Epithelial ovarian carcinomas are thought to arise from cells of ovarian surface epithelium (OSE) covering the free surface of the human ovary. Two immortalized human cell lines, OSE2a (non-tumorigenic) and OSE2b-2 (tumorigenic), were previously established from normal OSE cells of a reproductive-age patient. In the present study, we found that expression of luteinizing hormone (LH)/chorionic gonadotropin (CG) receptor (LH/CGR) is present in OSE2a cells and absent in OSE2b-2 cells. In OSE2a cells, a low concentration (10 3 mIU/ml) of CG enhanced anchorage-dependent growth via up-regulation of insulin-like growth factor-1 (IGF1), whereas a high concentration (10 5 mIU/ml) of CG induced anchorage-independent growth and down-regulation of IGF1 expression. To investigate involvement of other genes in LH/CGRrelated tumorigenicity, we compared cDNA expression arrays of OSE2a and OSE2b-2 cells, and found that the following genes had lower expression in OSE2b-2 than in OSE2a: integrin β β β β1, intercellular adhesion molecule-1 (ICAM1), and Waf1/Cip1. Subsequent semiquantitative reverse transcription polymerase chain reaction using OSE2a cells showed that expression of integrin β β β β1 pithelial ovarian carcinoma constitutes approximately 90% of ovarian malignancies, and is generally thought to derive from ovarian surface epithelium (OSE), 1) which descends from embryonic coelomic mesothelium and gives rise to the mülle-rian ducts.2) A number of gene alterations related to ovarian carcinogenesis have been found in studies using ovarian carcinoma specimens and cell lines. There have been reports of inactivation of tumor suppressor genes (p53, BRCA1, BRCA2 and PTEN) and activation of oncogenes (Ki-ras, c-erbB-2, c-myc, AKT2 and PIK3CA) in cases of epithelial ovarian carcinoma.3)