ArticleMolecular cancer2024
Joint single-cell genetic and transcriptomic analysis reveal pre-malignant SCP-like subclones in human neuroblastoma.
Article in Molecular cancer, 2024. 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.
- Alternative Splicing of the NF-Y Subunit, NF-YA, in Neuroblastoma Phenotype Heterogeneity.Cancers · 2026Review
- Neural crest gene regulatory networks as drivers of development, diversification and disease.Nature reviews. Molecular cell biology · 2026Review
- Article
- Ribosomal modifications are associated with mesenchymal fate selection in the neural crest lineage.Nature communications · 2026Article
- Repurposing statins and phenothiazines to treat chemoresistant neuroblastoma.EMBO molecular medicine · 2026Article
- Advances in multi-omics research on neuroblastoma.Frontiers in pediatrics · 2026Review
- Review
- Postnatal sustentacular cells as chromaffin progenitors and tumor cells of origin in VHL-related paragangliomas.NPJ precision oncology · 2025Article
- Restoring mitochondrial quantity and quality to reverse the Warburg effect and drive neuroblastoma differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Absolute copy number aware CNV calling of sub-megabase segments in ultra-low coverage single-cell DNA sequencing data.Nucleic acids research · 2025Article
- Transcriptionally distinct malignant neuroblastoma populations show selective response to adavosertib treatment.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Comparative Single-Cell Transcriptomics of Human Neuroblastoma and Preclinical Models Reveals Conservation of an Adrenergic Cell State.Cancer research · 2025Article
- Single-Cell Multi-Omics: Insights into Therapeutic Innovations to Advance Treatment in Cancer.International journal of molecular sciences · 2025Review
- Epidemiological characteristics and disease burden of childhood neuroblastoma in Asia: trends and regional differences over the past 30 years.Frontiers in pediatrics · 2025Article
- Epigenetic regulation of cell state by H2AFY governs immunogenicity in high-risk neuroblastoma.The Journal of clinical investigation · 2024Article
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Authors and funding
24 authors.
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Abstract
backgroundNeuroblastoma (NB) is a heterogeneous embryonal malignancy and the deadliest tumor of infancy. It is a complex disease that can result in diverse clinical outcomes. In some children, tumors regress spontaneously. Others respond well to existing treatments. But for the high-risk group, which constitutes approximately 40% of all patients, the prognosis remains dire despite collaborative efforts in basic and clinical research. While its exact cellular origin is still under debate, NB is assumed to arise from the neural crest cell lineage including multipotent Schwann cell precursors (SCPs), which differentiate into sympatho-adrenal cell states eventually producing chromaffin cells and sympathoblasts.
methodsTo investigate clonal development of neuroblastoma cell states, we performed haplotype-specific analysis of human tumor samples using single-cell multi-omics, including joint DNA/RNA sequencing of sorted single cells (DNTR-seq). Samples were also assessed using immunofluorescence stainings and fluorescence in-situ hybridization (FISH).
resultsBeyond adrenergic tumor cells, we identify subpopulations of aneuploid SCP-like cells, characterized by clonal expansion, whole-chromosome 17 gains, as well as expression programs of proliferation, apoptosis, and a non-immunomodulatory phenotype.
conclusionAneuploid pre-malignant SCP-like cells represent a novel feature of NB. Genetic evidence and tumor phylogeny suggest that these clones and malignant adrenergic populations originate from aneuploidy-prone cells of migrating neural crest or SCP origin, before lineage commitment to sympatho-adrenal cell states. Our findings expand the phenotypic spectrum of NB cell states. Considering the multipotency of SCPs in development, we suggest that the transformation of fetal SCPs may represent one possible mechanism of tumor initiation in NB with chromosome 17 aberrations as a characteristic element.
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