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

The addition of specific fiber supplements to semipurified diets has been shown to stimulate large bowel cell proliferation in laboratory rodents. Relatively insoluble fibers such as cellulose, which is poorly fermented, the more-soluble oat bran, and inert bulking agents such as kaolin produce little or no effect on cell growth. On the other hand, wheat bran, pectin, guar gum, and degraded carageenan all stimulate large bowel cell proliferation, the greatest growth response tending to occur in the cecum or proximal colon. The proximal large bowel is also the major site for the intestinal fermentation of dietary fiber and any other nonabsorbed carbohydrates. The fermentation of fiber by colonic microorganisms results in the production of short-chain fatty acids and a lower pH of large bowel contents, metabolic events known to be associated with increased epithelial cell growth. In general, factors that stimulate cell growth also enhance tumor development, a concept that holds true in the colon even for dietary fibers such as pectin and guar gum. Wheat bran can also stimulate colon carcinogenesis when fed only during carcinogen exposure. Oat bran and corn bran may stimulate colon carcinogenesis by increasing fecal bile acid excretion, a feature of many soluble fibers, while the acidification of large bowel contents is associated with an increased frequency of chemically induced colonic cancers. A greater understanding of colonic metabolism and cell physiology is needed to define fully the mechanisms by which dietary fibers modify colon cancer development.
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PMID:Effect of dietary fiber on colonic cell proliferation and its relationship to colon carcinogenesis. 281 52

A 2 X 2 X 2 factorial experimental design was used to investigate the effects of supplemental calcium (Ca) (0.5% versus 1.0% of diet as Ca gluconate) and vitamin D3 (D) (1000 IU/kg diet versus 2000 IU/kg diet) on 1,2-dimethylhydrazine-induced colon carcinogenesis in male F344 rats promoted with a 20% corn oil diet. Animals on the high-fat (HF) diet had an increased tumor incidence compared to the low-fat (LF) control diet (86% versus 53%, P less than 0.05) and supplemental Ca or D reduced this to or below the LF incidence (HF + Ca: 53%, HF + D: 47%). However, supplemental Ca or D had no inhibitory effect with LF diets (LF + Ca: 67%, LF + D: 60%). The results of this study indicate a possible role for supplemental Ca or D in the prevention of colon cancer, effective only in HF diets.
Carcinogenesis 1988 Jan
PMID:Inhibition of dietary fat-promoted colon carcinogenesis in rats by supplemental calcium or vitamin D3. 282 33

Dietary fibers may tend to enhance or inhibit chemically induced experimental colon cancer, depending on the particular fiber consumed. This study examined the relationship between colonic thymidine kinase enzyme activity and mucin histochemistry and the reported effects of various dietary fibers on chemically induced colon carcinogenesis. Fiber-supplemented diets containing fibers reported to inhibit (wheat bran) or enhance (guar gum, carrageenan) chemically induced colon carcinogenesis in the rat were selected. Four groups of male Fischer 344 rats consumed 10% wheat bran, 5% guar gum, 5% carrageenan, or fiber-free diets ad libitum for 4 weeks. At the completion of the treatment period, the distal 12 cm of colonic mucosa was scraped off and homogenized for determination of thymidine kinase activity, and a 0.5-cm section of midcolon was processed by the high-iron diamine/Alcian blue method for mucin histochemistry. Final animal weights did not differ significantly among groups. Thymidine kinase enzyme specific activity (mumole thymidine phosphate formed x 10(6)/min/mg protein, means +/- SEMs) was not significantly different in the fiber-free, wheat bran, and guar gum groups (10.98 +/- 1.50, 7.41 +/- 1.09, and 9.11 +/- 2.04, respectively) but was markedly elevated at 41.84 +/- 4.65 in the carrageenan group (alpha less than 0.001). Mucin histochemistry failed to reveal any significant differences among dietary groups.
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PMID:Alterations in colonic thymidine kinase enzyme activity induced by consumption of various dietary fibers. 284 79

