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

A method was developed for continuously exposing tracheal epithelium to measured amounts of carcinogen. Beeswax was the vehicle for sustained release of carcinogen, and tracheas transplanted to s.c. sites were target tissues. In the experiment reported here, transplanted rat tracheas were exposed to a potent carcinogen, 7,12-di-methyl benz(a)anthracene (DMBA). The rate of release of DMBA from the beeswax carrier within the tracheal lumen approached first order when the initial concentration of carcinogen was high (3200 to 325 microng in a 24.45-mg pellet). With lower concentrations, where the carcinogen was dissolved in the beeswax, initial release was rapid, and most of the carcinogen was delivered within 4 weeks. At high DMBA dose levels, the entire tracheal epithelium was uniformly replaced by keratinizing squamous metaplasia after 1 week of exposure, and after 2 months, when from 280 to 910 microng DMBA had been delivered, all transplants had developed invasive squamous carcinomas. Sarcomas also developed in 19% of the transplants. At lower dose levels the epithelial reactions were more varied, and tumor development was more protracted. The lowest DMBA dose presently known to diduce carcinomas in this experimental model is 40 microng, which is in the dose range used for tumor initiation in skin carcinogenesis studies in mice.
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PMID:Quantitative exposure of grafted rat tracheas to 7, 12-dimethylbenz(a)anthracene. 40 31

The previously observed alterations in the energy transducing system of rat liver mitochondria during 3'-methyl-4-(dimethylamino)azobenzene (3'-Me-DAB) carcinogenesis were investigated using aliphatic dicarbonyl compounds as molecular probes and the effect of temperature on the membrane-linked NADH-indophenol reductase. The vicinal diketone, diacetyl, uncouples oxidative phosphorylation in normal rat liver mitochondria while the higher diketones, acetylacetone and acetonylacetone, are increasingly less effective in that order; diacetyl totally abolishes respiratory control with substrates the oxidation of which involves the NADH leads to CoQ segment, but only partially with succinate which bypasses this segment. Diacetyl, likewise, uncouples oxidative phosphorylation in liver mitochondria from rats fed 3'-Me-DAB, but the mitochondria are most resistant to this uncoupling (in terms of the P/O ratio) at the time period when the respiratory control index (determined in the absence of diacetyl) is at the dye-induced minmum. This time period is at 3 to 4 weeks of dye administration, representing the cumulative dose for tumorigenesis threshold. At this threshold period of feeding 3'-Me-DAB, discontinuities in the Arrhenius plot of the mitochondrial membrane-localized NADH-indophenol reductase appear, with a return toward the control state (no break) at 8 weeks, only to reappear in the plot of the enzyme from tumor mitochondria, suggesting sequential membrane phase transitions in the mitochondria during azo dye carcinogenesis.
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PMID:Mitochondrial membrane-linked reactions in carcinogenesis: change in steroselective uncoupling of oxidative phosphorylation by aliphatic dicarbonyls and in the Arrhenius plot of NADH-indophenol reductase. 40 68

The formation of new hair follicles was quantitatively demonstrated in the tail skin of adult mice in the course of a two-stage carcinogenesis experiment with 7,12-dimethylbenz(a)anthracene as an initiator and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate as a promoter, as well as in experiments with 12-O-tetradecanoylphorbol-13-acetate alone. Two kinds of follicular neogenesis could be distinguished. The most frequently encountered type was characterized by the organization of new follicles from the upper neck and orifice regions of already existing follicles. During their development, these new follicles remained in close apposition to the original follicles but, after having reached a critical size, split off to form fully independent follicles. In the second, type of follicular neogenesis, which occurred very rarely, the new follicles seemed to arise directly from the epidermis between two sets of hair triads; however, these follicles never reached their final stage and did not produce hairs. The formation of new hair follicles may be explained by a "dedifferentiation" of epidermal cells caused by the tumor promoter. Because of the paucity and advanced stage of the papillomas formed in tail skin after long-term treatment with 12-O-tetradecanoylphorbol-13-acetate, no reliable comment as to whether the papillomas derive from the hair follicles can be made.
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PMID:Induction of the formation of new hair follicles in mouse tail epidermis by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate. 40 92

