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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Prolactin and estrogen dependency of rat mammary cancers at early and late stages of development. 81 59

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.
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PMID:Stimulation of carcinogen-induced mammary tumor growth in rats by adrenalectomy. 81 63

The persistence and proliferation rate of mouse skin papillomas were studied in HA/ICR mice initiated with 7,12-dimethylbenz(a)anthracene and promoted three times weekly with phorbol myristate acetate. When the promoter treatments were stopped, rapid (half-time, 24 days) and slow (half-time, greater than 140 days) components of papilloma regression were observed. When the promoter dose was increased, the major effect was an increase among the rapidly regressing papillomas. Increases in the epidermal pulse-labeling index and the number of dermal inflammatory cells produced by phorbol myristate acetate in normal skin were reversible when the phorbol myristate acetate was stopped, but high pulse-labeling index values in papillomas were not reversible. Antithymocyte serum had no effect on regression, although ethylphenylpropriolate, a nonpromoting irritant, slowed the regression sufficiently to increase the half-time from 24 to 57 days. The action of the promoter in overcoming the regression tendency of the papillomas may explain certain features of the role of nonspecific irritation and the importance of promotion frequency in determining tumor yield.
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PMID:Regression kinetics of mouse skin papillomas. 81 64

Female rats have been fed high fat diets containing either polyunsaturated or saturated fat. After being fed either of the diets for 4 weeks, some of the animals received an intragastric dose of 7,12-dimethylbenz(a)anthracene (DMBA). At this point, the diets of half of the animals were interchanged so that animals previously fed the polyunsaturated fat diet were fed the saturated fat diet and vice versa. The cumulative incidence of tumor-bearing rats among DMBA-dosed rats was greater when the polyunsaturated fat diet was fed. The mean induction time of tumors decreased and the proportion of tumor-bearing rats which developed malignant tumors increased when the polyunsaturated fat diet was fed. This promotional effect of the polyunsaturated fat diet was exerted only when the diet was fed after DMBA administration.
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PMID:Effect of dietary fats on the incidence of 7,12-dimethylbenz(a)-anthracene-induced tumors in rats. 81 1

After an introduction to the "Session on Skin" emphasizing that some early biochemical changes occurring in the two-stage model system for skin would be presented in the three following presentations, several background experiments were discussed. It was shown that a complete carcinogen for the skin (7,12-dimethylbenz[a]anthracene) provides both initiating and promoting components, but as the dose level of the carcinogen is lowered its promoting activity is lost while its initiating activity is retained. At the dose level that is completely carcinogenic, 7,12-dimethylbenz[a]anthracene exhibits the properties of a promoter; it stimulates RNA, protein, and DNA synthesis followed by cell division. At initiating doses, both the biochemical and morphological (increased mitosis) responses to treatment that are characteristic of promoters are lost; the remaining biochemical effects involve DNA and are attributed to initiating action. Some of the data supporting the concept that the mechanism of action of tumor promotion involves gene activation were reviewed.
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PMID:The biochemistry of preneoplasia in mouse skin. 81 31

Hyperplastic-metaplastic lesions were produced in transplanted rat tracheas by exposure to 310 or 75 mug 7,12-dimethylbenz(a)anthracene or to 650 mug benzo(a)pyrene delivered over a 2-week exposure period. Tissue recovery was studied for up to 16 weeks. After cessation of carcinogen exposure, most of the hyperplastic-metaplastic epithelium was rapidly replaced by mucociliary epithelium. In the 7,12-dimethylbenz(a)anthracene-exposed tracheas, a few mataplastic foci remained at 4 and 8 weeks. In all 3 exposure groups, portions of the mucosa were occupied by atrophic-pleomorphic epithelium that persisted throughout the observation period. The significance of these lesions in the evolution of neoplasia is as yet unknown. In vitro studies with epithelial cells derived from 7,12-dimethylbenz(a)anthracene-exposed tracheal transplants revealed that some cells have acquired a growth potential that is markedly different from that of normal mucociliary epithelium. This altered in vitro growth potential of epithelial cells may be an early indicator of an important event in the evolution of epithelial transformation in vivo.
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PMID:Fate of early carcinogen-induced lesions in tracheal epithelium. 81 32

