Immunohistochemical analysis of p53 protein and 72 kDa heat shock protein (HSP72) expression in ovarian carcinomas

Mutations of the tumour suppressor p53 gene have been reported in a variety of human malignant tumours, and are frequently associated with overexpression of p53 protein. To examine the significance of p53 gene alteration in malignant epithelial tumours of the ovary, we studied the immunohistochemical reactivity with a monoclonal antibody against p53 (PAb 1801) in 6 ovarian tumours of low malignant potential (LMP) and 32 ovarian carcinomas. The existence of any correlation of p53 overexpression with the clinicopathological features and with the immunohistochemical expression of 72 kDa heat shock protein (HSP72) and sex steroid receptors (oestrogen receptors; ER, progesterone receptors; PR) was also analysed. Expression of p53 was found in 2 of the 6 (33.3%) LMP tumours and in 15 of the 32 (46.9%) carcinomas. Strong expression of HSP72 was observed in 11 of the 17 (64.7%) p53-positive tumours, but only in 2 of the 21 (9.5%) p53-negative ones. Histologically, p53-positivity was observed in 7 of the 10 (70%) serous carcinomas, 4 of the 6 (66.7%) mucinous, 4 of the 10 (40%) endometrioid, and none of the 4 clear cell and 2 transitional cell carcinomas. Distribution of p53-positive cells in the tumour sections was homogenous in serous tumours, but heterogenous in mucinous lesions. All of the 4 carcinomas arising in endometriotic cysts were p53-negative. These differences support the thesis of heterogeneity in ovarian carcinogenesis. There was an inverse relationship between p53-positivity and sex steroid receptor status for ovarian carcinomas; 14 of the 15 p53-positive carcinomas were negative for both ER and PR, whereas 11 of the 17 p53-negative carcinomas were positive for ER and/or PR (P<0.01).