ArticleCancers2014
Targeting MET Amplification as a New Oncogenic Driver.
Article in Cancers, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 106 citations in OpenAlex.
- Phase 2 trial of crizotinib in Japanese patients with advanced NSCLC harboring a MET gene alteration: a Co-MET study.International journal of clinical oncology · 2024Trial
- Review
- Remarkable Efficacy of Capmatinib in a Patient with Cancer of Unknown Primary with MET Amplification.Internal medicine (Tokyo, Japan) · 2025Article
- MET (c-Met) protein overexpression is an emerging protein biomarker in non-small cell lung cancer.NPJ precision oncology · 2025Review
- MicroRNAs and lung cancer: overview of essential pathways and somatic mutations in cancer progression.Frontiers in oncology · 2025Review
- New therapeutic target molecules for gastric and gastroesophageal junction cancer.International journal of clinical oncology · 2024Review
- Exploration of molecular markers related to chemotherapy efficacy of hepatoid adenocarcinoma of the stomach.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Research progress on the role of bypass activation mechanisms in resistance to tyrosine kinase inhibitors in non-small cell lung cancer.Frontiers in oncology · 2024Review
- MET exon 14 skipping mutation is a hepatocyte growth factor (HGF)-dependent oncogenic driver in vitro and in humanised HGF knock-in mice.Molecular oncology · 2023Article
- TargetingCancers · 2023Review
- Detection of MET amplification by droplet digital PCR in peripheral blood samples of non-small cell lung cancer.Journal of cancer research and clinical oncology · 2023Article
- Comprehensive NGS profiling to enable detection ofFrontiers in oncology · 2023Article
- B cell linker protein (BLNK) is a regulator of Met receptor signaling and trafficking in non-small cell lung cancer.iScience · 2022Article
- Refining patient selection of MET-activated non-small cell lung cancer through biomarker precision.Cancer treatment reviews · 2022Review
- Bioinformatically Expanded Next-Generation Sequencing Analysis Optimizes Identification of Therapeutically Relevant MET Copy Number Alterations in >50,000 Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Phase Ia/Ib Study of the Selective MET Inhibitor, Savolitinib, in Patients with Advanced Solid Tumors: Safety, Efficacy, and Biomarkers.The oncologist · 2022Article
- Article
- Case Report: Gene Heterogeneity in the Recurrent and Metastatic Lesions of a Myxoid Chondrosarcoma Patient With Aggressive Transformation.Frontiers in genetics · 2022Article
- Comprehensive Genomic Profiling of Circulating Cell-Free DNA Distinguishes FocalCurrent oncology (Toronto, Ont.) · 2021Article
- Correlation between PD-L1 expression andOncotarget · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Certain genetically defined cancers are dependent on a single overactive oncogene for their proliferation and survival, a phenomenon known as "oncogene addiction". A new generation of drugs that selectively target such "driver oncogenes" manifests a clinical efficacy greater than that of conventional chemotherapy in appropriate genetically defined patients. MET is a proto-oncogene that encodes a receptor tyrosine kinase, and aberrant activation of MET signaling occurs in a subset of advanced cancers as result of various genetic alterations including gene amplification, polysomy, and gene mutation. Our preclinical studies have shown that inhibition of MET signaling either with the small-molecule MET inhibitor crizotinib or by RNA interference targeted to MET mRNA resulted in marked antitumor effects in cancer cell lines with MET amplification both in vitro and in vivo. Furthermore, patients with non-small cell lung cancer or gastric cancer positive for MET amplification have shown a pronounced clinical response to crizotinib. Accumulating preclinical and clinical evidence thus suggests that MET amplification is an "oncogenic driver" and therefore a valid target for treatment. However, the prevalence of MET amplification has not been fully determined, possibly in part because of the difficulty in evaluating gene amplification. In this review, we provide a rationale for targeting this genetic alteration in cancer therapy.
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.