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

Epidemiological and animal model studies indicate that increased calorie intake increases the risk for colon cancer development. Previous studies in animal models restricted the calorie intake severely, and none of these studies have investigated a dose-response effect of different levels of calorie restriction on colon carcinogenesis. The present study was designed to investigate the effect of various levels of calorie restriction on colon carcinogenesis in male F344 rats fed the low and high fat diets and the effect of these diets on the activities of colonic mucosal and tumor ornithine decarboxylase (ODC) and protein tyrosine kinase. Starting at 5 weeks of age, groups of male F344 rats were fed the low fat or high fat diets ad libitum. At 7 weeks of age, all animals except the vehicle-treated groups were given s.c. injections of azoxymethane (AOM) (15 mg/kg body weight, once weekly for 2 weeks). Four days after the second injection, groups of animals were restricted to 90, 80, or 70% of total calories consumed by the high fat ad libitum group (i.e., 10, 20, and 30% calorie restriction, respectively). In the low fat groups, animals were restricted to 80% of total calories consumed by the low fat ad libitum group (i.e., 20% restriction). Thirty-six weeks after AOM injections, all animals were necropsied and colon tumors were used for histopathology and ODC and protein tyrosine kinase analysis. In the second experiment, the protocol was the same as above except that the animals were sacrificed 5 days after the second AOM injection and colonic mucosal ODC and protein tyrosine kinase activities were assayed. The incidence and multiplicity of colon tumors were significantly inhibited in animals fed the high fat 20% calorie-restricted and high fat 30% calorie-restricted diets, as compared to those fed the high fat ad libitum diet. The regression coefficient representing the dose-response effect of different levels of calorie restriction in both high fat groups is significant. Results also indicate that AOM treatment significantly increased the colonic mucosal ODC and protein tyrosine kinase activities. This stimulation was inhibited by feeding the calorie-restricted diets. ODC and protein tyrosine kinase activities were lower in the colon tumors of animals fed the calorie-restricted diets.
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PMID:Effect of different levels of calorie restriction on azoxymethane-induced colon carcinogenesis in male F344 rats. 239 50

The effects of 2 levels of dietary calcium and 2 types of dietary fat on the promotional phase phase of azoxymethane-induced colon cancer in the F344 rat were investigated. During the initiation phase of carcinogenesis all animals were fed a 5% corn oil AIN-76A diet containing 0.32% Ca in the form of calcium lactate. Rats were then injected with azoxymethane (AOM) weekly for 8 weeks. Thereafter, the rats were fed 1 of 3 diet formulations: a 5% corn oil diet or a 20% corn oil or 20% American Blend oil fat diet, with the level of Ca set at either 0.32% of the diet, a nutrient density simulating a daily human intake of approximately 1700 mg Ca/day, or at 0.04% of the diet, reflecting a human daily intake of approximately 200-250 mg of Ca/day, thus modeling 2 human nutrient density levels for calcium. Measurements of fecal pH during the experiment indicated an acidic adaptation of the large bowel to the lactate anion. Analysis of collected fecal samples showed more total fatty acids to be present in the colon when higher amounts of calcium were consumed. However, results of the tumorigenesis study indicated that calcium lactate fed at the 0.32% level significantly inhibited the development of colonic adenocarcinoma in all dietary groups. Taken together, this investigation supports the hypothesis that calcium supplementation can inhibit colon neoplasia in rats fed a high fat diet; however, under the conditions of this study, the 20% fat level did not significantly promote colon cancer as compared to a 5% fat level.
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PMID:Inhibition of the promotional phase of azoxymethane-induced colon carcinogenesis in the F344 rat by calcium lactate: effect of simulating two human nutrient density levels. 239 78

