Overview
- University of Tokyo researchers used long-term in vivo lineage tracing and gene-expression profiling in mice to track melanocyte stem cell responses to DNA double-strand breaks.
- Damaged pigment stem cells underwent senescence-coupled differentiation, irreversibly leaving the stem cell pool and producing hair graying.
- Carcinogens and ultraviolet B exposure bypassed this protective program through niche KIT ligand signaling and altered arachidonic acid metabolism, enabling clonal expansion and melanoma founder clones.
- The study reframes hair graying and melanoma as divergent outcomes of the same stem cell population’s stress responses shaped by microenvironmental cues.
- Authors emphasize the findings are preclinical and do not show that graying prevents cancer, while pointing to KIT and metabolic pathways as targets for further research.