ArticleNature communications2022
Single-cell transcriptomics identifies potential cells of origin of MYC rhabdoid tumors.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- Variable latency between the founder genetic event and rhabdoid tumor expansion.bioRxiv : the preprint server for biology · 2026Article
- Rhabdoid tumors as a novel target for PSMA-directed CAR T cell therapy.Molecular therapy. Oncology · 2026Article
- Investigation of a global mouse methylome atlas reveals subtype-specific copy number alterations in pediatric cancer models.Nature genetics · 2026Article
- Histogenesis of Atypical Teratoid Rhabdoid Tumors: Anatomical and Embryological Perspectives.Cancers · 2025Article
- Disordered DNA methylation leads to targetable transcriptional plasticity in ATRT.Acta neuropathologica communications · 2025Article
- A cycling, progenitor-like cell population at the base of atypical teratoid rhabdoid tumor subtype differentiation trajectories.Neuro-oncology · 2025Article
- Learning the cellular origins across cancers using single-cell chromatin landscapes.Nature communications · 2025Article
- SMARCB1-related schwannomatosis and other SMARCB1-associated phenotypes: clinical spectrum and molecular pathogenesis.Familial cancer · 2025Review
- TAR RNA Mimicry of INI1 and Its Influence on Non-Integration Function of HIV-1 Integrase.Viruses · 2025Review
- Epigenetic modifications and their roles in pediatric brain tumor formation: emerging insights from chromatin dysregulation.Frontiers in oncology · 2025Review
- PPARγ and C/EBPα enable adipocyte differentiation upon inhibition of histone methyltransferase PRC2 in malignant tumors.The Journal of biological chemistry · 2024Article
- Spatial resolved transcriptomics reveals distinct cross-talk between cancer cells and tumor-associated macrophages in intrahepatic cholangiocarcinoma.Biomarker research · 2024Article
- Aberrant DNA methylation distorts developmental trajectories in atypical teratoid/rhabdoid tumors.Life science alliance · 2024Article
- Context-specific functions of chromatin remodellers in development and disease.Nature reviews. Genetics · 2024Review
- Organoids as a new approach for improving pediatric cancer research.Frontiers in oncology · 2024Review
- SMARCB1 loss activates patient-specific distal oncogenic enhancers in malignant rhabdoid tumors.Nature communications · 2023Article
- Imaging and multi-omics datasets converge to define different neural progenitor origins for ATRT-SHH subgroups.Nature communications · 2023Article
- A Carboxy-terminal Smarcb1 Point Mutation Induces Hydrocephalus Formation and Affects AP-1 and Neuronal Signalling Pathways in Mice.Cellular and molecular neurobiology · 2023Article
- Current advances in immunotherapy for atypical teratoid rhabdoid tumor (ATRT).Neuro-oncology practice · 2023Review
- Single-cell analysis of peripheral blood from high-altitude pulmonary hypertension patients identifies a distinct monocyte phenotype.Nature communications · 2023Article
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Authors and funding
24 authors at 9 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rhabdoid tumors (RT) are rare and highly aggressive pediatric neoplasms. Their epigenetically-driven intertumoral heterogeneity is well described; however, the cellular origin of RT remains an enigma. Here, we establish and characterize different genetically engineered mouse models driven under the control of distinct promoters and being active in early progenitor cell types with diverse embryonic onsets. From all models only Sox2-positive progenitor cells give rise to murine RT. Using single-cell analyses, we identify distinct cells of origin for the SHH and MYC subgroups of RT, rooting in early stages of embryogenesis. Intra- and extracranial MYC tumors harbor common genetic programs and potentially originate from fetal primordial germ cells (PGCs). Using PGC specific Smarcb1 knockout mouse models we validate that MYC RT originate from these progenitor cells. We uncover an epigenetic imbalance in MYC tumors compared to PGCs being sustained by epigenetically-driven subpopulations. Importantly, treatments with the DNA demethylating agent decitabine successfully impair tumor growth in vitro and in vivo. In summary, our work sheds light on the origin of RT and supports the clinical relevance of DNA methyltransferase inhibitors against this disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.