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7,12-Dimethylbenz[a]anthracene
About: 7,12-Dimethylbenz[a]anthracene is a research topic. Over the lifetime, 1717 publications have been published within this topic receiving 40892 citations.
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TL;DR: Oral administration of coumestrol did not appear to support the growth of DMBA-induced rat mammary tumors, nor did coummostrol act as an antiestrogen when administered orally in combination with 17 beta-estradiol, but coumstrol administered sc might, however, be able to supportThe growth of these tumors.
Abstract: A number of nonsteroidal estrogens, which are common naturally occurring substances in human foods, were examined for competitive binding to estrogen receptor proteins. These compounds bound competitively to estrogen receptor proteins in rat uterine cytosol, in tissue from 7,12-dimethylbenz[a]anthracene (DMBA)-induced rat mammary tumors, and in human mammary tumor tissue. The relative affinity of these estrogens for rat uterine cytosol receptors paralleled closely the affinities reported for other receptors. Oral administration of coumestrol did not appear to support the growth of DMBA-induced rat mammary tumors, nor did coumestrol act as an antiestrogen when administered orally in combination with 17 beta-estradiol. Coumestrol administered sc might, however, be able to support the growth of these tumors.
115 citations
Journal Article•
TL;DR: It is concluded that insulin administered in vivo appears to display intrinsic growth-stimulating properties on the mammary tumor tissue, similar to those previously demonstrated in organ culture.
Abstract: Summary Administration of insulin for 6 weeks at a daily dose of 2.5 i.u./100 g body weight, together with a 10% glucose solution as drinking fluid, increased tumor growth 8.3-fold as compared with a matched, untreated control group. Administration of insulin alone or of a 10% glucose solution alone produced a smaller yet statistically significant increase (4.8- and 2.2-fold, respectively). In oophorectomized rats, administration of the same dose of insulin, together with the 10% glucose solution for 4 weeks, failed to prevent tumor regression resulting from oophorectomy. On the other hand, in hypophysectomized rats, administration of insulin for 3 weeks at a daily dose of 0.4 to 0.8 i.u./100 g body weight significantly reactivated tumor growth, as compared with a matched control group, when started 21 days after hypophysectomy. Both insulin-treated and control groups received, in addition, a 10% glucose solution and daily s.c. injections of 1.5 mg ovine prolactin; the latter proved by itself incapable of significantly reactivating tumor growth. It is concluded that insulin administered in vivo appears to display intrinsic growth-stimulating properties on the mammary tumor tissue, similar to those previously demonstrated in organ culture. The present study, complementing earlier investigations in alloxan-diabetic rats, provides further evidence suggesting that the rat mammary carcinoma, in addition to being estrogen and prolactin dependent, is also insulin dependent.
115 citations
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110 citations
Journal Article•
TL;DR: The increased sensitivity of SENCAR's was apparent regardless of route of administration of initiator or the age or sex of the mice, which suggests that enhanced metabolic activation of hydrocarbon carcinogens by SENCAR mice is unlikely to account for their sensitivity.
Abstract: In order to define factors which determine susceptibility to chemical carcinogenesis, mice sensitive (SENCAR) and resistant (BALB/c) to epidermal carcinogenesis were studied under several treatment conditions for sensitivity to initiation by 7,12-dimethylbenz(a)anthracene or N -methyl- N ′-nitro- N -nitrosoguanidine and promotion by 12- O -tetradecanoylphorbol-13-acetate. In newborns of both strains, topical application of initiator was much less effective than in adults. However, initiation by i.p. injection of 7,12-dimethylbenz(a)anthracene is at least as effective in newborns as in adults, which may indicate that topically applied carcinogen is not delivered effectively to target cells in newborns. Thus, newborn epidermis can respond to 7,12-dimethylbenz(a)anthracene as well as adult epidermis when the initiator is appropriately administered. SENCAR mice are much more sensitive than are BALB/c mice to both initiators, which suggests that enhanced metabolic activation of hydrocarbon carcinogens by SENCAR mice is unlikely to account for their sensitivity. Newborn male SENCAR's developed approximately 50% more papillomas than did females in all groups. BALB/c newborn mice developed so few tumors that a meaningful comparison of sensitivity of males and females could not be made. Thus, the increased sensitivity of SENCAR's was apparent regardless of route of administration of initiator or the age or sex of the mice. SENCAR mice also developed a significant number of papillomas and squamous cell carcinomas with 12- O -tetradecanoylphorbol-13-acetate promotion in the absence of an exogenous initiator. Therefore, the skin of SENCAR mice may contain an initiated population of cells capable of responding to tumor promoters.
110 citations