Korean J Pathol.
2000 May;34(5):358-365.
Role of HSP70 Expression in the Development of Endometrial Adenocarcinoma Correlation of ER, PR, p53, and bcl-2 protein expressions and apoptosis
- Affiliations
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- 1Department of Anatomic Pathology, Pusan Paik Hospital, College of Medicine, Inje University, Pusan 614-735, Korea.
Abstract
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Heat shock protein of 72 kDa (HSP70) has a role in the functional modulation of sex steroid
hormone receptors and in p53-associated oncogenesis and inhibits apoptosis associated with bcl-2.
However, the exact role of HSP70 in the development of endometrial adenocarcinoma has not been
well established. The aim of this study is to evaluate the role of HSP70 in relation with ER, PR,
p53 and bcl-2 expressions and apoptosis in benign and malignant endometrial lesions.
Immunohistochemical studies for HSP70, ER, PR, p53, bcl-2 and TUNEL method for apoptosis
were performed in 30 cases of adenocarcinoma and 30 cases of benign endometrial lesions
consisted of each 10 cases of disordered proliferative endometrium (DP), simple or complex
hyperplasia (HP), and atypical hyperplasia (AH). There were no significant differences of HSP70
and bcl-2 expression rates and apoptotic index (AI) between DP, HP, AH, and adenocarcinoma.
p53 expression rate in adenocarcinoma was 36.7%, but no p53 expression was identified in DP, HP
and AH (p<0.05). In adenocarcinoma, HSP70 expression rate was higher in ER and PR negative
adenocarcinoma (p<0.05), and p53 expression rate was higher in nonendometrioid type and FIGO
grade II and III (p<0.05), but no significant difference of bcl-2 expression rate according to the
histological type and FIGO grade. AI was higher in nonendometrioid type (p<0.05). There was no
correlation between HSP70, p53 and bcl-2 expressions, and no significant difference of AI
according to HSP70, ER, PR, p53, and bcl-2 expressions. In conclusion, higher HSP70 expression
rate in poorly differentiated and ER and PR negative adenocarcinoma suggests that HSP70 inhibits
ER and PR expression and may be involved in the development of poorly differentiated
endometrial adenocarcinoma.