ReviewCancers2015
cMET in NSCLC: Can We Cut off the Head of the Hydra? From the Pathway to the Resistance.
Review in Cancers, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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
22 citing papers in PubMed, 40 citations in OpenAlex.
- ADC Target Profiling in NSCLC: Generalizable AI Separates TROP-2 and cMET Phenotypes.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- MET (c-Met) protein overexpression is an emerging protein biomarker in non-small cell lung cancer.NPJ precision oncology · 2025Review
- Design, synthesis and biological evaluation of thienopyridine derivatives as c-Met kinase inhibitors.Molecular diversity · 2025Article
- Neoadjuvant tepotinib in stage IIB N0 non-small cell lung carcinoma withTranslational lung cancer research · 2025Article
- Combined inhibition of MET and VEGF enhances therapeutic efficacy of EGFR TKIs in EGFR-mutant non-small cell lung cancer with concomitant aberrant MET activation.Experimental hematology & oncology · 2024Article
- Genomic instability in congenital lung malformations in children.Pediatric surgery international · 2024Article
- Savolitinib: A Promising Targeting Agent for Cancer.Cancers · 2023Review
- TargetingCancers · 2023Review
- SH005S7 Overcomes Primary and Acquired Resistance of Non-Small Cell Lung Cancer by Combined MET/EGFR/HER3 Inhibition.BioMed research international · 2022Article
- Targeting the cMET pathway to enhance immunotherapeutic approaches for mUM patients.Frontiers in oncology · 2022Review
- Proteasome Inhibitors Diminish c-Met Expression and Induce Cell Death in Non-Small Cell Lung Cancer Cells.Oncology research · 2020Article
- Article
- High-level gain of mesenchymal-epithelial transition factor (MET) copy number using next-generation sequencing as a predictive biomarker for MET inhibitor efficacy.Annals of translational medicine · 2020Article
- The Role of c-Met as a Biomarker and Player in Innate and Acquired Resistance in Non-Small-Cell Lung Cancer: Two New Mutations Warrant Further Studies.Molecules (Basel, Switzerland) · 2019Article
- Genome-wide mutation profiling and related risk signature for prognosis of papillary renal cell carcinoma.Annals of translational medicine · 2019Article
- Non-canonical cMet regulation by vimentin mediates Plk1 inhibitor-induced apoptosis.EMBO molecular medicine · 2019Article
- Detection of serum protein and circulating mRNA of cMET, HGF EGF and EGFR levels in lung cancer patients to guide individualized therapy.Cancer biomarkers : section A of Disease markers · 2019Article
- Simultaneous Monitoring of Cell-surface Receptor and Tumor-targeted Photodynamic Therapy via TdT-initiated Poly-G-Quadruplexes.Scientific reports · 2018Article
- Correlation ofOncotarget · 2018Article
- Better to be alone than in bad company: The antagonistic effect of cisplatin and crizotinib combination therapy in non-small cell lung cancer.World journal of clinical oncology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the last decade, the tyrosine kinase receptor cMET, together with its ligand hepatocyte growth factor (HGF), has become a target in non-small cell lung cancer (NSCLC). Signalization via cMET stimulates several oncological processes amongst which are cell motility, invasion and metastasis. It also confers resistance against several currently used targeted therapies, e.g., epidermal growth factor receptor (EGFR) inhibitors. In this review, we will discuss the basic structure of cMET and the most important signaling pathways. We will also look into aberrations in the signaling and the effects thereof in cancer growth, with the focus on NSCLC. Finally, we will discuss the role of cMET as resistance mechanism.
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.