Monoclonal antibody (MAb) B72.3 detects an epitope carried by high-molecular-weight mucins (tumor-associated glycoprotein, TAG-72) recently identified as sialyl-Tn. B72.3 MAb has a restricted pattern of reactivity with normal tissues but it reacts with a high proportion of epithelial cancers. To determine the possible relationship between neoplastic transformation and reactivity with B72.3 MAb, we have analyzed samples of normal colon, colon cancer and transitional mucosa (mucosa adjacent to colorectal cancer) or reactive mucosa (mucosa adjacent to squamous carcinoma of the anal canal, or mucosa overlying lymphoma). B72.3 MAb reacted strongly with 21/21 specimens of transitional mucosa and with 17/21 specimens of adjacent colon cancer. Reactivity of B72.3 MAb with transitional mucosa was strong and homogeneous, whereas reactivity with cancer tissue was weaker and more heterogeneous. Reactive mucosa adjacent to squamous carcinoma or lymphoma was also reactive with B72.3 MAb. Our findings show that, in the colon, expression of TAG-72 antigen occurs during the process of epithelial cell transformation but is also regulated by factors unrelated to the process of carcinogenesis.
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PMID:Expression of TAG-72 in normal colon, transitional mucosa, and colon cancer. 248 51

Epidemiologic studies of the relationship of diet to cancer etiology are hampered by methodologic difficulties which can be overcome by careful trial design. The use of appropriate dietary assessment instruments is necessary to minimize bias and improve accuracy of diet assessment. Population studies implicate dietary fat intake in the etiology of colorectal carcinogenesis, and the incidence of colorectal malignancies around the world is positively correlated with meat and fat consumption and total calorie intake. Retrospective studies of fat intake yield equivocal results, whereas prospective studies have failed to show a relationship between fat intake and colon cancer risk. An inverse relationship exists between fiber consumption and colorectal cancer incidence and mortality rates. The positive observational studies are supported by laboratory studies of experimental carcinogenesis which show a greater number of tumors in animals fed high-fat or high-calorie diets. Increased fiber intake appears to offer some protection against colorectal cancer. Plausible mechanisms have been proposed in animals for the role of fat and fiber in colorectal carcinogenesis; the mechanisms in human populations await further description. The interrelationships between fat consumption and consumption of dietary fiber and micronutrients have made it difficult to assess the roles of these substances in the etiology of colorectal cancer. Calcium offers protection in animal systems, and the data in humans are suggestive but not yet conclusive. Data on the role of alcohol in colorectal carcinogenesis remain inconclusive. Little evidence exists for a protective effect of retinoids and carotenoids; the evidence for selenium and vitamin C is limited and evolving.
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PMID:Dietary epidemiology of colon cancer. 253 85

In recent years molecular biology has been applied to the study of colonic carcinoma, both in the human and in the experimental animal. The data obtained have enriched our understanding of colonic carcinogenesis and are of potential interest for cancer diagnosis and prevention. In this paper we review part of the available literature on the molecular characterisation of colon tumors, with emphasis on the issues of clonality, in vitro cell lines, tumor progression and heredity of colon cancer.
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PMID:Molecular biology of colon cancer (review). 253 73

Although there have recently been reports in the literature indicating that vegetarian-type diets are protective against the development of human colon cancer, this is still far from clear. It was also recently indicated that the concentration of acidic lipids in the aqueous phase of stool constitutes a risk factor for the development of colon cancer. Thus, we examined the effect of a change from a mixed to a lactovegetarian diet on this fecal variable. The dietary change caused a decrease in the total concentration of soluble fecal fatty acids (4310 +/- 3020 to 1080 +/- 1040 mumol/L, p less than 0.05) and deoxycholic acid (125 +/- 42 to 73 +/- 35 mumol/L, p less than 0.05). However, there was no change in either the total bile acid concentration in (164 +/- 54 to 107 +/- 41 mumol/L) or the cellular toxicity of (0.94 +/- 0.55 to 1.60 +/- 0.63 mumol/L, relative survival) the aqueous phase of stool. Thus, the consumption of a lactovegetarian diet may reduce certain risk factors of potential significance in colon carcinogenesis.
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PMID:Shift from a mixed to a lactovegetarian diet: influence on acidic lipids in fecal water--a potential risk factor for colon cancer. 255 15

