Apoptosis in Uterine Cervical Intraepithelial Neoplasia and Cervical Carcinoma: Relationship with p53, MIB-1 and bcl-2 Expression.
- Author:
Kyu Wan LEE
1
;
Ki Hoon CHANG
;
Yong Ho LEE
;
Nak Woo LEE
;
Young Tae KIM
;
Pyong Sham KU
Author Information
1. Department of Obstetrics and Gynecology, College of Medicine, Korea University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Cervical cancer;
Cervical intraepithelial neoplasia;
Apoptosis;
MIB-1;
p53;
bcl-2
- MeSH:
Apoptosis*;
Cell Proliferation;
Cervical Intraepithelial Neoplasia*;
Immunohistochemistry;
Oncogene Proteins;
Oncogenes;
Uterine Cervical Neoplasms
- From:Korean Journal of Obstetrics and Gynecology
2001;44(6):1115-1122
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVES: Apoptosis may play a major role in determining the growth and progression of the tumors. Certain oncogenes and tumor supressor genes are known to modulate apoptosis. The aim of study was to investigate whether apoptosis is related to the degree of differentiation, MIB-1 indicies, and expression of mutated p53 and bcl-2 in cervical neoplasms. MATERIALS AND METHODS: We examined 57 samples of normal, premalignant(i.e. mild, moderate and severe dysplasia and carcinoma in situ), malignant cervical tissue to evaluate whether differences in the apoptotic activity. Apoptotic cells and bodies were visualized by 3' end labelling. Simultaneously, quantitative immunostaining was performed for bcl-2 and p53, two known regulators of apoptosis. RESULTS: The cell proliferation index as determined by MIB-1 immunohistochemistry increased with progression from normal to cervical intraepithelial neoplasm and invasive cancer. The apoptotic index(AI) also increased with grade of lesion and was significantly associated with cell proliferation. However, the extent of apoptosis did not correlate with the expression of p53 and bcl-2. CONCLUSIONS: These results suggest that the elevation of AI in cervical neoplasm is associated with cell proliferation activity but is independent of the expression of p53 and bcl-2. It is likely that the effects on apoptosis of bcl-2 and p53 are countered by those of other oncogene products and/or additional factors that regulate apoptosis in vivo.
