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[Cancer Research 40, 4628-4630, December 1, 1980]
© 1980 American Association for Cancer Research

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Effect of Ovariectomy on Hormone Receptors and Growth of N-Nitrosomethylurea-induced Mammary Tumors in the Rat1

Baha'uddin M. Arafah2, Pietro M. Gullino, Andrea Manni and Olof H. Pearson

Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106 [B. M. A., A. M., O. H. P.], and the National Cancer Institute, Bethesda, Maryland 20205 [P. M. G.]

Estrogen receptor(s) (ER), progesterone receptor(s) (PGR), androgen receptor(s) (ANR), and prolactin receptor(s) (PRLR) were measured in N-nitrosomethylurea-induced mammary tumors in intact female Sprague-Dawley rats and in rats 9 days after ovariectomy. Following ovariectomy, 12 of 15 tumors regressed to 47.7 ± 5.5% of the original size (hormone-dependent tumors), while the remaining three had arrest of growth reaching 88.8 ± 7.3% of their original sizes.

Cytosol ER level was 50.3 ± 6.6 fmol/mg protein in tumors of intact rats and was significantly lower (25.6 ± 8.3 fmol/mg, p < 0.025) in the ovariectomized group. PGR was abundantly present in ten of 13 tumors of intact rats (mean, 144.5 ± 46.8) but was undetectable in five of six hormone-dependent tumors after ovariectomy (p < 0.01). ANR was detectable at low levels in only four of 13 tumors of intact rats but in none of six hormone-dependent tumors after ovariectomy. PRLR was not significantly different in tumors of intact and ovariectomized rats (20.6 ± 2.4 and 15.6 ± 1.8 fmol/mg, respectively). In three tumors that had arrest of growth after ovariectomy, the levels of ER, PGR, ANR, and PRLR were not significantly different from those of the hormone-dependent tumors.

We conclude that the majority of N-nitrosomethylurea-induced rat mammary tumors are hormone dependent. ER, PGR, and PRLR were abundantly present in the majority of these tumors, while ANR was present in only four of 13 tumors. The levels of ER and PGR were significantly lower following ovariectomy, while PRLR was not significantly changed.

1 Supported in part by USPHS Grant CA-05197-20 and by Grant PDT-48V from the American Cancer Society, Inc.

2 To whom requests for reprints should be addressed.

Received 6/ 9/80. Accepted 9/11/80.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
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Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1980 by the American Association for Cancer Research.