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

Experiments were carried out in mice demonstrating that dietary carotenoids (beta-carotene or canthaxanthin), starting before cancer initiation and continuing throughout the experiment, have a protective effect against indirect skin carcinogenesis induced by benzo[a]pyrene +/- UVA and breast cancer induced by 8-methoxypsoralen + UVA. Experiments in rats demonstrated that carotenoids also prevent the direct gastric carcinogenesis induced by N-methyl-N'-nitro-nitroso-guanidine. Recently, prevention by beta-carotene against colon cancer induced in mice by dimethylhydrazine, another indirect carcinogen, was confirmed by others. The prospects for carotenoid intervention with humans were based on their antitumorigenic effect, which is quite independent of pro-vitamin A activity, their lack of toxicity even after prolonged administration, and their immunostimulating activity. These facts helped to build up a rationale predicting that any epithelial cancer, after radical surgery, can be chemoprevented with supplemental carotenoids. Thus, it is expected that the remaining initiated epithelial tissue will be protected by quenching oxygen radical formation, against the onset of a second primary malignancy. This type of prevention can be envisaged in organs like the lung, urinary bladder, breast, stomach, and colon-rectum. At present, human intervention protocols with a randomized drug/placebo method are underway under the supervision of the Centro Tumori of Pavia to chemoprevent with beta-carotene second primary lung or bladder cancer after radical surgery. Preliminary observations regarding findings in humans without randomization (1980-1988) in Pavia are also reported here. This consisted of chemoprevention with beta-carotene plus canthaxanthin against recurrence of different epithelial malignancies after radical treatment (surgery +/- chemoradiotherapy). None of the 11 cases recruited, on the basis of radical nature of treatment and patient adherence, have shown any recurrence beyond their expected disease-free intervals.
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PMID:Cancer chemoprevention by supplemental carotenoids in animals and humans. 269 58

Dietary calcium may inhibit colonic carcinogenesis promoted by high fat, phosphate, and low fibre diets. In persons at risk for colon cancer oral calcium supplements significantly suppress increased rectal epithelial proliferation. This was studied in a cohort of 35 volunteers: 26 first degree relatives of colorectal cancer patients and nine who had had colonic adenomas (mean age 51.6 years, 17 (49%) men, all negative for large bowel neoplasia). 1.25-1.5 g elemental calcium was given in divided daily doses for three months. Rectal pinch biopsies were taken without bowel preparation, before and mean 8.4 weeks during and 7.2 weeks after treatment and incubated with tritiated thymidine. The mean number of labelled cells, as a ratio of the total number of crypt cells (labelling index-LI), and their crypt position, were determined. The mean number of labelled cells decreased during treatment by 29%, especially in the basal three-fifths of crypts. There was also a significant 10% increase in mean number of crypt cells during treatment. [Mean LI decreased by 36% (p less than 0.001) during calcium treatment and almost returned to basal values after cessation.] If a raised LI is a marker of potential malignancy and a randomised clinical trial confirms that calcium suppresses it, dietary intervention studies in high risk persons are indicated.
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PMID:Oral calcium suppresses increased rectal epithelial proliferation of persons at risk of colorectal cancer. 273 58

Rectal mucosa from normal controls (n = 25) and tumor tissue and rectal mucosa from patients with colorectal cancer (n = 38) and adenoma (n = 35) were biopsied via colonoscopy. Ornithine decarboxylase (ODC) activity was determined in order to study the role of promoters in the process of colorectal carcinogenesis. ODC activity of cancer tissue was significantly higher than that of adenoma tissue. Normal mucosal ODC activity in rectum and sigmoid colon was 2 to 4 times higher than that in the proximal colon. Moreover, rectal mucosal ODC activity was significantly higher in patients with cancer or adenoma than that in normal controls. When ODC activity is regarded as an index of promoter, the possibility is suggested that cancer and adenoma developed in similar mucosa of the large bowel. Furthermore, ODC activity in colon cancer was significantly higher than that in rectal cancer. This suggests the possibility that TPA type promoter assumes a greater role in the process of carcinogenesis of colon cancer than that of rectal cancer.
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PMID:[A study of ornithine decarboxylase activity in tumor tissue and rectal mucosa in patients with colorectal cancer or adenoma]. 279 55


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