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

For more than 50 years, there has been documentation in the medical literature suggesting that regular sun exposure is associated with substantial decreases in death rates from certain cancers and a decrease in overall cancer death rates. Recent research suggests that this is a causal relationship that acts through the body's vitamin D metabolic pathways. The studies reviewed here show that (a) sunlight activation is our most effective source of vitamin D; (b) regular sunlight/vitamin D "intake" inhibits growth of breast and colon cancer cells and is associated with substantial decreases in death rates from these cancers; (c) metabolites of vitamin D have induced leukemia and lymphoma cells to differentiate, prolonged survival of leukemic mice, and produced complete and partial clinical responses in lymphoma patients having high vitamin D metabolite receptor levels in tumor tissue; (d) sunlight has a paradoxical relationship with melanoma, in that severe sunburning initiates melanoma whereas long-term regular sun exposure inhibits melanoma; (e) frequent regular sun exposure acts to cause cancers that have a 0.3% death rate with 2,000 U.S. fatalities per year and acts to prevent cancers that have death rates from 20-65% with 138,000 U.S. fatalities per year; (f) there is support in the medical literature to suggest that the 17% increase in breast cancer incidence during the 1991-1992 year may be the result of the past decade of pervasive anti-sun advisories from respected authorities, coinciding with effective sunscreen availability; and (g) trends in the epidemiological literature suggest that approximately 30,000 U.S. cancer deaths yearly would be averted by the widespread public adoption of regular, moderate sunning.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beneficial effects of sun exposure on cancer mortality. 847 9

Chemoprevention studies utilizing calcium have now progressed from basic measurements to clinical trials. Calcium's effects on epithelial cells have demonstrated decreased proliferation and induced cell differentiation with increasing levels of calcium in vitro, similar in vivo effects in rodent and human colon, and decreased carcinogen-induced colonic tumor formation in rodents. Current studies are attempting to inhibit colonic adenoma formation in human subjects. Most but not all epidemiologic studies also link increased dietary calcium with a decreased risk of colon cancer. In animal models, supplemental dietary calcium has decreased mammary epithelial cell hyperplasia and hyperproliferation and colonic cell hyperproliferation when the latter was induced by bile acids, fatty acids, and partial resection of the small intestine. Supplemental dietary calcium also decreased carcinogen-induced colonic tumors in several rodent models. In normal mice, and in mice carrying a targeted apc gene mutation, we recently increased colonic polypoid hyperplasias by a Western-style diet containing low calcium and vitamin D. In human subjects at increased risk for colon cancer, oral calcium supplementation significantly reduced colonic epithelial cell proliferation in most of the studies, including four randomized clinical trials. These studies have now progressed to short-term human clinical trials, including trials that measure the regrowth of transformed adenoma cells. Short-term adenoma-regrowth clinical trials, however, are limited in their ability to measure whether chemopreventive agents inhibit early genotoxic events, abnormal cellular metabolic activities involved in tumor promotion over many years, or the progression of adenoma cells to carcinoma.
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PMID:Calcium and the prevention of colon cancer. 853 12

To examine the associations between intakes of calcium, Vitamin D, and dairy foods and the risk of colon cancer, the authors analyzed data from a prospective study of 47,935 US male professionals, 40-75 years of age and free of cancer in 1986. Within this cohort, 203 new cases of colon cancer were documented between 1986 and 1992. After adjusting for age and total energy intake, the authors found that the intake of calcium from foods and supplements was inversely associated with colon cancer risk (relative risk (RR) = 0.58, 95% confidence interval (CI) 0.39-087 between high and low intakes of calcium). However, after adjusting for confounding variables, they found that the trend was no longer statistically significant (p = 0.22), and the relative risk for the highest quintile group of intake was attenuated: 0.75 (95% CI 0.48-1.15). Similar results were observed for total vitamin D intake; the age- and energy-adjusted relative risk was 0.54% (95% CI 0/34-0/85) for the highest versus lowest quintile group, and this was attenuated in the multivariate model (RR = 0.66, 95% CI 0.42-1.05). The inverse association was weaker for dietary vitamin D (RR highest vs. lowest quintile = 0.88. 95% CI 0.54-1.42) and strongest for vitamin D arising from vitamin supplements (RR = 0.48, 95% CI 0.22-1.02). Thus, it is possible that other components of multivitamin use rather than vitamin D accounted for the reduction in risk. Consumption of milk and fermented dairy products was not significantly associated with the risk of colon cancer; individuals consuming two or more glasses of "whole" or skim milk per day had a relative risk of 1.09 (95% CI 0.69-1.72), compared with those who consumed "whole or skim milk less than once a month. These prospective data do not support the hypothesis that calcium intake is strongly protective against colon cancer risk, although a modest association cannot be excluded.
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PMID:Calcium, vitamin D, and dairy foods and the occurrence of colon cancer in men. 861 Jul 4

