ArticleNature communications2024
Multi-omic and single-cell profiling of chromothriptic medulloblastoma reveals genomic and transcriptomic consequences of genome instability.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Cancer Heterogeneity and Cancer Cell Plasticity: Molecular Mechanisms and Precision Therapy.MedComm · 2026Review
- scCirclehunter delineates ecDNA-containing cells using single-cell ATAC-seq, with a focus on glioblastoma.Cell discovery · 2025Article
- Genome doubling as a dynamic driver of ovarian cancer evolution: insights from single-cell sequencing.Journal of ovarian research · 2025Review
- Dynamic association of H3K36me3 with pericentromeric heterochromatin regulates its replication time.EMBO reports · 2025Article
- Cancer therapy resistance from a spatial-omics perspective.Clinical and translational medicine · 2025Review
- Chromoanagenesis in Osteosarcoma.Biomolecules · 2025Review
- HIPSD&R-seq enables scalable genomic copy number and transcriptome profiling.Genome biology · 2024Article
- Spatio-temporal transcriptomics of chromothriptic SHH-medulloblastoma identifies multiple genetic clones that resist treatment and drive relapse.Nature communications · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
26 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromothripsis is a frequent form of genome instability, whereby a presumably single catastrophic event generates extensive genomic rearrangements of one or multiple chromosome(s). However, little is known about the heterogeneity of chromothripsis across different clones from the same tumour, as well as changes in response to treatment. Here we analyse single-cell genomic and transcriptomic alterations linked with chromothripsis in human p53-deficient medulloblastoma and neural stem cells (n = 9). We reconstruct the order of somatic events, identify early alterations likely linked to chromothripsis and depict the contribution of chromothripsis to malignancy. We characterise subclonal variation of chromothripsis and its effects on extrachromosomal circular DNA, cancer drivers and putatively druggable targets. Furthermore, we highlight the causative role and the fitness consequences of specific rearrangements in neural progenitors.
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