ArticleNeuro-oncology2023
Molecular heterogeneity of pediatric choroid plexus carcinomas determines the distinctions in clinical course and prognosis.
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 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Overactivation of SHH signaling induces a cascade of dedifferentiation and oncogenesis in a new mouse model for choroid plexus carcinoma.Acta neuropathologica communications · 2026Article
- The future of targeted therapies for pediatric central nervous system tumors.Neuro-oncology advances · 2026Review
- Report from the National Pediatric Cancer Foundation - infantile glioma and other non-embryonal central nervous system tumors: evolving molecular advances and current treatment landscape.Frontiers in oncology · 2026Review
- Decoding Gene Expression Changes in Cerebral Tumors: Before and After Radiotherapy.Medicinal research reviews · 2025Review
- SOX2 commands LIM homeobox transcription factors in choroid plexus development and tumorigenesis.Neuro-oncology · 2025Article
- Comprehensive multiomics analysis reveals distinct differences between pediatric choroid plexus papilloma and carcinoma.Acta neuropathologica communications · 2024Article
- Marrow-ablative consolidation chemotherapy and molecular targeted therapy delivered in a risk-adapted manner for newly diagnosed children with choroid plexus carcinoma:Neuro-oncology advancesArticle
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChoroid plexus carcinomas (CPCs) are rare aggressive pediatric tumors of the brain with no treatment standards. Genetic profiling of CPCs is often confined to possible association with Li-Fraumeni syndrome, though only about a half of CPCs develop from syndromic predispositions. Whole-chromosome gains and losses typical of CPCs reflect genomic instability of these tumors, but only partially explain the aggressive clinical course.
methodsThis retrospective study enrolled 25 pediatric patients with CPC, receiving treatment between January 2009 and June 2022. Molecular-genetic testing was performed for 20 cases with available tumor tissue and encompassed mutational status, chromosomal aberrations, and gene expression profiles. We analyzed several factors presumably influencing the outcomes, including molecular profiles and clinical parameters. The median follow-up constituted 5.2 years (absolute range 2.8-12.6 years).
resultsAll studied CPCs had smooth mutational profiles with the only recurrent event being TP53 variants, either germline or somatic, encountered in 13 cases. Unbalanced whole-chromosome aberrations, notably multiple monosomies, were highly typical. In 7 tumors, chromosome losses were combined with complex genomic rearrangements: segmental gains and losses or signs of chromothripsis. This phenomenon was associated with extremely low 5-year survival: 20.0 ± 17.9% vs 85.7 ± 13.2%; P = .009. Transcriptomically, the cohort split into 2 polar clusters Ped_CPC1 and Ped_CPC2 differing by survival: 31.3 ± 17.8% vs 100%; P = .012.
conclusionCPCs split into at least 2 molecular subtypes distinguished both genomically and transcriptomically. Clusterization of the tumors into Ped_CPC1 and Ped_CPC2 significantly correlates with survival. The distinction may prove relevant in clinical trials for dedicated and patient-oriented optimization of clinical protocols for these rare tumors.
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