ReviewJournal of neuro-oncology2026
Vestibular schwannoma: genetic and epigenetic mechanisms, hearing loss, and emerging therapies.
Review in Journal of neuro-oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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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Authors and funding
17 authors.
Funding
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Abstract
backgroundAlthough most vestibular schwannomas (VS) occur sporadically, both sporadic and hereditary tumors share common molecular features beyond the loss of NF2. New evidence highlights the role of interconnected signaling pathways and epigenetic regulation in Schwann cell tumorigenesis, pointing toward potential molecularly targeted therapeutic strategies.
methodsThis review synthesizes preclinical, molecular, and clinical evidence to examine genetic and epigenetic mechanisms underlying VS, therapeutic strategies, and contributors to hearing loss. A structured search of ClinicalTrials.gov identified 21 Phase 1-3 interventional therapeutic trials.
resultsVS pathogenesis is driven by NF2 loss and merlin deficiency, leading to dysregulation of Hippo/YAP-TAZ, PI3K/AKT/mTOR, VEGF, MAPK, and adhesion pathways. Epigenetic alterations, including DNA methylation, chromatin remodeling, non-coding RNAs, and SOX10 dysfunction, further shape tumor behavior. Clinical trial analysis revealed a predominance of early-phase, non-comparative studies, limited progression to later-phase trials, and incomplete results reporting, indicating gaps in high-quality evidence. Bevacizumab remains the most consistent systemic therapy for select NF2-related cases, while other agents such as icotinib, lapatinib, everolimus, selumetinib, and brigatinib have shown modest activity, primarily disease stabilization. Emerging approaches, including TEAD inhibition, PI3K/mTOR blockade, MEK inhibition, and combined signaling-epigenetic strategies, show preclinical promise. Hearing loss is multifactorial, involving tumor-secreted factors, inflammation, vascular changes, and inner ear damage alongside nerve compression.
conclusionVS biology reflects integrated genetic and epigenomic dysregulation. Advancing care will require multi-omic classification, biomarker-driven trials, and combination therapies targeting both signaling and epigenetic vulnerabilities. Future management is expected to shift toward personalized, mechanism-based strategies aimed at durable tumor control while preserving hearing and quality of life.
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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.