retinol-acetate and Adenocarcinoma

The analysis of clinical and immunologic findings indicate that retinol and decaris influence functional activity of immune cells at stage II of lung cancer irrespective of histological structure. In stage III, retinol induced changes in proportion of lymphocyte subpopulations, more evident in glandular cancer. Both immunomodulators lowered the number of purulent complications after surgical interventions. It is only retinol that influenced metastatic dissemination in lung cancer stage II-III.

Topics: Adenocarcinoma; Adjuvants, Immunologic; Adult; Carcinoma, Squamous Cell; Combined Modality Therapy; Diterpenes; Humans; Levamisole; Lung Neoplasms; Lymphocyte Subsets; Male; Middle Aged; Neoplasm Metastasis; Preoperative Care; Retinyl Esters; Vitamin A

The chemopreventive actions of sodium selenite (SS), magnesium chloride (MC), ascorbic acid (AA) and retinyl acetate (RA), given singly or in combinations, on mammary carcinogenesis induced by 30 mg of 7,12-dimethylbenz[a]anthracene (DMBA) in female adult rats were evaluated. Administration of modulators was carried out from the age of 40 +/- 3 days to 240 +/- 3 days. When DMBA alone was given 100% of the rats developed mammary tumors. When modulators were given singly the tumor incidences were reduced to 51.77% (SS), 46.4% (MC), 57.1% (AA) and 48.1% (RA). When the modulators were given in combination of twos, the tumor incidences were further reduced to 29.5% (SS + MC), 31% (SS + AA), 29.6% (SS + RA), 25.9% (MC + AA), 31.8% (MC + RA) and 34.6% (AA + RA). Administration of modulators in combinations of threes resulted in still further reduction of tumor incidences to 22.2% (SS + MC + AA), 19.2% (SS + MC + RA), 16% (MC + AA + RA) and 23.1% (AA + RA + SS). When all four modulators were given concurrently the tumor incidence was only 12%. Further, the number of tumors per tumor-bearing animal declined with the increase in the number of agents used in combination for modulation.

Topics: 9,10-Dimethyl-1,2-benzanthracene; Adenocarcinoma; Adenofibroma; Animals; Antineoplastic Combined Chemotherapy Protocols; Ascorbic Acid; Body Weight; Diterpenes; Drug Administration Schedule; Female; Magnesium Chloride; Mammary Neoplasms, Experimental; Rats; Retinyl Esters; Selenic Acid; Selenium; Selenium Compounds; Vitamin A

The effects of feeding menhaden oil (MO), rich in omega-3 fatty acids, or supplemental vitamin A [as retinyl acetate (RA)], on the growth of DU 145 human prostate cancer cells were studied in athymic nude mice. The mice were fed AIN-76A diets containing either 23% corn oil (CO), a mixture of 17% MO and 6% CO, or 23% CO plus RA. After irradiation sterilization, the RA-supplemented diet was found to contain approximately 15 times the amount of vitamin A present in the control diet. There were 24 mice in each dietary group. Three weeks after commencement of feeding the experimental diets, 1 x 10(6) or 5 x 10(6) DU 145 cells were inoculated into subgroups of 12 animals, and the appearance and growth of solid tumors followed over a 6-week period. There was no significant difference in tumor latency between mice fed MO plus CO, and those fed CO alone, regardless of the inoculum size. However, the appearance of palpable tumors was more rapid in mice inoculated with 5 x 10(6) cells and fed the RA-supplemented CO diet (91% after 17 days) compared with mice receiving the same tumor cell load but fed the unsupplemented CO diet (55% after 17 days). Growth of the solid tumors was retarded significantly in mice inoculated with 1 x 10(6) cells and fed the MO-containing diet compared with the CO controls; this effect was not evident in animals who received 5 x 10(6) cells. RA supplementation caused accelerated tumor growth, which, again, only achieved statistical significance in the group inoculated with 1 x 10(6) cells.

Topics: Adenocarcinoma; Animals; Cell Division; Diet; Diterpenes; Fish Oils; Humans; Male; Mice; Mice, Nude; Neoplasm Transplantation; Pancreatic Neoplasms; Retinyl Esters; Transplantation, Heterologous; Vitamin A

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

Pancreatic carcinomas have been induced in Wistar and W/LEW rats by administration of total azaserine doses of 150-520 mg/kg by injection or oral routes over periods of 5-52 weeks. The latent period for development of invasive carcinomas was 1-2 years, but focal abnormalities in acinar cells appear earlier. The incidence of carcinomas varied with total dose, route, and schedule of azaserine administration. The spectrum of histologic patterns of the carcinomas included well and poorly differentiated acinar cell, ductlike, and undifferentiated carcinomas. Rats fed a purified diet developed more pancreatic neoplasms than rats fed a commercial laboratory chow. Selective feeding of these diets during the administration of carcinogen and following completion of carcinogen treatment indicated that the inhibitory effect of chow on pancreatic carcinogenesis was exerted during the postinitiation phas. Supplementation of diet with 0.025% retinyl acetate during the postinitiation phase also inhibited the progression of azaserine-induced lesions in the pancreas.

Topics: Adenocarcinoma; Animals; Azaserine; Carcinoma; Cell Transformation, Neoplastic; Cytoplasmic Granules; Diet; Diterpenes; Enzyme Precursors; Male; Neoplasms, Experimental; Pancreatic Neoplasms; Rats; Rats, Inbred Lew; Rats, Inbred Strains; Retinyl Esters; Vitamin A

The effect of the duration of retinoid treatment on the inhibition of 1-methyl-1-nitrosourea-induced mammary carcinogenesis was studied. Female Sprague-Dawley rats were given i.v. injections of 50 mg 1-methyl-1-nitrosourea per kg body weight at both 50 and 57 days of age. Feeding of a placebo diet or diet supplemented with 323 mg retinyl acetate per kg diet (retinoid treatment) was initiated at 10 days after the first carcinogen injection. Retinoid treatment was either continued or discontinued after 60 days postcarcinogen, and the study was terminated at 182 days postcarcinogen. Retinoid treatment between 10 and 60 days postcarcinogen prolonged the cancer latency and reduced the average number of cancers per rat in comparison to that in placebo-treated rats. Continuation or cessation of retinoid treatment in 60-day tumor-bearing rats had no effect on the time of appearance of additional cancers. In 60-day tumor-free rats, continuation of retinoid treatment prolonged cancer latency in comparison to either 60-day tumor-free rats changed to placebo or rats continuously treated with placebo. The cessation of retinoid treatment in 60-day tumor-free rats resulted in a rapid increase in the appearance of cancers; at the termination of the study, the average number of cancers per rat was similar to that of animals fed only the placebo. The data indicated that some rats are more responsive to the retinoid than are others. Retinoid treatment apparently prevented the progression of early neoplastic lesions, and a continuous daily intake of the retinoid appears necessary to sustain the chemopreventive effect under the experimental conditions imposed.

Topics: Adenocarcinoma; Animals; Diterpenes; Female; Mammary Neoplasms, Experimental; Methylnitrosourea; Nitrosourea Compounds; Rats; Retinyl Esters; Time Factors; Vitamin A