ArticleBrain tumor pathology2020
Giant cell glioblastoma is a distinctive subtype of glioma characterized by vulnerability to DNA damage.
Article in Brain tumor pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- How survival time reshapes prognostic risk in giant cell glioblastoma.Discover oncology · 2026Article
- DNA methylation-based analysis reveals accelerated epigenetic aging in giant cell-enriched adult-type glioblastoma.Clinical epigenetics · 2024Article
- Prognosis prediction via histological evaluation of cellular heterogeneity in glioblastoma.Scientific reports · 2024Article
- Adult-type and Pediatric-type Diffuse Gliomas : What the Neuroradiologist Should Know.Clinical neuroradiology · 2023Review
- Article
- Ultra High-plex Spatial Proteogenomic Investigation of Giant Cell Glioblastoma Multiforme Immune Infiltrates Reveals Distinct Protein and RNA Expression Profiles.Cancer research communications · 2023Article
- Is Caperatic Acid the Only Compound Responsible for Activity of LichenAntioxidants (Basel, Switzerland) · 2022Article
- Morphogenetic and Imaging Characteristics in Giant Cell Glioblastoma.Current oncology (Toronto, Ont.) · 2022Article
- The evolution of pleomorphic xanthoastrocytoma: from genesis to molecular alterations and mimics.Laboratory investigation; a journal of technical methods and pathology · 2022Review
- Review
- Pediatric Giant Cell Glioblastoma Presenting with Intracranial Dissemination at Diagnosis: A Case Report.NMC case report journal · 2021Article
- Giants and monsters: Unexpected characters in the story of cancer recurrence.Advances in cancer research · 2020Review
- Near haploidization is a genomic hallmark which defines a molecular subgroup of giant cell glioblastoma.Neuro-oncology advancesArticle
- Glioma oncogenesis in the Constitutional mismatch repair deficiency (CMMRD) syndrome.Neuro-oncology advancesArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Giant cell glioblastoma (GC-GBM) consists of large cells with pleomorphic nuclei. As a contrast to GC-GBM, we defined monotonous small GBM (MS-GBM) as GBM that consists of small cells with monotonous small nuclei, and compared the DNA damage as well as other pathological features. GC-GBM showed minimal invasion (< 2 mm) and focal sarcomatous areas. TERTp was wild type in GC-GBM but mutant in MS-GBM. OLIG2 expression was significantly higher in MS-GBM (P < 0.01) (77% in MS-GBM and 7% in GC-GBM). GC-GBM showed significantly higher DNA double-strand breaks (DSBs) compared with MS-GBM (P < 0.01) (76% in GC-GBM and 15% in MS-GBM). Nearly, all large cells in GC-GBM underwent DSBs. Thus, significant DSBs in GC-GBM might be induced by an innate lesser stemness characteristic and be followed by mitotic slippage, resulting in polyploidization and the large pleomorphic nuclei. We conclude that GC-GBM is a distinctive subtype of glioma characterized by its vulnerability to DNA damage and that wild-type TERTp and lower OLIG2 function might induce this feature. Notably, even large pleomorphic nuclei with severe DSBs demonstrated Ki67 positivity, which alerts pathologists to the interpretation of Ki67 positivity, because cells with large nuclei undergoing severe DSBs cannot be recognized as proliferating cells that contribute to tumor aggressiveness.
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