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

Factors influencing the depression of natural killer (NK) activity and its prevention were studied in 57 esophageal cancer patients. NK activity off peripheral blood mononuclear cells was measured by a 51Cr-release assay against K-562 target cells. NK activity in esophageal cancer patients was significantly lower than that in healthy individuals and tended to be lower compared with those in stomach and colon cancer patients. The depression of NK activity was significantly correlated with the reduction of serum albumin level, creatinine height index of nutritional assessment. The activity was also suppressed in proportion to the size of cancer and its staging. Both preoperative radiation and surgery markedly depressed NK activity. Postoperative depression recovered to the Preoperative level 4 weeks after operation. These results indicated that malnutrition, cancer bearing and therapeutic stress were associated with the depression of NK activity. As the preventive measures against such depression of NK activity, avoidance of preoperative radiation and better selection for two-stage operation enhanced recovery of the depressed NK activity. Furthermore, the preoperative administration of OK-432, as n immuno-activator, could be effective to minimize a decrease of NK activity related to radiation and surgery, and to accelerate its recovery to the level before treatment.
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PMID:[Factors influencing depression of natural killer activity and its prevention in esophageal cancer patients]. 270 63

A series of recent studies has shown an association between low serum cholesterol level and cancer, particularly of the large bowel. To explore this issue, serum cholesterol measurements were collected from 244 patients with adenomatous polyps of the colon, 182 patients with Dukes' A or B colon cancer, and 688 hospital controls who were diagnosed between 1979 and 1981 at a New York City hospital. The mean serum cholesterol levels were lower for patients with cancer (207.2 mg/dL) than for controls (219.5 mg/dL), with patients with Dukes' B cancer accounting for most of the difference. Patients with adenomatous polyps (219.8 mg/dL) were similar to controls. After adjustments for nutritional status using the serum albumin level, there were no statistically significant differences among any of the groups. We conclude that the low serum cholesterol level previously associated with malignancies, and colon cancer in particular, is a consequence rather than a cause of the cancer.
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PMID:Serum cholesterol levels in adenomatous polyps and cancer of the colon. A case-control study. 394 15

A fraction of the alpha-globulins (NHG) from normal human serum was cytotoxic for mouse L-cells in culture and Meth A tumors in mice. NHG inhibited the growth in vitro of human colon cancer (HT-29), melanoma (RPMI 7931) and a neuroblastoma cell line. Survival of HeLa S-3 cell colonies after 24 h exposure to 25, 50, 75 or 100 micrograms NHG/ml medium was 86%, 77%, 40% and 10%, respectively. Whole human serum or purified serum albumin had no anti-HeLa cell activity. These results confirm the presence of a protein in human serum with antitumor activity. An assay for NHG using HeLa S-3 tumor cells is described.
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PMID:A protein fraction (NHG) from serum of normal humans which is cytotoxic for HeLa cells in culture. 617 Apr 26

Human monocytes from normal donors as well as breast or colon cancer patients were fractionated on five-step discontinuous bovine serum albumin (BSA) density gradients, and the monocytes from each fraction were allowed to mature into macrophages during a 5 day incubation period. The macrophages were then examined both for their ability to kill tumor cells after activation with lipopolysaccharide (LPS) and the quantity of prostaglandin E2 (PGE2) synthesized. When the macrophages obtained from normal donors were fractionated, fractions 2 and 4 which comprised 58% of the total cell population, were cytotoxic for tumor cells. In contrast, when the macrophages from breast cancer patients were fractionated, only the high density cells found in fraction 4 were cytotoxic. It is also conceivable that since fraction 4 comprises only 26% of the total macrophages recovered, this may be the reason unfractionated macrophages from breast cancer patients are unable to kill tumor cells. When the colon cancer patients' macrophages were fractionated on BSA density gradients, fractions 1, 2 and 4, which comprised 79% of the total cell population, were cytotoxic for tumor cells. Prostaglandin E2 synthesis was also analyzed and it was found that fraction 3 consistently synthesized increased quantities of PGE2 when compared with the other three fractions. Furthermore, since fraction 3 was non-cytotoxic for tumor cells, it is conceivable that the increased synthesis of PGE2 by fraction 3 rendered these macrophages non-cytotoxic.
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PMID:Separation of macrophages on discontinuous bovine serum albumin (BSA) density gradients: cytotoxic effects of fractionated cells from normal donors and cancer patients. 659 30

