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

Although selenium was once considered to be a toxic, undesirable and carcinogenic element, it is now recognized as an essential element with anticarcinogenic properties. Epidemiological studies in the United States have shown an inverse relationship between selenium intake and certain forms of cancer in humans, but other factors must be considered since cancer is not higher in people living in selenium-deficient areas of the world (Finland, New Zealand, and Keshan disease area, China). Under most dietary conditions, selenium has been shown to reduce the spontaneous mammary tumor incidence in an inbred strain of mice. In general, selenium will counteract to various degrees, the chemical carcinogens used to produce lesions of the skin [coal tar, 3-methylcholanthrene, alpha-pyrene, and 7,12 dimethylbenz(a) anthracene (DMBA)], liver (3-methyl-4-dimethyl-aminoazobenzene, aflatoxin B1, and 2-acetylaminofluorene), mammary gland (DMBA and N-methyl-N-nitrosurea), and intestinal tract [1,2-dimethylhydrazine, bis(2-oxopropyl)nitrosamine, and azoxymethane]. Dietary factors, such as fat, will modify the protective effects of selenium. High dietary unsaturated fats, for example, markedly increase the mammary tumors in rats treated with DMBA, and selenium will reduce the tumor incidence but not to the level of rats fed a low fat diet. Other factors known to affect the anticarcinogenic effects of selenium include synthetic antioxidants, vitamin E, vitamin A and ascorbic acid. The mechanisms of selenium counteraction of carcinogens remain unknown.
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PMID:Selenium interactions with carcinogens. 641 16

Forty-eight young male and female golden hamsters (Mesocricetus auratus) were divided into four groups of 12 animals each. The left buccal pouches of Group 1 and 2 animals were painted 3 times weekly with a 0.5% solution of 7,12-dimethylbenz(a)anthracene (DMBA) in heavy mineral oil for 7 weeks. At the end of this period, the left buccal pouches of Group 2 animals were painted 3 times weekly with vitamin E (DL-alpha-tocopherol, in pure form) for an additional 4 weeks. Group 3 animals were painted with vitamin E only, for 4 weeks. Group 4 animals were untreated controls. Group 2 animals demonstrated a significant delay in tumor formation in comparison with Group 1 animals. Gross observation revealed fewer and smaller tumors in the Group 2 animals; microscopic examination revealed smaller tumors with better cellular differentiation and less invasion. No tumors were observed in Group 3 and Group 4 animals. These observations were similar to those made in previous studies of oral carcinogenesis using systemic vitamin E to delay tumor formation.
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PMID:Retardation of experimental oral cancer by topical vitamin E. 644 34

The effect of the antioxidant vitamin E on the tumor-inducing ability of 1,2-dimethylhydrazine dihydrochloride (1,2-DMH) was investigated in randomly bred Swiss mice. Three groups of mice that were 6 weeks of age at the beginning of the experiment received the following treatments: a) vitamin E acetate [DL-alpha-tocopheryl acetate (TA)] at a 4% dose level in a powdered diet for life; b) 1,2-DMH, 10 weekly sc injections at 20 micrograms/g body weight; c) combination of a and b treatments. The administration of TA enhanced the tumorigenicity of 1,2-DMH, as evidenced by statistically significant incidences of tumors in the duodenum, cecum, colon, rectum, and anus. The present finding apparently is in contrast with the reported inhibitory effect of TA on colon carcinogenesis by 1,2-DMH.
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PMID:Enhancing effect of vitamin E on murine intestinal tumorigenesis by 1,2-dimethylhydrazine dihydrochloride. 657 81

