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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diet can play a key role in the pathogenesis of cancer. Diets high in fat and low in fiber predispose individuals to colon cancer. A high-fat diet is also implicated in breast cancer and prostate cancer. The dietary fat-cancer linkage is supported by epidemiological evidence, animal studies, and prospective trials. The antioxidants vitamin E, ascorbic acid, and beta-carotene have a protective effect and act as antipromoters of carcinogenesis. A diet of less than or equal to 10% of calories from fat and less than or equal to 40 g of fiber daily that includes fruits and vegetables will prevent up to 35% of cancers.
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PMID:Nutrition and cancer. 132 5

Retrovirally induced immunosuppression may elevate the incidence of chemically induced cancers. A proposed hypothesis to explain this relationship is the increased free radical activity observed during retroviral infection and carcinogen activation. We previously found that vitamin E retarded growth of esophageal tumors accompanied by reductions of free radical products. This study investigated the contribution that retroviral immunosuppression has on esophageal cancer induced by the carcinogen N-nitrosomethylbenzylamine (NMBzA), and the response that increased levels of dietary vitamin E has on this induced carcinogenesis. Female C57BL/6 mice received NMBzA or vehicle (corn oil) i.p. weekly for 3 weeks. Then some of the mice were infected with LP-BM5 murine retrovirus and fed diets containing 30 IU vitamin E or 172 IU vitamin E/kg of diet. As an assessment of free radical activity, exhaled ethane was measured prior to killing the animals at 26 weeks. Esophagi from the various mice groups were assessed for size and frequency of tumors. Livers homogenates were analyzed for vitamins A and E, lipid fluorescence, conjugated dienes and malondialdehyde. Hepatic levels of vitamin A and E were decreased (P < 0.05) and indices of lipid peroxidation were greater (P < 0.05) in NMBzA-treated mice relative to controls. Lipid peroxidation and serum transaminases (ALT and AST) were greatest in mice given NMBzA and infected with the retroviruses. Incidence of esophageal tumors were also greatest in the NMBzA-treated, immunocompromised animals. Mice fed vitamin E-supplemented diets showed increased (P < 0.05) hepatic concentrations of vitamin E and vitamin A, decreased activities of serum transaminases, decreased indices of lipid peroxidation, and decreased size and frequency of esophageal tumors in both the immunocompromised and non-immunocompromised mice. These results suggest that vitamin E plays an antioxidant function that retards the incidence of esophageal cancers in immunocompromised and non-immunocompromised animals.
Carcinogenesis 1992 Oct
PMID:Vitamin E protection against nitrosamine-induced esophageal tumor incidence in mice immunocompromised by retroviral infection. 133 Mar 43

Individually and in combination with other oils, the tropical oils impart into manufactured foods functional properties that appeal to consumers. The use of and/or labeling in the ingredient lists give the impression that these oils are used extensively in commercially processed foods. The estimated daily intake of tropical oils by adult males is slightly more than one fourth of a tablespoon (3.8 g), 75% of which consists of saturated fatty acids. Dietary fats containing saturated fatty acids at the beta-position tend to raise plasma total and LDL-cholesterol, which, of course, contribute to atherosclerosis and coronary heart disease. Health professionals express concern that consumers who choose foods containing tropical oils unknowingly increase their intake of saturated fatty acids. The saturated fatty acid-rich tropical oils, coconut oil, hydrogenated coconut oil, and palm kernel oil, raise cholesterol levels; studies demonstrating this effect are often confounded by a developing essential fatty acid deficiency. Palm oil, an essential fatty acid-sufficient tropical oil, raises plasma cholesterol only when an excess of cholesterol is presented in the diet. The failure of palm oil to elevate blood cholesterol as predicted by the regression equations developed by Keys et al. and Hegsted et al. might be due to the dominant alpha-position location of its constituent saturated fatty acids. If so, the substitution of interesterified artificial fats for palm oil in food formulations, a recommendation of some health professionals, has the potential of raising cholesterol levels. A second rationale addresses prospective roles minor constituents of palm oil might play in health maintenance. This rationale is founded on the following observations. Dietary palm oil does not raise plasma cholesterol. Single fat studies suggests that oils richer in polyunsaturated fatty acid content tend to decrease thrombus formation. Anomalously, palm oil differs from other of the more saturated fats in tending to decrease thrombus formation. Finally, in studies comparing palm oil with other fats and oils, experimental carcinogenesis is enhanced both by vegetable oils richer in linoleic acid content and by more highly saturated animal fats. The carotenoid constituents of red palm oil are potent dietary anticarcinogens. A second group of antioxidants, the tocotrienols, are present in both palm olein and red palm oil. These vitamin E-active constituents are potent suppressors of cholesterol biosynthesis; emerging data point to their anticarcinogenic and antithrombotic activities. This review does not support claims that foods containing palm oil have no place in a prudent diet.
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PMID:Tropical oils: nutritional and scientific issues. 134 19

