ArticleNeuro-oncology2018
EPH receptor signaling as a novel therapeutic target in NF2-deficient meningioma.
Article in Neuro-oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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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.
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
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Meningioma animal models: a systematic review and meta-analysis.Journal of translational medicine · 2023Pooled it
- Advancements in Preclinical Models forCancers · 2026Review
- Combining Brigatinib with mTOR Inhibition to Effectively Treat NF2-SWN-Associated and Sporadic NF2-Deficient Meningiomas.Cancer research communications · 2026Article
- Review
- Integrative bioinformatics analysis and elastic network modeling elucidate the role of cellular senescence in meningioma recurrence.Discover oncology · 2025Article
- Short‑term efficacy assessment of brigatinib for the treatment of neurofibromatosis type 2: A retrospective study.Oncology letters · 2025Article
- Cancer stem cells in meningiomas: novel insights and therapeutic implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Molecular Pharmacology of Dasatinib Provides Unique Insights into the Mechanistic Basis of Success and Failure of Targeted Cancer Therapy.ACS pharmacology & translational science · 2025Review
- Beyond cell-cell contact: therapeutic potential of Eph signaling in central nervous system tumors.Frontiers in molecular neuroscience · 2025Review
- Orthotopic meningioma rat model exhibits morphological and immunohistochemical congruency and epigenetic concordance with benign primary patient-derived tumors.Scientific reports · 2024Article
- CBX7 reprograms metabolic flux to protect against meningioma progression by modulating the USP44/c-MYC/LDHA axis.Journal of molecular cell biology · 2024Article
- The Clinical Relevance of the EPH/Ephrin Signaling Pathway in Pediatric Solid and Hematologic Malignancies.International journal of molecular sciences · 2024Review
- Proteasomal pathway inhibition as a potential therapy for NF2-associated meningioma and schwannoma.Neuro-oncology · 2023Article
- Preclinical Models of Meningioma.Advances in experimental medicine and biology · 2023Review
- Discovering the Molecular Landscape of Meningioma: The Struggle to Find New Therapeutic Targets.Diagnostics (Basel, Switzerland) · 2021Review
- Early phase clinical studies of AR-42, a histone deacetylase inhibitor, for neurofibromatosis type 2-associated vestibular schwannomas and meningiomas.Laryngoscope investigative otolaryngology · 2021Article
- Review
- Neurofibromatosis Type 2 (NF2) and the Implications for Vestibular Schwannoma and Meningioma Pathogenesis.International journal of molecular sciences · 2021Review
- Neurofibromatosis: Molecular Pathogenesis and Natural Compounds as Potential Treatments.Frontiers in oncology · 2021Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Meningiomas are the most common primary brain tumor in adults, and somatic loss of the neurofibromatosis 2 (NF2) tumor suppressor gene is a frequent genetic event. There is no effective treatment for tumors that recur or continue to grow despite surgery and/or radiation. Therefore, targeted therapies that either delay tumor progression or cause tumor shrinkage are much needed. Our earlier work established mammalian target of rapamycin complex mTORC1/mTORC2 activation in NF2-deficient meningiomas. Methods: High-throughput kinome analyses were performed in NF2-null human arachnoidal and meningioma cell lines to identify functional kinome changes upon NF2 loss. Immunoblotting confirmed the activation of kinases and demonstrated effectiveness of drugs to block the activation. Drugs, singly and in combination, were screened in cells for their growth inhibitory activity. Antitumor drug efficacy was tested in an orthotopic meningioma model. Results: Erythropoietin-producing hepatocellular receptor tyrosine kinases (EPH RTKs), c-KIT, and Src family kinase (SFK) members, which are biological targets of dasatinib, were among the top candidates activated in NF2-null cells. Dasatinib significantly inhibited phospho-EPH receptor A2 (pEPHA2), pEPHB1, c-KIT, and Src/SFK in NF2-null cells, showing no cross-talk with mTORC1/2 signaling. Posttreatment kinome analyses showed minimal adaptive changes. While dasatinib treatment showed some activity, dual mTORC1/2 inhibitor and its combination with dasatinib elicited stronger growth inhibition in meningiomas. Conclusion: Co-targeting mTORC1/2 and EPH RTK/SFK pathways could be a novel effective treatment strategy for NF2-deficient meningiomas.
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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.