A Mount Sinai team reporting in Science found that p53-deficient cells in mouse skin expand partly by reorganizing Wnt signaling across a clone: lower at its edge, higher toward its center. The cells tended to remain self-renewing rather than differentiate. Clones with uniformly elevated Wnt activity expanded less effectively even when their overall activity was higher; disrupting the gradient limited expansion. The experimental distinction is between the signal’s quantity and its spatial arrangement. This is mouse-tissue mechanism research, not a demonstrated treatment in people.

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