ReviewThe oncologist2013
The role of MET receptor tyrosine kinase in non-small cell lung cancer and clinical development of targeted anti-MET agents.
Review in The oncologist, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 75 citations in OpenAlex.
- MYC contributes to targeted therapy resistance in lung cancers driven by MET exon 14-skipping alteration.NPJ precision oncology · 2026Article
- Emrelis: A New Approach in Treating MET-high Locally Advanced or Metastatic Non-squamous NSCLC; A Mini Review.Thoracic research and practice · 2026Article
- The role and research progress of the MET signalling pathway in targeted therapy for osteosarcoma.Oncology reviews · 2025Review
- Efficacy and safety analysis of immunotherapy in non-small cell lung cancer patients with MET alterations.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Article
- MET alterations detection platforms and clinical implications in solid tumors: a comprehensive review of literature.Therapeutic advances in medical oncology · 2024Review
- The potential role of next-generation sequencing in identifyingFrontiers in oncology · 2024Article
- c-MetBiomedicines · 2023Article
- NEDD4L in human tumors: regulatory mechanisms and dual effects on anti-tumor and pro-tumor.Frontiers in pharmacology · 2023Review
- High expression of 14-3-3ơ indicates poor prognosis and progression of lung adenocarcinoma.Oncology letters · 2022Article
- Phase I Study of Glesatinib (MGCD265) in Combination with Erlotinib or Docetaxel in Patients with Advanced Solid Tumors.Targeted oncology · 2022Article
- Article
- NEDD4L-induced ubiquitination mediating UBE2T degradation inhibits progression of lung adenocarcinoma via PI3K-AKT signaling.Cancer cell international · 2021Article
- Perturbation of p38α MAPK as a Novel Strategy to Effectively Sensitize Chronic Myeloid Leukemia Cells to Therapeutic BCR-ABL Inhibitors.International journal of molecular sciences · 2021Article
- Comparison ofOncotarget · 2021Article
- Evolution of MET and NRAS gene amplification as acquired resistance mechanisms in EGFR mutant NSCLC.NPJ precision oncology · 2021Article
- The expression of miRNA-216b is negatively correlated with 18F-FDG uptake in non-small cell lung cancer.World journal of surgical oncology · 2021Article
- Cancer Stem Cells-Key Players in Tumor Relapse.Cancers · 2021Review
- Top-levelTranslational lung cancer research · 2020Article
- Mechanism of epithelial‑mesenchymal transition inhibited by miR‑203 in non‑small cell lung cancer.Oncology reports · 2020Article
- MicroRNA-216b regulated proliferation and invasion of non-small cell lung cancer by targeting SOX9.Oncology letters · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A better understanding of the pathophysiology and evolution of non-small cell lung cancer (NSCLC) has identified a number of molecular targets and spurred development of novel targeted therapeutic agents. The MET receptor tyrosine kinase and its ligand hepatocyte growth factor (HGF) are implicated in tumor cell proliferation, migration, invasion, and angiogenesis in a broad spectrum of human cancers, including NSCLC. Amplification of MET has been reported in approximately 5%-22% of lung tumors with acquired resistance to small-molecule inhibitors of the epidermal growth factor receptor (EGFR). Resistance to EGFR inhibitors is likely mediated through downstream activation of the phosphoinositide 3-kinase /AKT pathway. Simultaneous treatment of resistant tumors with a MET inhibitor plus an EGFR inhibitor can abrogate activation of downstream effectors of cell growth, proliferation, and survival, thereby overcoming acquired resistance to EGFR inhibitors. Development and preclinical testing of multiple agents targeting the HGF-MET pathway, including monoclonal antibodies targeting HGF or the MET receptor and small-molecule inhibitors of the MET tyrosine kinase, have confirmed the crucial role of this pathway in NSCLC. Several agents are now in phase III clinical development for the treatment of NSCLC. This review summarizes the role of MET in the pathophysiology of NSCLC and in acquired resistance to EGFR inhibitors and provides an update on progress in the clinical development of inhibitors of MET for treatment of NSCLC.
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.