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Updated: Feb 5, 2026
Cerebellar Regional Dissection for Molecular Analysis
Published on: December 5, 2020
Cerebellar glioblastoma: a clinical series with contemporary molecular analysis
Bujung Hong1, Rouzbeh Banan2, Arne Christians2
1Department of Neurosurgery, Hannover Medical School, MHH, Carl-Neuberg-Strasse 1, 30625, Hannover, Germany. hong.bujung@mh-hannover.de.
Background:
Glioblastomas (GBM) are localized in only less than 1% of patients in the cerebellum. Therefore, tumor characteristics, survival, and the efficacy of therapies are not yet well defined. The present study aims to characterize the molecular features of cerebellar GBM (GBMc) in 8 patients treated with contemporary modality in our institution.
Methods:
Patients' treatment history, progression-free survival (PFS), and overall survival (OS) were analyzed. All histopathological specimens were re-investigated. EGFR amplification was determined by FISH, H3F3A, and HIST1H3B mutation status and MGMT promoter methylation after bisulfite treatment by pyrosequencing and BRAF V600E by pyrosequencing and immunohistochemistry. TERT promoter mutations were analyzed by Sanger sequencing, CDKN2A/B deletions by digital PCR. The expression of IDH1 R132H, ATRX, and p53 was determined through immunohistochemistry.
Results:
Six adults and two children (mean age 36 years) underwent tumor resection via medial or lateral suboccipital craniotomy. The median overall survival (mOS) of the adult patients was 7 months. GBMc from two children demonstrated a H3F3A K27M mutation. One of these also harbored a BRAF V600E mutation and has already had a PFS of 74 months. Mutated IDH1 R132H protein was expressed in 2 GBM from adult patients with previous supratentorial anaplastic astrocytoma. One patient carried a TERT promoter mutation. Another patient initially presented with a thalamic pilocytic astrocytoma. The cerebellar tumor revealed neither a BRAF V600E nor a H3F3A mutation but a homozygous CDKN2A/B deletion.
Conclusions:
GBM located in the cerebellum can be found in all age groups. We provide novel molecular genetic data on these rare tumors. Mutated IDH1 R132H protein and H3F3A K27M mutations indicate that a substantial number of GBMc are "metastatic" or "diaschismatic" lesions. Mutation of BRAF V600E may have a stronger biological significance than H3F3A K27M alterations. In a subset of patients, GBM may arise primarily as a distinct entity in the cerebellum.
Insights
This study analyzes rare cerebellar glioblastomas (GBM), revealing diverse molecular features and mutations like H3F3A K27M and BRAF V600E. Findings suggest some GBMs may originate primarily in the cerebellum.
Area of Science:
- Neuro-oncology
- Molecular Pathology
- Genetics
Background:
- Cerebellar glioblastomas (GBMc) are rare, accounting for <1% of GBM cases.
- Limited data exists on their specific characteristics, survival outcomes, and treatment responses.
- This study investigates the molecular landscape of 8 cerebellar GBM patients.
Purpose of the Study:
- To molecularly characterize rare cerebellar glioblastomas (GBMc).
- To analyze survival data and treatment efficacy in patients with GBMc.
- To identify potential genetic drivers and subtypes of cerebellar GBM.
Main Methods:
- Histopathological re-investigation of all specimens.
- Analysis of EGFR amplification (FISH), H3F3A/HIST1H3B mutations (pyrosequencing), MGMT promoter methylation (pyrosequencing).
- Assessment of BRAF V600E (pyrosequencing/IHC), TERT promoter mutations (Sanger), CDKN2A/B deletions (dPCR), and protein expression (IHC for IDH1 R132H, ATRX, p53).
Main Results:
- Eight patients (6 adults, 2 children) with GBMc were analyzed.
- Median overall survival for adults was 7 months.
- Pediatric GBMc showed H3F3A K27M mutations; one also had BRAF V600E with 74 months PFS.
- IDH1 R132H mutations were found in 2 adult GBMc with prior astrocytoma history.
- One case presented with homozygous CDKN2A/B deletion without BRAF/H3F3A mutations.
Conclusions:
- Cerebellar GBM occurs across all age groups, with diverse molecular profiles.
- IDH1 R132H and H3F3A K27M mutations suggest potential metastatic or diachastic origins for some GBMc.
- BRAF V600E mutations may hold greater biological significance than H3F3A K27M.
- A subset of GBMc might represent a distinct primary cerebellar entity.
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