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

The purpose of this review is to study the literature concerning normal colon and colorectal cancer for evidencing that the location of the primary proximal or distal tumor may determine two categories of carcinogenesis. The proximal or distal normal colon can be considered as two different organs. Their embryologic origins are different, the splenic flexure starts the distal segment. Antigenic pattern as well as the use of metabolic pathways, such as that of glucose, butyrate and polyamines differ. Epidemiologic, macroscopic and histological features and the inherited and acquired genetic abnormalities allow in some cases to distinguish between two types of cancer according to their proximal or distal location. These two forms are not entirely different and these features can overlap. However the recognition of these two different forms of colon cancer, must be taken in account for clinical or basic research and evaluation of data.
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PMID:[Two colons--two cancers? Proximal or distal adenocarcinoma: arguments for a different carcinogenesis]. 774 9

Some factors related to Westernization or industrialization increase risk of colon cancer. It is believed widely that this increase in risk is related to the direct effects of dietary fat and fiber in the colonic lumen. However, the fat and fiber hypotheses, at least as originally formulated, do not explain adequately many emerging findings from recent epidemiologic studies. An alternative hypothesis, that hyperinsulinemia promotes colon carcinogenesis, is presented here. Insulin is an important growth factor of colonic epithelial cells and is a mitogen of tumor cell growth in vitro. Epidemiologic evidence supporting the insulin/colon-cancer hypothesis is largely indirect and based on the similarity of factors which produce elevated insulin levels with those related to colon cancer risk. Specifically, obesity--particularly central obesity, physical inactivity, and possibly a low dietary polyunsaturated fat to saturated fat ratio--are major determinants of insulin resistance and hyperinsulinemia, and appear related to colon cancer risk. Moreover, a diet high in refined carbohydrates and low in water-soluble fiber, which is associated with an increased risk of colon cancer, causes rapid intestinal absorption of glucose into the blood leading to postprandial hyperinsulinemia. The combination of insulin resistance and high glycemic load produces particularly high insulin levels. Thus, hyperinsulinemia may explain why obesity, physical inactivity, and a diet low in fruits and vegetables and high in red meat and extensively processed foods, all common in the West, increase colon cancer risk.
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PMID:Insulin and colon cancer. 774 56

Lignans and isoflavonoids are two groups of diphenolic phytoestrogens of plant origin which have gained increasing interest because of their possible cancer protective properties. High excretion of these compounds occur in populations at low risk of breast, prostate and colon cancer consuming either high amounts of whole-grain (lignans and some isoflavonoids) or soy products (isoflavonoids and some lignans). We determined the pattern of conjugation of the phytoestrogens in four urine samples from vegetarian or semivegetarian women and in two samples from men. Seven compounds were investigated: enterodiol, enterolactone, matairesinol, diadzein, equol, genistein and O-desmethylangolensin. The fractions quantified are the free fraction, mono- and disulfate, as well as the mono-, di- and sulfoglucuronide fractions. For the fractionation and purification we used ion-exchange chromatography and the determination of the concentrations of each compound in all fractions was done by isotope dilution gas chromatography-mass spectrometry (GLC-MS) using deuterated internal standards of all diphenols. More than 60% of all compounds determined, occurred in the monoglucuronide fraction. Daidzein, enterodiol and equol are excreted to a relatively high extent as sulfoglucuronides and genistein as diglucuronide. We conclude that the general pattern of lignan and isoflavonoid conjugates in urine is similar to that of endogenous estrogens.
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PMID:Lignan and isoflavonoid conjugates in human urine. 785 79

