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

Female Sprague-Dawley rats were fed semipurified diets containing various fats, either alone or in combination, to provide different amounts of dietary fat and linoleic acid. One week before commencing the diets, each rat received an intra-gastric dose of the carcinogen 7,12-dimethylbenz[a]anthracene. Rats fed diets containing mixtures of 3% sunflower seed oil and 17% of either tallow or coconut oil developed twice as many tumors as those fed 3% sunflower seed oil or 20% of either saturated fat alone. Tumor yields in the rats fed these mixed-fat diets were comparable to those in rats fed a 20% lard diet, which provided about the same amount of linoleic acid. No further increase in tumor yield was observed in rats fed a 20% sunflower seed oil diet that contained more than five times as much linoleic acid. These results show that a certain amount of polyunsaturated fat, as well as a high level of dietary fat, is required to promote mammary carcinogenesis.
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PMID:Relationship between amount and type of dietary fat in promotion of mammary carcinogenesis induced by 7,12-dimethylbenz[a]anthracene. 10 58

The abilities of the racemic trans-3,4-, 5,6-, and 8,9-dihydrodiols of 7,12-dimethylbenz(a)anthracene to initiate skin tumors in mice were determined by using a two-stage system of tumorigenesis. The 7,12-dimethylbenz(a)anthracene trans-3,4-dihydrodiol was found to be much more active as a tumor initiator than the parent hydrocarbon. The 7,12-dimethylbenz(a)anthracene trans-5,6- and 8,9-dihydrodiols were essentially inactive as skin tumor initiators. Our results suggest that the 3,4-dihydrodiol of 7,12-dimethylbenz(a)anthracene is a proximal carcinogen and that the "bay region" diol-epoxide may be the ultimate carcinogenic form of DMBA.
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PMID:Potent tumor-initiating activity of the 3,4-dihydrodiol of 7,12-dimethylbenz(a)anthracene in mouse skin. 10 89

4a alpha-Phorbol-9,9a-didecanoate, 4a alpha-phorbol-9-myristate-9a-acetate, and phorbol-9-myristate-9a-acetate-3-aldehyde were tested for skin tumor-promoting activity by using 7,12-dimethylbenz(a)anthracene as the initiating agent. There were 30 female ICR/Ha mice/group, and tests were continued for 434 to 461 days. 4a alpha-Phorbol-9,9a-didecanoate and 4a alpha-phorbol-9-myristate-9a-acetate were devoid of tumor-promoting activity. Phorbol-9-myristate-9a-acetate-3-aldehyde resulted in 10 mice with papillomas, 2 of which also bore squamous carcinomas of the skin. The positive control group, in which phorbol myristate acetate was used as promoting agent, resulted in 30 mice bearing multiple papillomas and 15 bearing squamous carcinomas of the skin. The effects of structural and stereochemical changes on tumor-promoting activity suggest that a primary interaction of the phorbol ester series is binding at specific sites on the plasma membrane.
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PMID:Effects of structural changes on the tumor-promoting activity of phorbol myristate acetate on mouse skin. 10 95

Prophylactic effect of repeated intravenous administrations of oil-attached BCG cell-wall skeleton (BCG-CWS) on the induction of tumor by 7,12-dimethylbenz[a]anthracene (DMBA) was investigated in various strains of mice. The subcutaneous injection of DMBA emulsified in oil induced squamous cell carcinoma in almost all of the strains of mice. Treatment of C57BL/6, BALB/c, and ddO strains with BCG-CWS with appropriate route and timing resulted in the retardation of DMBA-induced tumor development manifested by a prolonged latent period of tumor outgrowth. In contrast, the same BCG-CWS treatment of C3H/He and BTK mice was incapable in preventing such DMBA-induced carcinogenesis. Thus, the treatment with BCG-CWS was effective for preventing the DMBA-induced carcinogenesis in certain strains of mice, but the effectiveness varied depending on the strain. The implication of such a strain variationof the BCG-CWS effect on the prophylaxis of chemical carcinogenesis was discussed in the context of differences in the magnitude of immunopotentiation of the host by BCG-CWS.
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PMID:Prophylactic effect of BCG cell-wall skeleton on the tumor induction by 7,12-dimethylbenz[a]anthracene in mice: strain difference. 10 42

