C. J. Bradley

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J. Meites

Michigan State University

G. S. Kledzik

Centre hospitalier de l'Université Laval

Stephen Marshall

University of Manchester

Gerald A. Campbell

The University of Texas MD Anderson Cancer Center

H. J. Chen

Kaohsiung Chang Gung Memorial Hospital

Hsien-Jen J. Chen

Cooperative Institutions

Michigan State University

Kansas State University

Suez Canal University

Rutgers, The State University of New Jersey

University of California, San Diego

National Institute on Aging

Institute of Art

Max Planck Institute for Biophysical Chemistry

Heim Pál Gyermekkórház

Columbia University

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Stimulation of growth of carcinogen-induced mammary cancers in rats by thyrotropin-releasing hormone.

PubMed (1977)

H. J. Chen C. J. Bradley J. Meites

Twice-daily injections of three different doses of synthetic thyrotropin-releasing hormone (TRH), a hormone normally produced by the hypothalamus, produced significant increases in size and number of 7,12-dimethylbenz(a)anthracene-induced mammary cancers over 0.87% NaCl solution-injected control rats. When thyroidectomized rats, bearing 7,12-dimethylbenz(a)anthracene-induced mammary tumors were given the same twice-daily injections of TRH, mammary tumor growth was increased to the same extent as in intact rats given TRH, showing that the effects of TRH were not exerted via stimulation of thyroid function. The TRH-induced increments in mammary tumor growth were accompanied by significant increases in serum prolactin levels over 0.87% NaCl solution-injected controls. A single daily injection of 2-bromo-alpha-ergocryptine (CB-154), a prolactin-release inhibitor completely blocked TRH-induced mammary tumor growth and reduced serum prolactin values. These results indicate that a twice-daily pulse of TRH can stimulate mammary tumor growth by releasing prolactin from the anterior pituitary.

Mammary tumor

7,12-Dimethylbenz[a]anthracene

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Stimulation of carcinogen-induced mammary tumor growth in rats by adrenalectomy.

PubMed (1976)

Hsien-Jen J. Chen C. J. Bradley J. Meites

The effect of adrenalectomy on 7,12-dimethylbenz(a)anthracene-induced mammary tumor growth was studied in Sprague-Dawley female rats. Weekly measurements revealed that adrenalectomy significantly increased both mammary tumor size and number and elevated serum prolactin levels as compared to the intact controls. Daily injection of 1 mg hydrocortisone acetate into the intact 7,12-dimethylbenz(a)anthracene-tumor bearing rats did not significantly alter tumor size, number, or serum prolactin levels but, when injected into adrenalectomized rats, it prevented increased tumor growth and prolactin release. Daily injection of ovine prolactin and hydrocortisone suppressed endogenous prolactin release but significantly increased tumore size and number. Ergocornine, a prolactin-inhibiting drug, blocked adrenalectomy-induced tumor growth and partially blocked prolactin release. These results indicate that adrenalectomy in rats stimulates tumor growth by increasing prolactin release.

Mammary tumor

7,12-Dimethylbenz[a]anthracene

Pituitary Tumors

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Equality : toward a working definition : [an honors thesis (HONRS 499)]

C. J. Bradley

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Reduction of carcinogen-induced mammary cancer incidence in rats by early treatment with hormones or drugs.

PubMed (1974)

G. S. Kledzik C. J. Bradley J. Meites

This investigation attempted to determine whether early limited treatment with agents that either depress or elevate ovarian hormones and/or prolactin could protect rats against induction of mammary cancers by a carcinogen. 155 virgin female rats were treated with hormones or drugs daily for 20 days before and 20 days after a single iv injection of a lipid emulsion containing 5 mg of 7-12-dimethylbenz(a)anthracene (DMBA). Groups received either 20 mcg estradiol benzoate 4 mg progesterone 5 mcg estradiol benzoate and 4 mg progesterone 120 mcg haloperidol 20 mg L-dopa or 5 mg MER-25. Control groups received saline or corn oil injections. At Days 100 114 and 128 after DMBA treatment tumor sizes were recorded and at Day 135 the animals sacrificed. The percentage of animals with tumors the number of tumors per rat and the size of tumors were all reduced in all the treatment groups as compared to controls. The most effective agents were the female steroid hormones. No mammary cancers appeared in the rats given the combination of estrogen and progesterone. L-dopa haloperidol and MER-25 were least effective. Only rats given 20 mcg estradiol benzoate showed a marked loss of body weight and a high mortality rate. The mean latency period of mammary cancers was longer in the treated groups. This investigation showed that early treatment with L-dopa can inhibit development of mammary cancers in DMBA treated rats but that more frequent treatment would have been more effective. Also it was shown that early treatment during a critical period in development of mammary glands in female Sprague-Dawley rats with hormones or drugs that either reduce or elevate ovarian hormones and/or prolactin can act as prophylactic agents against the onset of DMBA-induced mammary cancers. A critical period may also exist for mammary cancer in women and it is possible that with limited early treatment with agents that depress or enhance prolactin and/or gonadal hormone secretion women with high breast cancer risk might be protected against the onset of this disease.

7,12-Dimethylbenz[a]anthracene

Mammary tumor

Corn oil

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Effects of high hoses of estrogen on prolactin-binding activity and growth of carcinogen-induced mammary cancers in rats.

PubMed (1976)

G. S. Kledzik C. J. Bradley Stephen Marshall Gerald A. Campbell J. Meites

Specific binding sites for prolactin (PRL) were present in membrane preparations from 7,12-dimethylbenz(a)-anthracene-induced rat mammary tumors. The specific binding of PRL was time and temperature dependent. A significant negative correlation was noted between administered doses of estrogen and the subsequent binding of PRL to tumor cell membranes. Injections of 10 or 25 mug estradiol benzoate daily for 10 days effectively inhibited mammary tumor growth and significantly reduced specific PRL binding to mammary tumor cell membranes.

Mammary tumor

7,12-Dimethylbenz[a]anthracene

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Prolactin and estrogen dependency of rat mammary cancers at early and late stages of development.

PubMed (1976)

C. J. Bradley G. S. Kledzik J. Meites

An attempt was made to separate estrogen from prolactin dependency of 7,12-dimethylbenz(a)anthracene (DMBA)-induced rat mammary tumors at 2.5 and 5 months after DMBA injection. Ovariectomy and drug and/or hormone treatments were used to produce an estrogen or prolactin deficiency for 2 weeks, followed by a 2-week period in which the deficiency was corrected. Tumors were classified as estrogen or prolactin dependent based upon regression in the absence of the hormone and resumption of growth upon hormone replacement. At 2.5 months and 5 months after DMBA injection, about 29 and 33% of the tumors, respectively, were classified as prolactin dependent, and 35 and 45%, respectively, were classified as estrogen dependent. However, the percentage of estrogen-dependent tumors was reduced to 2.2 and 9.7%, respectively, when prolactin levels were maintained after ovarierctomy. These results indicate that most DMBA-induced mammary tumors in Sprague-Dawley female rats are dependent on both estrogen and prolactin but that ovariectomy or estrogen administration do not accurately reflect estrogen dependency, since prolactin secretion also is altered by these procedures.

Prolactin cell

7,12-Dimethylbenz[a]anthracene

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Citations (55)