Most normal mammalian cells have a finite lifespan, thought to constitute a protective
mechanism against unlimited proliferation,,. This phenomenon, called senescence, is driven
by telomere attrition, which triggers the induction of tumour suppressors including p16INK4a
(ref.). In cultured cells, senescence can be elicited prematurely by oncogenes; however,
whether such oncogene-induced senescence represents a physiological process has long
been debated. Human naevi (moles) are benign tumours of melanocytes that frequently …