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Ageing and cancer are often seen as divergent tissue fates. In our study, we identify a protective programme, called senescence-coupled differentiation (or seno-differentiation), that eliminates cancer-prone stem cells by pushing them to differentiate. Whether melanocyte stem cells follow this path or bypass it under carcinogenic stress determines tissue outcomes: hair greying or melanoma development.
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References
Cohn, R. L. et al. The heterogeneity of cellular senescence: insights at the single-cell level. Trends Cell Biol. 33, 9–17 (2023). A review that provides valuable insights into the heterogeneity of senescent cells.
Gil, J. The challenge of identifying senescent cells. Nat. Cell Biol. 25, 1554–1556 (2023). A comment that discusses the difficulties of identifying senescent cells.
Inomata, K. et al. Genotoxic stress abrogates renewal of melanocyte stem cells by triggering their differentiation. Cell 137, 1088–1099 (2009). This study demonstrates that DNA damage induces stem cell differentiation within the niche through the stemness checkpoint.
Nishimura, E. K. et al. Mechanism of hair graying: incomplete melanocyte stem cell maintenance in the niche. Science 307, 720–724 (2005). This paper demonstrates that age-associated exhaustion of McSCs causes hair greying.
Chan, C. et al. Spontaneous hair repigmentation in an 80-year-old man: a case of melanoma-associated hair repigmentation and review of the literature. Am. J. Dermatopathol. 41, 671–674 (2019). A case report and literature review describing spontaneous grey hair repigmentation associated with lentigo maligna (a type of melanoma).
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This is a summary of: Mohri, Y. et al. Antagonistic stem cell fates under stress govern decisions between hair greying and melanoma. Nat. Cell Biol. https://doi.org/10.1038/s41556-025-01769-9 (2025).
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Senescence-coupled differentiation selectively eliminates cancer-prone stem cells. Nat Cell Biol (2025). https://doi.org/10.1038/s41556-025-01783-x
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DOI: https://doi.org/10.1038/s41556-025-01783-x