The epidemiology of large bowel cancer suggests an etiological role for dietary factors. Although the evidence is inconsistent, several studies have suggested an inverse association between dietary vitamin D or calcium and colorectal cancer risk. We conducted a population-based case-control study to examine the relationship between dietary vitamin D and calcium and colorectal cancer among residents of Stockholm, Sweden. Between January 1986 and March 1988, 352 cases of colon cancer and 217 cases of rectal cancer diagnosed among living persons residing in Stockholm County were identified via a cancer surveillance network established among all the hospitals in Sweden and the Stockholm Regional Cancer Registry. Controls (512) were randomly selected from a computerized population registry. Dietary intake was assessed using a quantitative food frequency questionnaire focusing on average consumption during the preceding 5 years. Supplemental intake of vitamin D and calcium was not ascertained. Logistic regression was used to calculate odds ratios (ORs) as the measure of association between the exposure of interest (vitamin D or calcium) and cancer risk. Increasing levels of dietary vitamin D were inversely associated with the risk of colorectal cancer. The association was somewhat more pronounced for cancers of the rectum [OR, 0.5; 95% confidence interval (CI), 0.3-0.9 between the highest and lowest quartiles] than for cancers of the colon (OR, 0.6; 95% CI, 0.4-1.0) after adjustment for age, sex, and total caloric and protein intake. Dietary calcium was not associated with the adjusted risk of colon (OR, 1.2; 95% CI, 0.7-2.1) or rectal cancer (OR, 1.0; 95% CI, 0.5-1.9). Further adjustments for fat and dietary fiber intake, body mass index, and physical activity had little or no effect on the results. These results suggest that dietary vitamin D may reduce the risk of large bowel cancer, particularly rectal cancer. In addition, although some of the previous data suggested a protective effect for calcium against cancers of the large bowel, we could not document such an effect.
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PMID:Dietary calcium, vitamin D, and the risk of colorectal cancer in Stockholm, Sweden. 892 97

Low serum levels of vitamin D metabolites have been associated with an increased risk for colon cancer. To investigate the effects of vitamin D deficiency on the colon, 4-week-old mice were fed a diet either containing (100,000 IU/kg diet) or lacking this vitamin for 3 weeks. Food consumption and body weight gain were similar in both groups. Following injection with 3H-thymidine to label dividing cells, cellular proliferation and migration up the colonic crypt were determined autoradiographically. Although overall crypt lengths were similar in both groups, there was hyperplasia and hyperproliferation in crypts of the deficient animals. Also, their epithelial cells migrated up the crypt at a significantly slower rate (maximum 0.78 micron/h) than did those from control mice (1.42 microns/h). There was no difference in cellularity, proliferation or migration in duodenal epithelium. These results indicate that vitamin D deficiency significantly alters colonic but not duodenal epithelial cells.
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PMID:Hyperplasia, hyperproliferation and decreased migration rate of colonic epithelial cells in mice fed a diet deficient in vitamin D. 900 93

The relationship between vitamin supplement use and colon cancer was assessed in a population-based case-control study among men and women aged 30-62 years. Cases were 251 men and 193 women diagnosed with colon cancer in 1985-1989 in three counties in the Seattle metropolitan area who were identified from the Surveillance, Epidemiology, and End Results cancer registry. Controls were 233 men and 194 women identified by random digit dialing. Supplement use was assessed by questions on frequency, duration, and dose per day (for individual supplements) or type (for multivitamins) during the 10-year period ending 2 years before diagnosis. All results were adjusted for age and sex and were not confounded by other measured behaviors. The average daily intake of supplemental vitamins A, C, E, folic acid, calcium, and multivitamins during the reference period were each associated with reduced risk of colon cancer (all P for trend < 0.03). The strongest associations were for use of vitamin E (odds ratio, 0.43; 95% confidence interval, 0.26-0.71 for > or = 200 IU/day versus none) and multivitamins (odds ratio, 0.49; 95% confidence interval, 0.35-0.69 for daily use versus no use; both P for trend < 0.001). These two associations were also significant using a stricter test of trend limited to supplement users, which reduces the effect of colinearity among these exposures. Because almost all vitamin D supplementation comes from multivitamin pills, the association of vitamin D use with colon cancer could not be distinguished from that of multivitamin use. Clinical trials or cohort studies with long-term assessment would be needed before public health recommendations could be made about supplement use.
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PMID:Relationship between vitamin and calcium supplement use and colon cancer. 933 57

