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

Epidemiological studies have suggested that the intake of green-yellow vegetables decrease the risk of cancer. Vitamin A, which is abundantly present in green-yellow vegetables in the form of provitamin A, was demonstrated to inhibit chemical and viral-carcinogenesis in experimental animals. However, little is known about the mechanism of anti-carcinogenic effect of vitamin A. Our data seem to support a hypothesis that vitamin A may contribute to the prevention of cancer by augmenting an immunosurveillance system. We found that vitamin A and provitamin A, beta-carotene, enhanced tumor immunity using a syngeneic murine tumor system.
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PMID:[The immunological role of carotenoids in the prevention of cancer]. 348 10

One promising area of current research in chemoprevention is the possibility that micronutrients, including vitamin A analogues, may decrease cancer incidence. The term "vitamin A" refers either to retinol (preformed vitamin A) and its synthetic analogues, or to certain carotenoids (provitamin A), which are converted to retinol in the body, as needed. Retinol and the other retinoids are integrally involved in cell growth and differentiation, which may affect carcinogenesis. Such a role has been supported by a large number of in vitro and animal experiments. Data from studies among humans are sparse, in part because most dietary studies have been conducted in populations in which the vast majority of vitamin A intake is actually beta-carotene and other carotenoids, found in carrots and other vegetables and fruits. Although the carotenoids do not have the hormone-like properties of retinol, they do have a potent antioxidant effect and could thus reduce cancer risk by preventing tissue damage due to oxidation. This possibility is supported by data from a large number of observational epidemiologic studies, most of which have consistently found an inverse relation between consumption of carotene-rich vegetables and cancer risk. However, the only direct way to determine whether carotenoids have a beneficial effect is through large, carefully conducted randomized trials. Several such studies are currently underway and should provide sound evidence on which future medical policy and practice can be based.
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PMID:Vitamin A, carotenoids, and retinoids. 353 Apr 30

The effects of vitamins A, C, and E and of selenium on carcinogenesis are briefly summarized and updated. These vitamins and minerals were selected because they have been studied extensively in recent years with a variety of carcinogenesis models. The consumption of vitamin A and its precursors (carotenoids) has been negatively correlated with cancer at a number of sites, particularly the lung. Animal investigations on vitamin A involvement in carcinogenesis have generally been of three types: those assessing the effect of vitamin A deficiency, the effect of excess vitamin A, or the effect of supplementation with synthetic analogs of vitamin A. Vitamin A deficiency had no effect on salivary gland carcinogenesis, enhanced urinary bladder, lung, and liver carcinogenesis, and inhibited colon carcinogenesis. Excess of various forms of vitamin A enhanced or inhibited skin tumorigenesis, inhibited mammary carcinogenesis in rats (but not in mice), and carcinogenesis of the forestomach, liver, and urinary bladder (with one model, but not with another), or enhanced or did not influence lung carcinogenesis. Vitamin A analogs have enhanced or inhibited skin tumorigenesis, inhibited salivary gland, mammary, and urinary bladder carcinogenesis, enhanced tracheal and liver carcinogenesis, and either enhanced or inhibited pancreas carcinogenesis, depending upon the model employed. Although retinoids have been shown to inhibit carcinogenesis at many sites, numerous negative studies have been reported and some reports have indicated enhanced carcinogenesis. The most convincing evidence for the involvement of vitamin C in cancer prevention is the ability of ascorbic acid to prevent formation of nitrosamine and of other N-nitroso compounds. In addition vitamin C supplementation was shown to inhibit skin, nose, tracheal, lung, and kidney carcinogenesis, to either not influence or enhance skin, mammary gland, and colon carcinogenesis, and to enhance urinary bladder carcinogenesis, when given as sodium ascorbate, but not when given as ascorbic acid. Like vitamin C, vitamin E can inhibit nitrosation. Vitamin E was shown to inhibit skin, cheek pouch, and forestomach carcinogenesis, to enhance or inhibit colon carcinogenesis, and to have no effect on or to inhibit mammary gland carcinogenesis, depending upon the method of vitamin E administration or the level of dietary selenium or dietary fat. Selenium effects on carcinogenesis have been recently reviewed and the present discussion only updates this area by indicating that enhancement of carcinogenesis by dietary selenium supplements has been observed in the liver, pancreas, and skin.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Update on the effects of vitamins A, C, and E and selenium on carcinogenesis. 354 Sep 70

