesis in vivo. Mutational analysis of 66 tumor tissues and 8 cell lines identified novel mutations in the semaphorin (T230M/E168D/N375S), juxtamembrane (T1010I/R988C), and tyrosine kinase (T1275I/V1333I) domains (incidence: 13.5%). Increased MET gene copy number was present with >10 copies in 3 of 23 (13%) tumor tissues. A greater-than-additive inhibition of cell growth was observed when combining a MET inhibitor with cisplatin or erlotinib and synergy may be mediated via erbB3/AKT signaling. MET is functionally important in HNSCC with prominent overexpression, increased gene copy number, and mutations. MET inhibition abrogated MET functions, including proliferation, migration/motility, and angiogenesis. MET is a promising, novel target for HNSCC and combination approaches with cisplatin or EGFR inhibitors should be explored.
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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.