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Journal ArticleDOI

Comparison of Ovariectomy and Retinyl Acetate on the Growth of Established 7,12-Dimethylbenz[a]anthracene-Induced Mammary Tumors in the Rat

TLDR
If treatment with RA is delayed until 6 months after carcinogen administration, the protective effect of RA can still be observed although its effectiveness is less dramatic than when it is administered earlier.
Abstract
Prolonged exposure to retinyl acetate (RA) in the diet inhibits the development of 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary cancers in rats. The effectiveness of RA was examined when given 6 months after the administration of DMBA. Non-inbred female Sprague-Dawley rats with DMBA-induced mammary tumors were divided into 3 groups and treated for 4 weeks as follows: Group 1 served as controls, group 2 was ovariectomized, and group 3 received 328 mg RA/kg diet. Ovariectomy (OVX) markedly reduced both the number and size of the tumors. RA administration failed to induce any significant regression in tumor number but significantly retarded tumor growth when compared to tumor growth in group 1 controls. The levels of estradiol, progestin, and prolactin (PRL) receptors were significantly reduced after OVX, whereas only the levels of PRL receptors declined significantly after RA administration. Circulating progesterone concentrations were not affected in the RA-treated group but the plasma PRL level was significantly increased. The present studies show that if treatment with RA is delayed until 6 months after carcinogen administration, the protective effect of RA can still be observed although its effectiveness is less dramatic than when it is administered earlier.

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Journal ArticleDOI

Timing of Dietary Estrogenic Exposures and Breast Cancer Risk

TL;DR: The results indicate that the estrogen receptor, mitogen‐activated protein kinase (MAPK), and the tumor suppressors BRCA1, p53, and caveolin‐1 are among the genes affected by diet‐induced alterations in programming/reprogramming.
Journal ArticleDOI

Modulation of normal mammary epithelial cell proliferation, morphogenesis, and functional differentiation by retinoids: a comparison of the retinobenzoic acid derivative RE80 with retinoic acid.

TL;DR: Several mechanisms may contribute to the chemopreventive and/or therapeutic efficacy of retinoids in breast cancer, including inhibition of proliferation, stimulation of cell death, and/ or induction of differentiation.
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Metabolism of Retinol and Retinoic Acid in N-Methyl-N-nitrosourea-induced Mammary Carcinomas in Rats

TL;DR: In this study, endogenous retinol and retinyl esters were present in normal mammary epithelial cells, but were undetectable in N-methyl-N-nitrosourea-induced mammary carcinomas in rats as determined by high-pressure liquid chromatography.
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Comparison of the Therapeutic Effects of a New Arotinoid, Ro 40-8757, and All-trans- and 13-cis-Retinoic Acids on Rat Breast Cancer

TL;DR: The high efficacy and relatively low toxicity of 4-((2-(p-[(E)-2-(5,6,7,8-tetrahydro-5,5,8,8 -tetramethyl-2- naphthyl)propenyl]phenoxy)ethyl))-morpholine suggest that it may be a promising new anticancer agent.
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Inhibition of growth of established N-methyl-N-nitrosourea-induced mammary cancer in rats by retinoic acid and ovariectomy.

TL;DR: The dietary supplementation with RA decreased the progression or stabilized the growth of the majority of tumors and only rarely induced tumor regression, and no additive or synergistic effects were found with the combination of RA and ovariectomy.
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