retinol-acetate has been researched along with Ovarian-Neoplasms* in 2 studies
2 other study(ies) available for retinol-acetate and Ovarian-Neoplasms
Article | Year |
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Retinyl acetate effects on the life span and the incidence of cryptogenic neoplasms in C3H mice.
The effect of feeding 0.02% retinyl acetate on the development of cryptogenic neoplasms and the life span of C3H/HeJ (+) mice of both sexes was studied. The survival at 105 weeks was 58% in untreated males and 28% in untreated females vs. 39% in treated males and 14% in treated females. The average weight in treated groups was also 10-15% lower. The incidence (percent) of neoplasm-bearing animals and total neoplasms was 87% and 57, respectively, in female controls vs. 93% and 55 in treated females. In male controls, these values were 57% and 39 compared with 50% and 38 in treated males. In treated animals, there was no reduction in the most common neoplasms, that is, neoplasms of the mammary gland and liver. The numbers of ovarian neoplasms and lung adenomas were slightly lower. Therefore, retinyl acetate exerted, at best, only a slight inhibitory effect on development of some types of cryptogenic neoplasms in mice. Topics: Animals; Body Weight; Diterpenes; Female; Hemangioma; Liver Neoplasms, Experimental; Longevity; Lung Neoplasms; Male; Mammary Neoplasms, Experimental; Mice; Mice, Inbred C3H; Neoplasms, Experimental; Ovarian Neoplasms; Retinyl Esters; Vitamin A | 1987 |
Effect of retinyl acetate on the occurrence of ovarian hormone-responsive and -nonresponsive mammary cancers in the rat.
The inhibitory activity of retinyl acetate against the induction of ovarian hormone-responsive and -nonresponsive mammary gland adenocarcinomas was studied in intact and castrated female Sprague-Dawley rats. Three experiments were conducted. Mammary cancer was induced by a single p.o. administration of 7,12-dimethylbenz(a)anthracene (DMBA) at 50 days of age. Animals in Experiments 1 and 2 each received 20 mg DMBA, whereas those in Experiment 3 received 15 mg. In all experiments, animals were fed a chow diet supplemented per kg with either a placebo or 328 mg retinyl acetate starting 7 days after carcinogen treatment. In Experiment 1, rats were castrated at either 7, 60, or 90 days postcarcinogen and were killed 120 days after DMBA was given. In Experiment 2, rats were castrated 30 days after DMBA and were killed 240 days after carcinogen treatment. In Experiment 3, rats were castrated when a detected tumor attained a measurable diameter, and the hormone responsiveness of their tumors was subsequently determined. The experiment was terminated 279 days after DMBA treatment. In both intact and castrated rats, mammary tumor occurrence was inhibited by treatment with retinyl acetate. However, there were no differences in the latency to appearance time of hormone-responsive and -nonresponsive cancers in intact animals receiving either placebo or retinyl acetate. The data indicate that retinyl acetate inhibits DMBA-induced mammary tumorigenesis in either the presence or the absence of the ovaries. It appears that retinyl acetate is effective in inhibiting both ovarian hormone-responsive and -nonresponsive mammary tumors. Topics: 9,10-Dimethyl-1,2-benzanthracene; Adenocarcinoma; Animals; Castration; Diet; Diterpenes; Female; Mammary Neoplasms, Experimental; Ovarian Neoplasms; Rats; Rats, Inbred Strains; Retinyl Esters; Time Factors; Vitamin A | 1982 |