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

Until now, carcinoma of the large intestine resected previously for benign disease has not been published. However an increasing number of patients resected for Crohn's disease, diverticulitis or trauma may reach nowadays a high lifespan. On the other hand, it is known that the gastroenteral anastomosis is predisposed to cancer development. In this study, the question of whether the large intestine following colotomy or ileotransversostomy is sensitive to carcinogenesis is examined. Male Wistar rats, subjected to colotomy or resection and ileotransversostomy, were treated weekly by subcutaneous injection of 1,2-dimethylhydrazine (12 mg/kg body weight) for seven weeks. The animals were killed 54 weeks after the first injection. At autopsy, 21 out of 29 operated rats had developed adenocarcinomas of the remaining colon. Intact control animals had the same incidence of malignant degeneration of the large bowel. When the anastomosis is chronically irritated by inflammation or by formation of a diverticulum, development, of carcinoma near the stoma was observed. This was the case in three rats of 28 animals. The results demonstrate that the resected colon of the rat is not more sensitive to experimental carcinogenesis than the intact one.
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PMID:Experimental carcinogenesis in the resected colon of the rat. 14

Patients with chronic ulcerative colitis are at increased risk of developing carcinoma of the colon. It has been shown that the concentration of fecal bile acids and neutral sterols was higher in cancer patients than in the comparable healthy controls. Fecal neutral steroids and bile acids were measured in patients with ulcerative colitis, family controls who were immediate relatives of patients, patients with other digestive diseases, and healthy unrelated controls. The fecal excretion of cholesterol, coprostanol, and cholestane-3beta, 5alpha, 6beta-triol was higher in patients with ulcerative colitis than in other groups. Patients with other diseases, family controls, and unrelated controls excreted comparable levels of neutral sterols. Patients with ulcerative colitis excreted levels of bile acids in their feces comparable to those excreted by other groups. These findings suggest that possible interactions between cholesterol metabolites and colonic epithelial cells may be relevant in colon carcinogenesis.
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PMID:Fecal bile acids and cholesterol metabolites of patients with ulcerative colitis, a high-risk group for development of colon cancer. 32 59

Experimental models of colonic carcinoma chemically induced in rats explored the effects of several factors involved in colon carcinogenesis: high fat level of the diet, quality and quantity of fat, fecal excretion of neutral and acid steroids, intestinal microflora and fiber content of the diet. They suggested an association linking colon cancer to dietary fat and fecal acids and neutral sterols.
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PMID:[Experimental models: nutrition and intestinal cancers]. 35 44

Several pre-malignant diseases are known to have a genetic etiology. This study focuses attention upon precancerous disorders wherein the mode of inheritance is either well established or wherein it remains unclear even though familial aggregation of the particular diseases have been amply documented. These conditions will be discussed as useful models for systematic investigations of the host etiologic component in carcinogenesis. Our survey of hereditary precancerous syndromes includes multiple polyposis of the coli, the multiple mucosal neuroma syndrome, the Cancer Family Syndrome, Sipple's syndrome, Von Recklinghausen's neurofibromatosus, the multiple nevoid basal cell carcinoma syndrome, tuberous sclerosis, familial cutaneous malignant melanoma, and carcinoma of the breast. We have emphasized the heterogeneous character of many forms of familial cancer. Familial breast cancer associations clearly show such heterogeneity, as do colon cancer syndromes. Certain of these precancerous states are characterized by phenotypes which are clinically apparent, polyposis coli being the classic example. Others, such as Sipple's syndrome are amenable to routine screening for biochemical markers. The bulk of putative genetic cancer-predisposing problems require further basic investigation of modes of inheritance. Cancer control may be enhanced through communication of useful genetic and diagnostic information to primary care physicians. Referral of cancer clusters of possible genetic etiology from clinicians to human geneticists facilitates the necessary basic research.
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PMID:Familial cancer syndromes: a survey. 40 22

Dietary plant fibre, or plantix, is thought to play a significant role in the pathogenesis of colon cancer in humans. It is a complex polymeric substance that has several distinct components resistant to hydrolysis by the digestive enzymes of humans. These components include cellulose, hemicelluloses, pectins, lignin, gums, mucilages and, in certain instances, algal polysaccharides. These polymers have different physicochemical properties, and recent evidence from experimental studies in animals treated with carcinogens suggests that some may exert protective effects in the intestine and others may enhance colon carcinogenesis. This review synthesizes information on the chemical composition, methods of analysis and physicochemical properties of dietary plant fibre and reviews available studies examining the role of fibre in colonic neoplasia in animals and humans.
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PMID:Dietary fibre and colonic neoplasia. 46 3