The tumor-enhancing effect of hydrogen peroxide (H2O2) in N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-initiated rainbow trout hepatocarcinogenesis was investigated and correlated with the levels of the mutagenic DNA adduct 8-hydroxy-2'-deoxyguanosine (oh8dG). In addition, the protective role of vitamin E was examined in relation to tumor enhancement and oh8dG levels in liver DNA. Trout were fed diets containing two levels of vitamin E (1000 or 20 mg/kg wet wt), each of which were made up to contain three levels of H2O2 (0, 600 or 3000 p.p.m.). Dietary vitamin E levels had no significant effect on tumor incidence or levels of oh8dG in liver DNA. On the other hand, dietary H2O2 enhanced liver tumors in a dose-dependent manner. Liver tumor incidence correlated significantly with the mean level of liver DNA oh8dG content (r = 0.87). We conclude that the H2O2 tumor-enhancing effect coincides with higher levels of oh8dG in the trout liver genome. Thus, rainbow trout may be a useful model for the study of the relationship of oh8dG levels in vivo to enhancement or promotion of carcinogenesis and its modulation by dietary enhancers and inhibitors of oxidative stress.
Carcinogenesis 1992 Sep
PMID:Dietary hydrogen peroxide enhances hepatocarcinogenesis in trout: correlation with 8-hydroxy-2'-deoxyguanosine levels in liver DNA. 139 49

Feeding rainbow trout for 16 weeks a diet in which the levels of vitamin E were reduced 70-fold resulted in marked depletion (18-fold) of vitamin E levels in liver microsomes from these fish. The susceptibility of hepatic microsomes to lipid peroxidation in vitro and the levels of plasma and liver microsomal lipid hydroperoxides generated in vivo were markedly elevated in vitamin E-depleted trout. No appreciable alterations were observed in the liver microsomal cytochrome P450-dependent mixed-function oxidase system or in the fatty acid composition of trout liver microsomal membranes. Livers from rats fed a vitamin E-deficient diet for 10 weeks also had significantly lower levels of microsomal vitamin E. In addition, total cytochrome P450 levels were depressed (15%) and cytosolic glutathione was enhanced (40%) in livers from rats fed the vitamin E-depleted diet. Covalent binding of [3H]-(+)-benzo[a]pyrene-7,8-dihydrodiol to exogenous DNA in vitro was enhanced with liver microsomes from vitamin E-deficient trout and these fish were much more sensitive to the acute toxicity of this carcinogenic polycyclic aromatic hydrocarbon. These results indicate that trout may be a useful model for studying the significance of peroxidative pathways in carcinogenesis and their manipulation by dietary antioxidants.
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PMID:Alterations in lipid peroxidation, antioxidant enzymes, and carcinogen metabolism in liver microsomes of vitamin E-deficient trout and rat. 152 56

Case-control differences in prediagnostic serum levels of retinol, beta-carotene, vitamin E, and selenium are compared for 10 cancer sites in 10 study populations. For all four nutrients, the majority of results showed lower levels among persons who subsequently became cases than among controls. Low levels of beta-carotene were most likely to be associated with subsequent cancer, but there were marked differences by cancer site. The results indicate that it is unlikely that any of these serum micronutrients are associated with protection against carcinogenesis at all sites. A plea is made for greater emphasis on replication of results, for reporting findings for all sites no matter how small the number of cases may be, and for keeping constantly in mind the fact that observational associations are not necessarily causal in nature.
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PMID:Serum retinol, beta-carotene, vitamin E, and selenium as related to subsequent cancer of specific sites. 153 30

The effects of combined dietary vitamin E supplementation and a relatively low increase in selenium levels on 7,12-dimethylbenz[a]anthracene (DMBA) induction of lipid peroxidation in the short term and development of mammary tumors in the long term were investigated in female Sprague-Dawley rats. Control animals were fed the basal diet (20 mg/kg vitamin E and 0.6 mg/kg selenium) throughout the experiment. Three other groups received a high vitamin E diet (235 mg/kg vitamin E and 0.6 mg/kg selenium) at different times, the first two from three weeks after DMBA treatment and the other throughout the experiment. When the vitamin E diet with selenium supplementation was applied until three weeks after DMBA or until the termination of the experiment, tumor yields (tumors per rat) were significantly inhibited compared with the control group. On the other hand, delaying the supplementation of vitamin E until three weeks postcarcinogen produced no prophylactic effect. The elevation of lipid peroxidation levels observed immediately after DMBA administration was also significantly inhibited in both mammary fat pads and livers of animals in the high vitamin E group. It was therefore concluded that the inhibitory effect of vitamin E in combination with selenium on tumorigenesis might be causally related to reduction of carcinogen treatment associated with lipid peroxidation, the latter presumably playing an important role in DMBA-induced mammary carcinogenesis.
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PMID:Inhibition of 7,12-dimethylbenz[a]anthracene-induced lipid peroxidation and mammary tumor development in rats by vitamin E in conjunction with selenium. 158 6

