Starring role for p16

Abstract

Two mutant mouse models of malignant melanoma, based on the genetic region that is commonly disrupted in human cancer, have been reported in recent back-to-back articles in Nature. The knockout mice lack a protein called p16INK4a while leaving p19ARF intact, not an easy feat because the sequences that encode each protein overlap on the same gene – a cell therefore makes only one protein or the other according to where transcription is initiated. Both p16 and p19 stop the formation of cancer by inhibiting cell division, but unlike mice devoid of p19, the p16 knockouts are much less likely to develop tumours spontaneously and are highly sensitive to carcinogens, features that make these mice useful for the study of malignant melanoma and other carcinogen-induced cancers. [Krimpenfort, P. et al. (2001) Nature 413, 83–86; Sharpless, N.E. et al. (2001) Nature 413, 86–91] DC