The human evidence that dietary fiber prevents the development of colon cancer has been reviewed. The correlational studies are consistent with a protective effect in 61.9 per cent of reports. However, these studies are all retrospective and largely uncontrolled. The case-control studies provide evidence of a protective effect in only 48 per cent of reports. It is of additional concern that some human studies have found an association between tumor enhancement and some fiber-containing foods. Whereas this is not sufficient evidence to implicate dietary fiber as a promoter of human colon cancer, it does perhaps argue for a more conservative approach to recommending high-fiber diets as a means of cancer prevention. The animal data show that different sources of dietary fiber produce markedly different effects on colon carcinogenesis. Although some fibers exhibit protective properties, others clearly promote tumor development. The mechanisms behind these opposing actions require further investigation. However, one thing is clear and that is that dietary fibers do modulate the carcinogenic process and as such provide a valuable tool for probing the mechanisms and stages of colon tumor development. Dietary fiber appears to play a major role in the regulation of normal intestinal function and in the maintenance of a healthy intestinal mucosa. Although there is some evidence that a fiber-deficient diet predisposes to colon carcinogenesis, it is still not known whether an increase in fiber consumption will prevent the development of colon cancer. This is further complicated by not knowing what constitutes a normal level of fiber intake. In the interim, physicians should perhaps advise their patients to consume a moderate diet that contains vegetables, fruits, and whole grains. This will provide a varied source of fiber-containing foods and if consumed in sufficient quantity will optimize intestinal transit and bulk according to individual needs. Isolated fiber supplements have not been shown to be effective in colon cancer prevention. Further attempts to be more specific about what type of fiber to recommend seem premature at this time. However, an intake in the range of 20 to 35 gm per day of dietary fiber from foods has recently been recommended by an Expert Panel.
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PMID:Fiber and colon cancer. 285 41

The effect of butylated hydroxyanisole (BHA) or butylated hydroxytoluene (BHT) on the carcinogenicity in rats of aflatoxin B1 (AFB1) was investigated. AFB1 was administered by gastric intubation to male F344 rats at 25 micrograms/kg body wt three times a week such that a total dose of 1.5 mg/kg (0.48 mmol/kg) body wt was given over a period of 20 weeks and diets containing either 1000 or 6000 p.p.m. BHA or BHT were fed starting one more week before carcinogen, during administration and for one week after cessation. Animals were killed during exposure and at intervals up to 24 weeks after cessation. Liver altered foci and neoplasms were quantified using the exclusion of cellular iron after iron-loading and gamma-glutamyl transpeptidase reaction, as well as conventional staining for identification. Exposure to AFB1 alone induced substantial numbers of altered foci after 20 weeks, and at 24 weeks after cessation of exposure, the incidence of hepatocellular neoplasms was 63%. In the groups receiving BHA or BHT together with AFB1, the numbers of altered foci were decreased at all time points and at termination, the final incidence of liver cell neoplasms and number of neoplasms per animal were also reduced in a dose-related manner. Neoplasms in other organs were rare and were not affected by antioxidant treatment, except for a possible reduction of colon cancer. Thus, BHA and BHT inhibited the hepatocarcinogenesis of concurrently administered AFB1 without shifting the organotropism.
Carcinogenesis 1986 Jul
PMID:Dose-related inhibition of aflatoxin B1 induced hepatocarcinogenesis by the phenolic antioxidants, butylated hydroxyanisole and butylated hydroxytoluene. 287 75

Naturally occurring fecal mutagens, called fecapentaenes, are hypothesized to contribute to large bowel carcinogenesis. To understand health risks it is necessary to relate fecal mutagen concentrations to intestinal pathologies, i.e. colon cancer. However, fast and reliable methods for analysis of stool for fecapentaene levels are not available. This study presents an evaluation of stabilizing effects on synthetic fecapentaene-12 of various antioxidants, indicating tri-ethylamine to give the best results. Furthermore, it describes a fast extraction procedure for human stool and a subsequent HPLC-analysis which produces quantitative data on fecapentaene-12 concentrations within 30 min.
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PMID:Stabilization and quantitative analysis of fecapentaenes in human feces, using synthetic fecapentaene-12. 291 40

Aberrant crypt foci can be identified in the colons of rodents treated 3 wk earlier with azoxymethane, a known colon carcinogen. These crypts can easily be visualized in the unsectioned methylene blue-stained colons under light microscopy, where they are distinguished by their increased size, more prominent epithelial cells, and pericryptal space. They occur as single aberrant crypts or as two, three, or four aberrant crypts in a cluster. We compared the reported ability of carcinogens associated with the human diet to induce colon cancer with the measured rate of induction of aberrant crypts in female CF1 mice and Sprague-Dawley rats. The carcinogens used were 1,2-dimethylhydrazine, methyl nitrosourea, N-nitrosodimethylamine, benzo(a)pyrene, aflatoxin B1, 2-amino-6-methyldipyrido[1,2-alpha:3',2'-d]imidazole, 2-amino-3-methylimidazo[4,5-P]quinoline, 2-amino-3,4-dimethylimidazo[4,5-P]quinoline, and 3-amino-1-methyl-5H-pyrido[4,3-b]indole. Graded doses of these compounds were given to the animals by gavage twice with a 4-day interval, and the animals were terminated 3 wk later. All colon carcinogens induced aberrant crypts in a dose-related fashion. N-Nitrosodimethylamine and 3-amino-1-methyl-5H-pyrido[4,3-b]indole, carcinogenic compounds that do not induce colon cancer, did not induce them. The ability of the studied compounds to induce aberrant crypts was species specific; e.g., aflatoxin B1 and 2-amino-3,4-dimethylimidazo[4,5-P]quinoline induce about 20 times more in rats than mice. This relationship was consistent with their reported ability to induce colon cancer in these species. Results of the present study support the use of the aberrant crypt assays to screen colon-specific carcinogens and to study the process of colon carcinogenesis.
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PMID:Foci of aberrant crypts in the colons of mice and rats exposed to carcinogens associated with foods. 291 53

