| PrefaceOvarian cancer is one of the most common malignancies in adult females . It is the leading cause of death from gynecologic cancer and has the worse prognosis. Risk for ovarian cancer increases as a woman gets older ( a rate of 30 cases per 100 ovarian cancer after 70 year age group). In 1994, a susceptibility gene was cloned by Skolnick reseach group which is a breast and ovarian cancer susceptibility gene . BRCAl was mapped by genetic linkage to the long arm of chromosome 17, in the interval 17q21. The BRCAl gene has been found to contain 24 exons and 22 intons that encode a protein of 1,863 amino acids. BRCAl is a tumor suppressor gene. BRCAl regulates multiple nuclear processes including DNA repair and ercombination, checkpoint control of the cell cycle, and transcription. Abnomal expression of BRCAl was observed in many tumors. Reduction of BRCAl expression may play a role in development , progression and prognosis of maglignant tumors. Like other tumors, development of ovarian cancer was related with the overexpression of oncogenes and the dysfunction of tumor suppressor genes. The purpose of this study was to examine BRCAl expression and its relationship to clinical pathological parameters in ovarian serous tumors.Material and methodsMaterial : All tumor samples were obtained from 62 patients who under -went surgery in China Medical University. Formalin - fixed, paraffin - embedded tumor specimens were studied from 62 patients with 42 ovarian serous cystad- enocarcinomas, 10 borderline serous cystadenomas, and 10 serous cystadeno-mas. All the cases were classified as serous cystadenocarcinomas according to WHO Histoloical Clsssifcation ;10 were classified as grad I , 17 were classified as grad II ,15 were classified as grad III ; All the cases were classified as serous cystadenomas according to FIGO Clinical Stage :21 were classified as stage I and stage II ,21 were classified as stage Mand stage IV .Methords: Immunohistochemical analysis was used to detect the expression cf BRCA1 protein in Formalin - fixed and paraffin embedded sections using the streptavidin - biotin - peroxidase methodology. 4jxm - thick sections were cut from paraffin blocks . Paraffin sections on solane - coated slides were dewaxed with xylene and rehydrated through a graded alcohol series. For antigen retrieval , they were immersed in citrate - phosphate buffer and microwaved. Then endogenous peroxidase activity was blocked in absolute methanol solution containing 3% hydrogen peroxide and the slides were washed in 10mM phosphate - buffered saline. After the buffer had cooled , normal serum was reacted with the slides. The slides were reacted with monoclonal antibody for BRCA1 with a dilution of 1:40. Antigen - antibody reaction were visualized using a streptavidin -biotin - peroxidase conjugate. Staining without antibody was performed as a negative control.Assessment of staining for BRCA1: Assessment of IHC results for BRCA1 was based on the brown precipitate located in the nuclear. Percentages of positively stained cells were calculated after counting a total of 500 epithial tumor cell from each ovarian serious tumor. Tumors staining <5% were scored ( - ) , 5% -25% were scored ( + ) , 25% -75% were scored ( ++ ) , >75% were scored ( +-H- ).Statistical analysis: Descriptive statistics comparing BRCA1 expression with other paramets were analyzed by standard Chi - square tests, or Fisher' s exact test as appropriate. All p values were two - tailed and the 0. 05 level was considered statistically significant . SPSS10. 0 computer package system was used for all statistical testing and management.
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