Epidemiologic studies of the relationships between vitamins and 3 types of cancer are reviewed. First, the widely reported association between vitamin A and beta-carotene and risk of lung cancer is considered. In a large population-based case-control study of lung cancer among white males in New Jersey, increased intake of vegetables, dark green vegetables, dark yellow-orange vegetables, and carotenoids were each associated with reduced risk, but intake of retinol or total vitamin A was not related. The protective effect of vegetables was limited to current and recent cigarette smokers, which suggests that vegetable intake prevents a late-stage event in carcinogenesis. Consumption of dark yellow-orange vegetables was consistently more predictive of reduced risk than either the total carotenoid index or consumption of any other food group, possible because of the high content of beta-carotene in this food group. The results and limitations of other epidemiologic studies of diet and lung cancer are reviewed. Second, the evolving relationship between multiple micronutrient deficiencies and esophageal cancer is discussed. In a death certificate-based case-control study of esophageal cancer in black males in Washington, D.C., several indicators of general nutritional status, including consumption of fresh or frozen meat and fish, dairy products and eggs, and fruit and vegetables, and the number of meals eaten per day, were inversely and independently correlated with the risk of esophageal cancer. Estimates of intake of micronutrients, such as carotenoids, vitamin C, thiamin, and riboflavin, were less strongly associated with reduced risk than were the broad food groups that provide most of each micronutrient. Thus no single micronutrient deficiency was identified. Other studies suggest that generally poor nutrition may partially explain the susceptibility of urban black men to esophageal cancer. Finally, the postulated association between low folacin levels and risk of cervical cancer is examined. Among women who use oral contraceptives, serum and red blood cell folacin levels were reported to be lower among those with cervical dysplasia. In a clinical trial involving oral contraceptive users, cervical dysplasia gradually decreased in the group supplemented with oral folate but remained unchanged in the group given the placebo. Other epidemiologic studies of diet and cervical cancer are discussed.
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PMID:Epidemiologic studies of vitamins and cancer of the lung, esophagus, and cervix. 359 17

A population-based incident case-control study of lung cancer in white males was conducted during 1980-1981 in six high-risk areas in New Jersey. Interviews were completed for 763 cases and 900 controls. To assess whether dietary intake of carotenoids, preformed retinol, or total vitamin A influences the risk of lung cancer, the authors asked the respondents about the usual frequency of consumption, approximately four years earlier, of 44 food items which provide 83% of the vitamin A in the US diet and about the use of vitamin supplements. The men in the lowest quartile of carotenoid intake had a relative risk of 1.3 compared with those in the highest quartile after adjusting for smoking. No increase in risk was associated with low consumption of retinol or total vitamin A. Intake of vegetables, dark green vegetables, and dark yellow-orange vegetables showed stronger associations than did the carotenoid index; the smoking-adjusted risks of those in the lowest quartiles of consumption of these food groups reached relative risks of 1.4-1.5 compared with the risks of those in the highest quartiles. The protective effect of vegetables was limited to current and recent cigarette smokers; the smoking-adjusted relative risks for low consumers reached 1.7, 1.8, and 2.2 compared with the risks for high consumers for vegetables, dark green vegetables, and dark yellow-orange vegetables, respectively. The reduction in risk with vegetable intake was most apparent for squamous cell carcinomas, but it extended to adenocarcinomas and most other cell types when only current and recent smokers were analyzed. This protection among current and recent smokers is consistent with the model that vegetable intake prevents a late-stage event of carcinogenesis. Consumption of dark yellow-orange vegetables was consistently more predictive of reduced risk than consumption of any other food group or the total carotenoid index, possibly because of the high content of beta-carotene relative to other carotenoids in this particular food group.
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PMID:Carotenoid intake, vegetables, and the risk of lung cancer among white men in New Jersey. 370 78

