Affiliation:
1. From the Department of Pathology and Laboratory Medicine, University of Calgary, and Calgary Laboratory Services, Calgary, AB
Abstract
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, p16INK4a, p21WAF1, and p27KIP1 in SK. Methods: We assessed acanthotic SKs ( n = 10) and irritated SKs ( n = 10) for Ki67, p16INK4a, p21WAF1, and p27KIP1 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 p16INK4A index was 6.0% (range 0–16%), and the p21WAF1 index was 4.8% (range 0–25%). p27KIP1 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 p27KIP1 expression. Conclusions: We conclude that in SKs, strong expression of the cyclin-dependent kinase inhibitor p27KIP1 appears to be a major mechanism controlling keratinocyte proliferation.
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5 articles.
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