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[Cancer Research 45, 5746-5750, November 1, 1985]
© 1985 American Association for Cancer Research

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Stimulative Effect of Physiological Doses of Androgen or Pharmacological Doses of Estrogen on Growth of Shionogi Carcinoma 115 in Mice1

Shinzaburo Noguchi, Yasuko Nishizawa, Naomi Uchida, Kenji Yamaguchi, Bunzo Sato, Yukihiko Kitamura and Keishi Matsumoto2

Departments of Pathology [S. N., Y. N., K. M.] and Internal Medicine [B. S.] and Institute for Cancer Research [Y. K.], Osaka University Medical School, Kita-ku, Osaka 530; Shionogi Research Laboratory [N. U.], Fukushima-ku, Osaka 553; and Kobe Women's College [K. Y.], Chuo-ku, Kobe 650, Japan

It was generally accepted for 20 yr that the growth of Shionogi carcinoma 115 (SC115) is stimulated only by androgen. In the present study, the growth-stimulative effect of estrogen alone on SC115 tumors was examined in castrated mice. Daily injections of physiological doses of 17ß-estradiol did not enhance the tumor growth. However, high doses of 17ß-estradiol (10–100 µg/mouse/day) significantly stimulated the growth of tumors in a dose-dependent manner. Since high doses of diethylstilbestrol (10–50 µg/mouse/day), which does not bind to androgen receptor, could markedly stimulate the growth of tumors and since antiandrogen (cyproterone acetate) failed to inhibit the growth stimulation induced by high doses of 17ß-estradiol, it is concluded that high doses of 17ß-estradiol, which binds to androgen receptor with relatively low but significant affinity, enhance the tumor growth not via the androgen receptor system. The growth speed, histological type, content, and affinity of androgen, estrogen, and progesterone receptors and pattern of newly synthesized proteins labeled in vitro with [35S]methionine of tumors grown by high doses of estrogen were not significantly different from those of the original SC115 tumors grown in normal males. Furthermore, seed tumors from one to six generations grown by pharmacological doses of estrogen alone could rapidly grow only in normal males and not in castrated males. The present findings demonstrate that the growth of SC115 tumors in vivo is stimulated by physiological doses of androgen or pharmacological doses of estrogen.

1 Supported in part by a grant-in-aid for cancer research from the Ministry of Education, Science, and Culture and from the Ministry of Health and Welfare.

2 To whom requests for reprints should be addressed.

Received 3/ 6/85. Revised 7/24/85. Accepted 7/29/85.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1985 by the American Association for Cancer Research.