An experimental model of rat mammary carcinoma induced by oral administration of ethyl methanesulphonate (EMS) was characterized with reference to estrogen receptors (ER) and hormone dependency. After the administration of EMS, the mammary carcinomas developed more rapidly in the 4-week old rats than in the 16-week old rats. The developed mammary carcinomas were related to the ER status. Tumor development was prevented by ablative oophorectomy prior to EMS administration, but only partially, by adrenalectomy. These inhibitory effects on tumor development were more obvious when ablative surgery was performed on younger rats at age 4 weeks. In rats subjected to oophorectomy at after EMS administration at age 16 weeks, tumor induction was retarded but not completely prevented. Thus, it appears that mammary tumors induced by EMS are dependent on ovarian hormones and that mammary glands of the younger female rats are more sensitive to carcinogenic actions of EMS.