A study was made on the effects of long-term dietary administration of beta-carotene, vitamin C, vitamin E and selenium, either alone or in combination, on azaserine-induced pancreatic carcinogenesis in rats. Male Wistar rats were given two i.p. injections of 30 mg azaserine per kg body weight at 19 and 26 days of age. The rats were allocated to eight groups of 40 animals each and were fed an AIN-76 diet rich in saturated fat (20% lard), either as such or after supplementation with beta-carotene, vitamin C, beta-carotene + vitamin C, vitamin E, selenium, vitamin E + selenium, or the combination of all micronutrients investigated. Fifteen months after the last treatment with azaserine the survivors were killed. The pancreata were examined for the number and size of advanced putative preneoplastic lesions and the number of neoplasms as well. Rats maintained on a diet high in either beta-carotene, vitamin C or selenium developed significantly less atypical acinar cells nodules, adenomas and carcinomas as compared to controls. The number of tumour-bearing animals was significantly lower in the groups fed the diet high in beta-carotene or selenium. In animals of the group given a diet high in all micronutrients investigated, both the number and incidence of pancreatic tumours was lower than in all other groups. It was concluded that selenium, beta-carotene and vitamin C, alone as well as in combination, have an inhibitory effect on pancreatic carcinogenesis induced in rats by azaserine.
Carcinogenesis 1991 Nov
PMID:Inhibitory effects of micronutrients on pancreatic carcinogenesis in azaserine-treated rats. 193 4

Experiments were conducted to determine the dietary levels of selenium and vitamin E that could be fed chronically to induce a deficiency of one or both nutrients. It was observed that diets containing less than 0.02 mg Se/kg and 3 IU vitamin E/kg induced a deficiency without drastically altering growth performance or survival. Once established, these dietary conditions were used to investigate the effect of single or combined deficiencies of selenium and vitamin E on the promotion phase of mammary carcinogenesis induced by 1-methyl-1-nitrosourea (MNU). In the carcinogenesis experiment, 21 day old female Sprague-Dawley rats were fed a torula yeast formulated diet deficient in selenium and vitamin E until they were 50 days of age. At that time, each rat was injected i.p. with 12.5 mg MNU/kg body weight. Seven days thereafter, rats were randomly assigned to one of four treatment groups that were deficient or adequate in selenium and/or vitamin E. The experiment was terminated 30 weeks after carcinogen treatment. In comparison to rats fed the adequate diet, final cancer incidence and number were higher and cancer latency shortened in rats consuming the diet deficient in both selenium and vitamin E. Single deficiencies of either nutrient failed to significantly alter the tumorigenic response.
Carcinogenesis 1991 Nov
PMID:Effect of deficiencies of selenium and vitamin E alone or in combination on the induction of mammary carcinogenesis by 1-methyl-1-nitrosourea. 193 7

The role of the consumption of fat, animal protein and vitamins on breast-cancer risk was investigated in a hospital-based case-control study of 924 patients (409 cases and 515 controls) in Montpellier (France). A dietary history questionnaire, administered by interview, comprising 55 key food items as well as beverage consumption, and including food frequencies and portion sizes, was used to measure the intake of total fat and its constituents, animal protein, retinol, beta-carotene, vitamin E and alcohol consumption. The questionnaire also elicited information on relevant medical history and personal characteristics. All food items which showed significantly elevated odds ratio (high-fat cheese, desserts and chocolate and processed pork meat) in a multivariate analysis contained a high proportion of animal fat. This is reflected in the nutrient analysis, which showed a significant linear trend as well as an elevated odds ratio for the highest tertile of consumption of total fat [OR3 = 1.6 (1.1-2.2)], animal fat [OR3 = 1.6 (1.1-2.2)], saturated fat [OR3 = 1.9 (1.3-2.6)] and mono-unsaturated fat [OR3 = 1.7 (1.2-2.5)]. For post-menopausal women, there is a particularly strong association with saturated fat [OR3 = 3.3 (1.4-7.8)] in a multivariate analysis including all other significant nutrients. There is no evidence of an increase of risk with the intake of animal protein and no evidence of risk reduction with increased consumption of vegetables, beta-carotene or vitamin E. Along with some recent studies, our results give support to the hypothesis that dietary fat is a risk factor in breast carcinogenesis.
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PMID:The role of fat, animal protein and some vitamin consumption in breast cancer: a case control study in southern France. 201 49


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