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

Mortality rates from multiple sclerosis show a well-known north-south gradient, both within the United States and internationally. Mortality rates from prostate cancer show a similar gradient and are significantly correlated with multiple sclerosis (MS) mortality and MS prevalence. This finding adds prostate cancer to the set of diseases whose geographic distributions are significantly correlated with MS and whose members include colon cancer, dental caries, and Parkinson's disease. Review of the literature indicates that these clinically dissimilar diseases may share an aberration in vitamin (hormone) D. Recent evidence demonstrating a multi-faceted role for vitamin D in immunoregulation suggests that a vitamin D aberration may also contribute to the etiology of MS. A vitamin D hypothesis can illuminate several unexplained features of the epidemiology of MS and suggests opportunities for epidemiologic, laboratory, and clinical investigation.
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PMID:Multiple sclerosis and prostate cancer: what do their similar geographies suggest? 129 88

Like calcium, vitamin D may protect against colorectal neoplasia as it reduces epithelial cell proliferation and induces differentiation. Although its therapeutic use is limited by its effects on calcium metabolism, analogues such as calcipotriol produce little hypercalcaemia. Stathmokinetic and immunohistochemical techniques were used to study the effect of 1,25 (OH)2 D3 and its analogues on cell proliferation in human rectal mucosa and a colon cancer cell line. Paired sigmoidoscopic biopsy specimens were obtained from 17 control patients and five patients with familial adenomatous polyposis. Explants were established in organ culture, with or without the addition of vitamin D. Proliferation was assessed using (1) metaphase arrest to determine the crypt cell production rate (CCPR) and (2) Ki-67 monoclonal antibody directed against an antigen present in proliferating cells. 1,25 (OH)2 D3 in concentrations of 1 microM-100 pM (10(-6)-10(-10) M) reduced the CCPR (cells/crypt/hour) from 4.74 to 2.15-2.67 (p < 0.001), and the Ki-67 labelling index from 7.28-3.74 (p < 0.01). Likewise, vitamin D2, 10 nM (10(-8) M) reduced the CCPR from 4.74-2.74 (p < 0.05) and calcipotriol from 4.86-2.38 (p < 0.05). In familial adenomatous polyposis patients 1,25 (OH)2 D3 100 pM (10(-10) M) halved the CCPR from 8.75-4.22. Calcipotriol (10(-5) M to 10(-9) M) produced a clearcut dose response inhibition of HT-29 cell growth. Thus, vitamin D and its metabolites inhibit proliferation in normal and premalignant rectal epithelium and suppress growth in a colorectal cancer cell line.
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PMID:Vitamin D and its metabolites inhibit cell proliferation in human rectal mucosa and a colon cancer cell line. 133 58

It has been suggested that sunlight might have a role in the prevention of colorectal cancer via a mechanism involving vitamin D. We used data from nine population-based cancer registries in the United States to analyze incidence rates for colon and rectal cancer during 1973-84 as a function of regional variation in the levels of available solar radiation. Data were restricted to include only those persons born and diagnosed in the same state. Incidence rates of colon and rectal cancer among men tended to increase with decreasing levels of solar radiation. Compared to rates in New Mexico and Utah, for example, rates in the Detroit area (MI), Connecticut, and western Washington were 50 percent to 80 percent higher. Among women, colon cancer rates showed a similar trend, though of smaller magnitudes; rates of rectal cancer among women did not vary in relation to levels of available solar radiation.
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PMID:Colorectal cancer and solar radiation. 153 21

Calcium contributes to the progression of epithelial cells through all phases of the proliferative cycle and into stages of cell differentiation; intracellular concentrations of calcium that are required for cell renewal, however, are lower than those required for epithelial-cell differentiation. These effects of calcium are modulated by interactions with 1,25-dihydroxy-vitamin D3, phosphate, and fatty acids, all of which are partly dependent on dietary intake. In rodent models, increased dietary calcium inhibited hyperproliferation of colon epithelial cells induced by increased levels of fatty acids or bile acids present in the colon. When carcinogens induced hyperproliferation of colon epithelial cells the hyperproliferation was decreased by added dietary calcium, and in several animal models the occurrence of carcinogen-induced carcinomas of the colon decreased with increased dietary calcium. A nutritional stress diet, designed to represent human Western dietary intake of calcium, phosphate, vitamin D, and fat, produced hyperproliferation and hyperplasia in the colons of rodents; these effects were reduced by increasing dietary levels of calcium. Decreased levels of ornithine decarboxylase also were reported in human and rodent colon mucosa exposed to increasing levels of calcium. In human subjects at increased risk for familial colon cancer, hyperproliferation of colon epithelial cells was reduced after oral dietary supplementation with calcium. In epidemiological studies, several investigators reported inverse correlations between levels of dietary calcium intake and the incidence of colon cancer. Extrapolation of the data have suggested a protective effect of total calcium intakes above 1500 to 1800 mg/day.
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PMID:Calcium, vitamin D, and colon cancer. 154 42