High-resolution 31P NMR spectroscopy at 11.7 T was used to examine the influence of medium formulation (medium and serum type, and concentrations of glucose and inositol) on the cellular phosphate metabolism of CX-1 cells, a human colon cancer cell line derived from HT-29 cells. Striking differences in the 31P spectra of harvested CX-1 cells were observed. The largest variation was seen in the phosphocholine and UDP-hexose levels (up to seven-fold changes), with smaller differences in the levels of other phosphate metabolites. The major UDP-hexose species were found to be UDP-N-acetylglucosamine and UDP-N-acetylgalactosamine (ca 2:1 ratio), which have been proposed in the literature to be markers of cell differentiation status. Medium-induced alterations in metabolite levels were much greater than the normal variations seen in CX-1 control samples grown under identical conditions. They even exceeded the characteristic differences observed between different human tumor cell lines grown under one set of culture conditions. The remarkable sensitivity of CX-1 cellular phosphate metabolism to the culture environment has implications for the comparison of in vitro vs in vivo spectra, and for the interpretation of effects due to growth and therapy.
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PMID:The influence of medium formulation on phosphomonoester and UDP-hexose levels in cultured human colon tumor cells as observed by 31P NMR spectroscopy. 821 27

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

We have studied the effects of 1,25-dihydroxyvitamin D [1,25-(OH)2D3] on cellular differentiation in the HT-29 human colon cancer cell line. Our aim was to evaluate the regulation of 1,25-dihydroxyvitamin D receptor (VDR) abundance and hormone responsiveness during the transition of rapidly proliferating to differentiated cells. Differentiation was induced by three means: cells were cultured in galactose-supplemented medium without glucose (GAL), grown on Matrigel-coated surfaces (MTG), or treated with 1,25(OH)2D3. Cell proliferation, assessed by [3H]thymidine incorporation, was equivalently inhibited by treatment with 1,25(OH)2D3, GAL or MTG. Differentiation was assessed by the induction of amino-oligo peptidase activity which was low in the proliferating cells. Following treatment with 1,25(OH)2D3, or growth in GAL or on MTG, amino-oligo peptidase activity increased 8- to 9-fold. The abundance of VDR measured by [3H]1,25(OH)2D3 binding, decreased to half without significant change in affinity, in cells differentiated by all three means compared to proliferating cells. Northern blot analyses of differentiated cells showed decreased steady-state levels of VDR messenger RNA (mRNA), indicating that all three treatments similarly decreased the abundance of VDR, at least in part, at the mRNA level. When exposed to 1,25(OH)2D3, the proliferating cells exhibited homologous up-regulation of VDR as well as the induction of 24-hydroxylase mRNA; the differentiated cells failed to exhibit both of these biological responses. Our findings demonstrate that 1,25(OH)2D3, GAL and MTG treatment all inhibit HT-29 cell proliferation and stimulate differentiation. Postproliferative differentiation achieved by the three approaches was associated with decreased VDR abundance, loss of VDR homologous up-regulation, and development of hormone unresponsiveness to 1,25(OH)2D3.
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PMID:Regulation of vitamin D receptor abundance and responsiveness during differentiation of HT-29 human colon cancer cells. 838 98

The effect of glucose and fructose and fetal bovine serum on the expression of the fructose transporter GLUT5 was studied in clone PD7 of the human colon cancer cell line Caco-2, which has been characterized previously [Chantret, Rodoloswe, Barbat et al. (1994) J. Cell Sci. 107, 213-225; Mahraoui, Rodolosse, Barbat et al. (1994) Biochem. J. 298, 629-633]. Culture of the cells in dialysed serum and hexose-free media, down-regulated the expression of GLUT5, which was below detection within 3-4 days. This effect was reversed by fructose and glucose feeding of the cells. Fructose feeding yielded a 3-fold higher abundance of GLUT5 protein and mRNA as compared with that expressed in glucose-fed cells. Cells fed normal serum exhibited an inverse hierarchy of expression, with glucose being a better inducer than fructose for the expression of GLUT5. The GLUT5 mRNA and protein abundances obtained in fructose-fed cells did not depend on the type of serum. A linear relationship between cyclic AMP (cAMP) levels and GLUT5 mRNA abundance was found in cells fed dialysed serum, whereas in cells fed normal serum, mRNA abundances were not correlated to cAMP levels. These results indicate that glucose and fructose, together with serum-related factors and cAMP, have combined effects on the expression of GLUT5 in Caco-2 cells.
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PMID:Sugar-dependent expression of the fructose transporter GLUT5 in Caco-2 cells. 855 16