In liver microsomes of ethanol-fed rats, retinol competitively inhibited the hydroxylation of aniline, the demethylation of dimethylnitrosamine, and the oxidation of ethanol to acetaldehyde, whereas the inhibition of benzphetamine demethylation was of the mixed type in microsomes of phenobarbital-treated, ethanol-treated or control rats. Conversely, benzphetamine exerted a striking inhibition of the 4-hydroxylation of retinol in microsomes of phenobarbital-treated rats. At the concentration used, ethanol (100 mM) and dimethylnitrosamine (10 mM) had no such effect. In vivo administration of phenobarbital resulted in a 9-fold increase in the Vmax of the microsomal retinol 4-hydroxylase activity, with a 3-fold increase of the Km, whereas ethanol feeding resulted in a doubling of the Vmax with no significant change in the Km. The induction of this microsomal retinol-metabolizing system may contribute to the hepatic vitamin A depletion that has been reported previously after either ethanol or drug administration. Conversely, the observed inhibition, by retinol, of microsomal drug metabolism, including the demethylation of dimethylnitrosamine, may be of significance with regards to the interaction of retinol with carcinogenesis.
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PMID:Interaction of drugs and retinol. 377 19

Experiments on rats were made to study the action of 7 anticarcinogenic substances administered postnatally for a long time (sodium selenite, retinol acetate, phenformin, amber acid, low-molecular polypeptide factors of the thymus, pineal gland, and bone marrow) on the transplacental carcinogenic effect of N-ethyl-N-nitrosourea (ENU) The polypeptide factors of the thymus and pineal gland and phenformin inhibited the development of nervous system and renal tumors induced transplacentally by ENU. The rest of the substances did not influence the transplacental carcinogenesis.
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PMID:[Influence of anticarcinogenic agents on the transplacental carcinogenic effect of N-nitroso-N-ethylurea]. 401 44

Groups of 40 hamsters of each sex were fed natural ingredient diets containing 600, 4000 or 100 000 IU vitamin A/kg. After an adaptation period of 170 days on the diets, respiratory tract tumours were induced by intratracheal instillation of benzo[a]pyrene + ferric oxide suspended in saline. Mortality was statistically significantly increased in the high dose group as compared with the mid (control) and low dose group. Microscopy of the respiratory tract did not reveal any significant differences in tumour response between the various dose groups. However, the incidence of preneoplastic respiratory tract lesions was distinctly inversely correlated with the oral vitamin A dose. The serum retinol values were similar in the various dose groups, without any indication of a dose related increase. It was concluded that under the experimental conditions used vitamin A did not influence benzo[a]pyrene-induced respiratory tract cancer in hamsters.
Carcinogenesis 1984 Aug
PMID:Modifying effect of vitamin A on benzo[a]pyrene-induced respiratory tract tumours in hamsters. 608 67

The tumor promotor, 12-O-tetradecanoylphorbol-13-acetate (TPA) inhibits DNA synthesis in allogenic, mixed cultures of bovine lymphocytes. Retinoic acid, an antagonist of TPA in in vivo skin promotion, was tested for its ability to counteract the effect of TPA on lymphocyte proliferation. Retinoic acid or related compounds, retinol or retinol acetate, did not reverse or prevent the inhibitory effect of TPA. Instead retinoic acid also inhibited DNA synthesis in mixed lymphocyte cultures. On the average, about 8 microM retinoic acid inhibited the mixed lymphocyte response by 50%. The mitogenic response of lymphocytes to phytohemagglutinin (PHA) was also inhibited by retinoic acid. The degree of inhibition depended both on the concentration of PHA and of retinoic acid. Therefore, in regard to bovine lymphocytes, retinoic acid depresses DNA synthesis in both allogenic and lectin stimulated responses. Such suppression should be taken into account in the use of retinoic acid in chemotherapy.
Carcinogenesis 1982
PMID:The effects of retinoic acid and a tumor promoter, 12-O-tetradecanoylphorbol-13-acetate, on lymphocyte proliferation. 621 57

Both the provitamin beta-carotene and natural vitamin A and its derivatives (the retinoids) are being proposed as potential chemopreventive agents. The biochemistry and pharmacology of vitamin A suggest a number of mechanisms whereby carcinogenesis can be affected. Epidemiologic studies have consistently demonstrated an increased relative risk of cancer for people with low vitamin A intake or low-to-normal serum retinol values. Chemoprevention trials in humans are only now beginning. In the interim, daily consumption of vitamin-A-containing foods may be a "prescription" worth following.
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PMID:Vitamin A: evidence for its preventive role in human cancer. 635 74


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