ArticleCancer research2025
Comparative Single-Cell Transcriptomics of Human Neuroblastoma and Preclinical Models Reveals Conservation of an Adrenergic Cell State.
Article in Cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Immune remodeling and myeloid signature in the bone marrow niche of MYCN-driven neuroblastoma.BJC reports · 2026Article
- Mutated FGFR1 is an oncogenic driver and therapeutic target in high-risk neuroblastoma.The Journal of clinical investigation · 2026Article
- Review
- Three-Dimensional Culture Systems in Neuroblastoma Research.Organoids · 2025Article
- A drug that induces the microRNA miR-124 enables differentiation of retinoic acid-resistant neuroblastoma cells.Science signaling · 2025Article
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17 authors.
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Abstract
Transgenic mice and organoid models, such as three-dimensional tumoroid cultures, have emerged as powerful tools for investigating cancer development and targeted therapies. Yet, the extent to which these preclinical models recapitulate the cellular identity of heterogeneous malignancies, like neuroblastoma, remains to be validated. In this study, we characterized the transcriptional landscape of TH-MYCN tumors by single-cell RNA sequencing and developed ex vivo tumoroids. Integrated analysis with murine fetal adrenal samples confirmed that both TH-MYCN tumors and tumoroids closely mirror the cellular profiles of normal embryonic sympathoblasts and chromaffin cells. Comprehensive comparison between tumors from patients with neuroblastoma and TH-MYCN mice demonstrated similarities in adrenergic tumor cell composition. Ex vivo tumoroid cultures displayed histologic resemblance and shared transcriptional profiles with the originating TH-MYCN tumors and human neuroblastoma tumors. Importantly, subpopulations within tumoroids exhibited gene expression associated with poor survival of patients with neuroblastoma. Notably, recurrent observations of a low-proliferative chromaffin phenotype connected to the highly proliferative sympathetic phenotype suggested that pushing sympathoblasts into a chromaffin-like state may offer an interesting therapeutic strategy for neuroblastoma. Together, this study not only deepens our understanding of a widely used transgenic mouse neuroblastoma model but also introduces an ex vivo model that maintains critical adrenergic cell state identity, thereby enhancing its translational potential for neuroblastoma research. Significance: Transgenic mouse models and ex vivo tumoroids, characterized through single-cell RNA sequencing, faithfully recapitulate neuroblastoma cellular identity, offering a useful platform for investigating potential therapeutic strategies.
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