Relation between HPV and cyclooxygenase 2 overexpression in cervical carcinoma in situ and carcinoma.
- Author:
Youn Seok CHOI
1
;
Tae Sung LEE
;
Ju Hyun KIM
;
Hong Tae KIM
;
Hun Kyu OH
;
Chi Dong HAN
Author Information
1. Department of Obstetrics and Gynecology, School of Medicine, Catholic University of Daegu, Daegu, Korea. cdhan@cu.ac.kr
- Publication Type:Original Article
- Keywords:
Cyclooxygenase 2;
COX-2;
Uterine cervical cancer;
HPV;
Human papilloma virus
- MeSH:
Carcinoma in Situ;
Cyclooxygenase 2;
Disease Progression;
Humans;
Immunohistochemistry;
Multivariate Analysis;
Myoma;
Polymerase Chain Reaction;
Prostaglandin-Endoperoxide Synthases;
Uterine Cervical Neoplasms
- From:Korean Journal of Obstetrics and Gynecology
2008;51(8):866-873
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVE: The aim of this study was to identify the relation between HPV infection and cyclooxygenase 2 (COX-2) overexpression in cervical carcinoma in situ (CIS) and carcinoma. METHODS: Fourteen patients with CIS, 14 patients with invasive cervical carcinoma, and 14 patients with myoma as control were enrolled. Polymerase chain reaction was used to detect high risk types of HPV, and immunohistochemistry was used to detect COX-2 expression. RESULTS: The frequencies of high risk types of HPV infections in CIS or carcinoma were significantly higher than control [CIS: 11 (78.6%), carcinoma: 14 (100%), control: 1 (7.1%), P-value>0.001]. COX-2 expressions in CIS were higher than control (P=0.037), and those in carcinoma were higher than CIS (P=0.002). Three patients with CIS did not show HPV infection and showed lower COX-2 expression than the other patients with HPV infection in CIS group (P=0.013). There was strong correlation between COX-2 expression and HPV infection (P>0.001). However, in multivariate analysis, disease progression from normal to invasive carcinoma was the only independent factor to affect COX-2 overexpression. CONCLUSION: Disease progression from normal to invasive carcinoma might be more important factor to affect COX-2 overexpression than high risk types of HPV infection.
