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

The experience of a professorial unit over a four-year period of carcinoma of the colon and rectum is described. The high incidence of anaemia in lesions proximal to the splenic flexure is shown. The distressing misdiagnosis of the cause of this anaemia is pointed out, and the consequent misuse of haematinics in the form of blood transfusion, iron and vitamin B12 is shown.
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PMID:Anaemia in the elderly: caveat caecum. 105 85

People who refuse to eat meat animal products mostly adhere to vegetarianism, veganism, crudivorism or macrobiotism, But these food habits are only one part of life-style chosen for spiritual, ethic or hygienic and healthy motivations. Except vitamin B12 deficiencies these regimens do not produce other deficiencies if they are correctly followed and if the energy intake is in agreement with the RDA'S. They reduce the risks of metabolic diseases, coronaropathies, arterial hypertension, colon cancer, diverticular disease of the colon, kidney and gallstones. Nevertheless crudivorism and macrobiotism are associated with high risks of deficiencies especially in children and pregnant women.
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PMID:[Diet peculiarities. Vegetarianism, veganism, crudivorism, macrobiotism]. 206 9

A diverse number of hematologic abnormalities may occur in association with gastrointestinal disease. For example, deficiencies of iron, folate, and vitamin B12 often accompany and may be the first clue to diseases such as colon cancer, celiac sprue, and chronic gastritis, respectively. A compilation of the hematologic disorders associated with diseases of the gastrointestinal tract, liver, and pancreas is provided.
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PMID:Hematologic manifestations of gastrointestinal disease. 330 21

Reduced growth in methionine-deficient, homocysteine-, folic acid-, and vitamin B12-supplemented medium, a characteristic of tumor and transformed cell lines, was investigated in skin fibroblasts of patients affected with hereditary colon neoplasms. The presence or absence of this phenotype was studied in 37 cell lines from either low-risk subjects or members of families with Gardner's syndrome (GS) or familial colon cancer (FCC). Growth constants of skin fibroblasts of the low-risk group were not significantly different in the presence of methionine (Kme) or absence of methionine (Kho) (0.106 +/- 0.011 and 0.098 +/- 0.011, respectively). However, growth constants of skin fibroblasts of both GS and FCC were significantly reduced in the absence of methionine. In GS, Kho = 0.086 +/- 0.006 and Kme = 0.120 +/- 0.006 (P less than .01). In FCC, Kho = 0.048 +/- 0.007 and Kme = 0.084 +/- 0.009 (P less than .01). Thus the growth of skin fibroblasts from both GS and FCC was methionine dependent. This phenotype was expressed in skin fibroblasts of an individual several years before any clinical manifestation of GS. In all populations studied the phenotype was independent of the age or sex of the individuals, aging of the cell lines, low serum concentration, and acute carcinogen treatment. In addition, there is a significant correlation (r = -0.85, P less than .001) between the disorganization of actin cables of the skin fibroblasts and the ratio of the growth constants. These data constitute the first report demonstrating methionine dependence in cell lines that are not derived from transformed cells, tumor cells, or fetal cells but are derived from skin fibroblasts of patients with hereditary colonic neoplasms. Inasmuch as these cells are not target cells related to colon cancer, the phenotype appears to be the expression of an inherited autosomal dominant genotype related to the oncogenic transformation.
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PMID:Methionine dependence in skin fibroblasts of humans affected with familial colon cancer or Gardner's syndrome. 658 98

Evidence is accumulating that folate, a B vitamin found in green leafy vegetables, may affect the development of neoplasia. We examined the relationship between folate status and colorectal cancer in a case-control study nested within the Alpha-Tocopherol Beta-Carotene Study cohort of male smokers 50-69 years old. Serum folate was measured in 144 incident cases (91 colon, 53 rectum) and 276 controls matched to cases on baseline age, clinic, and time of blood collection. Baseline dietary folate was available from a food-use questionnaire for 386 of these men (92%). Conditional logistic regression modeling was used. No statistically significant association was observed between serum folate and colon or rectal cancer. Although a 2-fold increase in rectal cancer risk was suggested for men with serum folate > 2.9 ng/ml and those in the highest quartile of energy-adjusted folate intake, there was no evidence of a monotonic dose-response, and all confidence intervals included unity. For dietary folate and colon cancer, odds ratios of 0.40 [95% confidence interval (CI), 0.16-0.96], 0.34 (95% CI, 0.13-0.88), and 0.51 (95% CI, 0.20-1.31) were obtained for the second through fourth quartiles of energy-adjusted folate intake, respectively, compared to the first (P for trend = 0.15). Furthermore, men with a high-alcohol, low-folate, low-protein diet were at higher risk for colon cancer than men who consumed a low-alcohol, high-folate, high-protein diet (OR, 4.79; 95% CI, 1.36-16.93). This study suggests a possible association between low folate intake and increased risk of colon cancer (but not rectal cancer) and highlights the need for further studies that measure dietary folate and methionine, along with biochemical measures of folate (i.e., erythrocyte and serum), homocysteine, and vitamin B12.
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PMID:Colorectal cancer and folate status: a nested case-control study among male smokers. 882 51

