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

Food contains a large number of inhibitors of carcinogenesis, including phenols, indoles, aromatic isothiocyanates, methylated flavones, coumarins, plant sterols, selenium salts, protease inhibitors, ascorbic acid, tocopherols, retinol, and carotenes. The diversity and widespread occurrence of these compounds in food make it virtually impossible to consume a diet that does not contain inhibitors of carcinogenesis. Inhibitors can be classified as to the time in the carcinogenic process at which they act. Some prevent formation of carcinogens. Others, termed "blocking agents," prevent carcinogens from reaching or reacting with critical target sites. A third group called "suppressing agents" are effective when fed subsequent to administration of carcinogens. Some compounds inhibit at more than one time point. The major emphasis in this paper is on blocking agents, in particular those that act by enhancing host detoxification systems. Mary blocking agents produce a coordinated enhancement of multiple detoxification systems. Two distinctive patterns termed type A and type B have been identified. One enzyme system commonly induced by blocking agents is glutathione S-transferase. On the basis of this information, induction of glutathione S-transferase activity is being used to detect the presence of blocking agents in complex natural products. Green coffee beans induce increased glutathione S-transferase activity and inhibit mammary neoplasia in the rat resulting from administration of 7,12-dimethylbenz(a)anthracene. Two potent inducers of increased glutathione S-transferase activity have been isolated from green coffee beans. These are kahweol palmitate and cafestol palmitate. In recent work, several plant materials have been found to inhibit carcinogenesis when fed after carcinogen exposure. The identification and further investigation of inhibitors present in food are of importance so that their impact on the occurrence of neoplasia in humans can be ascertained.
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PMID:Inhibition of neoplasia by minor dietary constituents. 640 36

The chemopreventive action of beta-carotene during chemically-induced transformation of the epithelial cells in organ culture of the whole mammary glands from BALB/c female mice was studied. The mammary epithelial cells in the whole mammary organ in a hormone supplemented, serum-free medium were transformed after 24 h exposure to 7.8 microM 7,12-dimethylbenz[a]anthracene (DMBA) between 3rd and 4th day of a total 10 day culture period. The transformation process was associated with appearance of nodule-like alveolar lesions (NLAL) in glands in vitro. The epithelial cells transformed by DMBA are potentially neoplastic, and NLAL serves as a morphological marker of preneoplasia in the glands in vitro. Treatment with beta-carotene (10(-6) M) during DMBA exposure (3rd-4th day) caused 68% inhibition in the number of glands with incidence of NLAL. A 49% inhibition of NLAL was evident when the glands were incubated with beta-carotene (days 4-10) after exposure to DMBA. Results indicate that beta-carotene inhibits DMBA-induced transformation of the mammary glands in vitro acting both at the initiation and the promotional stages. This inhibitory effect is likely due to the action of beta-carotene itself since no accumulation of retinol, the metabolic derivative of the vitamin A precursor, was detectable in the mammary glands during the 10 day culture period.
Carcinogenesis 1984 Jul
PMID:Beta-carotene inhibition of 7,12-dimethylbenz[a]anthracene-induced transformation of murine mammary cells in vitro. 642 68

Forty-two compounds belonging to various chemical groups have been tested for their ability to suppress formation of aflatoxin B1--DNA adduct mediated by microsome in vitro. While many of these compounds have either marginal or no modulating effect, some have been identified as effective inhibitors. The strong inhibition of DNA adduct formation by retinoids (retinol, retinal, retinoic acid and retinyl acetate), riboflavin, riboflavin 5'-phosphate, flavin adenine dinucleotide, Cu2+, 7,8-benzoflavone, disulfiram, butylated hydroxyanisole, butylated hydroxytoluene and phenothiazine suggests that these agents may have potential anticarcinogenic activity against aflatoxin B1.
Carcinogenesis 1984 Oct
PMID:Factors modulating the formation of DNA adduct by aflatoxin B1 in vitro. 643

The influence of high doses of retinol acetate (RA) fed with the diet and carbon tetrachloride (CCl4) injected intraperitoneally into rat offspring on transplacental carcinogenic effect of N-nitrosoethylurea (NEU) was studied. Neither RA nor CCl4 affected significantly the development of the nervous system and kidney tumors induced transplacentally by NEU. CCl4 did not induce liver tumors either under these conditions. Obviously, it is rather difficult to modify the transplacental carcinogenesis.
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PMID:[Influence of retinol acetate and carbon tetrachloride on the transplacental carcinogenic effect of N-nitrosoethylurea]. 650 38