The periodic exam for the healthy midlife patient (age 45 to 65) includes blood pressure testing, cholesterol screening, and a baseline ECG. Counseling is appropriate for proper diet, exercise, and smoking cessation Screening tests are indicated for colon cancer for men and women, and for breast and cervical cancer for women. A check of immunization status can detect a need for recommended vaccines, including tetanus-diphtheria. Question patients about hearing problems, and test as needed. Counsel women about risk factors for osteoporosis and the need for adequate calcium and vitamin D intake. Ask about symptoms of urinary incontinence and sexual problems. Screen women for thyroid disease.
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PMID:Midlife periodic health exam in the primary care practice. 933 6

Several epidemiologic studies have suggested that dairy product intake is associated with a decreased incidence of colon cancer. To determine whether the cytotoxicity and genotoxicity of the aqueous portion of human stool (two potential risk markers for the disease) were affected by a change in dairy product intake, 18 healthy male and female volunteers were randomly divided into two groups. In a crossover design, the volunteers shifted from their normal dairy product-rich diet to a dairy product-free diet. Nutritional analysis of the food consumed during the study period showed a significant decrease in energy intake from 9000 to 7866 kJ/d because of a decreased intake of protein and fat. Carbohydrate and fiber intakes remained unchanged during the intervention. Calcium intake decreased significantly from 1488 to 372 mg/d, with similar significant decreases in phosphate and vitamin D intakes. Cytotoxicity of fecal water, analyzed by the HT-29 cytotoxicity assay, indicated a significant decrease in cell survival from 34% to 20% when dairy products were excluded from the participants' diets. Single-cell gel electrophoresis (COMET assay), used to analyze genotoxicity of fecal waters, indicated no differences brought about by the dietary intervention. In conclusion, our findings indicate that a shift from a dairy product-rich to a dairy product-free diet resulted in a significant effect on an accepted risk marker for colon cancer and may suggest that the mechanism by which dairy products are protective is at the level of tumor promotion rather than initiation.
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PMID:Shift from a dairy product-rich to a dairy product-free diet: influence on cytotoxicity and genotoxicity of fecal water--potential risk factors for colon cancer. 958 55

The relationship between various micronutrients and colorectal cancer risk was investigated using data from a case-control study conducted between January 1992 and June 1996 in Italy. Cases were 1,953 incident, histologically confirmed colorectal cancers (1,225 of the colon and 728 of the rectum), admitted to the major teaching and general hospitals in the study areas, and 4,154 controls with no history of cancer, admitted to hospitals in the same catchment areas for acute, non-neoplastic diseases unrelated to the digestive tract and requiring no long-term modifications of the diet. Dietary habits were investigated using a validated food-frequency questionnaire. Odds ratio (ORs) were computed after allowance for age, sex and other potential confounding factors, including physical activity, total energy and fibre intake. For most micronutrients, ORs were below unity with increasing quintile of intake. The most consistent protective effects were for carotene, riboflavin and vitamin C (Multivariate ORs from the continuous model, with unit set as the difference between the upper cut-point of the 4th quintile and that of the 1st one, were 0.65, 0.73 and 0.80, respectively). Inverse relationships were observed also for calcium and vitamin D (ORs of 0.85 and 0.93, respectively). When the combined effect of calcium and vitamin D and selected anti-oxidants was considered, the OR reached 0.46 in subjects reporting high calcium/vitamin D and high anti-oxidant intake compared to those reporting low intake of both groups of micronutrients. Most results were apparently stronger for colon cancer and among females. Our results provide further support for a protective effect of several micronutrients on colorectal cancer risk and some indications for a specific and stronger effect of selected anti-oxidants.
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PMID:Intake of selected micronutrients and risk of colorectal cancer. 1047 41

The physiologically active form of vitamin D, 1alpha,25-dihydroxyvitamin D3, plays an important role not only in the establishment and maintenance of calcium metabolism, but also in regulating cell growth and differentiation. As the clinical usefulness of 1alpha,25-dihydroxyvitamin D3 is limited by its tendency to cause hypercalcemia, new analogs with a better therapeutic profile have been synthesized. One of these new synthetic vitamin D analogs is EB 1089, which is characterized by an altered side chain structure featuring 26,27-dimethyl groups and two double bonds. This analog has been shown to be more potent than 1,25-dihydroxyvitamin D3 in inhibiting proliferation, stimulating differentiation, and inducing apoptosis in a number of different cell types, including cancer cells. Despite being more potent than 1alpha,25-dihydroxyvitamin D3 with respect to its cell regulatory effects, EB 1089 displays weaker calcemic side-effects. These characteristics make EB 1089 a potentially useful compound for the treatment of a diversity of clinical disorders, including cancer and metabolic bone diseases. A promising phase I study with EB 1089 in patients with advanced breast and colon cancer has already been carried out, and more clinical trials evaluating the clinical effectiveness of EB 1089 in other types of cancer are in progress.
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PMID:EB 1089, a novel vitamin D analog with strong antiproliferative and differentiation-inducing effects on target cells. 941 68


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