Disturbances in DNA methylation have been hypothesized as being involved in carcinogenesis. It has been proposed that dietary factors such as folate, alcohol, and methionine may be associated with colon cancer because of their involvement in DNA methylation processes. Data from a large retrospective population-based case-control study of incident colon cancer were used to evaluate whether intake of alcohol and other dietary factors involved in DNA methylation are associated with colon cancer. Dietary data were obtained using a detailed diet history questionnaire. We did not observe strong independent associations between folate, vitamin B6, vitamin B12, methionine, or alcohol and risk of colon cancer after adjusting for body size, physical activity, cigarette smoking patterns, energy intake, and dietary intake of fiber and calcium. However, when assessing the associations between colon cancer and a composite dietary profile based on alcohol intake, methionine, folate, vitamin B12, and vitamin B6, we observed a trend of increasing risk as one moved from a low- to a high-risk group. This trend was modest and most marked in those diagnosed at a younger age [odds ratio (OR) for men = 1.3, 95% confidence interval (CI) = 0.9-1.9; OR for women = 1.6, 95% CI = 1.0-2.6]. We observed that associations with this high-risk dietary profile were greater among those who took aspirin or nonsteroidal anti-inflammatory drugs on a regular basis and were younger at the time of diagnosis (men OR = 1.7, 95% CI = 1.0-3.2; women OR = 2.2, 95% CI = 1.0-4.8) and for distal tumors (men OR = 1.4, 95% CI = 0.9-2.3; women OR = 2.0, 95% CI = 1.0-3.8). Findings from this study provide only limited support for previously reported associations between dietary factors involved in DNA methylation and risk of colon cancer.
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PMID:Are dietary factors involved in DNA methylation associated with colon cancer? 920 Jan 51

Individuals with different forms of the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene, carriers of the C677T mutation versus wild type, show differences in enzyme levels; these differences have been hypothesized to be related to DNA methylation and, perhaps, to the nucleotide pool size. Using data from an incident case-control study, we evaluated the combined effect of dietary intake of folate, methionine, vitamin B6, vitamin B12, and alcohol and various forms of the MTHFR gene on risk of colon cancer. Individuals homozygous for the variant form of the MTHFR gene (TT) had a slightly lower risk of colon cancer than did individuals who were wild type [CC, odds ratio (OR) = 0.8, 95% confidence interval (CI) = 0.6-1.1 for men; and OR = 0.9, 95% CI = 0.6-1.2 for women]. High levels of intake of folate, vitamin B6, and vitamin B12 were associated with a 30-40% reduction in risk of colon cancer among those with the TT relative to those with low levels of intake who were CC genotype. Associations were stronger for proximal tumors, in which high levels of intake of these nutrients were associated with a halving of risk among those with the TT genotype. The inverse association with high levels of these nutrients in those with the TT genotype was stronger among those diagnosed at an older age. Although imprecise, the inverse association with the low-risk diet that was high in folate and methionine and without alcohol was observed for both the TT genotype (OR = 0.4 95% CI = 0.1-0.9) and the CC/CT genotype (OR = 0.6, 95% CI = 0.4-1.0), but this association was not seen with the high-risk diet for either the TT or CC/CT genotype. Although associations were generally weak, these findings suggest that those with differing MTHFR genotypes may have different susceptibilities to colon cancer, based on dietary consumption of folate, vitamin B6, and vitamin B12.
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PMID:Methylenetetrahydrofolate reductase, diet, and risk of colon cancer. 1038 41

Deficiencies of the vitamins B12, B6, C, E, folate, or niacin, or of iron or zinc mimic radiation in damaging DNA by causing single- and double-strand breaks, oxidative lesions, or both. The percentage of the population of the United States that has a low intake (< 50% of the RDA) for each of these eight micronutrients ranges from 2% to 20+ percent. A level of folate deficiency causing chromosome breaks occurred in approximately 10% of the population of the United States, and in a much higher percentage of the poor. Folate deficiency causes extensive incorporation of uracil into human DNA (4 million/cell), leading to chromosomal breaks. This mechanism is the likely cause of the increased colon cancer risk associated with low folate intake. Some evidence, and mechanistic considerations, suggest that vitamin B12 and B6 deficiencies also cause high uracil and chromosome breaks. Micronutrient deficiency may explain, in good part, why the quarter of the population that eats the fewest fruits and vegetables (five portions a day is advised) has about double the cancer rate for most types of cancer when compared to the quarter with the highest intake. Eighty percent of American children and adolescents and 68% of adults do not eat five portions a day. Common micronutrient deficiencies are likely to damage DNA by the same mechanism as radiation and many chemicals, appear to be orders of magnitude more important, and should be compared for perspective. Remedying micronutrient deficiencies is likely to lead to a major improvement in health and an increase in longevity at low cost.
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PMID:Micronutrient deficiencies. A major cause of DNA damage. 1066 86