Biochemical analyses were conducted to evaluate the nutritional status of a high esophageal cancer risk population in Linxian, People's Republic of China. A study was conducted in September 1980 in which plasma levels of vitamins A, B2, and C were analyzed. In a second study in 1983, the plasma fat-soluble vitamins were analyzed with a newly developed high-performance liquid chromatography method that allowed the simultaneous determination of retinol, alpha-tocopherol, beta-carotene, alpha-carotene, and lycopene in 0.1 ml of plasma sample. The average plasma retinol levels ranged from 24 to 27 micrograms/dl among the population groups, with 20-35% of the individuals having levels under 20 micrograms/dl. Low plasma beta-carotene levels averaging 8-12 micrograms/dl were observed among the population groups. Low plasma alpha-tocopherol levels with average values around 700 micrograms/dl were also observed; about half the individuals were either low or deficient in vitamin E. After 4 months of supplementation with daily multivitamin tablets, the plasma contents of retinol and alpha-tocopherol were significantly increased. The plasma alpha-carotene and beta-carotene were also increased, possibly as a reflection of seasonal changes in the diet or a sparing effect of vitamins A and E on these carotenes. Low plasma ascorbate levels with an average of 567 micrograms/dl were observed, and about 23% of the individuals had values under 200 micrograms/dl. Riboflavin deficiency was prevalent, with about 90% of the subjects having an erythrocyte glutathione activation coefficient over 1.2. The study establishes the low nutritional status in vitamins of the population in Linxian and provides the background for further studies on the effects of nutritional deficiency on carcinogenesis.
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PMID:Vitamin A and other deficiencies in Linxian, a high esophageal cancer incidence area in northern China. 659 53

In the Basel study (BS) (1960-73) on cardiovascular and peripheral arterial diseases, a mortality follow-up was completed for the period 1965-80. Of the 4,224 men at risk for these diseases, 531 died. The causes of death were established from the death certificates and classified into 8 groups. For each case 2 age- and sex-matched controls were selected and compared with the corresponding cases with regard to the various variables obtained at the three examinations (1960, 1965, 1971). This report dealth with cancer mortality, plasma lipids, plasma vitamins, alcohol and cigarette consumption, and intake of milk and citrus fruits. The results were all obtained at the second follow-up examination (BS III, 1971-73). Cancer of the lung, stomach, large bowel, and all other sites were treated separately. The average follow-up from BS III until death varied from 3.7 years (other sites) to 4.9 years (cancer of the lung). Of 129 cancer deaths, the highest incidence was found for cancer of the lung (38) followed by stomach (19) and large bowel, (15) and the remainder (57) was for other sites. Plasma lipids did not differ significantly among cases and controls. However, the lowest values were observed in colorectal cancer and gastric carcinoma (mean cholesterol, 213 mg/dl). beta-Carotene was significantly lower in cancer cases of the lung than in controls (14.8 micrograms/dl vs. 23.7; P less than .05). It was also low in gastric cancer cases (13.0 micrograms/dl). Vitamin A was below average only in cases with gastric cancer (difference due to the small number not significant). Vitamin C was consistently lower in cancer cases than in controls. The lowest value was found for cancer of the stomach and corresponded to a below-average consumption of citrus fruits. Vitamin E was low in cancer of the colon. Plasma lipids correlated strongly with vitamin E (tau = 0.5) and to a lesser extent with vitamin A (tau = 0.25). beta-Carotene correlated poorly with beta-lipoproteins (low-density and very low-density lipoproteins) but significantly with total cholesterol. Smoking was inversely related, as was alcohol consumption, to the beta-carotene level. From these results, the conclusion was that vitamins influence carcinogenesis in humans.
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PMID:Cancer, vitamins, and plasma lipids: prospective Basel study. 659 56

