ArticleInternational journal of oral science2024
Single-cell transcriptomics reveals cell atlas and identifies cycling tumor cells responsible for recurrence in ameloblastoma.
Article in International journal of oral science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Oncogenic signaling pathways in ameloblastoma and their implications for precision based therapy.Discover oncology · 2026Review
- Spatial transcriptomics uncovers TAC-OGEs heterogeneity and FN1/MMP9 signature in ameloblastoma.Frontiers in immunology · 2026Article
- Programmed death-ligand 1 regulates ameloblastoma growth and recurrence.International journal of oral science · 2025Article
- A novel perspective on bone tumors: advances in organoid research.Frontiers in pharmacology · 2025Review
- Wnt signaling aberrant activation drives ameloblastoma invasion and recurrence: bioinformatics and in vitro insights.BMC oral health · 2024Article
- Differentially expressed extracellular matrix genes functionally separate ameloblastoma from odontogenic keratocyst.BMC oral health · 2024Article
Corrections and comments
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Authors and funding
20 authors at 5 institutions in 1 country.
Funding
Abstract
Ameloblastoma is a benign tumor characterized by locally invasive phenotypes, leading to facial bone destruction and a high recurrence rate. However, the mechanisms governing tumor initiation and recurrence are poorly understood. Here, we uncovered cellular landscapes and mechanisms that underlie tumor recurrence in ameloblastoma at single-cell resolution. Our results revealed that ameloblastoma exhibits five tumor subpopulations varying with respect to immune response (IR), bone remodeling (BR), tooth development (TD), epithelial development (ED), and cell cycle (CC) signatures. Of note, we found that CC ameloblastoma cells were endowed with stemness and contributed to tumor recurrence, which was dominated by the EZH2-mediated program. Targeting EZH2 effectively eliminated CC ameloblastoma cells and inhibited tumor growth in ameloblastoma patient-derived organoids. These data described the tumor subpopulation and clarified the identity, function, and regulatory mechanism of CC ameloblastoma cells, providing a potential therapeutic target for ameloblastoma.
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Registered trials
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