Overexpression of p27KIP1 in seborrheic keratosis.

Background: The pathogenesis of seborrheic keratosis (SK) is not well understood. SKs are slow growing, but the details of cell cycle control in these lesions are not known. We hypothesized that cyclin-dependent kinase inhibitors would be strongly expressed in SKs and that the proliferation rate would be low.

Objectives: To quantify the expression of Ki67, p16(INK4a), p21(WAF1), and p27(KIP1 )in SK.

Methods: We assessed acanthotic SKs (n=10) and irritated SKs (n=10) for Ki67, p16(INK4a), p21(WAF1), and p27(KIP1 )expression using immunohistochemistry.

Results: For nonirritated acanthotic pattern SKs, the Ki67 index was 3.4% (range 0.6-6.5%), confirming a low proliferation rate. The p16(INK4A) index was 6.0% (range 0-16%), and the p21(WAF1) index was 4.8% (range 0-25%). p27(KIP1) was strongly and diffusely expressed in all SKs, with a labeling index of 78% (range 75-85%). The labeling indices were similar in irritated SK lesions with a slightly increased proliferation rate and corresponding decrease in p27(KIP1) expression.

Conclusions: We conclude that in SKs, strong expression of the cyclin-dependent kinase inhibitor p27(KIP1) appears to be a major mechanism controlling keratinocyte proliferation.