Overview
- Experiments in mice show melanocyte stem cells with DNA damage can undergo 'seno-differentiation,' maturing and exiting the stem pool, which leads to greying.
- Under potent carcinogens or UV exposure, the same stem cells sometimes bypass this fate and self‑renew despite damage, creating conditions conducive to melanoma.
- Scientists describe these opposing outcomes as 'antagonistic fates' governed by microenvironmental signals and the nature of the cellular stress.
- Grey hair is framed as a byproduct of a protective process that culls risky cells rather than a direct shield against cancer.
- Findings are preclinical and drawn from mouse models, and researchers say human relevance remains uncertain pending further studies to map the signaling pathways involved.