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Query: UMLS:C0699790 (colon cancer)
 28,837 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

Several studies have demonstrated that certain essential fatty acids present a specific cytotoxicity for tumor cells. However, no investigation of this type has been performed on human colon cancer cells to date. This study investigated the effect of gamma-linolenic acid (GLA), eicosapentaenoic acid (EPA) and prostaglandin (PG) E1 on the proliferation and metabolism of three human colon cancer cell lines: HT 29, HRT 18, and CACO 2. GLA, EPA and PGE1 all inhibited the proliferation of the three cell lines, but with a decreasing gradient of sensitivity: HRT 18 > HT 29 > CACO 2, and with different IC50 values. PGE1 was markedly less effective than the other two. GLA and EPA increased lipid peroxidation and membrane fluidity in a dose-dependent manner. The presence of indomethacin did not modify the effects of GLA and EPA. In addition, PGE1 had little effect on membrane fluidity and lipid peroxidation. The antitumoral effect thus does not appear to be mediated by PGE1. Addition of vitamin E decreased the effects of GLA and EPA, which supports the hypothesis of direct action by these fatty acids. In conclusion, while EPA and GLA have an antitumoral effect in vitro, their effect on primary cultures of normal human colon cells must be investigated to determine whether this effect is specific to tumoral cells, as has been observed for other cell types.
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PMID:Effects of eicosapentaenoic acid, gamma-linolenic acid and prostaglandin E1 on three human colon carcinoma cell lines. 133 9

This review of corn oil provides a scientific assessment of the current knowledge of its contribution to the American diet. Refined corn oil is composed of 99% triacylglycerols with polyunsaturated fatty acid (PUFA) 59%, monounsaturated fatty acid 24%, and saturated fatty acid (SFA) 13%. The PUFA is linoleic acid (C18:2n-6) primarily, with a small amount of linolenic acid (C18:3n-3) giving a n-6/n-3 ratio of 83. Corn oil contains a significant amount of ubiquinone and high amounts of alpha- and gamma-tocopherols (vitamin E) that protect it from oxidative rancidity. It has good sensory qualities for use as a salad and cooking oil. Corn oil is highly digestible and provides energy and essential fatty acids (EFA). Linoleic acid is a dietary essential that is necessary for integrity of the skin, cell membranes, the immune system, and for synthesis of icosanoids. Icosanoids are necessary for reproductive, cardiovascular, renal, and gastrointestinal functions and resistance to disease. Corn oil is a highly effective food oil for lowering serum cholesterol. Because of its low content of SFAs which raises cholesterol and its high content of PUFAs which lowers cholesterol, consumption of corn oil can replace SFAs with PUFAs, and the combination is more effective in lowering cholesterol than simple reduction of SFA. PUFA primarily lowers low-density-lipoprotein cholesterol (LDL-C) which is atherogenic. Research shows that PUFA has little effect on high-density-lipoprotein cholesterol (HDL-C) which is protective against atherosclerosis. PUFA generally improves the ratio of LDL-C to HDL-C. Studies in animals show that PUFA is required for the growth of cancers; the amount required is considered to be greater than that which satisfies the EFA requirement of the host. At this time there is no indication from epidemiological studies that PUFA intake is associated with increased risk of breast or colon cancer, which have been suggested to be promoted by high-fat diets in humans. Recommendations for minimum PUFA intake to prevent gross EFA deficiency are about 3% of energy (en%). Recommendations for prevention of heart disease are 8-10 en%. Consumption of PUFA in the United States is 5-7 en%. The use of corn oil to contribute to a PUFA intake of 10 en% in the diet would be beneficial to heart health. No single source of salad or cooking oil provides an optimum fatty acid (FA) composition. Many questions remain to be answered about the relation of FA composition of the diet to various physiological functions and disease processes.
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PMID:Food uses and health effects of corn oil. 225 33

