Abstract

This study was accomplished by using a technology (Tissue microarrays (TMA) and Fluorescence In Situ Hybridization (FISH)) on different type of ovarian tumors, The method of FISH applied on TMA with HER1 and HER2 specific probes proved itself as the most commonly used and valuable analysis for routine HER1 status detection and copy number changes. The results showed in Out of all 417 ovarian carcinomas examined, the number of successfully hybridized for HER1 oncogene is 376 (90.61%), 224 of them are malignancies tumors (218 epithelial and 6 non epithelial ) ,25 low malignant ovarian tumors(just epithelial), 127 – Benign ovarian tumors(103 epithelial and 24 non epithelial ). We established HER1 amplification in malignancies tumors only 11 (4.91%) ,10 (4.58%) epithelial and in 1 (1.16%) non epithelial ). Not found amplification in tumors with low malignant potential & Benign ovarian tumors. While we established HER1 gains in malignancies tumors, low malignant ovarian tumors and Benign ovarian tumors only 28, malignancies 18 about (8.03%), low malignant 2 ( 8% ) and in Benign ovarian tumors 8 (6.29% ). Epithelial malignant tumors among the highest incidence of HER1 amplification was detected in Serous (4.71%), Mucinous (4%), Combined (4.54%), Undifferentiated tumors(4.34%) and Unclassification (14.28%). HER1 amplification is found in 1 of 6 non epithelial malignant tumors, Sex-cord stromal tumour (16.16%). HER1 gains in malignancies tumors was detected in serous (5.71%), Mucinous (8%), endometrioid (10.52%), Clear cell (11.11%), Combined ( 13.63%), Undifferentiated tumors(8.69%) and Unclassification (7.14%).and in epithelial malignant tumors was detected only in Embryonal carcinoma (16.16%). In low malignant ovarian tumors we was detected HER1 gain only in Mucinous (18.18%).