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Query: UMLS:C0699790 (colon cancer)
28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 1971-1973 at the third examination of the Basel Study started in 1959, the major antioxidant vitamins and carotene were measured in the plasma of 2974 men. A subsample and their families were reinvestigated in 1977-79. During the 12-y observation period (1973-85) 553 men died, 204 of cancer (lung cancer 68, stomach cancer 20; colon cancer 17, all other malignancies 99). We found significantly lower mean carotene levels for all cancer, bronchus cancer, and stomach cancer (all P less than 0.01) compared with the 2421 survivors. The relative risk of subjects with low carotene (less than 0.23 mumol/L) was significantly elevated (P less than 0.05) for lung cancer (Cox's model). Higher risks were noted for all cancer (P less than 0.01) if both carotene and retinol were low. Low plasma carotene which is known to reflect carotene intake is in our study associated with increased cancer risk.
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PMID:Beta-carotene and cancer prevention: the Basel Study. 198 97

The prevention of cancer by agents in our diet has led to the concept that oxygen radicals are a necessary component of a variety of human cancers including breast, colon and prostatic cancer. These cancers are putatively promoted by estradiol, bile acids and androgens. Epidemiological studies have shown that these cancers are suppressed in vegetarian populations. Vegetable components that may be responsible for this cancer prevention are Vitamin A, retinoids and protease inhibitors (PIs). These agents have been shown to suppress the formation of hydrogen peroxide in promoter-induced neutrophils. They also have been shown to block two-stage carcinogenesis and breast cancer when fed to animals. PIs also suppress experimentally-induced colon cancer and spontaneous liver cancer. Moreover, a new series of cancer-preventive agents, Sarcophytols (isolated by Fujiki and co-workers), are capable of suppressing two-stage carcinogenesis, breast and colon cancers in rodents when given in low concentrations. Sarcophytols were also active suppressors of H2O2 formation of 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced neutrophils. These observations point to an essential role of oxygen radicals in carcinogenesis. Suppression of the oxygen radical response of neutrophils in relation to cancer preventive agents is a facile assay of these important substances. The mechanism of action of oxygen radicals in promoting carcinogenesis is a multiple one, including: (1) activation of oncogenes, (2) modification of DNA bases, and (3) formation of single-strand breaks leading to poly(ADP)ribose polymerase activation.
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PMID:Prevention of cancer by agents that suppress oxygen radical formation. 206 Aug 47

A search of the literature using National Library of Medicine databases and individual cancer journal articles yielded over 500 compounds with published chemopreventive activity in animals. From these, an initial 16 agents or agent combinations have been evaluated in the following animal tumor models: mouse skin papillomas/carcinomas induced by 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-acetate; rat breast adenocarcinoma induced by N-methyl-N-nitrosourea or 7,12-dimethylbenz(a)anthracene; hamster lung carcinoma induced by N-methyl-N-nitrosourea or diethylnitrosamine; mouse bladder papillary carcinoma induced by N-butyl-N-(4-hydroxybutyl)nitrosamine; and rat and mouse colon cancer induced by azoxymethane/methylazoxymethanol acetate. Some of the most interesting positive results observed include 4-hydroxyphenyl retinamide plus tamoxifen in breast cancer, piroxicam in colon cancer, dimethylfluoroornithine in breast and bladder cancer, oltipraz in lung cancer, dehydroepiandrosterone in colon cancer, and molybdate in bladder cancer. Eighteen human intervention trials in progress are described that involve the following agents: beta-carotene (eight trials). Retinol/retinoic acid (seven trials), vitamins C and E (three trials), 4-hydroxyphenyl retinamide (one trial), piroxicam (one trial), and calcium (one trial). By organ site these studies involve cancer of the lung (six studies), skin (five studies), colon (four studies), breast (one study), and uterine cervix (two studies).
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PMID:Identification of candidate cancer chemopreventive agents and their evaluation in animal models and human clinical trials: a review. 240 15

