ReviewOncogene2021
When the MET receptor kicks in to resist targeted therapies.
Review in Oncogene, 2021. 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.
- Evaluating the Impact of CYP1A2 Inhibition on the Pharmacokinetics of Savolitinib: A Phase 1 Open-Label Study.Pharmacology research & perspectives · 2026Article
- Targeting MET and mTOR Synergistically Overcomes Adaptive Resistance in Glioblastoma.International journal of molecular sciences · 2026Article
- C-MET tyrosine kinase receptor: mechanisms, clinical applications and future perspectives in cancer therapy.Signal transduction and targeted therapy · 2026Review
- Golgi Retention and Oncogenic Signaling of KIT Tyrosine Kinase in Gastrointestinal Stromal Tumor.Sub-cellular biochemistry · 2026Review
- BNIP3-mTOR Signaling Mediates Resistance to MET Inhibition in Glioblastoma.bioRxiv : the preprint server for biology · 2025Article
- State-of-the-Art Liver Cancer Organoids: Modeling Cancer Stem Cell Heterogeneity for Personalized Treatment.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2025Review
- Article
- Functional interaction between receptor tyrosine kinase MET and ETS transcription factors promotes prostate cancer progression.Molecular oncology · 2025Article
- HER2-positive gastric cancer: from targeted therapy to CAR-T cell therapy.Frontiers in immunology · 2025Review
- Single-cell and Bulk Transcriptomic Analyses Reveal a Stemness and Circadian Rhythm Disturbance-related Signature Predicting Clinical Outcome and Immunotherapy Response in Hepatocellular Carcinoma.Current gene therapy · 2025Article
- Mapping kinase domain resistance mechanisms for the MET receptor tyrosine kinase via deep mutational scanning.bioRxiv : the preprint server for biology · 2024Article
- Article
- Design and Synthesis of c-Met and HDAC Dual Inhibitors for the Treatment of Breast Cancer.ACS medicinal chemistry letters · 2024Article
- Patient-derived tumor organoids: a new avenue for preclinical research and precision medicine in oncology.Experimental & molecular medicine · 2024Review
- 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
- Targeting MET in NSCLC: An Ever-Expanding Territory.JTO clinical and research reports · 2024Review
- Advances and challenges in gene therapy strategies for pediatric cancer: a comprehensive update.Frontiers in molecular biosciences · 2024Review
- Discovery of novel exceptionally potent and orally active c-MET PROTACs for the treatment of tumors withActa pharmaceutica Sinica. B · 2023Article
- MET Signaling Pathways, Resistance Mechanisms, and Opportunities for Target Therapies.International journal of molecular sciences · 2022Review
- c-Met-integrin cooperation: Mechanisms, tumorigenic effects, and therapeutic relevance.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although targeted therapies have increased the life expectancy of patients with druggable molecular alterations directly involved in tumor development, the efficacy of these therapies is limited by acquired resistances leading to treatment failure. Most targeted therapies, including ones exploiting therapeutic antibodies and kinase inhibitors, are directed against receptor tyrosine kinases (RTKs) or major signaling hubs. Resistances to these therapies arise when inhibition of these targets is bypassed through activation of alternative signaling pathways. In recent years, activation of the receptor tyrosine kinase MET has been shown to promote resistance to various targeted therapies. This casts MET as important actor in resistance. In this review, we describe how the MET receptor triggers resistance to targeted therapies against RTKs such as EGFR, VEGFR, and HER2 and against signaling hubs such as BRAF. We also describe how MET can be its own resistance factor, as illustrated by on-target resistance of lung tumors harboring activating mutations causing MET exon 14 skipping. Interestingly, investigation of all these situations reveals functional physiological relationships between MET and the target of the therapy to which the cancer becomes resistant, suggesting that resistance stems from preexisting mechanisms. Identification of MET as a resistance factor opens the way to co-treatment strategies that are being tested in current clinical trials.
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.