Retinol (vitamin A alcohol) at the doses tested neither induced an increase of frequency of sister chromatid exchanges (SCE) nor cell cycle delay in Chinese hamster V79 cells with or without the metabolic activation of S-9 mix. However, it inhibited SCE frequencies and cell cycle delay in V79 cells induced by the indirect mutagen cyclophosphamide or aflatoxin B1. The inhibition was found to be dose and time dependent. These results suggest that retinol itself may have no direct effect on the genetic materials but rather exert its effects possibly by inhibiting the metabolic activation of an indirect mutagen or carcinogen. Thus, the antitumor activities of retinoids may not be limited to the widely accepted role of preventing the promotion step but also the initiation step of carcinogenesis.
Carcinogenesis 1982
PMID:Retinol (vitamin A) inhibits sister chromatid exchanges and cell cycle delay induced by cyclophosphamide and aflatoxin B1 in Chinese hamster V79 cells. 680 8

Zinc deficiency enhances experimental esophageal tumor induction. Vitamin A supplementation inhibits carcinogenesis in animals. Plasma zinc and plasma vitamin A levels are reduced in several human squamous cancers, but have not been studied in a US population with esophageal cancer. Therefore, we measured plasma zinc and vitamin A in patients with newly diagnosed esophageal cancer. In addition, we assessed hepatic and nutritional status and attempted to control for other factors known to influence plasma zinc and vitamin A levels. Plasma zinc and vitamin A were both significantly less in esophageal carcinoma than in age-matched healthy controls (plasma zinc 65.7 +/- 3.3 micrograms/dl [mean +/- SEM] in esophageal cancer versus 80.5 +/- 2.4 micrograms/dl in controls, P less than 0.01; plasma vitamin A 32.6 +/- 3.4 micrograms/dl in esophageal cancer versus 60.2 +/- 4.2 in controls, P less than 0.001). Overall, 15 of 17 patients with esophageal cancer had decreased plasma zinc and/or decreased plasma vitamin A. Our findings are compatible with a hypothesis that zinc or vitamin A deficiency may be co-factors in the induction of human esophageal carcinoma.
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PMID:Plasma zinc and vitamin A in human squamous carcinoma of the esophagus. 683 64

Nutrition and cancer interact in a number of important ways and nutritional factors are increasingly recognized as relevant to both the prevention and treatment of cancer. The role of several nutrients in cancer development is considered briefly here. Deficiency of riboflavin (Vitamin B2) prolongs the survival of tumor-bearing animals, but may accelerate carcinogenesis caused by certain agents, as flavin cofactors are involved in drug and carcinogen metabolism. Deficiency of Vitamin A may enhance the development of tumors of epithelial origin, particularly lung. Evidence is accumulating that Vitamin A and/or its precursors, the B-carotenes, may possibly have an effect in chemoprevention of certain of these epithelial cancers both in animals and in man. The consumption of dietary fat among various nations is correlated closely with increased development of cancers of the breast, colon, and prostate, and possibly of other organs. Studies of migrant populations from Japan to the United States show changes in prevalence of stomach and colon cancer in the direction of the native United States population. Sources of nitrites are of concern because of their potential conversion to carcinogenic nitrosamines. Limitation of the delivery of nitrites may be difficult to accomplish so investigators are exploring the blockade of conversion of nitrites to nitrosamines. Nutrition should not be viewed as the sole means of cancer prevention and treatment but rather as a vital component of any treatment plan.
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PMID:Nutrition and cancer: state of the art relationship of several nutrients to the development of cancer. 718 45

The inhibitory effect of dietary supplementation of certain retinoids on mammary carcinogenesis in the rat has been reported from our laboratory. Specific cytosolic retinoic acid binding proteins (cRABP) as well as retinol binding proteins sedimenting as 2S components have been detected in the mammary tissue during normal and neoplastic differentiation. Relatively higher levels of cRABP were observed in the mammary glands from pregnant animals as well as in ovarian hormone independent tumors; whereas in glands obtained from lactating rats and in hormone dependent tumors, lower levels of cRABP were evident. Exogenous treatment of such animals with estradiol-17 beta enhanced the levels of cRABP. The results indicate a possible correlation between endocrine and retinoid function in both normal and neoplastic differentiation of mammary tissue. [3H]retinoic acid-RABP complex, under appropriate conditions, translocates into th nucleus. Unbound [3H]retinoic acid, however, failed to associate with the nuclear sites. Additional studies indicate a possible selective inhibition of ovarian hormones independent tumors by the retinoids.
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PMID:Retinoid binding in normal and neoplastic mammary tissue. 720 Jul 17


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