ArticleModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc2021
Utility of methylthioadenosine phosphorylase immunohistochemical deficiency as a surrogate for CDKN2A homozygous deletion in the assessment of adult-type infiltrating astrocytoma.
Article in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- MTAP immunohistochemistry as a surrogate marker of CDKN2A loss in brain tumors: A meta-analysis and literature review.Journal of neuropathology and experimental neurology · 2025Pooled it
- Prevalence of heterozygous and homozygous 9p21 deletions in human cancer: a tissue microarray study on 4,999 tumors from 125 different tumor types.Molecular medicine (Cambridge, Mass.) · 2026Article
- Association of CDKN2A/B and MTAP deletions in adult-type diffuse gliomas.Journal of neuropathology and experimental neurology · 2026Article
- Association of CDKN2A/B Homozygous Deletion and Extent of Resection With Survival of Patients With WHO CNS5 Grade 4 Astrocytoma.Annals of clinical and translational neurology · 2026Article
- CDKN2A/B status and histological grade independently predict post-recurrence survival in recurrent IDH-mutant astrocytoma.Brain tumor pathology · 2026Article
- T2-FLAIR mismatch sign in nonenhancing astrocytoma, IDH-mutant: impact of tumor area on diagnostic sensitivity.Journal of neuro-oncology · 2026Article
- AOSNP-ADAPTR resource level-based recommendations on practical diagnostic strategies for WHO CNS5 adult-type diffuse gliomas.Brain pathology (Zurich, Switzerland) · 2026Review
- Review
- Loss of MTAP expression is not an accurate surrogate for CDKN2A homozygous deletions in peritoneal mesothelioma.Histopathology · 2025Article
- Challenging CDKN2A assessment in BRAF-altered gliomas: lessons from a pleomorphic xanthoastrocytoma-enriched cohort.Acta neuropathologica communications · 2025Article
- Article
- Assessment of CDKN2A homozygous and heterozygous deletions in gliomas across multiple detection platforms.BMC cancer · 2025Article
- Article
- Comparing loss of p16 and MTAP expression in detecting CDKN2A homozygous deletion in pleomorphic xanthoastrocytoma.Journal of neuropathology and experimental neurology · 2024Article
- Usefulness of synthetic MRI for differentiation of IDH-mutant diffuse gliomas and its comparison with the T2-FLAIR mismatch sign.Journal of neuro-oncology · 2024Article
- Article
- T2-FLAIR mismatch sign, an imaging biomarker for CDKN2A-intact in non-enhancing astrocytoma, IDH-mutant.Neurosurgical review · 2024Article
- Loss of methylthioadenosine phosphorylase immunoreactivity correlates with poor prognosis and elevated uptake ofJournal of neuro-oncology · 2024Article
- Intratumoral heterogeneity of CDKN2A deletions in IDH-mutant astrocytoma.Brain tumor pathology · 2024Article
- CDKN2A/B deletion in IDH-mutant astrocytomas: An evaluation by Fluorescence in-situ hybridization.Journal of neuro-oncology · 2024Article
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Authors and funding
8 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Homozygous deletion (HD) of CDKN2A is one of the most promising biomarkers for predicting poor prognosis of IDH-mutant diffuse gliomas. The Consortium to Inform Molecular and Practical Approaches to CNS Tumor Taxonomy (cIMPACT-NOW) recommendations propose that IDH-mutant lower-grade astrocytomas with CDKN2A/B HD be classified as grade IV tumors. Loss of methylthioadenosine phosphorylase (MTAP) immunohistochemistry staining has been proposed as a surrogate of CDKN2A HD in various tumors but its performance has not been fully investigated in diffuse glioma. This study determined whether MTAP immunoreactivity could serve as a proxy for CDKN2A HD in adult-type diffuse glioma, thereby contributing to stratifying patient outcome. MTAP immunohistochemistry staining using clone EPR6893 was scored in 178 diffuse glioma specimens consisting of 77 IDH-mutant astrocytomas, 13 IDH-mutant oligodendrogliomas, and 88 IDH-wildtype glioblastomas. The use of MTAP immunohistochemical deficiency to predict CDKN2A HD was good for IDH-mutant astrocytomas (sensitivity, 88%; specificity, 98%) and IDH-wildtype glioblastomas (sensitivity, 89%; specificity, 100%), but poor for IDH-mutant oligodendrogliomas (sensitivity, 67%; specificity, 57%). Both CDKN2A HD and MTAP immunohistochemical deficiency were significant adverse prognostic factors of overall survival for IDH-mutant astrocytoma (P < 0.001 each), but neither were prognostically significant for oligodendroglioma or IDH-wildtype glioblastoma. IDH-mutant lower-grade astrocytoma with CDKN2A HD and deficient MTAP immunoreactivity exhibited overlapping unfavorable outcome with IDH-mutant glioblastoma. MTAP immunostaining was easily interpreted in 61% of the cases tested, but scoring required greater care in the remaining cases. An alternative MTAP antibody clone (2G4) produced identical scoring results in all but 1 case, and a slightly larger proportion (66%) of cases were considered easy to interpret compared to using EPR6893. In summary, loss of MTAP immunoreactivity could serve as a reasonable predictive surrogate for CDKN2A HD in IDH-mutant astrocytomas and IDH-wildtype glioblastomas and could provide significant prognostic value for IDH-mutant astrocytoma, comparable to CDKN2A HD.
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