ABSTRACT
BACKGROUND AND OBJECTIVES: Inverted papillomas (IPs) are rare benign tumors of nasal epithelium with high recurrence rates and malignant transformation potential. Tumor development results from imbalance between cell proliferation and "programmed cell death", also named apoptosis. The purpose of this study was to compare cell proliferation, apoptosis, and apoptosis inhibition in hyperplastic epithelium from IPs and nasal polyps (NPs), and also to understand the mechanism of growth and malignant transformation of IPs. MATERIALS AND METHODS: IP samples were obtained after surgical removal of tumor in 15 patients, and NPs were sampled during endoscopic sinus surgery in 7 patients as a control. IP samples were classified in three groups: group I (n=9) -IP without dysplasia or carcinoma, group II (n=3) -IP with dysplasia, group III (n=3) -IP with carcinoma. Cell proliferation and apoptosis inhibition, respectively, were assessed by immunohistochemical identification of the Ki-67 and the oncoprotein Bcl-2. Apoptosis was evaluated by analyzing the DNA fragmentation using TUNEL method. RESULTS: Ki-67 index was increased in IPs compared to NPs (p=0.001). Of the IPs, Ki-67 index was increased progressively from IP without dysplasia or caccinoma, through IP with dysplasia, to reach the highest level in IP with carcinoma. Apoptotic index was also increased in IPs (p=0.002) with the highest level in IP without dysplasia or carcinoma. Of the IPs, apoptotic index was decreased as the tumor progress. Bcl-2 index was decreased in IPs (p=0.004), but, of the IPs, as the tumor progress, bcl-2 index was more decreased. CONCLUSION: Tumor development of IPs could result from the imbalance between hugely increasing epithelial cell proliferation and slightly increasing apoptosis, and the inhibition of apoptosis via bcl-2 oncoprotein seems to be involved in the growing process of IPs. Although we can not exactly mention due to limited number of cases, these imbalance may be involved in dysplastic or malignant transformation of IPs, but may be independent of the expression of bcl-2.