Prolactin levels and molecular heterogeneity in rat strains with high and low incidence of DMBA-induced mammary tumors

Lawson, David M.; Sensui, Naoto; Haisenleder, D.H.; Kaufman, PA; Gala, Richard R.

doi:10.1007/bf01806395

Cited by 3 publications

(4 citation statements)

References 13 publications

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“…Evans rat, but such surges were not well-organized in Sprague-Dawley rats of the same age (7). The current data did not show a circadian pattern comparable to that shown in our earlier report, but the full 24-hr day was not examined in the current study.…”

Section: Discussioncontrasting

confidence: 59%

“…Carcinogens like 7,12-dimethylbenz [a] anthracene are most effective when administered to susceptible strains of rats at 10-20 days after the onset of puberty, and this is apparently due to rapid cell division in the mammary gland at this time (9). We (7), and others (lo), have shown that strains of rats that are susceptible to mammary tumor induction have different patterns of prolactin secretion than those strains that are resistant to mammary tumor formation. This is particularly true in rats at the time when carcinogen is most effective.…”

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confidence: 96%

“…Sprague-Dawley rats are quite susceptible to carcinogen-induced mammary tumors, whereas the Long-Evans rat is very resistant (7,8). Carcinogens like 7,12-dimethylbenz [a] anthracene are most effective when administered to susceptible strains of rats at 10-20 days after the onset of puberty, and this is apparently due to rapid cell division in the mammary gland at this time (9).…”

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confidence: 97%

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A Comparison of Plasma Prolactin Levels in Young Female Long-Evans and Holtzman Rats as Measured by Nb2 Lymphoma Bioassay and Radioimmunoassay

Cannon

et al. 1991

Experimental Biology and Medicine

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This study was conducted to determine the plasma levels of prolactin in prepubertal and young, postpubertal, proestrus rats of mammary tumor-susceptible (Sprague-Dawley) and tumor-resistant (Long-Evans) strains using a sensitive bioassay-Nb2 lymphoma cell replication. Prepubertal Long-Evans rats had significantly higher levels of prolactin than did Holtzman Sprague-Dawley rats of the same age. Likewise, Long-Evans rats secreted significantly more prolactin into the blood on the afternoon and evening of proestrus than did Holtzman rats. Finally, ovariectomized Long-Evans rats released more prolactin into the blood at 1 day, but not at 8 or 15 days, of treatment with diethylstilbestrol. Prolactin levels determined by conventional radioimmunoassay and by bioassay were similar except on the afternoon of proestrus, when, in both strains of rats, the bioassay to radioimmunoassay ratio increased significantly above 1.0 during the late evening. In addition, the ratio was significantly less than 1.0 in the early and late afternoon in the Holtzman rats, but not Long-Evans rats. These data indicate that a strain of rats that is resistant to experimentally induced mammary cancer has higher prolactin levels in the blood than does a strain that is susceptible to mammary cancer at a time when mammary gland growth is rapid. Furthermore, there are times during the proestrus prolactin surge when the bioassay yielded higher and lower values of prolactin than radioimmunoassay of the same samples, suggesting functional heterogeneity of prolactin that may impact on mammary gland or other target tissue function.

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Section: Discussioncontrasting

confidence: 59%

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confidence: 96%

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confidence: 97%

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A Comparison of Plasma Prolactin Levels in Young Female Long-Evans and Holtzman Rats as Measured by Nb2 Lymphoma Bioassay and Radioimmunoassay

Cannon

et al. 1991

Experimental Biology and Medicine

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“…The involvement of prolactin (PRL) and growth hormone (GH) in growth regulation of human breast cancer cells is still unclear, although numerous experimental data obtained with rodents support the contention that PRL is important in growth and development of their mammary tumors [e.g. [1][2][3]. The binding of human GH to the lactogenic receptor of human breast cancer cells in vitro and in vivo may also cause growth stimulatory effects [4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