A plasma membrane preparation from human amnion (WISH) cells contained uridine diphosphate sugars and methyl-uridine diphosphate (mUDP) sugars. The synthesis of mUDP-glucose, mUDP-mannose, and mUDP-fucose by the membrane preparation occurred when supplemented with uridine-5'-diphosphate-glucose and S-adenosyl-L-methionine. It is suggested that this newly recognized route for fucose biosynthesis might be employed by certain transformed cells, and may partly account for the methionine dependence of certain human tumors. Additionally, it is suggested that, in colon cancer, a deficiency of folic acid and methionine might affect mUDP-sugar biosynthesis rather than the methylation of DNA.
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PMID:Involvement of methionine in the synthesis of certain membrane-associated nucleotide sugars by human amnion (WISH) cells. 862 Apr 51

Glucose-regulated proteins (GRPs) are induced in cells by a variety of stress conditions such as treatment with 2-deoxyglucose, glucosamine, or the calcium ionophore A23187. We found that resistance to topoisomerase II (topo II) inhibitors, VP-16 and adriamycin, was induced by these treatments in human colon cancer HT-29 cells. Similar VP-16 resistance occurred in human ovarian cancer A2780 and breast cancer MCF-7 cells. The VP-16 resistance was reversible, since the sensitivity of the cells to VP-16 recovered within 24 h after the stresses were removed. Western blotting analysis showed that under these stress conditions the cellular contents of topo II alpha were decreased. The decreased expression of topo II was reversed to control levels within 24 h following removal of the stresses. The decrease in topo II levels under the stress conditions correlated well with the induction of GRP78 and 94. The close correlation between topo II and GRPs suggests that topo II is a protein sensitive to the glucose-regulated stresses. Since hypoxia and nutrient deprivation, which are also GRP-inducing conditions, could occur naturally in the solid tumors, the stress-associated cellular resistance through decrease in topo II levels may be a mechanism of the natural resistance of the solid tumors to topo II-directed chemotherapy.
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PMID:Glucose-regulated stresses confer resistance to VP-16 in human cancer cells through a decreased expression of DNA topoisomerase II. 870 75

To study the effect of dietary sugars and starches on parameters linked to colon carcinogenesis, female Sprague-Dawley rats were fed for one month five different diets containing sucrose, glucose, fructose, cornstarch, or Hylon 7, a starch with a high amylose content. After this period, colon proliferation, assessed by [3H] thymidine incorporation in vitro, was higher (p < 0.05) in rats fed sucrose than in rats fed glucose, fructose, or cornstarch [labeling index was 7.17 +/- 0.75, 5.03 +/- 0.07, 4.55 +/- 0.72, 4.00 +/- 0.70, and 5.89 +/- 1.05 (SE) in sucrose, glucose, fructose, cornstarch, and Hylon 7 diets, respectively]. Cecal pH was lower in rats fed cornstarch and Hylon 7 than in rats fed sucrose, glucose, or fructose. Content of short-chain fatty acids (SCFAs) in the cecum was higher in rats fed Hylon 7 than in those fed glucose and fructose. In conclusion, glucose and fructose, compared with sucrose, decrease mucosal proliferation and may be considered protective factors in colon carcinogenesis, although they do not affect SCFA production and cecal pH. On the contrary, Hylon 7 does not change mucosal proliferation but increases SCFAs and lowers cecal pH, two conditions associated with a lower risk of colon cancer.
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PMID:Dietary sucrose, glucose, fructose, and starches affect colonic functions in rats. 871 Jun 87


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