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

Established cancer in the liver can, in selected patients who have a good arterial circulation in these tumors, be effectively treated by intrahepatic artery radioactive yttrium-90 resin microspheres. Even in unselected patients treated in the last five years by the author, 17 of 25 patients treated have had good objective regression of cancers, improvement of symptoms and prolongation of life. Treatment is relatively simple and associated with few side effects. For adjuvant therapy of colon cancer having positive nodes (Dukes C), internal radiation therapy of the liver is best done with Phosphorus-32 Colloid passed through the circulation of the gut to be effectively and homogeneously trapped by the Kupffer cells of the liver. Four such patients have been subjected to a pilot study--three of the four are doing well without significant side effects and no evidence of liver cancer after two years. When the fourth died of brain metastases, he too had less liver cancer than would be expected.
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PMID:Internal radiation therapy of hepatic cancer. 49 90

Food intake during the preceding 15 years was evaluated in detail in 41 patients treated for colorectal cancer and an equal number of matched control subjects by means of a dietary history technique that permitted quantitation of nutrients. Dietary habits of the control group could be compared against two larger groups of 371 hospital control and 430 population control subjects. Patients with cancer, who were interviewed after complete recovery from surgery, consumed more fat, protein, and carbohydrates, and thus more energy, than control subjects although these differences were not statistically significant. Per unit energy, the habitual diet of patients with cancer contained less cereal fiber (P less than 0.001), less riboflavin (P less than 0.05), less calcium (P less than 0.05), and less phosphorus (P less than 0.05) than the diet of the control subjects. A high intake of either cereal fiber, total fiber, calcium, and phosphorus in relation to energy intake was found to be associated with a reduced risk ratio of colorectal cancer. For colon cancer separately, a high intake of calcium and cereal fiber was associated with a reduced risk ratio. For rectal cancer, a high intake of total fiber and cereal fiber was associated with a reduced risk ratio. High alcohol consumption correlated with an increased risk ratio. These data are compatible with previous Scandinavian studies relating food consumption to the incidence and mortality of colorectal cancer.
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PMID:Cereal fiber, calcium, and colorectal cancer. 131 77

One common nutrient postulated to be protective against osteoporosis, hypertension, and colon cancer is dietary calcium. We report here nutrient patterns by calcium intake in older adult residents of a geographically defined community in Southern California. The analysis included all 426 men and 531 women aged 50-79 y with complete 24-h diet data. Nutrient-density-adjusted calcium intake was divided into tertiles: low intake (less than 284 mg/1000 kcal), mid intake (284-440 mg/1000 kcal), and high intake (greater than 440 mg/1000 kcal). The distribution of the reported 24-h nutrient density of protein, fat, fiber, caffeine, trace minerals, vitamin D, and vitamin C was examined in relation to the calcium-intake tertiles. In both men and women, the adjusted intakes of protein, saturated fatty acids, vitamin D, magnesium, and phosphorus were significantly higher in the high-calcium-intake group than in the low- and mid-calcium-intake groups. In both men and women, alcohol intake was significantly lower in the high-calcium-intake group. Studies postulating a protective role for calcium will need to consider the multicolinearity in the Western diet.
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PMID:Calcium intake: covariates and confounders. 184 36

To determine whether supplemental dietary calcium and/or vitamin D deficiency are involved in modulating colon cancer induced by 1,2-dimethylhydrazine (DMH), Sprague-Dawley rats were fed diets containing either: (a) a normal content of calcium (0.87%) and phosphorus (0.60%) with 2.2 IU of vitamin D3 per g of feed (group A); (b) the same diet as group A, but with calcium and phosphorus increased to 1.80 and 0.80%, respectively (group B); or (c) a vitamin D-deficient diet with supplemental calcium (1.80%) and phosphorus (0.80%) (group C). After 6 weeks on their respective diets, one-half the animals in each group were given s.c. injections of either vehicle or DMH (20 mg/kg body weight/week) for 26 weeks. Animals were then sacrificed and the incidence of tumors as well as the number of tumors per tumor-bearing rat were determined. Colonic mucosal polyamine levels were measured after 15 weeks of exposure to vehicle or DMH, before development of histologically recognizable neoplasms. The results of these experiments demonstrated that neither calcium supplementation alone nor supplemental calcium in conjunction with vitamin D deficiency altered the incidence of colonic cancer induced by this carcinogen. Supplemental calcium, however, significantly decreased the number of rats with multiple tumors and reduced tumor size. Moreover, vitamin D deficiency abolished these protective effects of calcium on colon cancer in this experimental model. DMH treatment increased polyamine levels in the premalignant colonic mucosa in group A rats. This carcinogen-induced effect was blunted by high dietary calcium. Vitamin D-deficient, calcium-supplemented rats (group C) showed an increase in N1-acetylspermidine, but not the other polyamines, with DMH treatment.
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PMID:Dietary calcium and vitamin D modulate 1,2-dimethylhydrazine-induced colonic carcinogenesis in the rat. 191 78