This paper provides an overview of our knowledge on the involvement in cancer of vitamins A, C and E and of calcium, selenium and zinc. This work is a background for studies on dietary magnesium's effects on cancer. Consumption of vitamin A and its dietary precursors has been associated with reduced cancer at several sites in human and animal studies. Carcinogenesis studies using several models of cancer have been conducted on the influence of vitamin A deficiency, vitamin A excess and supplementation of vitamin A analogues. Vitamins C and E are effective in the prevention of N-nitroso compound (nitrosamine) formation. Vitamin C is effective in aqueous and vitamin E is effective in non-aqueous media. Both of these vitamins also have inhibited carcinogenesis by preformed carcinogens at several sites, but enhancement has been observed at some sites when excess vitamin treatment was studied. The potential role of calcium in the prevention of colon cancer is being pursed. Few experimental studies have been conducted but data support an effect of calcium on colonic epithelial proliferation. Epidemiological and especially experimental results suggest an inhibition of cancer by dietary selenium. In animal studies, selenium supplementation has been particularly effective in inhibiting colon and mammary carcinogenesis, but enhanced carcinogenesis was observed in some studies on skin, liver and pancreas cancer. Data suggest that zinc deficiency may be a factor in esophageal cancer; however, studies on tumor growth have demonstrated retarded tumor growth in zinc-deficient animals.
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PMID:Effects of the intake of selected vitamins and minerals on cancer prevention. 266 27

It has been hypothesized that selenium, vitamin E, and fiber reduce the risk of specific human cancers. Evidence for a role of selenium is based primarily on animal studies, inverse geographic correlations between intake and site-specific cancer incidence, and an inverse association between serum selenium and subsequent risk of cancer. Certain geographic areas with high fiber intakes have lower rates of colon cancer and, in several case-control studies, consumption of fruits and vegetables has been associated with a lower risk of large bowel cancer. Suspicion that vitamin E might reduce the risk of human cancer is largely theoretical; a protective association has been observed in only 1 small study of breast cancer. The evidence that these 3 dietary factors reduce the risk of human cancer remains incomplete. Future epidemiologic investigations should simultaneously assess a wide variety of dietary factors to address potential confounding and interacting effects. Prospective study designs should be used whenever possible to avoid any influence of cancer on dietary intake or its measurement.
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PMID:Selenium, vitamin E, fiber, and the incidence of human cancer: an epidemiologic perspective. 303 99

Chemoprevention of various epithelial cancers with vitamins or minerals has been the subject of multiple intervention trials to assess the impact of supplementation. These include several trials in patients with adenomatous polyps of the colon, a precursor lesion for colon cancer. The authors interviewed 255 women who underwent colonoscopy at Columbia Presbyterian Medical Center between 1983 and 1985 with a telephone-administered structured questionnaire. Eleven interviews were excluded for various reasons. Overall, 57.7 percent of the 244 interviewees used vitamin pills on a regular basis (at least once a week for a year); 6.6 percent of the interviewees used vitamin A, 20.7 percent used vitamin C, and 16.2 percent used vitamin E. There were no statistically significant differences in vitamin usage among women with adenomatous polyps of the colon (105 cases), women with colon cancer (56 cases), and women without colonic neoplasia (83 cases). Despite widespread use of supplementary vitamins, this study failed to demonstrate major benefits in preventing colon polyps or cancer.
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PMID:Vitamin supplements among women with adenomatous polyps and cancer of the colon. Preliminary findings. 337 66

The effects of cabbage and vitamin E on colon carcinogenesis were investigated in Swiss mice treated with 1,2-dimethylhydrazine. Throughout the experiment the mice were fed a laboratory chow diet (46 mg vitamin E per kg) or chow containing 13 g cabbage per 100 g or 180 mg vitamin E per kg. Starting after 31 days of diet treatment the mice received 7 weekly s.c. injections of DMH. They were sacrificed 17 weeks after the first dose of DMH. While diet did not significantly alter colon tumor response, some trends were observed. Female mice given cabbage had a higher incidence (percent of mice with a tumor) and multiplicity (tumors per tumor bearing mouse) of colon tumors. Males were little affected by cabbage apart from a lower incidence of adenocarcinomas. Compared with mice fed the control diet those given vitamin E had a higher colon tumor incidence. This effect, which was stronger in females, was due to an increased incidence of adenomas. Vitamin E had little apparent affect on tumor multiplicity apart from a reduction in adenocarcinomas in females and adenomas in males. The data do not support the view that cabbage and vitamin E are protective against colon cancer.
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PMID:Cabbage and vitamin E: their effect on colon tumor formation in mice. 356 89