The relationship between food intake and cancer of the large bowel was assessed by calculating the average intakes of foods, nutrients and dietary fibre in the different regions of Great Britain and relating these to the regional pattern of death from colon and rectal cancers between 1969 and 1973. No significant associations were found with the consumption of fat, animal protein or beer, nor with current estimates of total dietary fibre intake. Average intakes of the pentose fraction of total dietary fibres, and of vegetables other than potatoes, were negatively correlated with the truncated age- and sex-standardized death rates from colon cancer (r = -0.960 and -0.940). Specific components of dietary fibre may therefore inhibit colon carcinogenesis.
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PMID:Dietary fibre and regional large-bowel cancer mortality in Britain. 57 89

Epidemiological data indicate that colon cancer incidence is associated mainly with high dietary fat intake. Studies in metabolic epidemiology have shown a strong association between dietary fat intake, level of fecal bacteria, fecal acid, and neutral sterols, and the risk of colon cancer among different populations. Current concepts visualize that colonic bile acids and cholesterol metabolities play a modifying role in large bowel carcinogenesis, and that these compounds are derived from dietary factors, directly or indirectly, and subsequently are modified by the intestinal bacteria. In animal models, lithocholic acid and dexycholic acid, which are present in high concentration in the large bowel of man, acted as promoters of colon carcinogenesis. The carcinogenic effect of azoxymethane in rats was enhanced by the increase of bile salts in the colon induced by surgical means. Animals fed a high fat diet were more susceptable to colon tumor induction by dimethylhydrazine compared with rats fed a normal diet. Our data also demonstrate that the intestinal microflora played a modifying role in accelerating colon tumor production by dimethylhydrazine.
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PMID:Role of bile metabolites in colon carcinogenesis. Animal models. 76 59

Because of potential significance of bile acids and cholesterol metabolites in the pathogenesis of colon cancer, fecal neutral sterols, and bile acids were determined in patients with colon cancer, adenomatous polyps or other digestive diseases and American or Japanese controls. The fecal excretion of cholesterol, coprostanol, coprostanone, total bile acids, deoxycholic acid, lithocholic acid was higher in patients with colon cancer and patients with adenomatous polyps compared to normal American and Japanese controls as well as patients with other digestive diseases. Patients with other digestive diseases excreted comparable levels of fecal bile acids and cholesterol metabolites compared to normal American controls; Japanese controls excreted reduced levels compared to normal American controls. These findings suggest that possible interactions between bile acids and cholesterol metabolites and colonic epithelial cells may be relevant in colon carcinogenesis.
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PMID:Metabolic epidemiology of colon cancer. Fecal bile acids and neutral sterols in colon cancer patients and patients with adenomatous polyps. 87 53

BD-II and BD-IX male and female rats received weekly subcutaneous (s.c.) injections of 15 mg/kg 1,2-dimethylhydrazine dihydrochloride (DMH) beginning at either 35, 120 or 210 days of age and continuing for 20 weeks. Control animals received only the DMH vehicle. Additional BD-II and BD-IX male and female rats of the three age groups were gonadectomized at 21, 106 and 196 days. Beginning 14 days after gonadectomy, the rats received 15 mg/kg of DMH by s.c. injection once a week for 20 weeks. Animals were sacrificed 35 weeks after the initial DMH injection. Control rats of the appropriate age and sex did not develop colon tumors. BD-IX rats are apparently more sensitive to DMH than BD-II rats. The incidence of DMH-induced cancer is less in females than in males in both the BD-II and BD-IX animals. Gonadectomy does not affect cancer incidence in either BD-II males or females nor in the BD-IX females but reduced the incidence in BD-IX males exposed initially at either 120 or 210 days. Administration of androgen to castrate BD-IX males (120-day-old group) increases the incidence of colon cancer to that approaching the intact animal but has little effect in the BD-II castrate male. These data suggest a genetically influenced susceptibility to DMH-induced colon carcinogenesis between BD-II and BD-IX rats. Furthermore, a sex difference is evident in both BD lines but age appears to be a factor only in older BD-IX females. Apparently, androgens influence DMH-induced tumorigenesis in BD-IX males only if the initial exposure of DMH occurs after sexual maturity.
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PMID:Influence of gonadal hormones and age on 1,2-dimethylhydrazine-induced colon carcinogenesis. 92 91

Carcinoma of the colon was studied in Omaha-Douglas County, Nebraska (population 345,000). A total of 154 cases of colon cancer were diagnosed in 1964 (44.7/100,000). The frequency distribution of these patients in specific census tracts of this community was determined. Statistical analysis of the data showed a greater frequency of colon cancer in patients living in census tracts with higher average income. Colon cancer appears to be nonrandomly distributed with respect to the income and socioeconomic status of its victims, suggesting that hypotheses consistent with environmental variables--particularly those characterizing extremely high versus extremely low socioeconomic groups, including occupation, diet and other life patterns--should be pursued. All of these data have implications for cancer epidemiology, cancer control, and carcinogenesis.
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PMID:Cancer of the colon: socioeconomic variables in a community. 115 41


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