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PubMed1988

Localization of villin, a cytoskeletal protein specific to microvilli, in human ileum and colon and in colonic neoplasms.

Villin is a cytoskeletal protein of microvilli of epithelial cell brush borders found principally in absorptive cells of the intestine and proximal renal tubule. A marker of both enterocyte differentiation and epithelial cell polarity, it has been studied mainly in experimental animals. We raised monoclonal antibodies to villin and used them to localize it in human ileum and colon and in 22 colonic neoplasms. Villin is localized in the brush border of normal ileum and in the luminal border of normal colon and is expressed with increasing staining intensity as cells migrate from crypt to surface. It was present in the luminal border in all five adenomas and in 16 of 17 adenocarcinomas studied. In addition, villin staining was observed in the cytoplasm of 10 tumors, and in the basement membrane area surrounding tumor in 10 cases. In "transitional" mucosa adjacent to carcinomas it was confined to the luminal border. Abnormal expression of villin by a significant proportion of colonic tumors suggests that it may have a role as a marker of colorectal neoplasia.

Adenocarcinoma↗
PubMed1993

Effects of new somatostatin analogs on the cell proliferation of colonic crypts and colonic cancers in rats.

The antiproliferative activity of two new somatostatin (SS) analogs: ASS-51 and ASS-52 have been tested in this study. We assessed their ability to inhibit the DNA synthesis in normal colon crypt cells and in the cells of chemically (dimethylhydrazine)-induced colon cancer in the rats. The incorporation of bromodeoxyuridine (BrDU) into appropriate cell nuclei was used as an index of DNA synthesis. It was found that: 1) Only ASS-51 significantly decreases the colon crypt cell proliferation in the rat when compared to controls. Since both analogs were previously shown to inhibit GH release, these data indicate that the antiproliferogenic effect of ASS-51 is independent of the inhibition of GH release. 2) Both examined analogs did not significantly effect the BrDU incorporation into cell nuclei of chemically-induced colon cancer.

Adenocarcinoma↗
PubMed1987

Observation and quantification of aberrant crypts in the murine colon treated with a colon carcinogen: preliminary findings.

In the present study a methodological approach is taken which quantitates aberrant dysplastic crypts in the unsectioned murine colon. C57BL/6J or CF1 female mice (7-8 weeks old) were injected (i.p.) with azoxymethane (5 mg/kg body wt./week) for 4 weeks. Their colons were excised, cut open on the median axis and fixed flat in buffered formalin. Unsectioned colons were stained with methylene blue. The mucosal side was examined under a light microscope. The aberrant crypts, which are larger and have a thicker epithelial lining, were easily visualized using X 4 or X 10 objectives. CF1 mice, which are more sensitive to developing colon tumors, had a higher number of aberrant crypts/colon than their less sensitive counterparts, C57BL/6J mice (5.0 +/- 0.7 vs. 2.4 +/- 0.7). The usefulness of this observation as a possible measure of neoplastic events is discussed in the animal and human situation.

Animals↗
PubMed2005

Proteomic analysis of colonic myofibroblasts and effect on colon cancer cell proliferation.

BACKGROUND: The stromal microenvironment influences many steps of tumor progression through the elaboration of signals from myofibroblasts. The phosphatidylinositol 3-kinase (PI3K)/Akt pathway transduces signals initiated by growth factors and is involved in colonic epithelial proliferation. The purpose of this study was to determine (1) the influence of myofibroblasts on colon cancer cell proliferation and PI3K activity, and (2) the protein alterations associated with myofibroblasts derived from polyp versus normal margins. METHODS: Myofibroblasts were derived from polyps and corresponding normal mucosa. Myofibroblasts were cocultured with colon cancer cells HT29 stably transfected with green fluorescent protein and KM20 cells. Proliferation was quantitated by green fluorescent protein count and cytokeratin enzyme-linked immunosorbent assay. HT29 cells were incubated with conditioned medium from myofibroblasts, and the effect on proliferation and PI3K activity was determined by 5-bromo 2-deoxyuridine incorporation and Akt kinase assay, respectively. Protein profiles were obtained by SELDI-TOF MS analysis. RESULTS: In coculture experiments, all myofibroblasts significantly enhanced HT29 and KM20 cell proliferation. However, polyp myofibroblasts enhanced proliferation of the cancer cells to a greater extent than normal myofibroblasts. Conditioned medium from all myofibroblasts stimulated Akt kinase activity. SELDI-TOF MS profiles showed more than 40 protein peaks for each isolate. One protein was differentially expressed in polyps versus normal cells. CONCLUSIONS: Utilizing a novel proteomic approach, we identify distinct protein profiles in myofibroblasts of polyps compared with stromal cells of normal mucosa. Moreover, myofibroblasts can stimulate indirectly PI3K activity and enhance colon cancer cell proliferation. These findings suggest that targeted therapy to signaling pathways in myofibroblasts may be useful in colorectal cancer chemoprevention and possible treatment.

