ArticleBrain pathology (Zurich, Switzerland)2001
Low frequency of chromosomal imbalances in anaplastic ependymomas as detected by comparative genomic hybridization.
Article in Brain pathology (Zurich, Switzerland), 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.
- Genetic differences on intracranial versus spinal cord ependymal tumors: a meta-analysis of genetic researches.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2016Pooled it
- Definition of parameters and thresholds to detect MYCN amplification in retinoblastomas.Virchows Archiv : an international journal of pathology · 2026Article
- Primary intracranial myxopapillary ependymoma: two case reports and literature review.Frontiers in oncology · 2026Article
- MYCN immunohistochemistry as surrogate marker for MYCN-amplified spinal ependymomas.Human cell · 2024Article
- Epigenetic Regulation in Primary CNS Tumors: An Opportunity to Bridge Old and New WHO Classifications.Cancers · 2023Review
- Spinal ependymoma in adults: from molecular advances to new treatment perspectives.Frontiers in oncology · 2023Review
- Ependymomas.Pathologica · 2022Review
- Updates in the classification of ependymal neoplasms: The 2021 WHO Classification and beyond.Brain pathology (Zurich, Switzerland) · 2022Review
- The biology of ependymomas and emerging novel therapies.Nature reviews. Cancer · 2022Review
- Clinically aggressive pediatric spinal ependymoma with novel MYC amplification demonstrates molecular and histopathologic similarity to newly described MYCN-amplified spinal ependymomas.Acta neuropathologica communications · 2021Article
- Review
- Ultra high-risk PFA ependymoma is characterized by loss of chromosome 6q.Neuro-oncology · 2021Article
- Pediatric ependymoma: an overview of a complex disease.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2021Review
- High level MYCN amplification and distinct methylation signature define an aggressive subtype of spinal cord ependymoma.Acta neuropathologica communications · 2020Article
- MYCN amplification drives an aggressive form of spinal ependymoma.Acta neuropathologica · 2019Article
- Evaluation of chromosome 1q gain in intracranial ependymomas.Journal of neuro-oncology · 2016Article
- The Similarities and Differences between Intracranial and Spinal Ependymomas : A Review from a Genetic Research Perspective.Journal of Korean Neurosurgical Society · 2016Review
- Diagnostic application of high resolution single nucleotide polymorphism array analysis for children with brain tumors.Cancer genetics · 2014Article
- Study of chromosome 9q gain, Notch pathway regulators and Tenascin-C in ependymomas.Journal of neuro-oncology · 2014Article
- Spinal cord tumours: advances in genetics and their implications for treatment.Nature reviews. Neurology · 2013Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We screened 26 ependymomas in 22 patients (7 WHO grade I, myxopapillary, myE; 6 WHO grade II, E; 13 WHO grade III, anaplastic, aE) using comparative genomic hybridization (CGH) and fluorescence in situ hybridization (FISH). 25 out of 26 tumors showed chromosomal imbalances on CGH analysis. The chromosomal region most frequently affected by losses of genomic material clustered on 13q (9/26). 6/7 myE showed a loss on 13q14-q31. Other chromosomes affected by genomic losses were 6q (5/26), 4q (5/26), 10 (5/26), and 2q (4/26). The most consistent chromosomal abnormality in ependymomas so far reported, is monosomy 22 or structural abnormality 22q, identified in approximately one third of Giemsa-banded cases with abnormal karyotypes. Using FISH, loss or monosomy 22q was detected in small subpopulations of tumor cells in 36% of cases. The most frequent gains involved chromosome arms 17 (8/26), 9q (7/26), 20q (7/26), and 22q (6/26). Gains on 1q were found exclusively in pediatric ependymomas (5/10). Using FISH, MYCN proto-oncogene DNA amplifications mapped to 2p23-p24 were found in 2 spinal ependymomas of adults. On average, myE demonstrated 9.14, E 5.33, and aE 1.77 gains and/or losses on different chromosomes per tumor using CGH. Thus, and quite paradoxically, in ependymomas, a high frequency of imbalanced chromosomal regions as revealed by CGH does not indicate a high WHO grade of the tumor but is more frequent in grade I tumors.
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