Mouse peritoneal macrophages (MPM) from C57BL/6J, BALB/c, A strains, and (BALB/ cfemale X C57BL/ 6Jmale )F1 offspring were treated with the oxidative burst (OB)-stimulant 12-O-tetradecanoylphorbol 13-acetate, and their in vitro tumoricidal, tumorostatic , and OB activities were examined. Paraffin oil-elicited, but not thioglycollate (TG)-elicited, MPM exhibited cytotoxicity only toward Yac-1 cells and cytostatic activity toward Yac-1, EL 4, RBL-5, and RLmale 1 lymphoma cells. This activity was in correlation with the reduced capacity of TG-elicited cells to generate OB products. The toxic effect of such activated MPM was partially inhibited by catalase, superoxide dismutase, cytochrome c, and vitamin E (alpha-tocopherol) and was augmented by horseradish peroxidase and the catalase inhibitor aminotriazole (3-amino-1H-1,2,4-triazole), thus indicating the involvement of oxygen-derived toxic reagents, mainly hydrogen peroxide, in the MPM-mediated damage inflicted on the tumor cells. EL 4 cells incubated with nonstimulated MPM exhibited enhanced growth both in vitro and in vivo, whereas OB-stimulated MPM inhibited the growth of such cells in the same experimental systems.
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PMID:Oxidative burst-dependent tumoricidal and tumorostatic activities of paraffin oil-elicited mouse macrophages. 658 55

d- and dl-alpha-tocopheryl succinate inhibited growth and caused morphological changes in mouse melanoma (B-16), mouse neuroblastoma (NBP2), and rat glioma (C-6) cells in culture. To study whether the effects of alpha-tocopheryl (vitamin E) succinate on tumor cells are mediated by antioxidant mechanisms, the effects of lipid-soluble antioxidants, butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) were compared with those of vitamin E succinate. Results showed that these antioxidants produced alterations on the growth and morphology of neuroblastoma, melanoma, and glioma cells which are similar to those produced by vitamin E succinate; however, the extent of the effect depended upon the type of antioxidant and the form of tumor cells. These data suggest that the effects of vitamin E succinate on tumor cells may be mediated, in part, by antioxidant mechanisms.
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PMID:Study on the specificity of alpha-tocopheryl (vitamin E) acid succinate effects on melanoma, glioma and neuroblastoma cells in culture. 663 22

The antitumor effects of vitamin A and its related substances, vitamin E, vitamin K, beta-carotene, ubiquinone, phytol, and squalene, were examined using a syngeneic murine tumor system. Intraperitoneal administration of these substances (0.19 mumol/mouse/day) slightly suppressed the growth of Meth A fibrosarcoma cells inoculated s.c. into Balb/c mice. Administration of all test substances except beta-carotene significantly suppressed the growth of Meth A fibrosarcoma cells rechallenged in Meth A-primed mice on day 10, but did not influence the growth of Meth 1 fibrosarcoma cells (another syngeneic tumor of Balb/c origin) rechallenged in Meth A-primed mice on day 10. The growth of Meth A tumor cells was suppressed when Meth A was inoculated together with lymph node cells obtained from the Meth A-primed Balb/c mice treated with vitamin A, vitamin E, phytol, or squalene. Our findings suggest that certain constituents in green-yellow vegetables may contribute to the prevention of cancer by augmenting an immunological response against tumor cells in the early stages of carcinogenesis.
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PMID:Immunological role of vitamin A and its related substances in prevention of cancer. 666 79

Mice fed vitamin E at a level of 0.5 g DL-alpha-tocopheryl acetate/kg diet demonstrated decreased incidence and rate of appearance of tumors produced by transplanted sarcoma cells (K3T3), compared to control groups fed diets without the vitamin supplement. Protection was dependent on the degree of unsaturation of dietary fat and on the size of the tumor cell challenge. When vitamin E was increased 10-fold (to 5 g/kg diet), the protective effect was no longer observed. Protection may be mediated through the host immune system, because sublethal, whole-body X-irradiation abrogated differences in tumor development between the +E and the -E mice. Studies with in vitro immunization showed that treatment of the K3T3 cell with vitamin E enhanced its ability to induce a cytotoxic response. It appears that the direct effect of vitamin E is on the tumor cell rather than on the immune system, since spleen cells from mice fed diets with and without vitamin E supplementation were indistinguishable in their response to untreated K3T3 cells. K3T3 cells treated with excessive levels of vitamin E were unable to induce a cytotoxic response, a result that correlates with the loss of protection against tumor development when massive doses of vitamin E were fed.
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PMID:Vitamin E protection against tumor formation by transplanted murine sarcoma cells. 676 53

