ReviewAnnals of translational medicine2015
Biology of MET: a double life between normal tissue repair and tumor progression.
Review in Annals of translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 75 citations in OpenAlex.
- Distinct genetic profiles of obesity have different effects on breast cancer risk: leveraging Mendelian randomisation to interrogate causal pathways and identify mediating proteins.Breast cancer research : BCR · 2026Article
- Single-Molecule FRET-Tracking of InlB-Activated MET Receptors in Living Cells.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- Autoregulation of the MET receptor tyrosine kinase by its intracellular juxtamembrane domain.The Biochemical journal · 2025Article
- Global gene expression landscape of gallbladder cancer and advances in targeted therapeutic strategies.World journal of clinical oncology · 2025Review
- Article
- Urolithins' interaction with hepatocyte growth factor receptor: a mechanistic basis for anticancer activity in gastric adenocarcinoma cells.Discover oncology · 2025Article
- Identification of Novel Compounds That Bind to the HGF β-Chain In Silico, Verification by Molecular Mechanics and Quantum Mechanics, and Validation of Their HGF Inhibitory Activity In Vitro.Molecules (Basel, Switzerland) · 2025Article
- HGF, HNRPD, and sFLT1 Interfere with the Induction of VEGF in Patients with Severe Psoriasis.Current molecular medicine · 2025Article
- Article
- Diagnosis and treatment of non-small cell lung cancer (NSCLC) harboringTranslational lung cancer research · 2024Article
- Conserved regulatory motifs in the juxtamembrane domain and kinase N-lobe revealed through deep mutational scanning of the MET receptor tyrosine kinase domain.bioRxiv : the preprint server for biology · 2024Article
- Reducing target binding affinity improves the therapeutic index of anti-MET antibody-drug conjugate in tumor bearing animals.PloS one · 2024Article
- Airborne fine particulate matter exposure induces transcriptomic alterations resembling asthmatic signatures: insights from integrated omics analysis.Environmental epigenetics · 2024Article
- Review
- Landscape of Genetic Mutations in Appendiceal Cancers.Cancers · 2023Review
- [Expert Consensus on Targeted Therapy of NSCLC with MET Exon 14 Skipping Mutation].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023Article
- An In silico Approach towards Finding the Cancer-Causing Mutations in Human MET Gene.International journal of genomics · 2023Article
- Efficacy of CAR-T immunotherapy in MET overexpressing tumors not eligible for anti-MET targeted therapy.Journal of experimental & clinical cancer research : CR · 2022Article
- Practical Significance of Biomarkers in Axial Spondyloarthritis: Updates on Diagnosis, Disease Activity, and Prognosis.International journal of molecular sciences · 2022Review
- Leukocyte cell-derived chemotaxin 2 is an antiviral regulator acting through the proto-oncogene MET.Nature communications · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MNNG HOS transforming gene (MET) is a class IV receptor tyrosine kinase, expressed on the surface of epithelial cells. The interaction with the hepatocyte grow factor (HGF) induces MET dimerization and the activation of multiple intracellular pathways leading to cell proliferation, anti-apoptosis, morphogenic differentiation, motility, invasion, and angiogenesis. Knock out mice have demonstrated that MET is necessary for normal embryogenesis including the formation of striate muscles, liver and trophoblastic structures. The overexpression of MET and HGF are common in solid tumors and contribute to determine their growth. Indeed, MET has been cloned as a transforming gene from a chemically induced human osteosarcoma cell line and therefore is considered a proto-oncogene. Germline MET mutations are characteristic of hereditary papillary kidney cancers and MET amplification is observed in tumors including lung and gastric adenocarcinomas. The inhibition of MET signaling is the target for specific drugs that are raising exciting expectation for medical treatment of cancer.
Indexed as
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.