OBJECTIVES: The cell cycle must be involved in cell proliferation of the epithelium of middle ear cholesteatoma Cyclins and cyclin-dependent kinase (CDK) complexes have important regulatory roles during cell cycle progression. Cyclin-CDK complexes are in turn regulated by the cyclin-dependent kinase inhibitors (CDKIs), which generally inhibit cell cycle progression. One of the important CDKI members is p27(Kip1). The goal of this study is to evaluate the expression of p27(Kip1) and Ki-67, a proliferation marker, in cholesteatoma and in the skin of the external ear canal. METHODS: The expressions of p27(Kip1) and Ki-67 in cholesteatoma epithelium (n = 20) and ear canal epithelium (n = 7) were investigated by an immunohistochemical technique. RESULTS: In cholesteatoma epithelium specimens, the expression of p27(Kip1) was observed from the parabasal layer to the granular layer, but not in the basal layer. Ki-67 was expressed dominantly in the basal and parabasal cell layers. Their expressions tend to be increased compared with their expressions in the normal ear canal skin. The expression pattern of the proliferation marker Ki-67 in the epithelial layers of two groups was inversely related to the expression of p27(Kip1). CONCLUSIONS: In cholesteatoma, the expressions of CDKI and Ki-67 were both increased in this study. The ability to inhibit proliferative activity was also increased in the cholesteatoma epithelium. The expression pattern of the proliferation marker Ki-67 in the epithelial layers was inversely related to the expression of p27(Kip1). Not only is the proliferation activity increased, but also the ability to inhibit hyperproliferation is increased in the cholesteatoma epidermis. Despite increased proliferative activity in the cholesteatoma epidermis, epithelial cells still retain the capability to prevent cell cycle arrest by means of p27(Kip1).
OBJECTIVES: The cell cycle must be involved in cell proliferation of the epithelium of middle ear cholesteatoma Cyclins and cyclin-dependent kinase (CDK) complexes have important regulatory roles during cell cycle progression. Cyclin-CDK complexes are in turn regulated by the cyclin-dependent kinase inhibitors (CDKIs), which generally inhibit cell cycle progression. One of the important CDKI members is p27(Kip1). The goal of this study is to evaluate the expression of p27(Kip1) and Ki-67, a proliferation marker, in cholesteatoma and in the skin of the external ear canal. METHODS: The expressions of p27(Kip1) and Ki-67 in cholesteatoma epithelium (n = 20) and ear canal epithelium (n = 7) were investigated by an immunohistochemical technique. RESULTS: In cholesteatoma epithelium specimens, the expression of p27(Kip1) was observed from the parabasal layer to the granular layer, but not in the basal layer. Ki-67 was expressed dominantly in the basal and parabasal cell layers. Their expressions tend to be increased compared with their expressions in the normal ear canal skin. The expression pattern of the proliferation marker Ki-67 in the epithelial layers of two groups was inversely related to the expression of p27(Kip1). CONCLUSIONS: In cholesteatoma, the expressions of CDKI and Ki-67 were both increased in this study. The ability to inhibit proliferative activity was also increased in the cholesteatoma epithelium. The expression pattern of the proliferation marker Ki-67 in the epithelial layers was inversely related to the expression of p27(Kip1). Not only is the proliferation activity increased, but also the ability to inhibit hyperproliferation is increased in the cholesteatoma epidermis. Despite increased proliferative activity in the cholesteatoma epidermis, epithelial cells still retain the capability to prevent cell cycle arrest by means of p27(Kip1).