The presence or absence of estrogen receptors in the nuclei of human breast tumor may be a useful tool in determining whether the tumor will or will not respond to endocrine therapy. This paper describes an assay which measures both unoccupied and occupied nuclear receptors in human breast cancer tumors. The assay was predicated on the fact that at low salt concentration, the nuclear receptor is bound to chromatin particles and can be separated from the soluble components containing proteolytic acitivity. Nuclear estradiol receptors were measured in human breast cancer tissue (MCF-7 cell line) and in DMBA (dimethylbenz(a)anthracene-induced rat mammary carcinomas) tumors. Complete translocation of the cytoplasmic receptor in the MCF-7 cells was observed compared to only 35-50% of the cytoplasmic receptors seen in the nucleus of the DMBA tumor after estradiol injection. The study also showed 6 pmol/mg DNA for total unoccupied nuclei and cytoplasmic estrogen receptors, and 25% of it in the nucleus; this finding differed from Zava et al's finding of 2 pmol/mg DNA and 75% in the nucleus, probably because of differing methodology or use of a later passage of cell line. 29 out of the 34 tumors with cytoplasmic receptors were found to contain unoccupied nuclear receptors, indicating that free nuclear receptors are not exceptions. The assay used in this study is currently being used to determine the translocative ability of the cytoplasmic receptors in human breast carcinomas.
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PMID:Estradiol binding to nuclear receptors in human breast cancer tissue (MCF-7 cell line) and in dimethylbenz(a)anthracene-induced mammary carcinoma. 10 64

The effects of repeated low-dose-rate, high-dose-rate X-radiation of the head and neck on lingual tumor induction by 7,12-dimethylbenz[a]anthracene (DMBA) in Syrian golden hamsters were studied. Animals received either topical application as 0.5% DMBA in acetone on the lateral middle third of the tongue three times a week for 15 consecutive weeks, 20-R X-radiation exposures of the head and neck once a week for 15 consecutive weeks, or concurrent radiation and DMBA treatments for 15 consecutive weeks. Animals were examined visually at regular intervals, and all were killed 35 weeks after the start of treatments. All tissues were than examined histopathologically. Animals receiving radiation alone had no detectable changes. Animals receiving DMBA plus radiation had an excess of papillomas compared to animals receiving only DMBA (35% vs. 15%). In addition, an excess of nonlingual oral tumors (lip, gingiva, and floor of mouth) was found in DMBA-treated plus radiation-treated animals versus DMBA-treated animals. These results suggest that repeated, localized, low-level X-radiation exposures enhance chemical tumorigenesis in a variety of oral tissues of Syrian golden hamsters.
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PMID:Effects of low-level X-radiation on 7,12-dimethylbenz[a]anthracene-induced lingual tumors in Syrian golden hamsters. 10 94

Benzo[e]pyrene (B[e]P) inhibited 7,12-dimethylbenz[a]anthracene (DMBA) skin tumor-initiation in mice by 84%, whereas pyrene and fluoranthene inhibited DMBA initiation by 50 and 34%, respectively. However, B[e]P, pyrene and fluoranthene had either no significant effect or a slight enhancing effect on benzo[a]pyrene (B[a]P) skin tumor-initiation. In addition, B[e]P had essentially no effect on the initiating ability of (+/-)B[a]P-7 beta,8 alpha-diol-9 alpha,10 alpha-epoxide. As a tumor-initiator, B[e]P was found to have very weak activity at a 252 microgram/level (0.4 papillomas/mouse at 40 weeks) and no activity at 100 microgram. When given at a dose of 100 microgram twice weekly, B[e]P induced 2.1 papillomas/mouse at 30 weeks, and 25% of the mice had carcinomas at 40 weeks. However, B[e]P carcinogenic activity is weak when compared to B[a]P, which can induce a comparable tumor response at a dose of 5 microgram twice weekly. When B[e]P was tested as a tumor promoter at a dose of 100 microgram twice weekly after DMBA initiation, it induced 4.5 papillomas/mouse at 30 weeks and a 45% carcinoma incidence at 40 weeks, which was approximately twice as effective as B[e]P alone. The data show that B[e]P is a very weak tumor initiator, a weak complete carcinogen, a moderate tumor promoter, possibly a weak co-tumor-initiator when given with B[a]P, and a potent anit-tumor-initiator when given with DMBA. The anti-tumor initiating and co-tumor-initiating effects of B[e]P appear to be related to its ability to modify the conversion of the tumor initiator into an electrophilic intermediate(s) which are capable of covalently binding to DNA. In addition, B[e]P induced epidermal cellular proliferation which may be related to its promoting ability.
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PMID:The effects of weak or non-carcinogenic polycyclic hydrocarbons on 7,12-dimethylbenz[a]anthracene and benzo[a]pyrene skin tumor-initiation. 11 Apr 41