The effects of dietary calcium, magnesium, and butterfat on intestinal function and flora in rats initiated with 1,2-dimethylhydrazine (DMH) were studied. Male weanling rats were assigned to six isocaloric diets that varied in their levels of calcium and magnesium (0.25% Ca with 0.05% Mg, 1.0% Ca with 0.05% Mg, or 0.625% Ca with 0.50% Mg) and butterfat (5% or 20%). One-half of the rats in each treatment were injected subcutaneously with DMH weekly for four weeks. This short-term exposure to DMH increased colonic ornithine decarboxylase (ODC) activity and the mass of cecal contents. Ingestion of the high levels of either calcium or magnesium depressed colonic ODC activity and depressed apparent absorption of organic matter, calcium, magnesium, and phosphorus. Ingestion of excess magnesium increased the mass of the cecal contents by twofold, caused hypertrophy of cecal walls, and increased the total amount of protein and total nitroreductase and beta-glucuronidase activity in the ceca of rats. Ingestion of supplemental calcium had less dramatic effects and increased the mass of cecal contents by only 28% and decreased the total amount of protein in the ceca. On the basis of their different effects on cecal microflora, magnesium appears to have less potential than does calcium as a protective agent against colon cancer.
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PMID:Changes in intestinal function of rats initiated with DMH and fed varying levels of butterfat, calcium, and magnesium. 230 74

In a prospective cohort study, 8006 men of Japanese ancestry were examined from 1965 to 1968. A 24-h dietary recall questionnaire was administered to each subject as part of the baseline clinical examination. Dietary data were analyzed for intake of calcium, phosphorus, and total fat in 99 colon cancer cases and in 378 controls chosen from the cancer-free men. This was a nested case-control study design with 14-17 yr of prospective followup for colon cancer incidence. We found no significant association between dietary calcium intake and colon cancer risk. This held true whether phosphorus intake was low (less than 1032 mg/day) or high (greater than or equal to 1032 mg/day), and whether total fat intake was low (less than 61 g/day) or high (greater than or equal to 61 g/day). Adjusted-odds ratios were 0.7-1.4 across eight subgroups of low and high intakes of the three nutrients studied. These data do not support a recent hypothesis that calcium intake might be negatively associated with colon cancer risk, depending on the level of fat and phosphorus intake.
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PMID:Colon cancer and dietary fat, phosphorus, and calcium in Hawaiian-Japanese men. 394 95

A Phase I trial of tricyclic nucleoside phosphate (1,4,5,6,8-pentaazaacenaphthylene-3-amino-1, 5-dihydro-5-methyl-1-beta-D-ribofuranosyl 5'-phosphate ester; NSC 280594) was conducted using a 5-day continuous infusion schedule. Thirty-seven patients with advanced cancer were entered on the study, of whom 33 patients were evaluable for response and toxicity. Dose levels ranged from 10 mg/sq m/day X 5 days to 40 mg/sq m/day X 5 days. Initially, courses were repeated every 3 to 4 weeks. As cumulative toxicity became manifested, the interval between courses was changed to every 6 weeks. Major toxicities included hyperglycemia, hepatotoxicity, and thrombocytopenia. Patients with a prior history of diabetes mellitus, extensive radiation therapy, or significant liver metastases were prone to severe toxicity. Other toxicities noted were nausea and vomiting, abdominal discomfort, anemia, and reduction in serum calcium, phosphorus, and albumin levels. Rare side effects included hypertriglyceridemia, hyperamylasemia, diarrhea, and stomatitis. Antitumor activity observed include improvement in s.c. metastases in a patient with papillary thyroid carcinoma, stabilization of disease in a patient with mesothelioma, and mixed responses in three patients (colon cancer, sarcoma, and tonsillar squamous cell cancer). Recommended schedule for Phase II studies is 20 mg/sq m/day for 5 days every 6 weeks.
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PMID:Phase I study of tricyclic nucleoside phosphate using a five-day continuous infusion schedule. 674 83