A study was undertaken to determine whether prediagnostic serum levels of retinol, beta-carotene, vitamin E, and selenium are lower in colon cancer cases compared with matched, population-based controls. Sera were available from 25,802 participants of a serum collection campaign conducted in Washington County, Maryland in 1974. The authors identified from these participants 72 white colon cancer cases, who were first diagnosed with colon cancer during 1975-1983, and 143 white, living, cancer-free controls, matched to cases on the basis of age, sex, month of serum collection, and enumeration in a 1975 private census of Washington County. The mean values of serum nutrients in cases and controls, respectively, were 59.1 micrograms/dl and 61.8 micrograms/dl for retinol (p = 0.22), 32.9 micrograms/dl and 34.4 micrograms/dl for beta carotene (p = 0.52), 1.17 mg/dl and 1.27 mg/dl for vitamin E (p = 0.10), and 11.0 micrograms/dl and 11.5 micrograms/dl for selenium (p = 0.07). There were no consistent trends in the relative odds of colon cancer by quintiles of serum levels for any of the nutrients; however, a relative odds of 3.2 (95% confidence interval = 1.1-8.7) was found when persons in the four lowest quintiles of retinol were compared with those in the highest. No interactions with matching factors or between serum nutrients and no confounding effects of covariables were identified through conditional logistic regression analysis. The findings of this study do not support a strong association of low serum levels of retinol, beta-carotene, vitamin E, and selenium with an increased risk of subsequent colon cancer.
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PMID:Serologic precursors of cancer. I. Prediagnostic serum nutrients and colon cancer risk. 368 15

Neoplasms affecting different subsections of the large bowel appear to have different risk factors. For the major type of neoplastic disease in the large bowel, that in the descending and sigmoid colon, a good association with nutrition and specific nutritional elements has been found. The risk of this type of colon cancer is proportional to the customary dietary fat intake--high in the Western World and low in the Orient. It is inversely proportional to stool bulk, which is itself modulated by cereal fibre intake. Fat and fibre, as the two major elements implicated, are sufficiently secure with regard to underlying scientific data and understanding of mechanisms, to permit utilising them to modify risk. Thus, a dietary regimen low in total fat, 20% of calories, and higher in cereal fibre, of the order of 30 grams/day, is indicated. Such a modified nutritional intake could be expected to reduce risk, not only in the general population, but most likely also in patients who have been treated successfully by conventional means. Additional evidence suggests that regular intake of yellow and green vegetables, of foods containing calcium salts, selenium and other micro-nutrients, lower the risk even more. More research is needed to provide the data necessary for deliberate intervention with these agents. Gastric cancer, on the other hand, has a distinct set of risk factors, namely, intake of pickled and salted fish or beans. Other risk factors are associated with residence in areas where the geochemical or agricultural sources of nitrate intake are not balanced by the presence of vitamin C, vitamin E, or certain phenolic antioxidants and nitrite traps such as pyrogallol, tannins, or peptides. The possible genotoxic carcinogen is not yet known, but it could be an alkyl-nitrosamide type of aryldiazonium chemical. The formation of such compounds is inhibited by vitamin C, vitamin E, and certain antioxidants. This fact can be used to decrease deliberately the risk of gastric cancer.
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PMID:Human and laboratory studies on the causes and prevention of gastrointestinal cancer. 609 59

The relationship between estimated intake of selected micronutrients and the risk of colorectal cancer was analysed using data from a case-control study conducted in northern Italy. The study was based on 828 patients with colon cancer, 498 with rectal cancer and 2,024 controls in hospital for acute, non-neoplastic, non-digestive tract diseases. Relative risks (RRs) of intake quintiles were computed after allowance for age, sex and other major potential confounding factors, including an estimate of total energy intake. No apparent trend in risk across intake quintiles was evident for retinol, vitamin D, methionine and calcium. For beta-carotene, ascorbic acid, vitamin E and folate there was a trend of a protective effect with increasing consumption: the RR for the highest versus the lowest quintile was 0.32 for beta-carotene, 0.40 for ascorbic acid, 0.60 for vitamin E and 0.52 for folate. These inverse associations were similar for colon and rectal cancer, and consistent across strata of sex and age. When simultaneous allowance was made for all these micronutrients, besides other covariates, the only persistent protective effects were for beta-carotene (RR = 0.38 for the highest quintile) and ascorbic acid (RR = 0.52). Whether this reflects a specific, or stronger, effect of these micronutrients, rather than problems of collinearity between micronutrients or other limitations of the data, remains open to discussion. Still, this study suggests that specific micronutrients may exert an independent protective effect against colorectal carcinogenesis.
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PMID:Selected micronutrient intake and the risk of colorectal cancer. 798 Oct 67


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