Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Benz(a)anthracene (BA) and its five possible trans-dihydrodiols were evaluated for determination of their skin tumor-initiating activity and their mutagenic activity in Chinese hamster V79 cells. In addition, the skin tumor-initiating abilities of five diol-epoxides of BA were tested. Results showed (+/-)-trans-3,4-dihydroxy-3,4-dihydrobenz(a)anthracene (BA 3,4-dihydrodiol) to be approximately 10 times more mutagenic than was BA and about 20 times more mutagenic than were the other possible dihydrodiols in the V79 cells cocultivated with irradiated hamster embryo cells. As a skin tumor initiator, BA 3,4-dihydrodiol was approximately 5 times more active than BA, whereas the other BA dihydrodiols were all less active tumor initiators. (+/-)-trans-3alpha,4beta-Dihydroxy-1alpha,2alpha-epoxy-1,2,3,4-tetrahydrobenz(a)anthracene was found to be approximately 20% more active as a tumor initiator than was BA 3,4-dihydrodiol, whereas the other diol-epoxides of BA were less active than BA itself. The results suggest that the bay-region diol-epoxide of BA may be the ultimate carcinogen and mutagenic form of BA.
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PMID:Carcinogenicity and mutagenicity of benz(a)anthracene diols and diol-epoxides. 64 80

The inhibitory effect of actinomycin D on the induction of tumors by in vitro exposure of mammary glands to 7,12-dimethylbenz(a)anthracene was studied. When actinomycin D was given i.p. 24 hr before excision of the mammary glands, the induction of tumors by in vitro exposure of the glands to 7,12-dimethylbenz(a)anthracene was significantly decreased. On the other hand, when actinomycin D was administered 24 hr after excision, it had no effect on the induction of tumors. In vitro exposure of excised glands to 7,12-dimethylbenz(a)anthracene and actinomycin D significant decreased tumor induction. However, the order of exposure to 7,12-dimethylbenz(a)anthracene and actinomycin D influenced the inhibitory effect of actinomycin D on tumor induction. Results indicated that this might be due to a difference in the amounts of 7,12-dimethylbenz(a)anthracene and actinomycin D bound to the mammary glands.
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PMID:Inhibitory effect of actinomycin D on the inductio of rat mammary tumors by in vitro exposure to 7,12-dimethylbenz(a)anthracene. 80 63

The effect of L-arginine on growth of rat mammary tumors induced by 7,12-dimethylbenz(a)anthracene was studied. Growth of induced tumors was inhibited by feeding rats an arginine-enriched diet containing 5% L-arginine in addition to the necessary components for rats, including 15% milk casein. The diet significantly reduced both the rate of tumor induction and the number of tumors induced per rat. Histological examination showed that the tumors induced were more benign in rats fed the arginine-enriched diet than in those fed the control diet. A possible mechanism of the inhibitory effect of L-agrinine id discussed.
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PMID:Inhibitory effect of L-arginine on growth of rat mammary tumors induced by 7,12-dimethylbenz(a)anthracene. 80 24

The induction of ornithine decarboxylase and S-adenosyl-L-methionine decarboxylase in mouse epidermis by various classes of tumor-promoting and nonpromoting compounds has been studied in order to determine the specificity of this response for tumor promotion. The effect of topical applications of a series of phorbol esters on these enzyme activities correlated well with their promoting abilities. Iodoacetic acid, anthralin, and Tween 60, all promoting compounds, also stimulated both of these enzyme activities after single and multiple applications. The hyperplastic agents acetic acid, cantharidin, and ethyl phenylpropriolate, however, had little effect on ornithine decarboxylase activity but a pronounced effect on epidermal S-adenosyl-L-methionine decarboxylase activity. The specificity of the ornithine decarboxylase response for tumor promotion was suggested by the results of the above experiments as well as the stimulatory effect of a completely carcinogenic dose of 7,12-dimethylbenz[a]anthracene; a lower initiating dose had no effect. In addition, epidermal tumors produced by a two-stage procedure showed consistently high levels of ornithine decarboxylase activity but variable levels of S-adenosyl-L-methionine decarboxylase activity.
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PMID:Induction of the polyamine-biosynthetic enzymes in mouse epidermis and their specificity for tumor promotion. 80 25

The association between mammary carcinogenesis induced by 7,12-dimethylbenz(alpha)anthracene (DMBA) in the rat, the influence by manipulations of its hepatic metabolism and the secretion of prolactin has been investigated. Various test compounds: coumarin, 4-methylcoumarin, phenobarbital and CCl4 all elevated serum prolactin level, but only coumarin and 4-methylcoumarin reduced tumor incidence. These observations do not support the assumption that the suppression of DMBA-induced breast adenocarcinoma by coumarin and 4-methylcoumarin is mediated via prolactin.
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PMID:Is there any association between elevated serum prolactin level and mammary adenocarcinoma induced by 7,12-dimethylbenz(alpha)anthracene. 80 60

