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[Cancer Research 38, 2077-2083, July 1, 1978]
© 1978 American Association for Cancer Research

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Effect of Estradiol and Prolactin on Galactosyltransferase and {alpha}-Lactalbumin Activities in Rat Mammary Gland and Mammary Tumor1

Clement Ip and Thomas L. Dao2

Department of Breast Surgery and Breast Cancer Research Unit, Roswell Park Memorial Institute, Buffalo, New York 14263

We have reported the conditions for the in vivo stimulation of galactosyltransferase and {alpha}-lactalbumin activities in the mammary gland of virgin ovariectomized rats by exogenous hormones. Administration of 1 µg estradiol and 1 mg prolactin daily for 6 days produces a maximal effect, provided the mammary tissue has already been primed by a combination of 1 µg estradiol and 3 mg progesterone daily for 14 days to promote cellular proliferation. Although the data suggest that prolactin may be the key hormone that triggers the expression of both proteins, estrogen is necessary, especially for maximal stimulation of {alpha}-lactalbumin activity. A high dosage of estradiol (10 µg/day), however, results in an inhibitory response.

Of the 15 dimethylbenz(a)anthracene-induced mammary tumors studied, only 4 have detectable {alpha}-lactalbumin activity, although they all contain different levels of galactosyltransferase. Estradiol and prolactin administration causes a slight increase in the level of both proteins in these 4 tumors, but the remaining 11 tumors are unresponsive to the effect of this hormonal combination. There does not seem to be an absolute correlation between the estrogen-binding capacity and the production of {alpha}-lactalbumin. However, preliminary data show that of the four tumors with the highest estrogen-binding capacity, three are positive for {alpha}-lactalbumin. The inability of most of these tumors to synthesize {alpha}-lactalbumin, even when the hosts have undergone pregnancy and lactation, suggests that in the majority of cases the gene coding for this tissue-specific protein is probably not expressed as a result of malignant transformation.

1 This investigation was supported by Grant CA 14812-03, awarded by the National Cancer Institute, Department of Health, Education and Welfare.

2 To whom requests for reprints should be addressed, at Roswell Park Memorial Institute, 666 Elm Street, Buffalo, N. Y. 14263.

Received 10/ 6/77. Accepted 4/ 4/78.







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 © 1978 by the American Association for Cancer Research.