ReviewOncogene2018
The multiple paths towards MET receptor addiction in cancer.
Review in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Pooled it
- The HGF/MET Axis in Advanced Prostate Cancer: From Context-Dependent Biology to Biomarker-Driven Therapeutic Strategies.Cancers · 2026Review
- MEK inhibitor mirdametinib promotes fracture healing in osteofibrous dysplasia RASopathy.The Journal of clinical investigation · 2026Article
- MET (c-Met) protein overexpression is an emerging protein biomarker in non-small cell lung cancer.NPJ precision oncology · 2025Review
- Deciphering context-specific Axitinib escape pathways via multi-omics and explainable machine learning.Journal of translational medicine · 2025Article
- MET variants with activating N-lobe mutations identified in hereditary papillary renal cell carcinomas still require ligand stimulation.Molecular oncology · 2025Article
- Unique characteristics of autoantibodies targeting MET in patients with breast and lung cancer.JCI insight · 2025Article
- Article
- 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
- 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
- Review
- Radiomics Based on Contrast-Enhanced CT for Recognizing c-Met-Positive Hepatocellular Carcinoma: a Noninvasive Approach to Predict the Outcome of Sorafenib Resistance.Molecular imaging and biology · 2023Article
- Fully automated radiolabeling of [EJNMMI radiopharmacy and chemistry · 2023Article
- Real-World Treatment Outcomes of MET Exon14 Skipping in Non-small Cell Lung Cancer: GFPC 03-18 Study.Targeted oncology · 2023Article
- Overview of Molecular Detection Technologies forCancers · 2023Review
- Efficacy of CAR-T immunotherapy in MET overexpressing tumors not eligible for anti-MET targeted therapy.Journal of experimental & clinical cancer research : CR · 2022Article
- Deciphering signal transduction networks in the liver by mechanistic mathematical modelling.The Biochemical journal · 2022Article
- hOA-DN30: a highly effective humanized single-arm MET antibody inducing remission of 'MET-addicted' cancers.Journal of experimental & clinical cancer research : CR · 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
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Targeted therapies against receptor tyrosine kinases (RTKs) are currently used with success on a small proportion of patients displaying clear oncogene activation. Lung cancers with a mutated EGFR provide a good illustration. The efficacy of targeted treatments relies on oncogene addiction, a situation in which the growth or survival of the cancer cells depends on a single deregulated oncogene. MET, a member of the RTK family, is a promising target because it displays many deregulations in a broad panel of cancers. Although clinical trials having evaluated MET inhibitors in large populations have yielded disappointing results, many recent case reports suggest that MET inhibition may be effective in a subset of patients with unambiguous MET activation and thus, most probably, oncogene addiction. Interestingly, preclinical studies have revealed a particularity of MET addiction: it can arise through several mechanisms, and the mechanism involved can differ according to the cancer type. The present review describes the different mechanisms of MET addiction and their consequences for diagnosis and therapeutic strategies. Although in each cancer type MET addiction affects a restricted number of patients, pooling of these patients across all cancer types yields a targetable population liable to benefit from addiction-targeting therapies.
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.