Human Papillomavirus Prevalence and Cell Cycle Related Protein Expression in Tonsillar Squamous Cell Carcinomas of Korean Patients with Clinicopathologic Analysis.
- Author:
Miji LEE
1
;
Sung Bae KIM
;
Sang Wook LEE
;
Jong Lyel ROH
;
Seung Ho CHOI
;
Soon Yuhl NAM
;
Sang Yoon KIM
;
Kyung Ja CHO
Author Information
1. Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. kjc@amc.seoul.kr
- Publication Type:Original Article
- Keywords:
Human papillomavirus;
Tonsillar neoplasm;
Carcinoma, squamous cell;
Cyclin-dependent kinase inhibitor p16;
Tumor suppressor protein p53
- MeSH:
Carcinoma, Squamous Cell;
Cell Cycle;
Cyclin D1;
Cyclin-Dependent Kinase Inhibitor p16;
DNA;
Down-Regulation;
Humans;
In Situ Hybridization;
Prevalence;
Prognosis;
Tonsillar Neoplasms;
Tumor Suppressor Protein p53
- From:Korean Journal of Pathology
2013;47(2):148-157
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Human papillomavirus (HPV)-related tonsillar squamous cell carcinoma (TSCC) has recently been characterized as a distinct subset with a favorable prognosis. The prevalence and clinicopathologic significance of HPV-related TSCC in Koreans are not well known. METHODS: HPV in situ hybridization (ISH) accompanied by p53, p16, pRb, and cyclin D1 immunohistochemical staining were performed on 89 resection cases of TSCC from 2000 through 2010. RESULTS: HPV was detected by ISH in 59 of 89 cases (66.3%). HPV-positive TSCCs were more common in younger ages (p=0.005), and tumor sizes were smaller in the HPV-positive compared to the HPV-negative group (p=0.040). Positive HPV staining was significantly correlated with p16 expression (p<0.001), pRb inactivation (p=0.003), and cyclin D1 down-regulation (p<0.001) but not with p53 expression (p=0.334). Seventeen cases that showed p16-immunopositivity with HPV-negativity by ISH were retested by HPV typing; HPV DNA was not detected in all cases. There was no significant difference between HPV-positive and HPV-negative patients either in the disease-specific survival (DSS, p=0.857) or overall survival (p=0.910). Furthermore, pRb-inactivated cases showed better DSS (p=0.023), and p53-positive cases showed worse DSS (p=0.001). CONCLUSIONS: Although high HPV prevalence was noted, it was not correlated with histopathologic findings or survival benefit. In addition to p53 expression, pRb inactivation along with p16 overexpression and down-regulation of cyclin D1 are thought to be important pathogenetic steps for developing TSCCs.