Vitamin D3 and its metabolites, particularly 1 alpha,25-dihydroxyvitamin D3 (1 alpha, 25(OH)2D3), have received increasing attention as potential anticarcinogens in the prevention of cancers in a number of organs, including the colon. These agents, however, have the potential to induce hypercalcemia, thus limiting their practical use for these purposes. In the present studies it was, therefore, of interest to determine whether dietary supplementation with 1 alpha,25-dihydroxy-16-ene-23-yne-26,27-hexafluorocholecalcifero l (RO24-5531), a recently synthesized apparently noncalcemic analogue of 1 alpha,25(OH)2D3, inhibited colon cancer induced by azoxymethane (AOM). Rats were placed on a standard diet or fed this diet with supplemental RO24-5531 (2.5 nmol/kg feed) before and during (initiation arm), or after AOM or vehicle administration (postinitiation arm). After 34 weeks of study, animals in each group were sacrificed, and their colons were removed and examined macroscopically and microscopically for the presence of tumors. At the time of sacrifice, the animals' serum calcium, phosphorus, 25-hydroxyvitamin D3 and 1 alpha,25(OH)2D3 levels were also analyzed. The results of these studies demonstrated that dietary RO24-5531 supplementation during the initiation arm of these experiments significantly reduced (by 70%) the incidence of AOM-induced colonic tumors compared to rats on the standard diet without RO24-5531. Moreover, this dietary regimen abolished the development of adenocarcinomas in this model. Although there was also a trend for dietary RO24-5531 supplementation during the postinitiation arm of this study to reduce the incidence of colon tumors, this did not reach statistical significance (P > 0.05). In addition, neither dietary RO24-5531 supplementation regimen significantly influenced the animals' rates of growth or their serum levels of calcium, phosphorus, or 25-hydroxyvitamin D3. These studies, therefore, demonstrate for the first time that supplemental dietary RO24-5531 is a chemopreventive agent in the AOM model of experimental colonic carcinogenesis. They also suggest that this agent may ultimately prove useful in clinical colon cancer chemopreventive trials.
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PMID:1 alpha,25-Dihydroxy-16-ene-23-yne-26,27-hexafluorocholecalciferol, a noncalcemic analogue of 1 alpha,25-dihydroxyvitamin D3, inhibits azoxymethane-induced colonic tumorigenesis. 760 26

A population-based case-control study including 726 patients with colon cancer, 575 with rectum cancer, and 1400 population controls matched on age (+/- 5 yrs.) and sex was carried out to evaluate the association of ten inorganic elements, including potassium, sodium, calcium, magnesium, iron, manganese, zinc, copper, phosphorus and selenium, and other dietary factors with colorectal cancer. Single variable analysis adjusted for age and sex showed most of the ten elements, except sodium and selenium, may reduce the risk of the development of colorectal cancer. Correlation analysis indicated these eight elements correlated closely to the "vegetable factors", e.g., dietary fibre, and so on, since the major sources (about 80%) of these elements were from vegetables. Multi-variable logistic regression analysis showed nine elements (except sodium) may confound the effects of some dietary factors (such as dietary fibre and vitamin C) on the occurrence of colorectal cancer and only contribute to it. The results showed a close association between saturated fatty acid, mono-unsaturated fatty acid, dietary fibre, vitamins C and E, and colorectal cancer.
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PMID:[Relationship between colorectal cancer and ten inorganic elements]. 813 59

Rhodamine 123 is a lipophilic cationic compound that is selectively taken up by cancer cell mitochondria. This compound is toxic to epithelial cancer cells in vitro and displays significant anticancer activity in vivo. However, the mechanism of action of rhodamine 123 in intact, actively metabolizing cell preparations is unknown. We have used 31P- and 13C-nuclear magnetic resonance spectroscopy to quantitatively characterize how rhodamine 123 affects the energetics of human colon cancer cells (HCT-116) and spontaneously immortalized normal epithelial cells (CV-1). Rhodamine 123 differentially altered the phosphorus and glucose metabolism of HCT-116 and CV-1 cells. 31P-nuclear magnetic resonance detected mitochondrial poisoning in the HCT-116 human colon cancer cell line in its early stages after selective uptake of rhodamine 123. When we compared administration of rhodamine 123 and [1-C13]glucose to administration of [1-C13]glucose alone in the HCT-116 cells, we noted a marked decrease in intracellular pH to 6.7 +/- 0.06 (mean +/- SD) units, a 2.2-fold increase in lactate production, and a 1.8-fold increase in glucose consumption after 10 h. In addition, we found a 2-fold rise in intracellular free magnesium 12 h after rhodamine 123 administration. These results suggest that when rhodamine 123 inhibits mitochondrial ATP production, it initially stimulates cytoplasmic glycolysis in an attempt to maintain cellular energy demands. The marked fall in intracellular pH and rise in intracellular free magnesium after administration of rhodamine 123 may inhibit activity of several glycolytic enzymes: this effect would inhibit cytoplasmic ATP generation and interfere with multiple cell enzymatic processes, leading to cell death. The CV-1 cells showed no change in intracellular pH, intracellular free magnesium, or magnesium-bound ATP levels over the 24-h period following rhodamine 123 administration. Rhodamine 123 also failed to alter glucose utilization and lactate production levels significantly in the CV-1 cells. These results prove the usefulness of 31P- and 13C-nuclear magnetic resonance spectroscopy for quantifying differing effects of rhodamine 123 on the high energy phosphate metabolism and glucose metabolism of HCT-116 and CV-1 cells.
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PMID:Quantitative differential effects of rhodamine 123 on normal cells and human colon cancer cells by magnetic resonance spectroscopy. 824 40


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