ArticleJournal of neuro-oncology2019
Gliosarcoma: distinct molecular pathways and genomic alterations identified by DNA copy number/SNP microarray analysis.
Article in Journal of neuro-oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Gliosarcoma of the craniovertebral junction with loss of H3K27me3: a case report with molecular profiling.Brain tumor pathology · 2026Article
- NMR-Based Metabolomic Profiling for Brain Cancer Diagnosis and Treatment Guidance.Metabolites · 2025Review
- Molecular characterization of gliosarcoma reveals prognostic biomarkers and clinical parallels with glioblastoma.Journal of neuro-oncology · 2025Article
- Primary Intracranial Gliosarcoma: Is It Really a Variant of Glioblastoma? An Update of the Clinical, Radiological, and Biomolecular Characteristics.Journal of clinical medicine · 2023Review
- Pediatric gliosarcoma, a rare central nervous system tumor in children: Case report and literature review.Heliyon · 2023Article
- Survival outcomes associated with MGMT promoter methylation and temozolomide in gliosarcoma patients.Journal of neuro-oncology · 2022Article
- Sporadic and Lynch syndrome-associated mismatch repair-deficient brain tumors.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Gliosarcoma: The Distinct Genomic Alterations Identified by Comprehensive Analysis of Copy Number Variations.Analytical cellular pathology (Amsterdam) · 2022Article
- Genomic landscape of gliosarcoma: distinguishing features and targetable alterations.Scientific reports · 2021Article
- Noncoding RNAs involved in the STAT3 pathway in glioma.Cancer cell international · 2021Review
- Gliosarcoma vs. glioblastoma: a retrospective case series using molecular profiling.BMC neurology · 2021Article
- Review
- Gliosarcoma in patients under 20 years of age. A clinicopathologic study of 11 cases and detailed review of the literature.BMC pediatrics · 2021Review
- Machine Learning-Based Analysis of Magnetic Resonance Radiomics for the Classification of Gliosarcoma and Glioblastoma.Frontiers in oncology · 2021Article
- IDH1-mutant primary intraventricular gliosarcoma: Case report and systematic review of a rare location and molecular profile.Surgical neurology international · 2020Article
- Current Opinion on Molecular Characterization for GBM Classification in Guiding Clinical Diagnosis, Prognosis, and Therapy.Frontiers in molecular biosciences · 2020Review
- Evaluating Surgical Resection Extent and Adjuvant Therapy in the Management of Gliosarcoma.Frontiers in oncology · 2020Article
- GATAD1 gene amplification promotes glioma malignancy by directly regulating CCND1 transcription.Cancer medicine · 2019Article
- Clinical Characteristics of Gliosarcoma and Outcomes From Standardized Treatment Relative to Conventional Glioblastoma.Frontiers in oncology · 2019Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
purposeGliosarcoma is a histologic variant of glioblastoma (GBM), and like GBM carries a poor prognosis. Median survival is less than one (1) year with less than 5% of patients alive after 5 years. Although there is no cure, standard treatment includes surgery, radiation and chemotherapy. While very similar to GBM, gliosarcoma exhibits several distinct differences, morphologically and molecularly. Therefore, we report a comprehensive analysis of DNA copy number changes in gliosarcoma using a cytogenomic DNA copy number (CN) microarray (OncoScan
methodsCytogenomic DNA copy number microarray (OncoScan
resultsThe most frequent alteration was copy number loss, comprising 57% of total copy number changes. The number of losses far exceeded the number of amplifications (***, < 0.001) and loss of heterozygosity events (***, < 0.001). Amplifications were infrequent (4.6%), particularly for EGFR. Chromosomes 9 and 10 had the highest number of losses; a large portion of which correlated to CDKN2A/B loss. Copy number gains were the second most common alteration (26.2%), with the majority occurring on chromosome 7. MetaCore™ enrichment detected notable pathways for copy number gains including: HOXA, Rho family of GTPases, and EGFR; copy number loss including: WNT, NF-kß, and CDKN2A; and copy number loss of heterozygosity including: WNT and p53.
conclusionsThe pathways and copy number alterations detected in this study may represent key drivers in gliosarcoma oncogenesis and may provide a starting point toward targeted oncologic analysis with therapeutic potential.
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