We have evaluated the interaction of radiation and 1,2-dimethylhydrazine (DMH) with respect to colon carcinogenesis in the Fischer 344 rat and have demonstrated the utility of this model for future more detailed mechanistic studies. In initial experiments, single doses of abdomen-only radiation (9 Gy) or DMH (150 mg/kg) were employed alone or in combination. Radiation was administered 3.5 days prior to the DMH. At 8 months post-treatment, the incidence of DMH-induced colon tumors was doubled by prior radiation exposure. When the protocol was repeated employing a DMH dose of 135 mg/kg with a 6-month observation period, the incidence of tumors induced by DMH alone was reduced, but the combination of radiation plus DMH still resulted in an augmentation of tumor incidence. When the protocol of radiation plus DMH was repeated three times at monthly intervals, a 15-fold increase in tumor incidence (from 5 to 74%) was observed at 6 months post-treatment. This finding demonstrates an apparent synergy between the radiation and the chemical carcinogen. Throughout these studies, the appearance of carcinomas was associated with preexisting colonic lymphoid nodules. The reproducibility of tumor induction as well as range of tumor incidence generated by variations in this system may be adequately sensitive to examine the combination of much lower doses of radiation and/or chemical carcinogen. The relationship between existing lymphoid aggregates which alter local epithelial cell kinetics and which are associated with fenestrations in the basement membrane, and the development of colon cancer in congruent sites may assist in defining dose-response curves for combined agents as well as providing a system for evaluating the mechanisms underlying their interactions.
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PMID:Apparent synergism between radiation and the carcinogen 1,2-dimethylhydrazine in the induction of colonic tumors in rats. 292 75

Colon cancer is one of the most common tumours observed in the western population for which the relationship between epidemiological and laboratory findings and an overall assessment of the influence of diet on carcinogenesis is not straightforward. The aim of this review is to evaluate critically the experimental data which suggest a positive modulating effect of dietary lipids. Although a great number of data are available on the relation between the nature of fat in diet and colon cancer, no clear conclusions can be drawn from their analysis. The lack of consistent findings is due to the discrepancy of the results which may have arisen from methodological differences between the studies. Concerning the influence of the amount of dietary fat on colon cancer, it has been demonstrated that a high fat diet could increase the incidence and the number of colonic tumours in rats. Nevertheless, this positive modulating effect could be seen provided the fat amount in the diet was at least 20% (w/w). This observation is of first importance for colon cancer prevention and must be confirmed for fat of various nature. Systematic dose-effect studies are necessary. The question whether the effect of dietary fat on carcinogenesis is due to the specific action of fat or to an associated caloric effect has been raised several times. Although the previous studies concerned the role of caloric intake versus fat intake in carcinogenesis, the observed effects might have been due to a change in body weight or to changes in other dietary components such as non nutritive fibre, protein and micronutrients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Dietary lipids and experimental colonic carcinogenesis. Critical review of the literature]. 297 51

The multiple-step model of carcinogenesis discussed here identifies the two major stages of initiation and promotion. A more recent research development proposes that oncogenes present in chromosomes are activated by viral, chemical, or physical agents and cause cancer. A great variety of natural mutagens and carcinogens find their way into the modern US diet. Excessive fat and alcohol consumption have been studied in relation to many kinds of malignancies. Dietary anticarcinogens include vitamins A, C, and E, although under certain conditions some generally inhibitive substances can actually enhance carcinogenesis. A provocative hypothesis argues that a high-fiber diet can substantially reduce the likelihood of carcinoma of the colon.
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PMID:Diet, nutrition, and cancer. An update on a controversial relationship. 298 9


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