Adenomatous Polyps↗
PubMed1999

Ability of naloxone to enhance the colonoscopic appearance of normal colon vasculature and colon vascular ectasias.

BACKGROUND: Colon vascular ectasias are a common cause of lower intestinal bleeding among the elderly. The lesions may be difficult to diagnose at colonoscopy because they are small and their appearance may be influenced by the patient's blood pressure, blood volume, and narcotic sedation during the procedure. The purpose of this study was to determine whether naloxone influenced the appearance of colon vascular ectasias at colonoscopy. METHODS: One hundred forty-four patients older than 60 years undergoing complete colonoscopy participated in the study. Medications were given in the usual doses. After a 2-minute inspection of the cecum and ascending colon, naloxone was given, followed by another 2-minute observation period. Photographic documentation of areas of interest was obtained before and after administration of naloxone. RESULTS: One hundred fourteen patients (79%) had no ectasias before or after administration of naloxone. Fourteen (9.7%) initially had normal vessels, and the vessels became more prominent; 4 (2.7%) initially had no ectasias, but ectasias later developed. Four patients (2.7%) had ectasias before administration of naloxone that did not change; 8 (5.4%) had ectasias before administration of naloxone that increased in size (3 patients), number (7 patients), or both (2 patients). CONCLUSIONS: Naloxone can enhance the appearance of normal colonic vasculature and ectasias. Naloxone is an important adjunctive medication for patients undergoing examinations for lower intestinal bleeding.

Blood Vessels↗
PubMed2003

Effects of sphingomyelin on aberrant colonic crypt foci development, colon crypt cell proliferation and immune function in an aging rat tumor model.

Sphingomyelin (SPM) was assessed in older rats for in vivo effects on multiple immune responses and the development of colon preneoplastic lesions. Fifty-four-week-old rats were injected with 10 mg/kg body weight of the carcinogen azoxymethane (AOM), and then treated with 35 mg/kg body weight SPM orally for 6 weeks beginning 6 weeks after AOM treatment. None of the immune functions tested (antibody formation, delayed-type hypersensitivity or natural killer cell cytotoxicity) were significantly affected by SPM treatment. Natural killer (NK) cell activity was, however, decreased in all rats that were treated with AOM. There was a tendency for decreased aberrant crypt foci (ACF) numbers in the SPM-treated rats but this reduction was only significant for the largest lesions (> nine crypts per foci). The decreased ACF numbers were most evident in the proximal end of the colon. Colonic crypt cell proliferation was also decreased in SPM treated rats. This reduction was primarily in the base of the crypt column. Also, low numbers of ACF developed spontaneously in rats not treated with AOM, but no ACF were present in non-AOM rats that also received SPM. It appears that SPM may have effects on the post-initiation development of preneoplastic lesions in the rat colon but not on the immune functions assessed in this study.

Aging↗
PubMed1992

Mononuclear cells in normal colon and colonic carcinoma express the same T cell activation markers.

The proportion of mononuclear cells (MC) expressing some of the T cell activation markers in normal colon and colonic carcinomas was determined by immunoperoxidase staining and computer-assisted video image analysis (VIA). Tissue sections were stained with monoclonal antibodies against the T cell activation markers which included the MHC class II antigens DR, DP and DQ, interleukin 2 receptor (CD25) and the p180 (CD45RO) form of the leucocyte common antigen. The mean values for the proportion of leucocytes expressing these activation markers were 92% for DR, 61% for DP, 68% for DQ and 60% for CD45RO in tumours and 90, 62, 70 and 55% in normal tissue respectively. Few cells were stained for the IL2 receptor (mean values 7% for tumours and 5% for normal tissue) or the p220 form (CD45RA) of the leucocyte common antigen (mean values 6% for tumours and 4% for normal tissue). The proportion of MC bearing any of these markers in the normal colon was not significantly different from the matched colonic carcinomas.

Antibodies, Monoclonal↗
PubMed2001

Congenital pouch colon associated with segmental dilatation of the colon.

