ArticleBrain pathology (Zurich, Switzerland)2020
IDH mutant lower grade (WHO Grades II/III) astrocytomas can be stratified for risk by CDKN2A, CDK4 and PDGFRA copy number alterations.
Article in Brain pathology (Zurich, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 2 of them syntheses that pooled it.
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Who cites it
80 citing papers in PubMed, 2 syntheses or guidelines pooled it, 125 citations in OpenAlex.
- Molecular Biomarker Testing for the Diagnosis of Diffuse Gliomas.Archives of pathology & laboratory medicine · 2022Guideline
- The prognostic significance of CDKN2A homozygous deletion in IDH-mutant lower-grade glioma and glioblastoma: a systematic review of the contemporary literature.Journal of neuro-oncology · 2020Pooled it
- Phase II Study of Palbociclib in Patients with Tumors with CDK4 or CDK6 Amplification: Results from the NCI-MATCH ECOG-ACRIN Trial (EAY131) Subprotocol Z1C.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Trial
- Article
- DNA Methylation Profiling in IDH-Mutant Gliomas: Biological Evolution, Molecular Grading and Clinical Implementation.Neuropathology and applied neurobiology · 2026Review
- Expanding the molecular grading criteria in IDH-mutant astrocytoma.Neuro-oncology · 2026Article
- Association of CDKN2A/B and MTAP deletions in adult-type diffuse gliomas.Journal of neuropathology and experimental neurology · 2026Article
- Bibliometric mapping of glioma classification research through main path, key route, and K-core analyses.Oncotarget · 2026Review
- Prognostic significance of CDKN2A/B hemizygous deletion in IDH-mutant astrocytomas: a systematic review and meta-analysis.Brain tumor pathology · 2026Article
- Increased neural excitability and glioma synaptic activity drives glioma proliferation in human cortex.Nature neuroscience · 2026Article
- Clinicopathologic and FISH-Based Evaluation of CDKN2A/B and EGFR in IDH Mutant Astrocytomas.Noro psikiyatri arsivi · 2026Article
- Consequences of Hypoxic Events, Necrosis, and Microvascular Density, in Astrocytoma IDH-Mutant, CNS WHO Grade 4.Medical sciences (Basel, Switzerland) · 2025Article
- Clinical outcomes and management ofNeuro-oncology practice · 2025Article
- MYCN amplification defines an aggressive phenotype in IDH-mutant gliomas.The journal of pathology. Clinical research · 2025Article
- Assessment of CDKN2A homozygous and heterozygous deletions in gliomas across multiple detection platforms.BMC cancer · 2025Article
- Canonical amplifications and CDKN2A/B loss refine IDH1/2-mutant astrocytoma prognosis.Neuro-oncology · 2025Article
- CLINICAL utility of assessing CDKN2A status in recurrent astrocytomas.Brain tumor pathology · 2025Article
- Prognostic value of immunohistochemical staining for H3K27me3 and EZH2 in astrocytoma, IDH-mutant.Journal of neuro-oncology · 2025Article
- The molecular history of IDH-mutant astrocytomas without adjuvant treatment.Brain pathology (Zurich, Switzerland) · 2025Article
- Mutant IDH impairs chromatin binding by PDGFB to promote chromosome instability.bioRxiv : the preprint server for biology · 2025Article
20 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors at 3 institutions in 2 countries.
Funding
Abstract
In the 2016, WHO classification of tumors of the central nervous system, isocitrate dehydrogenase (IDH) mutation is a main classifier for lower grade astrocytomas and IDH-mutated astrocytomas is now regarded as a single group with longer survival. However, the molecular and clinical heterogeneity among IDH mutant lower grade (WHO Grades II/III) astrocytomas have only rarely been investigated. In this study, we recruited 160 IDH mutant lower grade (WHO Grades II/III) astrocytomas, and examined PDGFRA amplification, CDKN2A deletion and CDK4 amplification by FISH analysis, TERT promoter mutation by Sanger sequencing and ATRX loss and p53 expression by immunohistochemistry. We identified PDGFRA amplification, CDKN2A homozygous deletion and CDK4 amplification in 18.8%, 15.0% and 18.1% of our cohort respectively, and these alterations occurred in a mutually exclusive fashion. PDGFRA amplification was associated with shorter PFS (P = 0.0003) and OS (P < 0.0001). In tumors without PDGFRA amplification, CDKN2A homozygous deletion or CDK4 amplification was associated with a shorter OS (P = 0.035). Tumors were divided into three risk groups based on the presence of molecular alterations: high risk (PDGFRA amplification), intermediate risk (CDKN2A deletion or CDK4 amplification) and low risk (neither CDKN2A deletion and CDK4 amplification nor PDGFRA amplification). These three risk groups were significantly different in overall survival with mean survivals of 40.5, 62.9 and 71.5 months. The high-risk group also demonstrated a shorter PFS compared to intermediate- (P = 0.036) and low-risk (P < 0.0001) groups. One limitation of this study is the relatively short follow-up period, a common confounding factor for studies on low-grade tumors. Our data illustrate that IDH mutant lower grade astrocytomas is not a homogeneous group and should be molecularly stratified for risk.
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