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

The relationship between various dietary constituents and colon cancer has been demonstrated by previous research. This study was conducted to investigate the combined effects of several dietary constituents on the preneoplastic stage of azoxymethane (AOM)-induced colon cancer in rats. A nutritionally adequate, "low-risk" (LR) diet was formulated through the modulation of dietary fat, fiber, protein, vitamins A and E, and selenium. Female F344 rats were given three weekly subcutaneous injections of AOM and were maintained on either the LR diet or a "high-risk" (HR) diet. After 12 weeks, the rats were killed and the following parameters were determined: pH of colon contents, fecal beta-glucuronidase activity, tissue ornithine decarboxylase (ODC) activity, and colonic labeling index. The pH of the colon contents and incremental labeling index were lower in the group given the LR diet and treated with AOM compared with the group given the HR diet and treated with AOM; however, no statistically significant dietary effects were observed for beta-glucuronidase and ODC activities. The results of this study indicated that the colons of rats fed the LR diet exhibited different proliferative characteristics than did the colons of rats fed the HR diet.
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PMID:The effects of a "low-risk" diet on cell proliferation and enzymatic parameters of preneoplastic rat colon. 281 30

Research in varied populations, in appropriate animal models, and through other laboratory techniques, in great part fostered through the National Large Bowel Cancer Program of the National Cancer Institute, has provided a reasonable basis for assessing environmental elements as to risk for large bowel cancer. It was noted that the term large bowel cancer needs to be specifically related to subsections of the large bowel that appear to have different risk factors. For the major type of neoplastic disease in the large bowel, that in the descending and sigmoid colon, there is a good association with nutrition and specific nutritional elements. 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, itself related to cereal fiber intake. These two major elements are sufficiently secure as to underlying scientific data and understanding of mechanisms to permit utilizing them for personal modification of risk. Thus, a dietary regimen low in total fat, 20% of calories, and higher in cereal fiber, of the order of 30 g per day, are indicated and would serve to reduce risk not only in the general population, but most likely also in patients who have been successfully treated through conventional modalities. There are also suggestions that regular intake of yellow and green vegetables, of foods with calcium salts, selenium, and other micronutrients, lower risk even more. Further research is needed to provide the data base necessary for deliberate interventions with these agents.
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PMID:Potential for personal modification of risk for developing colon cancer. 299 20

Evidence pertaining to the role of dietary factors in carcinogenesis comes from both epidemiological studies and laboratory experiments. In 1982, the Committee on Diet, Nutrition, and Cancer of the National Research Council conducted a comprehensive evaluation of this evidence. That assessment as well as recent epidemiological and laboratory investigations suggest that a high fat diet is associated with increased susceptibility to cancer of different sites, particularly the breast and colon, and to a lesser extent, the prostate. Current data permit no definitive conclusions about other dietary macroconstituents including cholesterol, total caloric intake, protein, carbohydrates and total dietary fiber. Specific components of fiber, however, may have a protective effect against colon cancer. In epidemiological studies, frequent consumption of certain fruits and vegetables, especially citrus fruits and carotene-rich and cruciferous vegetables, is associated with a lower incidence of cancers at various sites. The specific components responsible for these effects are not clearly identified, although the epidemiological evidence appears to be most consistent for a protective effect of carotene on lung cancer and less so for vitamins A and C and various cancer sites. The laboratory evidence is most consistent for vitamin A deficiency and enhanced tumorigenesis, and for the ability of various nonnutritive components in cruciferous vegetables to block in-vivo carcinogenesis. The data for minerals and carcinogenesis are extremely limited, although preliminary evidence from both epidemiological and laboratory studies suggests that selenium may protect against overall cancer risk. Frequent consumption of cured, pickled, or smoked foods, possibly because they may contain nitrosamines or polycyclic aromatic hydrocarbons, appears to increase the risk of esophageal or stomach cancer, however, the specific causative agents in these foods are not clearly identified. Excessive alcohol consumption among smokers appears to be associated with an elevated risk of cancers of the oral cavity, esophagus, larynx, and respiratory tract. The mechanisms of action of dietary factors on carcinogenesis are poorly understood. The NRC committee, and more recently, the National Cancer Institute and the American Cancer Society have proposed interim dietary guidelines to lower the risk of cancer. These guidelines are consistent with general dietary recommendations proposed by U.S. government agencies for maintenance of good health.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diet, nutrition, and cancer. 301 Mar 79

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

Recombinant human interferon alpha inhibits growth of a human colon cancer cell line, Colo 205. To explore the mechanisms of IFN induced growth inhibition, quiescent Colo 205 cells were stimulated to proliferate in serum-free media by defined growth factors. Addition of insulin, transferrin and selenium (ITS) stimulated DNA synthesis, as measured by 3H-thymidine incorporation, in a dose-dependent manner. IFN-alpha (at concentrations greater than 100 U ml-1) inhibited ITS stimulated DNA synthesis by 63%. Inhibition of cell cycle traverse was confirmed by flow cytometric analysis. Although IFN inhibited growth of ITS-treated cells, steady state levels of c-myc mRNA remained above levels observed in unstimulated cells. IFN inhibited DNA synthesis only when added prior to mitogen stimulation. IFN, added 6 h after exposure of quiescent cells to ITS, failed to inhibit cell growth. Addition of increasing concentrations of ITS failed to overcome the IFN-induced growth inhibition. These results suggest IFN may inhibit cell growth in part by antagonizing the action of growth factors.
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PMID:Inhibition of mitogen stimulated growth of human colon cancer cells by interferon. 316 5

