ArticleNature communications2023
Reversible transitions between noradrenergic and mesenchymal tumor identities define cell plasticity in neuroblastoma.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed.
- Quantitative and sensitive neuroblastoma minimal residual disease detection using extrachromosomal DNA (ecDNA) breakpoints.bioRxiv : the preprint server for biology · 2026Article
- MYCN-driven metabolic remodelling of the tumour microenvironment in neuroblastoma: implications for stromal biology and CAF heterogeneity.Cancer metastasis reviews · 2026Review
- Review
- Alternative Splicing of the NF-Y Subunit, NF-YA, in Neuroblastoma Phenotype Heterogeneity.Cancers · 2026Review
- A Bayesian-Based Integrative Bioinformatics Analysis Nominates Oncogenic Drivers in Neuroblastoma.Clinical and translational science · 2026Article
- Efficacy and Tolerability of Topotecan/Cyclophosphamide/Dinutuximab in Relapsed and Refractory High-Risk Neuroblastoma: A Multi-Institutional Retrospective Study.Pediatric blood & cancer · 2026Article
- The protein phosphatase 2A-B56α complex regulates N-Myc degradation in neuroblastoma.The Journal of biological chemistry · 2026Article
- Ribosomal modifications are associated with mesenchymal fate selection in the neural crest lineage.Nature communications · 2026Article
- Multiscale modeling of the spatial structure of stem cells in neuroblastoma patient-derived tumoroids reveals a critical role for a short-range diffusive process.PLoS computational biology · 2026Article
- Hypoxia Promotes an Adrenergic to Mesenchymal Transcriptional Program Transition in Neuroblastoma.Clinical and translational science · 2026Article
- Growth rate-driven modelling suggests that phenotypic adaptation drives drug resistance in BRAFV600E-mutant melanoma.Communications biology · 2026Article
- Repurposing statins and phenothiazines to treat chemoresistant neuroblastoma.EMBO molecular medicine · 2026Article
- Review
- The hegemonic EWSR1::ETS oncoprotein overrules core regulatory circuitry principles in Ewing sarcoma.NPJ precision oncology · 2025Article
- Advances in Targeting Growth Factor Signalling in Neuroblastoma and Overcoming Drug Resistance.Cells · 2025Review
- Transcriptomic and epigenetic profiling of neuroblastoma states in response to RBM39 degrader.Scientific data · 2025Article
- Systematic Analysis of SH-SY5Y Differentiation Protocols and Neuronal Subtype Abundance.Cellular and molecular neurobiology · 2025Article
- Chromosomal instability degrades developmental phenotypes essential for anti-GD2 immunotherapy outcomes in high-risk neuroblastoma.Cell reports. Medicine · 2025Article
- Review
- RBM39 degrader invigorates innate immunity to eradicate neuroblastoma despite cancer cell plasticity.Nature communications · 2025Article
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Authors and funding
32 authors.
Funding
Abstract
Noradrenergic and mesenchymal identities have been characterized in neuroblastoma cell lines according to their epigenetic landscapes and core regulatory circuitries. However, their relationship and relative contribution in patient tumors remain poorly defined. We now document spontaneous and reversible plasticity between the two identities, associated with epigenetic reprogramming, in several neuroblastoma models. Interestingly, xenografts with cells from each identity eventually harbor a noradrenergic phenotype suggesting that the microenvironment provides a powerful pressure towards this phenotype. Accordingly, such a noradrenergic cell identity is systematically observed in single-cell RNA-seq of 18 tumor biopsies and 15 PDX models. Yet, a subpopulation of these noradrenergic tumor cells presents with mesenchymal features that are shared with plasticity models, indicating that the plasticity described in these models has relevance in neuroblastoma patients. This work therefore emphasizes that intrinsic plasticity properties of neuroblastoma cells are dependent upon external cues of the environment to drive cell identity.
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