Cycline-dependent kinase inhibitor, p27 (KIP1), is associated with cholesteatoma.

Abstract

Cyclin-dependent kinases (CDKis) can arrest the cell cycle, which in turn inhibits the cell proliferation. P27 (KIP1) is a CDKi and acts as a tumor suppressor gene. In this study, we aimed to investigate the role of p27 CDKi in cholesteatoma, a disease characterized by the presence of hyperproliferative squamous epithelium. Immunohistochemical staining of 15 cholesteatoma and 18 control ear canal skin samples, which were taken intraoperatively, was performed for p27 positivity. The monoclonal antibodies to p27 were used for immunohistochemical staining of the sections. The streptavidin-biotin horseradish method was used. The number of cells staining positive for p27 was calculated, and the intensity of p27 positivity was graded. P27 positivity was obtained in 9 (50%) of 18 skin tissues. In the cholesteatoma tissues, p27 positivity was found only in 2 (13.3%) tissue samples. The difference between the groups were statistically significant (P =.03). The mean numbers of p27 positivity were 11.8 +/- 15.5 and 1.4 +/- 3.8 (mean +/- standard deviation) in the skin and cholesteatoma samples, respectively. This difference was also statistically significant (P =.02). The p27 results of primary and secondary cholesteatoma samples were not significantly different (P =.3). The results of p27 were not related to the gender of the patients (P =.8). P27 is involved directly or indirectly in the occurrence of cholesteatoma. Alterations of p27 levels in keratinocytes can influence the proliferative state of the keratinocytes. Altered p27 levels in cholesteatoma may suggest a molecular pathology in cholesteatoma. The search for significance of CDKis seems promising to better understand the pathogenesis of cholesteatoma.