Female Sprague-Dawley rats, 36 days old, were pretreated for 2 weeks either with 100 ppm 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) or 250 ppm S-(1,2-dicarbeth-oxyethyl)OO-dimethyldithiophosphate (Malathion) in the diet. From day 50 they were given, via stomach tube, 21 consecutive daily doses of 0.714 mg 7,12-dimethylbenz[a]anthracene (DMBA). Pesticide diets and observation of the animals for mammary tumors continued until necropsy, 230 days after the start of DMBA administration. DDT-treated rats had a significantly lower mammary tumor incidence, prolonged tumor latency period, and fewer tumors per rat than did the control group. Animals given Malathion (an organophosphate pesticide) had a higher mammary tumor incidence, shortened latency period, more tumors per rat, and more actively growing tumors than did the control group (DMBA only). Leukemia incidence in rats surviving to necropsy (230 days after the start of DMBA administration) was 11/20 for control, 2/29 for DDT, and 8/12 for Malathion-treated rats. Leukemia was primarily myelogenous. DDT may inhibit DMBA-induced mammary tumors and leukemia by stimulating hepatic metabolism and excretion of DMBA so that less carcinogen is available to peripheral tissues. Malathion may potentiate DMBA induction of mammary tumors and leukemia by inhibiting the same enzyme systems induced by DDT.
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PMID:Protection by 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) against mammary tumors and leukemia during prolonged feeding of 7,12-dimethylbenz(a)anthracene to female rats. 80 43

By means of an implanted transmitter, a circadian rhythm of temperature was found both in 7,12-dimethylbenz(a)anthracene-induced tumors and in Walker 256 carcinosarcomas. There was no significant difference in the temperatures of the two tumors. The temperature was lowest in periods of rest, and the temperature difference between light and dark periods was about 1 degree. Both tumors were found to have a higher temperature than that of s.c. tissue. External temperature measurements of the skin covering the 7,12-dimethylbenz(a)anthracene-induced tumor by thermistor probe and by thermography showed a temperature 1-2 degrees below the temperature of surrounding skin areas. In the 7,12-dimethylbenz(a)anthracene-induced tumors the blood flow was low, which should correspond to a relatively small heat production, although the temperature was relatively high. Blood flow in skin overlying tumor was high, presumably a perifocal hyperemic reaction, although the temperature was relatively low in this area. Thus tissue temperatures was not indicative of blood flow.
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PMID:Temperature and blood flow measurements in and around 7,12-dimethylbenz(a)anthracene-induced tumor and Walker 256 carcinosarcomas in rats. 81 Feb 41

Cryostat sections of 29 squamous cell carcinomas, 13 keratoacanthomas, and 12 papillomas, induced by 7,12-dimethylbenz(a)anthracene in the skin of rabbits and rats were examined by indirect immunofluorescence with human serum containing antibody to smooth muscle. Linear or granular staining of the cell outlines of the basal squamous cell layers was seen most extensively in the carcinomas, less in keratoacanthomas, and least in papillomas. In addition, squamous cell carcinomas showed this pattern of staining at advancing tumor margins and in invasive cords and tumor cell nests in the dermis. Four keratoacanthomas also showed prominent staining of the basement membrane area. The specificity of the staining reaction was established by its prevention on neutralization absorptions of the serum with extracts or homogenates of smooth muscle. The epidermal cells of normal rabbit and rat skin gave negative staining reactions. The presence of smooth muscle-associated antigen probably corresponds to cellular microfilaments.
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PMID:Smooth muscle-associated antigen in experimental cutaneous squamous cell carcinoma, keratoacanthoma, and papilloma. 81 54

The peroxidase and estradiol-metabolizing activities of mammary tumors induced by 7,12-dimethylbenz(a)anthracene were determined in fresh and stored tissue. In both cases, a wide variation in peroxidase activity was observed in 47 different tumors tested. The properties of the enzyme found in the tumors were similar to those of lactoperoxidase. It is suggested that the amount of peroxidase present might reflect the ability of tumor cells to differentiate in response to hormonal stimulation and be indicative of the degree of tumor progression.
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PMID:Metabolism of (4-14C)estradiol by 7,12-dimethylbenz(a) anthracene-induced mammary tumor peroxidase. 81 11

Six of 70 female Sprague-Dawley rats given a single intravenous injection of 7,12-dimethylbenz[a]anthracene (DMBA) developed 7 pilosebaceous tumors. Two of the tumors showed differentiation toward the upper portion of the pilosebaceous unit while 5 showed differentiation toward the lower portion. Each tumor was examined histochemically for the presence of inner root sheath keratin of the hair follicle using the carbamido diacetyl reaction for citrulline and for hair shaft keratin using boiling ninhydrin reagent. The 2 tumors of the upper portion of the pilosebaceous unit were sebaceous adenomas which were accompained by a keratinizing epithelim like that of the sebaceous gland duct and upper pilosebaceous canal. Histochemically, the keratin was not like that of hair shaft nor inner root sheath. The 5 tumors showing differentiation toward components of the lower pilosebaceous unit were trichoepitheliomas. They were composed of structures which, to varying degrees, recapitulated the organization of the normal hair follicle. Within these follicular structures, both inner root sheath and hair shaft type keratins were found. The occurrence of skin tumors after the intravenous administration of DMBA was unexpected since it is uncommon for skin tumors to be produced by the systematic administration of chemical carcinogens and they have never been described after the oral administration of DMBA. That the route of administration may influence tumor production with this carcinogen is suggested by the fact that the only other reported tumors, which were squamous carcinomas, also followed intravenous injection of DMBA.
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PMID:Tumors of the pilosebaceous unit induced in the rat by the intravenous administration of 7,12-dimethylbenz(A)anthracene. 81 74


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