Colorectal hyperplastic polyps are benign lesions that share many risk factors with colorectal adenomas and cancers. Low folate intakes are associated with an increased risk of colon cancer. The enzyme 5,10-methylene-tetrahydrofolate reductase (MTHFR) may be linked to DNA methylation and nucleotide synthesis and thus play a role in the etiology of colorectal neoplasia. We investigated an association between the common MTHFR polymorphism (C677T) and colorectal hyperplastic polyps within the Minnesota Cancer Prevention Research Unit case-control study. Cases (n = 200) were diagnosed with colonoscopically confirmed hyperplastic polyps; controls (n = 645) were derived from the same gastroenterology practice and were polyp-free at colonoscopy. Dietary intakes were estimated from a self-administered food-frequency questionnaire prior to colonoscopy. Multivariate adjusted odds ratios (ORs) and 95% confidence intervals for MTHFR status were 0.8 (0.6-1.2; CT versus CC wild-type) and 0.9 (0.5-1.6; TT versus CC). In subgroup analyses stratified on dietary intakes of folate, vitamin B12, vitamin B6, or methionine, those with the TT genotype and either low intakes of folate or vitamin B6 were at increased risk relative to those with normal or high vitamin intake. However, most 95% confidence intervals included 1.0, and no consistent trends were observed. In contrast to our findings on colorectal adenomas, increasing alcohol consumption was associated with an elevated risk of colorectal hyperplastic polyps, regardless of genotype. The MTHFR (C677T) variant genotype does not appear to be related to risk of colorectal hyperplastic polyps, and there is no convincing evidence that MTHFR shows a different relation to risk, dependent on dietary intakes of nutrients related to its pathway.
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PMID:Lack of association between the C677T MTHFR polymorphism and colorectal hyperplastic polyps. 1079 88

Ki-ras mutations are thought to be early events in the carcinogenic process leading to colon tumors. Dietary factors associated with colon cancer may be associated with these mutations. Data from a population-based, multicenter, case-control study of colon cancer were used to determine whether dietary factors are associated with Ki-ras mutations. Ki-ras mutations were detected by direct sequencing of codons 12 and 13 of the Ki-ras gene on exon 1 from DNA obtained from archival tissue. Ki-ras data were available for 1428 cases with valid interview data; data from 2410 controls were available for comparison with cases positive and negative for Ki-ras mutations. Mutations in the Ki-ras gene were detected in 32% of tumors. Of these mutations, 32.8% were G-->A transitions in the second base of codon 12 (2G-->A). Other than cruciferous vegetables, there were no nutrients or foods associated specifically with Ki-ras mutations [odds ratio (OR) for high intake relative to low intake, 0.7; 95% confidence interval (CI), 0.5-1.0]. However, evaluation of specific types of Ki-ras mutations revealed that for each of the most common types of mutation, dietary associations existed. Dietary factors involved in DNA methylation pathways were associated with 2G-->A mutations. Comparison of individuals with and without Ki-ras mutations revealed that individuals with low levels of dietary folate (OR, 0.7; 95% CI, 0.4-1.3), vitamin B6 (OR, 0.5; 95% CI, 0.3-1.0), vitamin B12 (OR, 0.6; 95% CI, 0.3-1.1), and high levels of alcohol (OR, 0.7; 95% CI, 0.4-1.1) were less likely to have a 2G-->A mutation. Individuals with high levels of dietary carbohydrate (OR, 2.0; 95% CI, 0.9-4.4) and a high glycemic index (OR, 1.9; 95% CI, 0.8-4.6) were more likely to have a G-->A transition mutation in the second base of codon 13 (5G-->A). Individuals with high levels of dietary fat (OR, 1.6; 95% CI, 0.8-3.2), saturated fat (OR, 1.7; 95% CI, 0.8-3.5), and monounsaturated fat (OR, 1.9; 95% CI, 1.0-3.7) were more likely to harbor a 2G-->T mutation. Low levels of cruciferous vegetable intake and high levels of processed meat intake also were associated with fewer 5G-->A, as reflected by the ORs (OR, 0.4; 95% CI, 0.2-1.0 and OR, 0.4; 95% CI 0.2-0.8, respectively). These data suggest that diet may be involved in disease pathways represented by specific Ki-ras mutations. However, given the limited information currently available on associations between specific genetic mutations in colon tumors and diet, these findings also should be viewed as hypothesis generating.
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PMID:Associations between dietary intake and Ki-ras mutations in colon tumors: a population-based study. 1115 93


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