Sera from 111 patients with various gastro-intestinal (GI) diseases were studies for the presence of antibodies to human serum albumin (HSA), bovine serum albumin (BSA) and ovalbumin (OA) by passive haemagglutination assay. The antibody titre to BSA was higher than that to HSA or OA. The anti-BSA antibody was demonstrated in upper GI diseases i.e. esophageal cancer, gastric ulcer, gastric cancer and duodenal ulcer, and not in lower GI disease i.e. Crohn's disease, ulcerative colitis and colon cancer. Both the mean titre and the incidence of the anti-BSA antibody tended to be higher in women than in men, and the titre was in a positive correlation with serum gamma-globulin levels. Sephadex G-200 column chromatography revealed that the anti-BSA antibody was widely distributed between void volume and 7S fraction.
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PMID:Anti-albumin antibodies in sera of patients with gastro-intestinal disease. 714 Nov 96

Dietary cooked casein promotes colon cancer in rats. We speculated and tested the hypothesis that cooking reduces the digestibility of casein, and increases the yield of bacterial metabolites, which are potential promoters of cancer. We investigated dietary means to manipulate nitrogen transfer and fermentation in the caecum. The caecal digestion of casein (cooked or not), keratin (hydrolysed or not) and bovine serum albumin (oxidized or not) was measured in rats. Protein fermentation was estimated by assaying caecal ammonia and branched-chain fatty acids. Keratin and cooked casein were digested to a very low extent, and were poorly fermented. Rats given cooked casein had 2-3 times more ammonia in their caecum than animals given the other proteins. Antibiotics (bacitracin, chlortetracycline, neomycin and spiramycin, at either 20 and 80 micrograms/ml water) decreased caecal ammonia in rats eating cooked casein, with spiramycin being most efficient. These data support the hypothesis given above, and provide ways to manipulate caecal ammonia.
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PMID:Digestion and fermentation of proteins in rats fed keratin, albumin, cooked casein and antibiotics. 751 Apr 93

Initial attachment of leukocytes to the vessel wall at sites of inflammation is supported by a family of carbohydrate-binding adhesion molecules called the selectins. Selectin ligands include sialyl-Lewis x (sLex, Neu5Ac alpha 2-3Gal beta 1-4[Fuc alpha 1-3]GlcNAc--) and related structures. We report here that defined heparin oligosaccharides interact with the selectins. Heparin chains containing four or more monosaccharide residues inhibited the function of L- and P-selectin, but not E-selectin, in vitro. In a competition enzyme-linked immunosorbent assay measuring inhibition of solution-phase selectin-Ig fusion proteins (selectin-Ig) binding to immobilized bovine serum albumin-sLex neoglycoprotein, a heparin-derived tetrasaccharide mixture inhibited 50% of L- and P-selectin-Ig binding (IC50) at 200 +/- 40 mumol/L and 850 +/- 110 mumol/L, respectively. A single hexasulfated tetrasaccharide (delta UA2S alpha 1-4GlcNS6S alpha 1-4IdoA2S alpha 1-4GlcNS6S) was particularly active against L- and P-selectin-Ig (IC50 = 46 +/- 5 mumol/L and 341 +/- 24 mumol/L). By comparison, the tetrasaccharide sLex was not inhibitory at concentrations up to 1 mmol/L. In cell adhesion assays, heparin tetrasaccharides reduced binding of neutrophils to COS cells expressing P-selectin but not to COS cells expressing E-selectin. They also blocked colon cancer cell adhesion to L- and P-selectin but not E-selectin. In a model of acute inflammation, intravenously administered heparin tetrasaccharides diminished influx of neutrophils into the peritoneal cavities of thioglycollate-treated mice. We conclude that heparin oligosaccharides, including non-anticoagulant tetrasaccharides, are effective L- and P-selectin inhibitors in vitro and have anti-inflammatory activity in vivo.
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PMID:Heparin oligosaccharides bind L- and P-selectin and inhibit acute inflammation. 769 75

