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Androgen Dependency of a Tumor Produced by a Cell Line Derived from Androgen-responsive Shionogi Carcinoma 115¹

Departments of Pathology [N. T., T. T., H. T.], Gastrointestinal Oncology [R. Y.], and Gynecology [M. S.], The Center for Adult Diseases Osaka, Higashinari-Ku, Osaka 537; Shionogi Research Laboratories, Fukushima-Ku, Osaka 553 [N. U.]; Department of Physical Education, Nishinomiya, Hyogo 662 [D. T.]; Department of Pathology, Osaka Medical College, Takatsuki, Osaka 569 [M. T.]; Division of Cancer Pathology, Biomedical Research Center [Y. K.], and Department of Pathology [W. L., K. M.], Medical School, Osaka University, Fukushima-Ku, Osaka 530, Japan

An androgen-dependent tumor (SCC8 tumor) was obtained by inoculating an androgen-responsive cell line derived from the androgen-responsive Shionogi carcinoma 115 (SC115) into mice and then treating the mice with testosterone propionate (TP) at a pharmacological dose (400 µg/day). The SCC8 tumor differed in histological appearance from the SC115 tumor and its growth was less stimulated by androgen than that of the SC115 tumor. However, its growth was completely androgen dependent; SCC8 tumors did not develop in castrated mice and regressed when TP treatment was discontinued. The decreased sensitivity of the SCC8 tumor seemed to be attributable in part to its rapid metabolism of testosterone to metabolites with lower androgenic actions. The effects of TP at doses of 0, 100, 200, and 400 µg/day on cell division and cell death in SCC8 tumors of medium size were examined by measurements of the mitotic index and the retention of 5-[¹²⁵I]iodo-2'-deoxyuridine incorporated into the whole tumor. TP increased the mitotic index dose dependently and at all doses reduced the decrease in the retention of 5-[¹²⁵I]iodo-2'-deoxyuridine. These results suggest that steroids may not only stimulate cell division but also reduce cell death in steroid-dependent tumors.

¹ This work was supported in part by Grants-in-Aid for Cancer Research from the Ministry of Education, Science and Culture, the Osaka Anti-Cancer Campaign, and the Foundation for Promotion of Cancer Research.

² To whom requests for reprints should be addressed.

Received 3/16/88. Revised 10/ 3/88. Accepted 10/27/88.