Primary cell cultures need to be frequently passaged, which limits the study of long-term biological processes, such as how mutant clones colonize aging epithelia. Esophageal epithelioids self-maintain for months, recapitulating progenitor cell behavior in vivo. Epithelioid CRISPR–Cas9 screens reveal genes encoding molecules that control cell fitness.
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References
Fowler, J. C. & Jones, P. H. Somatic mutation: what shapes the mutational landscape of normal epithelia? Cancer Discov. 12, 1642–1655 (2022). A review of somatic mutations in epithelial tissues.
Abby, E. et al. Notch1 mutations drive clonal expansion in normal esophageal epithelium but impair tumor growth. Nat. Genet. 55, 232–245 (2023). A research paper showing how a colonizing somatic mutation can be anti-oncogenic.
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Herms, A. et al. Organismal metabolism regulates the expansion of oncogenic PIK3CA mutant clones in normal esophagus. Nat. Genet. https://doi.org/10.1038/s41588-024-01891-8 (2024). A recent paper that describes the use of epithelioids to discover potential interventions to restrict oncogenic clonal expansion.
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This is a summary of: Herms, A. et al. Self-sustaining long-term 3D epithelioid cultures reveal drivers of clonal expansion in esophageal epithelium. Nat. Genet. https://doi.org/10.1038/s41588-024-01875-8 (2024).
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Long-term 3D primary epithelioid cultures reveal genes that regulate esophageal cell fitness. Nat Genet 56, 2010–2011 (2024). https://doi.org/10.1038/s41588-024-01887-4
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DOI: https://doi.org/10.1038/s41588-024-01887-4
