To evaluate the possibility of the targeted therapy for human epidermal growth factor receptor (HER)-2 and epidermal growth factor receptor (EGFR) in ovarian cancers, we evaluated HER-2 and EGFR gene amplification by using chromogenic in-situ hybridization method in ovarian common epithelial tumors. The increased gene copy number of HER-2 was found in 20 of 90 primary cancers (22.2%), but not in benign and borderline tumors. There were 3 trisomy (3.3%), 10 polysomy (11.1%), and 7 amplification (7.8%). The increased gene copy number of HER-2 was more common in mucinous (45.5%) and clear cell carcinomas (41.7%) than in serous (17.5%) and endometrioid carcinomas (0%), but without statistical significance. The increased copy number of EGFR gene was found in 2 of 24 borderline tumors (8.3%) and 34 of 90 malignant tumors (37.8%), but none of benign tumors. There were 1 amplification (1.1%), 9 trisomy (10.0%), and 26 polysomy (28.9%). Serous (45.6%) and clear cell (50.0%) carcinomas showed more frequent EGFR gene copy number changes than in serous borderline tumors (11.8%), mucinous (9.1%), and endometrioid carcinomas (10%), but with statistical significance only between serous borderline tumors and serous carcinomas. Increased HER-2 gene copy number was not correlated with International Federation of Gynecology and Obstetrics stage as well as histologic and nuclear grades, whereas increased EGFR gene copy number was correlated with histologic and nuclear grade. From the above results, we conclude that chromogenic in-situ hybridization technique can be used in the evaluation of HER-2 and EGFR gene number changes in selecting the patients who need far more specific and effective therapeutic modalities, such as targeted therapy.