ArticleCancer discovery2025
Pan-Cancer Analysis of Oncogenic MET Fusions Reveals Distinct Pathogenomic Subsets with Differential Sensitivity to MET-Targeted Therapy.
Article in Cancer discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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Who cites it
16 citing papers in PubMed.
- MET-associated immune prognostic signature predicts survival and guides personalized therapy in glioma.Acta neuropathologica communications · 2026Article
- Article
- CLIP2::MET fusion identifies a molecularly distinct glioneuronal tumor.Discover oncology · 2026Article
- Advances in translational lung cancer research in 2025: a narrative review.Translational lung cancer research · 2026Review
- MYC contributes to targeted therapy resistance in lung cancers driven by MET exon 14-skipping alteration.NPJ precision oncology · 2026Article
- Liquid biopsy-based detection of acquired MET resistance enables sequential targeted therapy in MET fusion-positive NSCLC.The oncologist · 2026Article
- FGFR alterations and potential role of FGFR inhibitors in pediatric brain tumors.Neuro-oncology advances · 2026Review
- Efficacy of tepotinib in patients with high-grade glioma withNeuro-oncology practice · 2026Article
- From Classical to Emerging Biomarkers of Brain and Central Nervous System Tumors. An Evidence-Based Review with a Focus on Gliomas.Cellular and molecular neurobiology · 2026Review
- Cross-Cancer Detectability of ctDNA Biomarkers in Asian Populations: Implications for Pan-Cancer Detection.Cancer management and research · 2026Review
- Immune checkpoint inhibitor-based combinatory and alternative strategies for immune treatment of lung cancers.Frontiers in immunology · 2026Review
- Precision Oncology: Current Landscape, Emerging Trends, Challenges, and Future Perspectives.Cells · 2025Review
- Study on the in vitro and in vivo killing effects of PD-1 antibody-secreting c-Met-targeted CAR-T cells on esophageal cancer cell line ECA109.Discover oncology · 2025Article
- Clinical and preclinical insights into a novel MDM2::PDGFRA fusion in recurrent glioblastoma.NPJ precision oncology · 2025Article
- Responsiveness of different MET tumour alterations to type I and type II MET inhibitors.Clinical and translational medicine · 2025Article
- Targeting c-MET Alterations in Cancer: A Review of Genetic Drivers and Therapeutic Implications.Cancers · 2025Review
Corrections and comments
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Authors and funding
26 authors.
Funding
Abstract
MET fusions (MET-F) are oncogenic drivers that remain poorly characterized. Analysis of 56 MET-F-positive tumors from an institutional cohort of 91,119 patients (79,864 DNA sequencing plus 11,255 RNA sequencing) uncovered two forms of MET-F pathobiology. The first group featured 5' partners with homodimerization domains fused in-frame with the MET tyrosine kinase domain, primarily originated from translocations, frequently excluded MET exon 14, mediated oncogenesis through cytoplasmic aggregation and constitutive activation, and were markedly sensitive to MET tyrosine kinase inhibitors (TKI) in preclinical models and patients with lung cancer. The second group lacked partner homodimerization motifs and retained MET transmembrane and extracellular domains. Their pathogenesis involved intrachromosomal rearrangements, resulting in partner selection for promoter hijacking and fusion allele amplification. Membrane-bound fusions were enriched in gliomas with receptor tyrosine kinase co-alterations. We provide a framework to comprehend the heterogeneous landscape of MET-Fs, supporting that fusion oncogenicity and MET TKI sensitivity are determined by structural topology and pathogenomic context. SIGNIFICANCE: MET fusions are primary drivers of tumor growth in multiple tumor types - lung cancer and gliomas - and can be effectively targeted with either type I (crizotinib, capmatinib, tepotinib, and savolitinib) or type II (cabozantinib) MET TKIs, with best responses in tumors harboring fusions with partner homodimerization.
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Registered trials
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