ReviewMolecular cancer2018
Function of the c-Met receptor tyrosine kinase in carcinogenesis and associated therapeutic opportunities.
Review in Molecular cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 352 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
352 citing papers in PubMed, 1 synthesis or guideline pooled it, 554 citations in OpenAlex.
- Global research trends and hotspots for leukocyte cell-derived chemotaxin-2 from the past to 2023: a combined bibliometric review.Frontiers in immunology · 2024Pooled it
- Identification of Protein Biomarkers of the Dietary Approaches to Stop Hypertension Diet in Randomized Feeding Studies and Validation in an Observational Study.Journal of the American Heart Association · 2023Trial
- Targeting receptor tyrosine kinases: from molecular mechanisms to clinical therapeutics.Signal transduction and targeted therapy · 2026Review
- AI-Powered Marine Drug Discovery: A Putative Dual c-Met/VEGFR2 Lead Candidate for Hepatocellular Carcinoma via Deep Learning and Multiscale Simulation.Current issues in molecular biology · 2026Article
- PPIB interacts with MET to activate the PI3K-AKT pathway and promote head and neck squamous cell carcinoma pathogenesis.Molecular biology reports · 2026Article
- SPARC Promotes Corneal Epithelial Wound Healing Through β-catenin Nuclear Translocation and c-Met Activation.Investigative ophthalmology & visual science · 2026Article
- Circulating tumour cells as a window into lethality in prostate cancer.Nature reviews. Urology · 2026Review
- Recent Progress in Urea-Containing Compounds as Tyrosine Kinase Inhibitors.Chemistry & biodiversity · 2026Review
- Capmatinib and paclitaxel combination: a novel strategy for overcoming challenges in triple-negative breast cancer treatment.BMC cancer · 2026Article
- Tetrahedral framework nucleic acids: Nanokeys unlocking a new era of precision biomedicine.Journal of advanced research · 2026Review
- Targeting MET in 2025: From Exon 14 Skipping to MET-Amplified Acquired Resistance in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2026Review
- Article
- Discovery of 2H-Pyrrolo[3,4‑ACS medicinal chemistry letters · 2026Article
- Single-cell and deep learning identify hypoxia-responsive lncRNAs predicting outcomes in colorectal cancer.NPJ precision oncology · 2026Article
- CircNOLC1/KRT16 promotes colorectal cancer invasion and migration via c-met nuclear translocation and reprogramming of the oxidative pentose phosphate pathway.The Journal of biological chemistry · 2026Article
- Dual-Targeting Strategy in Cancer Therapy: The Emerging Role of Pyrrolopyrimidine Scaffolds.Chemistry & biodiversity · 2026Review
- Successful Tepotinib Rechallenge after Tepotinib-induced Adverse Events Following Pembrolizumab Failure in a Case of Non-small Cell Lung Carcinoma with MET Exon 14 Skipping.Internal medicine (Tokyo, Japan) · 2026Article
- Osteosarcoma cells promote intracellular iron detoxification to mitigate GPX4-mediated ferroptosis.Cancer gene therapy · 2026Article
- A molecular landscape tracking the progression of non-muscle invasive bladder cancer.World journal of urology · 2026Review
- Targeting MET in non-small cell lung cancer brain metastases: from molecular mechanism to precision therapy.Journal of translational medicine · 2026Review
292 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
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
c-Met is a receptor tyrosine kinase belonging to the MET (MNNG HOS transforming gene) family, and is expressed on the surfaces of various cells. Hepatocyte growth factor (HGF) is the ligand for this receptor. The binding of HGF to c-Met initiates a series of intracellular signals that mediate embryogenesis and wound healing in normal cells. However, in cancer cells, aberrant HGF/c-Met axis activation, which is closely related to c-Met gene mutations, overexpression, and amplification, promotes tumor development and progression by stimulating the PI3K/AKT, Ras/MAPK, JAK/STAT, SRC, Wnt/β-catenin, and other signaling pathways. Thus, c-Met and its associated signaling pathways are clinically important therapeutic targets. In this review, we elaborate on the molecular structure of c-Met and HGF and the mechanism through which their interaction activates the PI3K/AKT, Ras/MAPK, and Wnt signaling pathways. We also summarize the connection between c-Met and RON and EGFR, which are also receptor tyrosine kinases. Finally, we introduce the current therapeutic drugs that target c-Met in primary tumors, and their use in clinical research.
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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.