ArticleNeuro-oncology2023
Significant increase of high-risk chromosome 1q gain and 6q loss at recurrence in posterior fossa group A ependymoma: A multicenter study.
Article in Neuro-oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Tumor-derived cell-free DNA detected in cerebrospinal fluid enables minimally invasive profiling of pediatric brain tumors.The Journal of clinical investigation · 2026Trial
- AOSNP-ADAPTR resource level-based recommendations on practical diagnostic strategies for ependymomas.Brain pathology (Zurich, Switzerland) · 2026Article
- Supratentorial ependymoma: a comprehensive review of molecular classification, management strategies, and clinical outcomes (Part II of pediatric ependymomas across compartments).Journal of neuro-oncology · 2026Review
- Posterior fossa ependymoma: a comprehensive review of molecular classification, management guidelines, and clinical outcomes (Part I of ependymomas across compartments).Journal of neuro-oncology · 2026Review
- Pediatric ependymoma in the molecular era: real-world experience with diagnostic correlation and long-term clinical outcomes.Journal of neuro-oncology · 2026Article
- Cerebrospinal Fluid in Pediatric Neuro-Oncology: Molecular Diagnosis, Disease Monitoring, and Clinical Translation.International journal of molecular sciences · 2026Review
- A brief history of ependymoma.Neuro-oncology · 2026Review
- Thoracic metastasis of a pediatric posterior fossa group A ependymoma: a rare case and literature review.World journal of pediatric surgery · 2026Article
- Loss of LDOC1 by chromatin compaction in mesenchymal tumor cells is required for PFA1 ependymoma growth.Neuro-oncology · 2025Article
- Optimizing outcomes in intracranial ependymoma: a contemporary review.Frontiers in oncology · 2025Review
- Conditional survival estimates for ependymomas reveal the dynamic nature of prognostication.Discover oncology · 2024Article
- Glioma.Nature reviews. Disease primers · 2024Review
- Development of Chromosome 1q+ Specific Treatment for Highest Risk Pediatric Posterior Fossa Ependymoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Clinically relevant molecular hallmarks of PFA ependymomas display intratumoral heterogeneity and correlate with tumor morphology.Acta neuropathologica · 2024Article
- No safe harbors for recurrent posterior fossa group A ependymoma: A time for change in risk assignment?Neuro-oncology · 2023Article
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Abstract
backgroundEpendymoma (EPN) posterior fossa group A (PFA) has the highest rate of recurrence and the worst prognosis of all EPN molecular groups. At relapse, it is typically incurable even with re-resection and re-irradiation. The biology of recurrent PFA remains largely unknown; however, the increasing use of surgery at first recurrence has now provided access to clinical samples to facilitate a better understanding of this.
methodsIn this large longitudinal international multicenter study, we examined matched samples of primary and recurrent disease from PFA patients to investigate the biology of recurrence.
resultsDNA methylome derived copy number variants (CNVs) revealed large-scale chromosome gains and losses at recurrence in PFA. CNV changes were dominated by chromosome 1q gain and/or 6q loss, both previously identified as high-risk factors in PFA, which were present in 23% at presentation but increased to 61% at first recurrence. Multivariate survival analyses of this cohort showed that cases with 1q gain or 6q loss at first recurrence were significantly more likely to recur again. Predisposition to 1q+/6q- CNV changes at recurrence correlated with hypomethylation of heterochromatin-associated DNA at presentation. Cellular and molecular analyses revealed that 1q+/6q- PFA had significantly higher proportions of proliferative neuroepithelial undifferentiated progenitors and decreased differentiated neoplastic subpopulations.
conclusionsThis study provides clinically and preclinically actionable insights into the biology of PFA recurrence. The hypomethylation predisposition signature in PFA is a potential risk-classifier for trial stratification. We show that the cellular heterogeneity of PFAs evolves largely because of genetic evolution of neoplastic cells.
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