P53, bcl-2, ki-67 li (labeling index) status in benign, proliferative, and malignant ovarian surface epithelial neoplasms.

Journal: The Eurasian Journal Of Medicine
Published:
Abstract

Objective: Approximately 50% of human malignancies present with mutations in p53, which is the most common tumor suppressor gene involved with human malignancies. Bcl-2 is a protooncogene, and expression of its protein product is associated with a better prognosis in several malignancies. Ki-67 is a marker of cellular proliferation. The purpose of this study was to determine whether simultaneous detection of p53, bcl-2 and Ki-67 using immunohistochemical staining can be used as a diagnostic factor in the assessment of human ovarian epithelial tumors.

Methods: The study was performed on formalin-fixed, paraffin-embedded tissue samples from 75 epithelial ovarian tumors, 15 serous cystadenomas, 15 mucinous cystadenomas, 5 borderline serous cystadenomas, 5 borderline mucinous cystadenomas, 15 serous cystadenocarcinomas, 15 mucinous cystadenocarcinomas and 5 endometrioid carcinomas. Immunohistochemical staining was performed using monoclonal antibodies against p53, bcl-2, and Ki-67(MIB1).

Results: Anti-p53 reactivity was observed in 14 tumors, all of which were malignant tumors, and no reactivity was observed in borderline or benign tumors. Overexpression of bcl-2 was observed in 12 benign neoplasms (40%), 5 of which were borderline (50%), but was not observed in any of the malignant tumors. There was a statistically significantly higher level of Ki-67 LI positivity in the malignant tumors than in the benign and borderline tumors (p<0.005).

Conclusions: These data show significant differences in the expression of these markers in ovarian tumors and suggest a possible role for these tumor-associated genes as supplemental tools in diagnostic pathology. Furthermore, our findings support the redesignation of low malignant potential tumors (current nomenclature) to benign ovarian carcinoma.

Authors
Nesrin Gursan, Sare Sipal, Muhammed Calik, Cemal Gundogdu