ArticleJournal of neuro-oncology2025
Pitfalls in the evaluation of CDKN2A copy number status in meningioma.
Article in Journal of neuro-oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Prognostic Markers in Meningioma: Effectiveness of FISH-Assessed CDKN2A/B Homozygous Deletion and Limits of Surrogate p16/MTAP Immunohistochemistry in Predicting Disease-Specific Survival.Neuropathology and applied neurobiology · 2026Article
- The superior prognostic role of pRB1 over p16 immunohistochemistry as a biomarker in meningiomas.Acta neuropathologica communications · 2026Article
- Immunohistochemical Loss of MTAP as a Diagnostic and Prognostic Surrogate ofDiagnostics (Basel, Switzerland) · 2026Review
- Challenging CDKN2A assessment in BRAF-altered gliomas: lessons from a pleomorphic xanthoastrocytoma-enriched cohort.Acta neuropathologica communications · 2025Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeMeningiomas are the most common primary intracranial tumors, with anaplastic variants linked to a poor prognosis. CDKN2A deletions are key markers of malignancy and were integrated into the 2021 WHO classification for anaplastic meningiomas. Both p16 and MTAP immunohistochemistry (IHC) are employed to assess CDKN2A loss, though each marker has limitations in accuracy to varying degrees.
methodsThis study analyzed the concordance between molecular methods - DNA methylation profiling, molecular inversion probe (MIP) analysis, targeted next-generation sequencing (NGS), and fluorescence in situ hybridization (FISH) - and protein expression of p16 and MTAP in nine anaplastic meningiomas.
resultsWe showed that while p16 loss correlated well, MTAP protein was still expressed in three cases despite homozygous CDKN2A deletions. In those three cases the MTAP gene was hemizygously deleted. Additionally, a FISH probe encompassing both genes generated misleading results.
conclusionOur results suggest that MTAP IHC can be unreliable as a sole surrogate for CDKN2A loss in anaplastic meningioma. Quantitative copy-number analysis via high-resolution chromosomal arrays enables precise determination of CDKN2A deletions. Given the therapeutic implications of WHO grading, accurate molecular testing is critical. We conclude that negative p16/MTAP IHC in high-grade meningiomas should prompt molecular analysis for CDKN2A deletions, and MTAP IHC should not be solely relied upon for classification.
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