A 1-day-old boy who presented with an anorectal malformation (ARM) was found to have a segmental dilatation of the colon (SDC) associated with a typical congenital pouch colon (CPC) malformation. The distal colonic pouch terminated in a high colovesical fistula. The posterior portion of the perineal raphé was duplicated and ended in 2 anal dimples. Both dilated segments of the colon were excised. The similarity between CPC and SDC is highlighted, and the possible embryogenesis of both conditions is discussed.

Colon↗
PubMed2000

Colon heat and colon cancer.

Epidemiological findings on the relation between foods and colon cancer are inconsistent. Many, but far from all, found positive associations for meat and fat and negative ones for vegetables and fruits. Explanations so far have focused on direct biochemical conversions in the colon or transit time, but they remain unable to explain the contradictory observations. One aspect grossly ignored has been bacterially produced heat which is beyond somatic control. A present day affluent lifestyle includes a more sedentary life, the strongest of all risk factors for colon cancer, with more sitting and less diffusion of bacterial heat, more fat and sugar, rich in energy and less of energy poor foods like cereals. A temperature higher by less than 1 degrees C in the colon over decades may promote tumour growth to a distinguishable extent.

Animals↗
PubMed1989

Measurement of the proliferative status of colonic epithelium as a risk marker for colon carcinogenesis: effect of bile acid and dietary fiber.

The proliferative status of mouse colonic epithelium, as affected by dietary fibers with or without cholic acid (CA), was studied by autoradiography and the metaphase arrest technique. In the first study, groups of mice were fed natural ingredient (laboratory chow) or semisynthetic diets containing 0% (control) or 0.2% (test) CA. After the mice were fed two weeks, the effect of CA was significantly more pronounced in the semisynthetic diet group than in the natural ingredient diet group with respect to labeled cells/crypt section (7.8 +/- 0.8 vs. 2.9 +/- 0.4) and mitotic figure (MF)/crypt section (3.0 +/- 0.5 vs. 1.8 +/- 0.2). In the second study, diets formulated to contain 5 or 10% cellulose (C), pectin (P), or wheat bran (WB) with or without CA (0.2%) were fed to animals for two weeks and colonic proliferative indices were measured. When compared with 5% C group, the 10% WB group exhibited lower labeling index (LI) values (4.2 +/- 0.5 vs. 6.4 +/- 1.0) and the 10% P group exhibited higher LI values (10.0 +/- 1.1 vs. 6.4 +/- 1.0). CA-induced increases in the LI and MF values responded independently in some cases to dietary fiber. Among the CA-treated groups, only the 10% P diet resulted in lower LI when compared with the 5% C group (p less than 0.05) (7.4 +/- 0.8 vs. 12.5 +/- 2.8) but had no effect on MF/crypt section. However, the 5 or 10% WB diet resulted in lower MF values (1.7 +/- 0.2 and 1.8 +/- 0.6 vs. 2.6 +/- 0.3). A long-term feeding study comparing 10% P with 10% C diets also demonstrated that the LI was elevated in the 10% P group without any effect on the mitotic activity of the colonic epithelium. This paradoxical finding suggests that the value of the LI and/or mitotic index as a risk marker of colon carcinogenesis should be further investigated.

Animals↗
PubMed2002

Phytoestrogens regulate vitamin D metabolism in the mouse colon: relevance for colon tumor prevention and therapy.

Soybean products are highly represented in the traditional Asian diet. Major components of soy proteins are phytoestrogens, such as isoflavones. They may be responsible for the extremely low incidence of prostate and mammary tumors and possibly also of colon cancer in countries such as China and Japan. Serum 1,25-dihydroxyvitamin D3 level is inversely related to incidence of some cancers. Levels are determined by skin exposure to ultraviolet light or, to a minor extent, nutritional uptake and by subsequent conversion of the precursor vitamin D to the active hormone by the cytochrome P450 hydroxylases CYP27A1, CYP27B1 (responsible for synthesis) and CYP24 (responsible for catabolism) in liver and kidney. However, vitamin D synthesis is also found in colonocytes and is enhanced during incipient malignancy. This may indicate an autocrine/paracrine role for this differentiation-inducing hormone in defense against progression. We were able to demonstrate that either a single large oral dose of genistein or feeding soy protein for 4 mo elevated CYP27B1 and decreased CYP24 expression in the mouse colon. Our data therefore suggest that an inverse correlation of soy product consumption with colon tumor incidence may be consequent to enhanced colonic synthesis of the antimitotic hormone 1,25-dihydroxyvitamin D3.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed2006

Uranyl nitrilotriacetate, a stabilized salt of uranium, is genotoxic in nontransformed human colon cells and in the human colon adenoma cell line LT97.