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

It was proposed in 1980 that vitamin D and calcium could reduce the risk of colon cancer. This assertion was based on the decreasing gradient of mortality rates from north to south, suggesting a mechanism related to a favorable influence of ultraviolet-induced vitamin D metabolites on metabolism of calcium. A 19-y prospective study of 1954 Chicago men found that a dietary intake of greater than 3.75 micrograms vitamin D/d was associated with a 50% reduction in the incidence of colorectal cancer, whereas an intake of greater than or equal to 1200 mg Ca/d was associated with a 75% reduction. Clinical and laboratory studies further support these findings. A nested case-control study based on serum drawn from a cohort of 25,620 individuals reported that moderately elevated concentrations of 25-hydroxyvitamin D, in the range 65-100 nmol/L, were associated with large reductions (P less than 0.05) in the incidence of colorectal cancer.
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PMID:Can colon cancer incidence and death rates be reduced with calcium and vitamin D? 205 61

Effects of dietary calcium on mammary carcinogenesis in rats were investigated because of evidence that calcium counteracts the promotion of colon cancer by dietary fat and because experimental diets for rats normally contain higher amounts of calcium and vitamin D than do human diets. Our earlier experiments indicated that yields of tumors induced in young, Sprague-Dawley rats by 7,12-dimethylbenz(a)-anthracene (DMBA) were higher when dietary calcium, phosphate, and vitamin D were decreased. Results of an experiment in which dietary amounts of calcium, phosphate, and vitamin D were varied independently suggested that phosphate and vitamin D have interactive effects with calcium. Another experiment in which dietary vitamin D alone was varied provided evidence that higher amounts inhibited tumorigenesis in the presence of low amounts of calcium and phosphate but the results with a high-calcium and -phosphate diet were inconclusive. The findings suggest that low amounts of dietary calcium and vitamin D and high amounts of phosphate increase susceptibility to DMBA-induced mammary neoplasia.
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PMID:Calcium and carcinogenesis of the mammary gland. 205 63

Sulfur dioxide absorbs ultraviolet light in the region of the spectrum which is most active in forming vitamin D on the skin. Sulfate particles reflect light at this wavelength. High concentrations of these pollutants (acid haze) may lead to vitamin D deficiencies in exposed populations. Epidemiologic and laboratory evidence suggests that vitamin D plays a role in reducing risk of colon and breast cancer. We examined the association between sulfur dioxide and ultraviolet-light-blocking aerosols in 20 Canadian cities, and age-adjusted breast and colon cancer mortality rates in the census divisions encompassing these cities. Statistically significant positive associations were found between these two measures of air pollution and age-adjusted mortality rates for colon cancer in women (multiple r = +.74, p = 0.003), and men (multiple r = +.61, p = 0.03), and breast cancer in women (multiple r = +.69, p = 0.007). Mortality rates for all other reported cancer sites were also examined, and no statistically significant positive associations were found consistently in both sexes. The ecological nature of this study is emphasized, and the possibility that an indirect association could explain these findings is discussed.
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PMID:Acid haze air pollution and breast and colon cancer mortality in 20 Canadian cities. 272 May 47

Mortality rates from colon cancer in the USA are highest in populations exposed to the least amounts of natural sunlight; differences in endogenous vitamin D production and calcium absorption could be responsible. To investigate this possibility, the association of dietary vitamin D and calcium with 19-year risk of colorectal cancer was examined in 1954 men who had completed detailed, 28-day dietary histories in the period 1957-59. Risk of colorectal cancer was inversely correlated with dietary vitamin D and calcium. In the quartiles of a combined index of dietary vitamin D and calcium, from lowest to highest, observed risks of colorectal cancer were 38.9, 24.5, 22.5, and 14.3/1000 population. This association remained significant after adjustment for age, daily cigarette consumption, body mass index, ethanol consumption, and percentage of calories obtained from fat.
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PMID:Dietary vitamin D and calcium and risk of colorectal cancer: a 19-year prospective study in men. 285 64


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