The effect of Danazol, a synthetic gonadotropin inhibitor, on two groups of Sprague-Dawley rats with dimethylbenze (a) anthracine (DMBA) induced mammary carcinoma was studied. Twenty-four (83%) of 29 control animals developed mammary tumors. Forty-four rats in one treatment group received Danazol after tumor reached 0.5 cm in diameter. Twenty-nine (66%) demonstrated tumor regression (p less than 0.005) and in 16 (36%) tumor disappeared (p less than 0.005). In a second treatment group (given Danazol daily after administration of DMBA), only seven of 50 rats (14%) developed palpable mammary carcinoma (p less than 0.0005). Danazol therapy resulted in regression of established mammary carcinoma in rats, and produced a striking inhibition of carcinogenesis in those animals treated from the time DMBA was administered. Danazol is clinically safe; studies using it in the treatment of breast cancer in women who are candidates for hormonal ablative therapy seem warranted.
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PMID:Danazol therapy in hormone-sensitive mammary carcinoma. 41 78

Beryllium is a proven bone carcinogen in rabbits, and proven pulmonary carcinogen in rats. Median effective doses or concentrations can be computed only with considerable uncertainty; they appear to be in the 10 mg area (as total dose, in divided intravenous injections, expressed as Be for zinc beryllium silicate) for rabbits, and in the 20 alpha/m3 area (as atmospheric concentration for inhalation exposures lasting for at least three months, expressed as Be for beryllium sulfate) for rats. It is also proven that, at least from inhalation, guinea pigs do not develop beryllium cancers. Epidemiologic studies in humans are thus far unconfirmed but do not show increased cancer morbidity among beryllium workers. Current research is aimed at explaining the mechanism of carcinogenic action in the susceptible species, which seems to involve nucleic acid transcriptional interference, or the species specificity, which seems to involve immune mechanisms. No experiments were reported thus far besides the carcinogenesis studies to show that beryllium is a chemical mutagen. In the species thus far tested, there appeared to be mutual exclusion of development of a delayed (cell-mediated) hypersensitivity to beryllium and development of neoplasia from beryllium. Further research on this subject might lead to new possibilities in the understanding of cancer susceptibility.
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PMID:Beryllium carcinogenesis. 41 24

The effect of a diet containing either sunflower-seed oil (polyunsaturated fat diet) or tallow (saturated fat diet) on 7,12-dimethylbenz[a]anthracene (DMBA)-induced carcinogenesis in C3H-A vyfB mice was examined. After receiving either diet for 28 days, some of the mice were given an intragastric dose of 5 mg DMBA. To identify the stage of carcinogenesis that might be influenced by dietary fat, the diets of half of the mice were then interchanged so that those previously fed the saturated fat diet were fed the polyunsaturated fat diet and vice versa. The cumulative incidence of tumor-bearing mice was significantly greater among the females fed the polyunsaturated fat diet compared to those fed the saturated fat diet. This enhancement of carcinogenesis was observed only when the mice were fed the polyunsaturated fat diet after DMBA administration. Similar trends were observed in the male mice, but these mice developed fewer tumors and none of the differences between the tumor incidences were statistically significant. The most common sites for tumors in the male mice were the liver, lungs, and skin, whereas those for tumors in the females were the mammary glands and ovaries. The differences in tumor incidence suggest that carcinogenesis was enhanced by the polyunsaturated fat diet during the promotion stage of carcinogenesis.
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PMID:Carcinogenesis induced by 7,12-dimethylbenz[a]anthracene in c3H-A vyfB mice: influence of different dietary fats. 41 26

We find that colonic adenocarcinoma, which is an extremely rare neoplasm of all animals except man and carcinogen-treated rodents, occurs spontaneously in some marmosets. The cotton-topped Saguinus oedipus oedipus is particularly prone to develop it, but we have found it also at necropsy in Callimico goeldii (Goeldi's marmoset). Numerous metastases to regional lymph nodes develop. The cancers arise de novo in the mucosa and early invade the submucosa and lymphatic apparatus and paracolonic lymph nodes. These findings and the continuing occurrence of this cancer in our colony suggests that the marmoset may be the long-sought primate model for experimental intestinal carcinogenesis.
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PMID:Spontaneous colonic adenocarcinoma in marmosets. 41 16