A case-control study was carried out in the populations of two Belgian provinces that differed in food consumption habits, particularly fat intake. There were 453 colonic and 365 rectal cancer cases and 2,851 population controls. There were no significant differences in the average intake of the major nutrients, with the exception of carbohydrates; patients had a larger intake, limited to oligosaccharides. In both provinces, in males and females having cancer of the colon or the rectum, the intake of linoleic acid was lower than among controls; for dietary fibers, a smaller intake was observed among patients in one province. The relative risks were computed for four levels of daily intake of each nutrient. A positive trend was found for oligosaccharides in all subgroups, and a negative trend was found for polysaccharides, the latter for colon cancer patients only. There was a constant and significant negative trend for linoleic acid, with a similar negative trend for dietary fiber. None of these trends were affected by further adjustment for total calorie intake. For several vitamins and minerals, less marked, less constant effects were observed. They tended to be negative for vitamin B1, vitamin B6, and iron; they were positive for retinol and vitamin B2.
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PMID:Colorectal cancer and the intake of nutrients: oligosaccharides are a risk factor, fats are not. A case-control study in Belgium. 282 39

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

Seventeen patients with non-metastatic carcinoma of the colon (9 male, 8 female) were compared with age- and sex-matched controls in a study examining the relationship of diet and altered cholesterol metabolism with carcinoma of the colon. Bile acid excretion in the faeces was significantly less in cancer patients (P less than 0.001), and a significantly lower intake of retinol (P less than 0.01) and vitamin A (P less than 0.05) was demonstrated in female cancer patients. There was no difference between patients and controls in hepatic cholesterol enzyme activity or in fasting plasma lipid levels.
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PMID:Carcinoma of the colon--association with low dietary vitamin A in females: preliminary communication. 376 Dec 90

Epidemiologic studies of diet and cancer have been facilitated in Hawaii by the multiethnic composition of its population and the consequent heterogeneity in dietary intakes. Studies of migrant populations, particularly the Japanese, have firmly supported the conclusions that environmental factors are of predominant etiologic significance for most major sites of cancer, and that these factors may exert their influences at particular periods of life. Recent observations on Filipino migrants reproduce most of the findings in the Japanese, although they do not show the same abrupt increase in colon cancer rates to the high levels found in Caucasians. Data on dietary intakes in these populations support several of the prevailing hypotheses regarding the etiology of certain gastrointestinal and hormone-dependent cancers. Several case-control studies of diet and cancer have been completed or are ongoing in Hawaii. Some of these have included comparable studies in Japan, but the findings in Hawaii have generally not been reproduced in Japan. Weak associations with dietary fat have been found in Hawaii for breast cancer (particularly in Japanese women) and for prostate cancer (particularly in men greater than or equal to 70 years of age). Vitamin A (especially carotene) has been shown to be inversely associated with lung cancer risk in men, but positively associated with prostate cancer risk in older men. Vitamin C may be inversely related to bladder cancer risk, but has shown no relationship to lung or prostate cancer risk. These and other findings are discussed in terms of future needs for epidemiologic research in this field.
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PMID:Multiethnic studies of diet, nutrition, and cancer in Hawaii. 391

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 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

In this review we have examined epidemiological data from a variety of sources to assess the relation between vitamin A intake and cancer risk. The potential for recall bias in case-control studies makes their interpretation difficult, particularly if we are searching for modest associations. Prospective data are preferable, but sparse. Studies of blood levels of carotenoids may be informative if the blood is stored at ultra-low temperatures; however, studies of blood retinol levels are largely uninformative as an index of dietary intake because blood retinol is not well correlated with intake except in vitamin A-deficient populations. We have also reviewed the evidence for an influence of vitamin A intake on the incidence of cancer at the three major cancer sites accounting for a substantial portion of cancers in developed countries. The available data are compatible with a modest inverse association between intake of vitamin A and breast cancer, although it is not clear whether this effect may be due to preformed vitamin A, carotenoids, or both. The evidence that vitamin A protects against colon cancer is unconvincing. In the case of prostate cancer, early suggestions that vitamin A may increase incidence have not been confirmed by subsequent studies. Fortunately, prospective data from a number of large ongoing cohort studies in the United States and Europe should be available within the next 5 years or so. These data will permit further assessment of potential correlations between vitamin A and cancer at various sites by analysis of much larger numbers of cases than are presently available.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vitamin A and cancers of the breast, large bowel, and prostate: epidemiologic evidence. 820 83


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