Eighty young adult male and female Syrian golden hamsters (Mesocricetus auratus) were divided into 4 equal experimental groups. In group I animals the left buccal pouch was painted three times weekly with a 0.5% solution of 7,12-dimethylbenz[a]anthracene (DMBA) in heavy mineral oil. In group 2 animals the left buccal pouch was similarly painted with DMBA, but the animals also received orally 10 mg vitamin E (dl-alpha-tocopherol) in peanut oil twice weekly on alternate days with DMBA painting. Group 1 animals received a similar amount of peanut oil vehicle, group 3 animals received only vitamin E (vitamin E controls) in peanut oil, and group 4 animals served as untreated controls receiving only peanut oil. Four animals in each group (2 males and 2 females) were killed at 8, 10, 12, 14, and 16 weeks. Buccal pouches were photographed and excised, and tumors were noted and measured in the left buccal pouches. In group 2 animals receiving vitamin E, tumor formation was significantly delayed, so that by 14-16 weeks there were fewer tumors and their average size was smaller than that of tumors in group 1 animals that were painted with DMBA but received no vitamin E supplement. In group 2 there was also less invasion of underlying tissues and less surface necrosis.
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PMID:Oral mucosal carcinogenesis in hamsters: inhibition by vitamin E. 680 58

Sixty-four young adult male and female golden hamsters (Mesocricetus auratus) were divided into four equal experimental groups of sixteen animals. In Group 1 animals the left buccal pouch was painted three times weekly with a 0.25 percent solution of 7, 12-dimethylbenz(a)anthracene (DMBA) in heavy mineral oil. In Group 2 animals the left buccal pouch was similarly painted with DMBA, but the animals also received 7 I.U. of vitamin E (alpha tocopherol) twice weekly on days alternate to the DMBA painting. The vitamin E was administered orally via a fine pipette. Group 3 animals were similarly painted with DMBA and received vitamin E vehicle by pipette. Group 4 animals served as untreated controls. Four animals in each group (two male, two female) were killed at 8, 10, 12, and 14 weeks. Buccal pouches were photographed and excised. Tumors were noted and measured in the left buccal pouches. The buccal pouches as well as major organs were fixed in formalin, sectioned in paraffin, and stained with hematoxylin and eosin. In the Group 2 animals receiving vitamin E, there was a significant delay in tumor formation so that by 12 to 14 weeks there were fewer tumors and their average size was smaller than those in the Group 1 and Group 3 animals painted with DMBA but receiving no vitamin E supplement. Microscopic examination revealed that there was less invasion of underlying tissues and less surface necrosis. The tumors in both control and vitamin E groups were well-differentiated epidermoid carcinomas. No differences in the nature of the cellular patterns of the carcinomas in control and vitamin E groups were revealed by electron microscopic studies.
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PMID:Vitamin E inhibition of hamster buccal pouch carcinogenesis. A gross, histologic, and ultrastructural study. 681 90

Using the dimethylbenz[a]anthracene-induced mammary tumor model, the present study demonstrated that a low vitamin E intake (7.5 mg/kg of diet) had minimal effect on carcinoma development in rats fed a 5% stripped corn oil diet, but resulted in a marked enhancement in tumor incidence and yield in those rats fed a 25% stripped corn oil ration. Control animals in this experiment received an adequate supply of vitamin E (30 mg/kg as DL-alpha-tocopheryl acetate). Thus, the effect of vitamin E deficiency on mammary carcinogenesis was accentuated in rats maintained on a high polyunsaturated fat diet, an observation similar to that of selenium deficiency which was reported by the author in a previous publication. In view of the biochemical interaction between vitamin E and selenium as endogenous antioxidants, another experiment was conducted to determine whether supranutritional supplementation of vitamin E (1000 mg/kg) was able to block the enhancement in mammary tumorigenesis due to selenium deprivation. Results of this experiment indicated that vitamin E excess failed to overcome the augmented tumor yield in selenium-deficient rats, nor did it provide any protection in rats that received an adequate supply of selenium. In summary, vitamin E deficiency may increase the risk of neoplastic development, especially when coupled with a high polyunsaturated fat intake; however, a high vitamin E supplementation does not seem to have any prophylactic effect on tumorigenesis by itself.
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PMID:Dietary vitamin E intake and mammary carcinogenesis in rats. 681 42


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