The existence of at least two stages in bladder carcinogenesis was evaluated in male Fischer rats using N-[14-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) fed for six weeks at a level of 0.2% of the diet as the initiator. Sodium saccharin and DL-tryptophan were fed at levels of 5 and 2% of the diet, respectively, as possible promoting chemicals, and they were fed either immediately after FANFT administration or after six weeks of FANFT plus six weeks of control diet. All surviving rats were killed at the end of two years. Both chemicals significantly increased the incidence of bladder tumors following FANFT feeding compared to six weeks of FANFT feeding followed by control diet, and the results were similar whether saccharin or tryptophan feeding was started immediately after FANFT feeding was concluded or after a six-week delay. Saccharin was considerably more potent as a promoting agent than was tryptophan, inducing higher incidences of bladder tumors and having a shorter latent period. Long-term administration of FANFT induced a 100% incidence of bladder cancer. Sequential epithelial changes were observed by scanning and transmission electron microscopy as well as by light microscopy. Pleomorphic microvilli were present on the superficial cells of all tumors examined and on the surface cells of hyperplastic bladder epithelium after six weeks of FANFT plus six weeks of saccharin, but not after six weeks of FANFT and six weeks of control diet. Rats fed only saccharin tryptophan, or control diet did not have bladder tumors or pleomorphic microvilli on bladder epithelium. These data suggest that saccharin and tryptophan might act as tumor-promoting agents during bladder carcinogenesis.
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PMID:Promoting effect of saccharin and DL-tryptophan in urinary bladder carcinogenesis. 42 Dec 4

The importance of surface charge in foreign body carcinogenesis was evaluated by implanting in C3H/HeJ male mice, bipolar polystyrene thermoelectrets formed in variously charged electrical fields. Charged electrets had tumor rates similar to control groups. The cumulative probability of tumor development was highest in the charged electret group being 0.58 at 133 weeks after implantation. The tumor rate for all charged electrets was 27% as compared to 17% and 6% for the control groups. The latent period of tumor induction varied little between groups and averaged approximately 700 days. No conclusions regarding the tumorigenic effect of electropositive versus electronegative sides of the electret were made although the majority of tumors arose on the electronegative (body) side of the electrets. An occasional tumor (2/25) arose on both sides of a single electret. The antigenicities of tumors tested by excise and challenge techniques were weak. The immunologic relationship between top and bottom growing tumors on a single electret could not be adequately determined because of the weak antigenicity.
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PMID:Surface charge in foreign body carcinogenesis. 42 89

Carcinogenicity of phenacetin was tested using Sprague-Dawley rats. Two groups of animals containing 50 males and 50 females per group were fed respectively with 2.5% and 1.25% phenacetin diet for 18 months and fed thereafter with basal diet for 6 months. Control animals containing 65 males and 65 females were fed with basal diet for 24 months. Animals surviving more than 24 months were regarded as effective animals and killed. Rats that died of tumor development within 24 months were also regarded effective animals. Every organ from the killed and dead animals was fixed in 10% formaldehyde solution and examined histopathologically. Effective number of rats was 27 males and 27 females in 2.5% phenacetin feeding group, and 22 males and 25 females in 1.25% phenacetin feeding group. In control group, 19 males and 25 females were effective. Neoplasms including spontaneous tumors were detected in 26 out of 27 males (96.3%) and 21 out of 27 females (77.8%) of 2.5% phenacetin feeding group, and in 20 out of 22 males (90.9%) and 19 out of 25 females (76.0%) of 1.25% phenacetin feeding group. In control group, 1 out of 19 males (5.3%) and 6 out of 25 females (24.0%) showed spontaneous tumor development. Histopathologically, carcinomas of the nasal cavity, such as adenocarcinoma, squamous cell carcinoma, and transitional cell carcinoma, and the urinary passage, as renal cell carcinoma of the kidney pelvis, and transitional cell carcinoma of the urinary bladder, were most conspicuous, suggesting the target organs of phenacetin carcinogenesis. Males showed higher tumor incidence compared to females. The higher the concentration of phenacetin given, higher incidence of tumors was observed.
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PMID:Tumors of Sprague-Dawley rats induced by long-term feeding of phenacetin. 44 75


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