Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The overall importance of nutrition to favorable perinatal outcome is only beginning to be fully appreciated. Although nutritional status can be linked to such things as socioeconomic class and education, it is nutrition directly that exerts a biologic effect. This review has attempted to look at three elements and their relationship to maternal and fetal outcome. At the present time, there does not seem to be a role for routine magnesium supplementation during pregnancy. Magnesium deficiency, as an isolated nutritional deficiency, is rare, and the evidence is, at best, weak that magnesium supplementation reduces the risk of poor perinatal outcome. Zinc deficiency is also a very rare isolated nutritional finding. Our ability to measure zinc accurately, be it in leukocytes or serum, is improving, but the routine use of zinc supplements during pregnancy cannot be recommended at this time. It may be that zinc will be a useful diagnostic marker, rather than a therapeutic intervention. There is substantial evidence that the average American diet does not contain sufficient calcium. An expansive literature continues to grow in the areas of calcium and colon cancer, calcium and breast cancer, calcium and hypertension, and calcium and osteoporosis. Is it possible that our susceptibilities to these problems begin in utero? Obviously, the answer is unknown. What is known is that supplemental calcium to some degree is needed in the diets of most Americans and in about two thirds of pregnant women. Calcium supplementation seems to affect blood pressure favorably and, pending confirmation with larger trials, may significantly reduce prematurity and preeclampsia risk, thus improving perinatal outcome for a large number of our high-risk patients.
 ...
PMID:Calcium, magnesium, and zinc supplementation and perinatal outcome. 186 34

The role of nutrients in cancer causation has been a subject of considerable interest, research, and public discussion in recent years. Results from epidemiologic, clinical, and animal studies have suggested that: 1) a reduction in total calories decreases risk for a number of tumor types; 2) dietary protein is directly correlated with liver, prostate, and colon cancer, among others, with increasing dietary protein increasing the risk; 3) increased dietary fat is correlated with increased risk for breast cancer; the evidence for an effect of fat on colon cancer is equivocal in human and animal studies; 4) a deficiency of vitamin A may enhance lung and colon tumors in animal experiments but in human this is equivocal. Increasing vitamin A above normal levels, as an anticarcinogenic effect, has not been satisfactorily demonstrated in animal models. The synthetic retinoid, 13-cis retinoic acid, inhibits both colon and lung cancer in animal models; 5) zinc deficiency is associated with enhanced esophageal cancer in humans and markedly enhances animal tumors; selenium inhibits this form of neoplasia in animals, 6) diets low in lipotropes enhance liver cancer induced by a variety of hepatocarcinogens. Our data from studies in animal models agree in some cases with epidemiological observations, but disagree with others, particularly fat and colon cancer. Overall, some forms of cancer are enhanced by excessive calories, increased dietary protein and fat, and by deficiencies of vitamin A, selenium, zinc, and lipotropes. Decreasing total intake of calories, protein, and fat, and ensuring adequate dietary levels of vitamin A, selenium, zinc, and lipotropes decreases risk for some forms of cancer.
 ...
PMID:The role of nutrients in cancer causation. 243 54

As zinc status may influence susceptibility to colon cancer, we examined the effect of dietary zinc deficiency on the proliferation of epithelial cells (colonocytes) in the large bowel of rats. When compared to feed-restricted rats, those with zinc deficiency showed a significant reduction in proliferation in the distal colon as assessed by accumulated metaphase arrest and crypt cell production rates in vivo. Zinc deficiency had no apparent effect on thymidine kinase activity in colonocytes but was accompanied by minor changes in fecal mass and fecal pH. In rats, zinc deficiency is associated with a reduction in the rate of proliferation of colonocytes in the distal colon.
 ...
PMID:Zinc deficiency is associated with suppression of colonocyte proliferation in the distal large bowel of rats. 248 56

This paper provides an overview of our knowledge on the involvement in cancer of vitamins A, C and E and of calcium, selenium and zinc. This work is a background for studies on dietary magnesium's effects on cancer. Consumption of vitamin A and its dietary precursors has been associated with reduced cancer at several sites in human and animal studies. Carcinogenesis studies using several models of cancer have been conducted on the influence of vitamin A deficiency, vitamin A excess and supplementation of vitamin A analogues. Vitamins C and E are effective in the prevention of N-nitroso compound (nitrosamine) formation. Vitamin C is effective in aqueous and vitamin E is effective in non-aqueous media. Both of these vitamins also have inhibited carcinogenesis by preformed carcinogens at several sites, but enhancement has been observed at some sites when excess vitamin treatment was studied. The potential role of calcium in the prevention of colon cancer is being pursed. Few experimental studies have been conducted but data support an effect of calcium on colonic epithelial proliferation. Epidemiological and especially experimental results suggest an inhibition of cancer by dietary selenium. In animal studies, selenium supplementation has been particularly effective in inhibiting colon and mammary carcinogenesis, but enhanced carcinogenesis was observed in some studies on skin, liver and pancreas cancer. Data suggest that zinc deficiency may be a factor in esophageal cancer; however, studies on tumor growth have demonstrated retarded tumor growth in zinc-deficient animals.
 ...
PMID:Effects of the intake of selected vitamins and minerals on cancer prevention. 266 27