Two hemopoietic tumors induced in rats by Gross leukemia virus and dimethylbenz(a)anthracene, respectively, display distinctive and consistent patterns of metastases, the former in the thymus and lymph nodes, the latter in the liver and spleen. To investigate the role of circulatory anatomy in the localization of metastases, 51Cr-labeled cells were injected i.v., and their distribution was followed at various intervals. To explore the influence of immune mechanisms, Gross leukemia virus- and dimethylbenza(a)anthracene-induced leukemic cells as well as a line of antigenically modulated cells were administered to newborn, X-irradiated, and immunologically unresponsive recipients. The circulation of tumor cells through various organs was indiscriminate. The immune response of the host was operative in limiting the local and metastatic tumor growth but not in determining the site of secondary tumors. The conclusion of these experiments was that the selective organ distribution of tumor metastases was solely dependent on intrinsic cellular properties.
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PMID:Role of immune mechanisms in metastatic patterns of hemopoietic tumors in rats. 81 34

Experiments designed to study the changes in prolactin (PRL) binding to rat mammary tissue and liver during pregnancy and lactation, to study the relationship between PRL binding and growth in 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary tumors and to measure PRL binding in DMBA tumors, lactating mammary gland and liver following administration of pharmacological doses of estrogen are described. Specific binding of radioactive PRL binding to mammary gland increased throughout late pregnancy and early lactation, reached a maximum on Day 11 of lactation and then declined. Maximum binding to liver membrane preparations was observed during late pregnancy and declined throughout lactation. The administration of 20 mcg estradiol benzoate (EB/day on Days 5-10 of lactation, reduced PRL binding to mammary gland by 55%, increased binding to liver 2-fold and reduced litter weight gain by 25%. PRL binding to DMBA-induced mammary tumor was 3 times higher than that observed in lactating mammary gland. PRL administration enhanced tumor growth but decresed specific PRL binding to tumors. Lergotrile mesylate inhibited and 2 mcg EB enhanced tumor growth, but neither treatment affected PRL binding to tumor membrane preparations. However, 20 mcg EB inhibited tumor growth and reduced PRL binding. PRL binding varied widely within all groups of mammary tumors and was not clearly related to growth response or to altered circulating estrogen and/or PRL levels. It is concluded that hormone dependence in the rat tumor model is complex and may not be predicted on the basis of PRL-binding capacity alone.
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PMID:Prolactin binding to mammary gland, 7,12-dimethylbenz(a)-anthracene-induced mammary tumors, and liver in rats. 82 5

Malignant melanoma has been induced in the Weiser-Maple guinea pig by prolonged application of 7,12-dimethylbenz(a)anthracene. The tumor shows a biphasic growth pattern analogous to the radial and vertical growth phase of human cutaneous malignant melanoma. It evolves through a predictable series of cellular events classified as intraepidermal melanocytic hyperplasia, dermal melanocytosis, dermal melanocytoma, malignant melanoma without intralesional transformation, and, finally, malignant melanoma with intralesional transformation, which is characterized by the appearance of "new kinds of cells" and is associated with widespread metastases and massive lymph node involvement. Clinically, the lesions evolve from diffuse hyper-pigmentation to brown-black macules, to nodules of increasing size, to overt malignant melanoma associated with metastases, wasting, and death. Examples of intralesional transformation analogous to that in guinea pigs are found not only in human malignant melanomas, but in other human neoplastic systems, and such analogous cellular events are discussed in this paper.
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PMID:The developmental biology of induced malignant melanoma in guinea pigs and a comparison with other neoplastic systems. 82 48

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.
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PMID:Effects of high hoses of estrogen on prolactin-binding activity and growth of carcinogen-induced mammary cancers in rats. 82 50


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