A Study on the Expression of p53 and the Detection of Human Papilloma Virusin the Sinonasal Inverted Papilloma Associated with Carcinoma

Byun, Jae Yong; Cho, Joong Saeng; Hong, Il Hee; Kim, Woo Seok; Lee, Dong Yeup; Cha, Chang Il

Abstract

BACKGROUND AND OBJECTIVES: There have been some reports suggesting that the malignant and benign clinical courses are separable on the basis of HPV subtypes in the sinonasal inverted papilloma. The E6 protein of high risk HPV subtype including types 16 and 18 is known to be associated with p53. The viral E6 protein-p53 complex is responsible for the functional loss of p53 which then becomes immunohistochemically negative. The aim of this study was to determine the prevalence and types of HPV in this neoplasm and evaluate the relationship between expressions of the oncogenes and HPV. MATERIALS AND METHOD: The material was composed of 11 cases of inverted papilloma and 7 cases which were associated with carcinoma. Immunohistochemical staining for p53 was performed. A molecular study of the E6 gene of HPV DNA types 6, 11, 16 and 18 was also performed with separate nest-PCR on squamous cell lesions stainned p53 and papillomatous lesions by use of microdissection technique with paraffin embedded materials.
RESULTS
The carcinomatous and dysplastic areas were diffusely positive for p53 in all cases associated with carcinoma, whereas the control group was negative for p53. HPV types 6 and 11, generally known as the lower risk types were presented in the 80% of all cancers and papilloma lesions. A HPV DNA type 18 was solely positive in 2 cases on the p53 overexpressed lesion, associated with carcinoma.
CONCLUSION
p53 and HPV may be involved in the pathogenesis of malignant transformation in the inverted papilloma. Therefore, it can be disproved that the HPV subtypes are directly related to either benign or malignant clinical course. However, functional loss of the wild type p53 gene is deeply associated with malignant transformation. In addition to the classical E6 of HPV 16,18-p53, another mechanism could be involved in the functional inactivation of p53.