To better understand the biochemical mechanisms by which select fats and fibers modulate colonic cell proliferation, we determined the profile of protein kinase C (PKC) isozymes and cell proliferation in rat proximal and distal colonic mucosa following diet manipulation, because enhanced cell proliferation has been correlated with colon cancer incidence. Rats were assigned to one of four diets (each with 15 g fat + 6 g fiber/100 g diet) for 3 wk: fiber-free fish oil (FF), fiber-free corn oil (FC), cellulose + corn oil (CC), or pectin + corn oil (PC). Stead-state levels of colonic mucosal cytosolic and membrane PKC isozymes were determined. In vivo cell proliferation was determined by bromodeoxyuridine incorporation into DNA. In addition, viable exfoliated colonic epithelial cells were isolated from feces using Percoll-bovine serum albumin gradients. We found that 1) proximal and distal colonic mucosa possessed different steady-state levels and relative proportions of PKC isozymes; 2) PKC alpha and delta expression were significantly greater in distal membrane of the PC-fed group compared with the other dietary groups; 3) the number of exfoliated cells per 4-h fecal collection generally was proportional to the diet-induced changes in cell proliferation (PC > FC > CC > FF). These data demonstrate that dietary treatment altered colonic PKC isozyme expression, with animals fed the fiber-containing diets generally expressing higher steady-state levels of PKC alpha and delta.
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PMID:Dietary fat and fiber alter rat colonic protein kinase C isozyme expression. 781 76

Bombesin (BBS) stimulates cellular proliferation of both normal and transformed cells. The mouse colon cancer cells (MC-26) possess specific binding sites for BBS. The purpose of this study, therefore, was to examine the effect of chronic administration of BBS on in vivo growth of MC-26 tumours in Balb/c mice and on survival of tumour-bearing mice. Three groups of mice (n = 10 each) inoculated with MC-26 cells received either saline containing 0.1% bovine serum albumin (BSA), or BBS (5 micrograms kg-1 or 20 micrograms kg-1) dissolved with 0.1% BSA saline by intraperitoneal route three times a day for 15 days. BBS increased weight, DNA and RNA contents of MC-26 tumours. To examine the effect of BBS on survival rates of mice with MC-26 tumours, three groups of mice (n = 20 each) were treated for 31 days, as above. One group of mice inoculated with MC-26 cells received 0.1% BSA saline; the other group of MC-26-inoculated mice and the control group without tumour received BBS (5 micrograms kg-1) dissolved with 0.1% BSA saline. BBS significantly decreased the survival rate of mice bearing MC-26 tumours (median survival; saline group: 42.5 days, BBS group: 32.0 days, P = 0.037). None of the mice in the control group died during the experiment. BBS may stimulate in vivo growth of MC-26 cells through specific receptors.
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PMID:Bombesin stimulates growth of colon cancer in mice and decreases their survival. 825 6

Suramin is a polysulfonated compound currently under investigation for the treatment of various types of cancer. Pharmacokinetic studies from clinical trials in humans have shown that most of the circulating drug is associated with serum albumin. The objective of the present study was to investigate the intracellular localization of suramin and serum albumin in human colon cancer cells (HT-29-D4) upon suramin treatment. For this purpose, combined gold labeling and autoradiographic methods were performed on HT-29-D4 cells grown in serum free medium containing both [3H]suramin and colloidal gold-albumin. These morphological experiments demonstrated for the first time that suramin and serum albumin were co-localized in the same cellular compartment (i.e. the lysosomal system) of the suramin-treated HT-29-D4 cells. The albumin-directed targeting of suramin in lysosomes may allow the drug to inhibit the activity of several lysosomal hydrolases, resulting in a lysosomal storage disorder.
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PMID:Co-localization of suramin and serum albumin in lysosomes of suramin-treated human colon cancer cells. 862 Apr 67


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