The effects of a vitamin A analog, TMMP ethyl retinoate [or ethyl-9-(4-methoxy-2,3,6-trimethylphenyl)-3,7-dimethyl-trans-2,4,6,8-nonatetraenoate] (abbreviated Ro 10-9359), and an anti-inflammatory steroid, fluocinolone acetonide (or 6 alpha, 9 alpha-difluoro-11 beta, 16 alpha, 17,21-tetrahydroxypregna-1,4-diene-3,20-dione cyclic 16,17-acetal) (abbreviated FA), given alone or together were studied in a two-stage carcinogensis system. The phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) was used as the tumor promoter in a 7,12-dimethylbenz[a]anthracene (DMBA)-initiated mouse skin system. Two stocks of female mice, CD-1 and Sencar, which differ in their degrees of sensitivity to skin carcinogenesis, were used. A dose-dependent inhibition of carcinogenic expression, as determined by a decreased number of papillomas per animal, was observed in each mouse stock with the use of both FA and Ro 10-9359 when given alone. When FA and Ro 10-9359 were given together, an enhanced effect on the lowering of tumor incidence was noted. FA effectively inhibited tumor formation in the sensitive mouse stock even when the steroid was given 1 day prior to TPA treatment under conditions of unusually high doses of initiator (DMBA) and/or promoter (TPA). These results suggest that both anti-inflammatory steroids and retinoids inhibit tumor promotion and can be effectively used as a combination regimen for increased chemopreventive response.
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PMID:Inhibition of phorbol ester-induced tumor promotion in mice by vitamin A analog and anti-inflammatory steroid. 11 Sep 70

A gonadoliberin analog, (D-leucyl6, desglycyl-NH2(10), prolyl ethylamide9) gonadoliberin, is known to suppress ovarian function and plasma prolactin levels. Its antitumor activity was evaluated against mammary tumors induced in Sprague-Dawley rats by dimethylbenz(a)anthracene. Observations were made when the analog, referred to as A-43818, was given alone and together with estrogen replacement or perphenazine, A-43818, 10 microgram s.c. twice a day for 6 weeks, was highly effective in producing tumor remissions. All of the 11 animals survived throughout the observation period, complete regressions occurred in 8 of 13 tumors, and 2 were classified as static. None of the 16 tumors in 12 control rats regressed, and there were 4 deaths. When estradiol benzoate, 2 microgram s.c. each day, was administered with the A-43818, antitumor activity was suppressed; only 2 of 17 tumors regressed, 6 were static, and 5 of the 10 rats in this group died. Perphenazine, 1 mg i.m. daily, a dose known to cause hyperprolactinemia, also impaired the efficacy of A-43818. Three of 14 tumors regressed, 6 were static, and the rest continued to grow; 3 of the 12 rats died within 6 weeks of starting treatment.
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PMID:Modification of the effect of a gonadoliberin analog on 7,12-dimethylbenz(a)anthracene-induced rat mammary tumors by hormone replacement. 11 83

A single oral administration of 7,12-dimethylbenz[a]anthracene (DMBA) 2 weeks after intrasplenic grafting of ovarian tissue in unilaterally ovariectomized C3HeB/Fe mice resulted in a high tumor incidence (47%) in the grafted tissue, with only 1 tumor (3%) in the orthotopic ovary. No tumors were seen in the control group (unilaterally ovariectomized mice given intrasplenic grafts of ovarian tissue without subsequent DMBA administration), nor did tumors develop in response to DMBA treatment in mice with both ovaries in situ and no grafted tissue in the spleen. The results indicated that some local change caused by the grafting procedure rendered the tissues more sensitive to the action of DMBA and/or more responsive to gonadotropic stimulation.
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PMID:Mechanism of ovarian carcinogenesis: effect of 7,12-dimethylbenz[a]anthracene administration on intrasplenic ovarian grafts in unilaterally ovariectomized C3HeB/Fe mice. 11 53


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