Expression of Cyclins (D1, A, E, and B1) in N-butyl-N-(4-hydroxybutyl)nitrosamine-induced Rat Bladder Carcinogenesis.
- Author:
Gui Young KWON
1
;
Eon Sub PARK
;
Sung Geun BONG
;
Tae Jin LEE
;
Mi Kyung KIM
;
Jae Hyung YOO
;
Kye Yong SONG
Author Information
1. Department of Pathology, Chung-Ang University College of Medicine, Seoul, Korea. taejlee@chol.com
- Publication Type:Original Article
- Keywords:
Cyclins;
Carcinogenesis;
N-butyl-(4-hydroxybutyl)nitrosamine;
Rat;
Urinary bladder
- MeSH:
Animals;
Carcinogenesis*;
Cell Cycle;
Cell Cycle Proteins;
Cyclin B1;
Cyclin D1;
Cyclins*;
Humans;
Hyperplasia;
Male;
Mucous Membrane;
Papilloma;
Rats*;
Rats, Sprague-Dawley;
Urinary Bladder*
- From:Korean Journal of Pathology
2003;37(4):255-262
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Cell cycle deregulation plays a major role in chemical multistage carcinogenesis.Therefore, the evaluation of cell cycle proteins is important. METHODS: In order to induce carcinogenesis in the rat urinary bladder, 0.05% N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN)was administered to male Sprague-Dawley rats for 30 weeks. Expressions of cyclin D1, A, E, and B1 were examined by immunohistochemical stainings. RESULTS: Urothelial cell hyperplasia appeared at 5 weeks, followed by papilloma at 10 weeks. Superficial carcinoma was observed at 20 weeks, and invasive carcinoma developed in 40% (4/10) of the rats at 30 weeks. Expressions of cyclin D1 and A increased sequentially from normal mucosa throughhyperplasia, papilloma, and carcinoma (p<0.01). Expressions of cyclin D1, B1 and cyclin Ewere higher in invasive carcinomas than in superficial carcinomas (p<0.01). In contrast, therewas no significant difference in the expression of cyclin B1 between hyperplasia, papillomaand superficial carcinoma. CONCLUSIONS: The present results indicate the important roles of cyclin D1 and A in the development of BBN-induced urothelial carcinoma of rats. Aberrantexpression of cyclin B1 and E may contribute to the progression from superficial to invasivebladder cancer rather than tumorigenesis.
