Senescence suppresses tumors early but promotes them late—the switch happens when tissue architecture breaks down

Senescence is a double-edged sword: it arrests damaged cells (cancer protection) but secretes SASP factors (cancer promotion). The net effect depends on timing and context.

The hypothesis: senescence suppresses tumors in young tissue with intact architecture, but promotes them in aged tissue where chronic senescence and architectural disruption create a permissive environment for mutant clones.

The switch is not in the senescent cells themselves—it is in the tissue context they inhabit.