ReviewTranslational oncogenomics2015
c-Met as a Target for Personalized Therapy.
Review in Translational oncogenomics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 3 of them syntheses 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
80 citing papers in PubMed, 3 syntheses or guidelines pooled it, 135 citations in OpenAlex.
- MET-Targeted Therapies and Clinical Outcomes: A Systematic Literature Review.Molecular diagnosis & therapy · 2022Pooled it
- Incidence and risk of fatigue in cancer patients treated with MET inhibitors: A systematic review and meta-analysis.Medicine · 2019Pooled it
- The Efficacy and Risk Profile of c-Met inhibitors in Non-small Cell Lung Cancer: a Meta-analysis.Scientific reports · 2016Pooled it
- Tepotinib in Non-Small-Cell Lung Cancer withThe New England journal of medicine · 2020Trial
- Site-Specific Phosphoproteomic Profiling of CAV1 Reveals Co-Regulatory Kinase Networks in Cancer Signaling.International journal of molecular sciences · 2026Article
- CUX1::MET fusion defines an indolent subtype of diffuse low-grade glioma, MAPK pathway-altered.Acta neuropathologica communications · 2026Article
- Boolean Networks with Classic and New Updating Modes Applied to Genetic Regulation in Some Familial Diseases.International journal of molecular sciences · 2025Article
- Therapeutic potential of TAS-115 in 3D breast cancer models.Biofabrication · 2025Article
- Recent Advancement in Drug Designing as Small Molecules in Targeted Cancer Therapy: Challenges and Future Directions.Current cancer drug targets · 2025Review
- Advancements in Protein Kinase Inhibitors: From Discovery to Clinical Applications.Research (Washington, D.C.) · 2025Review
- Interleukin 6 and cancer resistance in glioblastoma multiforme.Neurosurgical review · 2024Review
- A Synopsis of Biomarkers in Glioblastoma: Past and Present.Current issues in molecular biology · 2024Review
- Targeting c-Met in breast cancer: From mechanisms of chemoresistance to novel therapeutic strategies.Current research in pharmacology and drug discovery · 2024Review
- TargetingCancers · 2023Review
- Article
- ETS-1/c-Met drives resistance to sorafenib in hepatocellular carcinoma.American journal of translational research · 2023Article
- [Research Progresses in the Treatment of NSCLC with MET Gene Variants: A Riview].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2022Review
- Refining patient selection of MET-activated non-small cell lung cancer through biomarker precision.Cancer treatment reviews · 2022Review
- Article
- Novel function of THEMIS2 in the enhancement of cancer stemness and chemoresistance by releasing PTP1B from MET.Oncogene · 2022Article
20 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
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MET and its ligand HGF are involved in many biological processes, both physiological and pathological, making this signaling pathway an attractive therapeutic target in oncology. Downstream signaling effects are transmitted via mitogen-activated protein kinase (MAPK), PI3K (phosphoinositide 3-kinase protein kinase B)/AKT, signal transducer and activator of transcription proteins (STAT), and nuclear factor-κB. The final output of the terminal effector components of these pathways is activation of cytoplasmic and nuclear processes leading to increases in cell proliferation, survival, mobilization and invasive capacity. In addition to its role as an oncogenic driver, increasing evidence implicates MET as a common mechanism of resistance to targeted therapies including EGFR and VEGFR inhibitors. In the present review, we summarize the current knowledge on the role of the HGF-MET signaling pathway in cancer and its therapeutic targeting (HGF activation inhibitors, HGF inhibitors, MET antagonists and selective/nonselective MET kinase inhibitors). Recent advances in understanding the role of this pathway in the resistance to current anticancer strategies used in lung, kidney and pancreatic cancer are discussed.
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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.