The somatostatin analog Sandostatin (SMS201-995) in treatment of DMBA-induced rat mammary tumors

Bakker

Setyono-Han

Foekens

et al. 1990

Breast Cancer Res Tr

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The effects of treatment with a somatostatin analog (Sandostatin, SMS201-995) were investigated in female rats with dimethylbenzanthracene (DMBA)-induced rat mammary tumors. A 3-week treatment was performed using sandostatin, the LHRH-agonist buserelin alone, or buserelin in combination with sandostatin. Twice daily sandostatin treatment was performed with dosages of 0.05 microgram, 0.2 microgram, 1 microgram, 5 micrograms, and 20 micrograms. Buserelin was used in a 2 x 5 micrograms/day dosage. The combined results from six different experiments show that the various dosages of sandostatin caused no tumor growth inhibition. Somatostatin receptors could not be demonstrated in these mammary tumors. Sandostatin treatment by daily injections did not suppress levels of growth hormone, prolactin, or epidermal growth factor-like activities. Estrogen (ER) and progesterone (PgR) receptor contents of the mammary tumors were not changed. In contrast, buserelin treatment caused highly significant tumor remission. The combined treatment with sandostatin and buserelin did not alter the treatment results obtained after treatment with buserelin alone. In conclusion, sandostatin treatment in this tumor model had no direct growth inhibitory effect and did not cause an endocrine inhibition of mammary tumor growth. However, these results do not exclude antitumor effects in human breast cancer in view of the presence of somatostatin receptors in approximately 20-45% of human tumors, besides possible different endocrine effects.

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Pineal melatonin inhibition of tumor promotion in theN-nitroso-N-methylurea model of mammary carcinogenesis: potential involvement of antiestrogenic mechanisms in vivo

Blask

Pelletier

Hill

et al. 1991

J Cancer Res Clin Oncol

103

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The N-methyl-N-nitrosourea (NMU) model of hormone-responsive rat mammary carcinogenesis was used to address the hypothesis that melatonin (Mel), the principle hormone of the pineal gland, inhibits tumorigenesis by acting as an anti-promoting rather than an anti-initiating agent. Daily late-afternoon injections of Mel (500 micrograms/day), restricted to the initiation phase of NMU mammary tumorigenesis, were ineffective in altering tumor growth over a 20-week period. When Mel treatment was delayed for 4 weeks after NMU and then continued through the remainder of the promotion phase, only tumor number was significantly lower than in controls. However, when Mel injections encompassed the entire promotion phase, both tumor incidence and number were significantly lower than in the controls. Although elimination of the endogenous Mel signal via pinealectomy promoted tumor growth, the effect was not statistically significant. Serum levels of estradiol and tumor estrogen receptor content were unaltered by either Mel or pinealectomy. While Mel treatment failed to affect circulating prolactin levels, pinealectomy caused a two-fold increase in serum prolactin. The estradiol-stimulated recrudescence of tumors following ovariectomy was completely blocked by either 20, 100 or 500 micrograms Mel/day or tamoxifen (20 micrograms/day). Thus, Mel appears to be an anti-promoting hormone that may antagonize the tumor-promoting actions of estradiol in this model of mammary tumorigenesis.

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Prolactin levels and molecular heterogeneity in rat strains with high and low incidence of DMBA-induced mammary tumors

Cited by 3 publications

References 13 publications

A Comparison of Plasma Prolactin Levels in Young Female Long-Evans and Holtzman Rats as Measured by Nb2 Lymphoma Bioassay and Radioimmunoassay

A Comparison of Plasma Prolactin Levels in Young Female Long-Evans and Holtzman Rats as Measured by Nb2 Lymphoma Bioassay and Radioimmunoassay

The somatostatin analog Sandostatin (SMS201-995) in treatment of DMBA-induced rat mammary tumors

Pineal melatonin inhibition of tumor promotion in theN-nitroso-N-methylurea model of mammary carcinogenesis: potential involvement of antiestrogenic mechanisms in vivo

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