Some lines of colon cancer cells are forced to undergo differentiation by 12-O-tetradecanoylphorbol-13-acetate (TPA). The increases in activities of both protein tyrosine phosphatase (PTP) and protein tyrosine kinase (PTK) have been reported to be associated with the TPA-induced differentiation of HL-60 leukemia cells. In the present study, a 2-fold increase in PTP activity was observed in SW620 human colon cancer cells after 30 min of TPA treatment; a maximal level (4- to 5-fold) was reached at 60 min and continued for more than 6 hr. In addition, two TPA-induced differentiated characteristics, morphological alteration and release of cellular surface proteoglycan, were effectively blocked by PTP inhibitors, such as sodium orthovanadate (50 microM), zinc chloride (100 microM), and iodoacetate (250 microM), but not by the protein serine/threonine phosphatase inhibitor okadaic acid (20 nM). On the other hand, although TPA induced a transient slight increase in PTK activity (1.4-fold) at 60 min, four PTK inhibitors (genistein, herbimycin A, tyrphostin-23 and quercetin) had different effects on the TPA-induced release of cell surface proteoglycan. Genistein (60 microM) potentiated this process, but in contrast, quercetin (45 microM) could partially inhibit the TPA effect. Taken together, these observations suggest that both PTP and PTK activities were increased in SW620 cells in response to TPA; however, the activation of PTP seems to be preferentially required for the TPA-induced differentiation of SW620 human colon cancer cells.
 ...
PMID:Preferential requirement for protein tyrosine phosphatase activity in the 12-O-tetradecanoylphorbol-13-acetate-induced differentiation of human colon cancer cells. 748 37

Ribosomal protein L37 mRNA is overexpressed in colon cancer. The nucleotide sequences of human L37 from several tumor and normal, colon and liver cDNA sources were determined to be identical. L37 mRNA was approximately 375 nucleotides long encoding 97 amino acids with M(r) = 11,070, pI = 12.6, multiple potential serine/threonine phosphorylation sites and a zinc-finger domain. The human sequence is compared to other species.
 ...
PMID:Human ribosomal protein L37 has motifs predicting serine/threonine phosphorylation and a zinc-finger domain. 754 44

For several human tumour types, allelic loss data suggest that one or more tumour suppressor genes reside telomeric to the p53 gene at chromosome 17p13.1. In the present study we have used a new strategy, involving molecular analysis of a DNA site hypermethylated in tumour DNA, to identify a candidate gene in this region (17p13.3). Our approach has led to identification of HIC-1 (hypermethylated in cancer), a new zinc-finger transcription factor gene which is ubiquitously expressed in normal tissues, but underexpressed in different tumour cells where it is hypermethylated. Multiple characteristics of this gene, including the presence of a p53 binding site in the 5' flanking region, activation of the gene by expression of a wild-type p53 gene and suppression of G418 selectability of cultured brain, breast and colon cancer cells following insertion of the gene, make HIC-1 gene a strong candidate for a tumour suppressor gene in region 17p13.3.
 ...
PMID:p53 activates expression of HIC-1, a new candidate tumour suppressor gene on 17p13.3. 758 25

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.
 ...
PMID:[Relationship between colorectal cancer and ten inorganic elements]. 813 59

Phytic acid (PA), a major phosphorus storage compound of most seeds and cereal grains, contributes about 1 to 7% of their dry weight. It may account for more than 70% of the total kernel phosphorus. PA has the strong ability to chelate multivalent metal ions, especially zinc, calcium, and iron. The binding can result in very insoluble salts that are poorly absorbed from the gastrointestinal tract, which results in poor bioavailability (BV) of minerals. Alternatively, the ability of PA to chelate minerals has been reported to have some protective effects, such as decreasing iron-mediated colon cancer risk and lowering serum cholesterol and triglycerides in experimental animals. Data from human studies are still lacking. PA is also considered to be a natural antioxidant and is suggested to have potential functions of reducing lipid peroxidation and as a preservative in foods. Finally, certain inositol phosphates, which may be derived from PA, have been noted to have a function in second messenger transduction systems. The potential nutritional significance of PA is discussed in this review.
 ...
PMID:Phytic acid in health and disease. 877 15

GL331 is a semisynthetic topoisomerase II inhibitor derived from a plant toxin podophyllotoxin. In 72-h exposure assays, LD50 values of GL331 range from 0.5 to 2 microM, which are three- to ten-fold lower than those of its homologous compound etoposide (VP-16), depending on different cancer cell lines including nasopharyngeal, hepatocellular, gastric, cervical and colon cancer types. Apoptotic DNA ladders could be detected when cancer cells were treated with GL331 for 24 h even if the Bcl-2 and Bax protein levels were not altered during the period. Besides acting as topoisomerase II inhibitors, both GL331 and VP-16 decrease the cellular protein tyrosine kinase (PTK) activities in cancer cells. The activities of protein tyrosine phosphatase (PTP) are significantly increased after GL331 treatment but are not affected by VP-16. GL331-induced internucleosomal cleavage can be efficiently prevented by two inhibitors of PTP, sodium orthovanadate and zinc chloride, but not by okadaic acid, which inhibits serine/threonine phosphatase activity. These results indicate that GL331 may induce apoptotic cell death, and that activation of protein tyrosine phosphatases may be involved in this process.
 ...
PMID:Protein tyrosine phosphatase activities are involved in apoptotic cancer cell death induced by GL331, a new homolog of etoposide. 901 84


1 2 3 4 5 6 7 8 9 10 Next >>