ArticleActa neuropathologica2015
Identification of a novel MET mutation in high-grade glioma resulting in an auto-active intracellular protein.
Article in Acta neuropathologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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.
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Who cites it
34 citing papers in PubMed, 43 citations in OpenAlex.
- Spatial enrichment of PTPRZ1 in the peritumoral niche drives glioblastoma migration via the OPA1/ROS/CDH2 axis.Journal of translational medicine · 2026Article
- C-MET tyrosine kinase receptor: mechanisms, clinical applications and future perspectives in cancer therapy.Signal transduction and targeted therapy · 2026Review
- Targeting Kinase Signaling in Glioblastoma: Structural Optimization, Blood-Brain Barrier Dynamics and Combinatorial Translational Strategies.International journal of molecular sciences · 2026Review
- CUX1::MET fusion defines an indolent subtype of diffuse low-grade glioma, MAPK pathway-altered.Acta neuropathologica communications · 2026Article
- Efficacy of MET-targeting CAR T cells against glioblastoma patient-derived xenograft models.Journal of translational medicine · 2025Article
- MET fusions and splicing variants is a strong adverse prognostic factor in astrocytoma, isocitrate dehydrogenase mutant.Brain pathology (Zurich, Switzerland) · 2024Article
- Clinical, pathologic, and genomic characteristics of two pediatric glioneuronal tumors with a CLIP2::MET fusion.Acta neuropathologica communications · 2024Article
- Progress in Glioma Stem Cell Research.Cancers · 2023Review
- From Biology to Diagnosis and Treatment: The Ariadne's Thread in Cancer of Unknown Primary.International journal of molecular sciences · 2023Review
- Mutated axon guidance gene PLXNB2 sustains growth and invasiveness of stem cells isolated from cancers of unknown primary.EMBO molecular medicine · 2023Article
- Advancements, Challenges, and Future Directions in Tackling Glioblastoma Resistance to Small Kinase Inhibitors.Cancers · 2022Review
- Review
- HGF/MET Signaling in Malignant Brain Tumors.International journal of molecular sciences · 2020Review
- SRC and PIM1 as potential co-targets to overcome resistance in MET deregulated non-small cell lung cancer.Translational lung cancer research · 2020Article
- Monotherapy efficacy of blood-brain barrier permeable small molecule reactivators of protein phosphatase 2A in glioblastoma.Brain communications · 2020Article
- Mapping actionable pathways and mutations in brain tumours using targeted RNA next generation sequencing.Acta neuropathologica communications · 2019Article
- MET in glioma: signaling pathways and targeted therapies.Journal of experimental & clinical cancer research : CR · 2019Review
- Glioblastoma Multiforme: An Overview of Emerging Therapeutic Targets.Frontiers in oncology · 2019Review
- Molecular Profiling of Druggable Targets in Clear Cell Renal Cell Carcinoma Through Targeted RNA Sequencing.Frontiers in oncology · 2019Article
- Adaptive adhesion systems mediate glioma cell invasion in complex environments.Journal of cell science · 2018Article
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MET has gained interest as a therapeutic target for a number of malignancies because of its involvement in tumorigenesis, invasion and metastasis. At present, a number of inhibitors, both antibodies against MET or its ligand hepatocyte growth factor, and small molecule MET tyrosine kinase inhibitors are in clinical trials. We here describe a novel variant of MET that is expressed in 6% of high-grade gliomas. Characterization of this mutation in a glioma cell line revealed that it consists of an intronic deletion, resulting in a splice event connecting an intact splice donor site in exon 6 with the next splice acceptor site being that of exon 9. The encoded protein lacks parts of the extracellular IPT domains 1 and 2, encoded by exons 7 and 8, resulting in a novel pseudo-IPT and is named MET(Δ7-8). MET(Δ7-8) is located predominantly in the cytosol and is constitutively active. The auto-activating nature of MET(Δ7-8), in combination with a lack of transmembrane localization, renders MET(Δ7-8) not targetable using antibodies, although the protein is efficiently deactivated by MET-specific tyrosine kinase inhibitors. Testing of MET-expressing tumors for the presence of this variant may be important for treatment decision making.
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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.