Breath methane and hydrogen, plasma acetate, serum selenium, vitamin A and beta-carotene were measured in 47 patients from whom colonic polyps had been removed by endoscopic polypectomy between 3 months and 2 years previously. Patients were compared with 39 control subjects in whom no abnormality was detected during colonoscopy. The proportion of methane exhalers was significantly (p less than 0.0005) higher in patients after polypectomy (66.0%) than in controls (28.2%). Mean plasma acetate was lower (p less than 0.025) in post-polypectomy patients (70.5 microM) than in control subjects (97.1 microM) while breath hydrogen was similar in both groups. The serum concentrations of the antioxidants selenium and beta-carotene showed no differences between the groups whereas vitamin A was higher (p less than 0.01) in serum samples of patients after polypectomy than of controls. These findings indicate that the colonic environment in post-polypectomy patients exhibits certain characteristics which may be related to the formation of benign tumors and possibly colon cancer.
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PMID:Metabolic and nutritional parameters in patients after colonic polypectomy. 322 Jan 81

Colon cancer is one of the most frequent forms of cancer in the Federal Republic of Germany and in most Western countries, but is, however, generally rare in Africa, Asia, and Latin America. Based on epidemiological investigations, differing dietary practices are considered to be main reason for these differences. A high fat and protein consumption was identified as a risk factor, while a high fibre content of the diet was found to be protective. Existing hypotheses of the etiology of colon cancer, which are based on the two-stage initiation-promotion model, regard interactions between initiators, promotors, and inhibitors as decisive for the final outcome of colon cancer. Possible initiators are pyrolysis products of protein-rich food (meat or fish), generated by heating, and products of metabolism of intestinal bacteria (e.g. faecal mutagens, N-nitroso compounds, transformation products of bile acids). Fats probably exert their influence only at the promotional stage. The diet-dependent bacterial formation of deoxycholic and lithocholic acids is a possible mechanism which has been experimentally substantiated. The protective effect of a diet rich in fibre seems to be mediated in particular by dilution and adsorption of harmful compounds. Further protective factors in human diet may be calcium, selenium, vitamin A and beta-carotene. In this paper, evidence, both supporting and refuting the existing hypotheses, is discussed, as well as the possibilities of dietary prevention of colon cancer.
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PMID:[Nutrition and the etiology of colon cancer: from descriptive epidemiology to dietary prevention]. 331 74

The relationship between various dietary constituents and colon cancer has been demonstrated by previous research. We conducted a study to investigate the combined effects of several dietary constituents on intestinal tumor incidence in azoxymethane (AOM)-induced colon cancer in rats. A nutritionally adequate, "low-risk" (LR) diet was formulated through nonextreme dietary manipulations of dietary fat, fiber, protein, vitamins A and E, and selenium. Seventy-two female F344 weanling rats were given three weekly subcutaneous injections of either AOM or physiological saline solution, and were maintained on either the LR or a "high-risk" (HR) diet. Food consumption and body weights were monitored on a weekly basis throughout the study. Tumor incidence was determined 36 weeks following the first injection of AOM. The incidence of adenocarcinomas in the LR diet group was 4.2% compared with 29.2% in the HR diet group. There were no significant differences in the incidence of small intestinal tumors or in the incidence of benign polyps between the diet groups. The results of the study indicated a significant protective effect of the various chemopreventive dietary factors when combined in an LR diet for colon cancer.
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PMID:The effects of a "low-risk" diet on tumor incidence in chemically induced colon cancer in rats. 335 10

Diminished blood selenium levels have been associated with increased risk of gastrointestinal cancers in man, while dietary selenium supplementation reduces the incidence of experimental colon cancer in rats. However, no previously published data are available concerning selenium and the evolution of colon cancer from benign neoplastic colonic polyps through localized and metastatic cancer. To assess any influence of selenium on this polyp to cancer sequence, we measured plasma and erythrocyte selenium levels in colonoscopically and histologically evaluated patients with adenomatous polyps (group I), locally resectable colon cancer (group II), metastatic colon cancer (group III), and selected colonoscopy negative controls (group IV). We found no difference in selenium levels between groups IV versus groups I or II. Likewise, within group I, no difference in selenium was present for different polyp histologies or numbers of polyps. However, selenium levels did drop progressively (p = 0.028, ANOVA) from polyp (group I) to local cancer (group II, p = NS vs group I) to metastatic cancer (group III, p less than 0.05 vs group I or group II). Parallel changes were seen in both plasma and erythrocyte levels, suggesting that these selenium abnormalities are of long duration, reflecting tissue stores, and therefore capable of influencing cancer risk. We conclude that selenium stores may not be an important factor in the de novo formation of benign neoplastic colonic polyps. Although these data suggest that selenium does not affect the polyp-cancer sequence, it is possible that a subset of patients with polyps and the lowest selenium levels are at higher risk for malignant transformation. However, these human data do not support a significant role for selenium in colon carcinogenesis.
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PMID:Selenium status and the polyp-cancer sequence: a colonoscopically controlled study. 338 7

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


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