ArticleCNS neuroscience & therapeutics2021
High-sensitive clinical diagnostic method for PTPRZ1-MET and the characteristic protein structure contributing to ligand-independent MET activation.
Article in CNS neuroscience & therapeutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Vebreltinib for Previously Treated Astrocytoma,Cancer communications (London, England) · 2026Trial
- Spatial enrichment of PTPRZ1 in the peritumoral niche drives glioblastoma migration via the OPA1/ROS/CDH2 axis.Journal of translational medicine · 2026Article
- Artificial intelligence-based diagnostic model for identifying PTPRZ1-MET fusion in a clinically defined secondary glioblastoma cohort.Molecular biomedicine · 2026Article
- MET-associated immune prognostic signature predicts survival and guides personalized therapy in glioma.Acta neuropathologica communications · 2026Article
- MET fusions and splicing variants in glioma: a landscape integrating clinical, pathological, and survival features.The journal of pathology. Clinical research · 2026Article
- Roles and Impacts of Integrative Medical Interventions in Central Nervous System Tumor Treatment: Multi-Technology Convergence and the Paradigm Shift Toward Functional Reconstruction.CNS neuroscience & therapeutics · 2025Review
- Pan-Cancer Analysis of Oncogenic MET Fusions Reveals Distinct Pathogenomic Subsets with Differential Sensitivity to MET-Targeted Therapy.Cancer discovery · 2025Article
- Prolonged complete response to adjuvant tepotinib in a patient with newly diagnosed disseminated glioblastoma harboring mesenchymal-epithelial transition fusion.The oncologist · 2025Article
- AberrantCells · 2024Review
- An Observatory for theCancers · 2023Review
- Protein Tyrosine Phosphatase Receptor Zeta 1 as a Potential Target in Cancer Therapy and Diagnosis.International journal of molecular sciences · 2023Review
- Multiomics integration reveals the effect of Orexin A on glioblastoma.Frontiers in pharmacology · 2023Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPTPRZ1-MET (ZM) is a critical genetic alteration driving the progression of lower-grade glioma. Glioma patients harboring ZM could benefit from MET inhibitors. According to the remarkable role of ZM as a driver of glioma progression and indicator of MET inhibitor sensitivity, it is necessary to detect this alteration even when it presents in glioma with relatively fewer copies.
methodsHerein, we proposed that ZM could be detected with a high-sensitive method of reverse transcriptase PCR with 50 amplification cycles. Via this newly proposed detection method, we depicted the incidence preference of ZM fusion in a cohort of 485 glioma patients. To further explore the oncogenic nature of ZM, we predicated the protein structure alteration of MET kinase brought by its fusion partner.
resultsThe incidence of ZM fusions was much higher than previous report. ZM fusions exhibited a striking preference in lower-grade glioma and secondary glioblastoma. By contrast, none of patients with primary glioblastoma was detected harboring ZM fusion. In each of the four variants of ZM, the fusion partner segment of MET contained a remarkable coiled-coil motif. In glioma cells expressing ZM, MET kinase could be activated in a ligand-independent manner, which might be contributed by the special coiled-coil structure brought by the fusion partner. Corresponding to the 3D structural analysis and cell line experiment, the ZM positive clinical specimens showed hyperactivations of MET signaling.
conclusionsZM fusions are critical drivers of glioma progression and effective target of MET inhibitor. Early detection could be performed with a high-sensitive method of reverse transcriptase PCR. The hyperactivations of MET signaling driving glioma progression might be contributed by a ligand-independent activation enabled by the protein structure modification of extracellular domain of MET in ZM fusions.
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