Previous uranium mining in the "Wismut" region in Germany enhanced environmental distribution of heavy metals and radionuclides. Carryover effects may now lead to contamination of locally produced foods. Compounds of "Wismut" origin are probably genotoxic via their irradiating components (radon) or by interacting directly with cellular macromolecules. To assess possible hazards, we investigated the genotoxic effects of uranyl nitrilotriacetate (U-NTA) in human colon tumor cells (HT29 clone 19A), adenoma cells (LT97), and nontransformed primary colon cells. These are target cells of oral exposure to environmentally contaminated foods and represent different cellular stages during colorectal carcinogenesis. Colon cells were incubated with U-NTA. Cell survival, cytotoxicity, cellular glutathione (GSH) levels, genotoxicity, and DNA repair capacity (comet assay), as well as gene- and chromosome-specific damage combination of comet assay and fluorescence in situ hybridization [FISH], 24-color FISH) were determined. U-NTA inhibited growth of HT29 clone 19A cells (75-2000 microM, 72 h) and increased GSH (125-2000 microM, 24 h). U-NTA was genotoxic (1000 microM, 30 min) but did not inhibit the repair of DNA damage caused by hydrogen peroxide (H(2)O(2)), 4-hydroxynonenal, and 2-hydroxyamino-1-methyl-6-phenylimidazo[4,5-b]-pyridine. U-NTA was also genotoxic in LT97 cells and primary colon cells, where it additionally increased migration of TP53 into the comet tail. In LT97 cells, 0.5-2mM U-NTA increased chromosomal aberrations in chromosomes 5, 12, and 17, which harbor the tumor-related genes APC, KRAS, and TP53. It may be concluded that uranium compounds could increase alimentary genotoxic exposure in humans if they reach the food chain in sufficient amounts.

Adenoma↗
PubMed1989

Epidemiology of the Bacteroides fragilis group in the colonic flora in 10 patients with colonic cancer.

We report the relative frequencies of members of the Bacteroides fragilis group in the faeces, in colon lavage fluid obtained pre-operatively, and in colonic tissue specimens obtained at operation from 10 patients with colonic cancer. B. vulgatus was the most and B. fragilis and B. ovatus were the least frequently isolated Bacteroides spp. in the faeces of the 10 subjects. B. uniformis and B. thetaiotaomicron ranked second and third in the faeces. The relative frequencies of all species except B. fragilis were lower in the lavage fluid and in cultures of mucosa. The relative frequency of B. fragilis increased from 4% in faeces to 39% in the final lavage fluid and to 42% in the colonic mucosa culture. Our results suggest that B. fragilis has a more intimate association with the gut mucosa than other members of the B. fragilis group, which might be one explanation for the high incidence of this species in gut-associated intra-abdominal infections.

Adult↗
PubMed2003

Effects of high amylose maize starch and Clostridium butyricum on metabolism in colonic microbiota and formation of azoxymethane-induced aberrant crypt foci in the rat colon.

High amylose maize starch (HAS) is not digested in the small intestine and most of it reaches the large intestine. In the large intestine, HAS is fermented by intestinal bacteria, resulting in production of short-chain fatty acids (SCFA), particularly butyrate. Clostridium butyricum can utilize HAS and produce butyrate and acetate. It has been proposed that butyrate inhibits carcinogenesis in the colon. In this study, we examined the inhibitory effects of HAS and C. butyricum strain MIYAIRI588 (CBM588) on azoxymethane-induced aberrant crypt foci (ACF) formation in rats. In the group of rats administered only CBM588 spores, the concentration of butyrate in the cecum increased, but there was no decrease in the number of ACF. In the group of rats fed an HAS diet, a decrease in the number of ACF was observed, and in the group of rats administered HAS and CBM588, the number of ACF decreased significantly. In these two groups, the concentrations of acetate and propionate in intestinal contents significantly increased, but the concentration of butyrate did not change. It was found that the beta-glucuronidase activity level of colonic contents decreased significantly in the two groups of rats fed HAS. This study showed that HAS and CBM588 changed the metabolism of colonic microbiota and decreased the level of beta-glucuronidase activity, phenomena that may play a role in the inhibition of ACF formation in the rat colon.

Amylose↗
PubMedDate not supplied

The influence of dibutyryl adenosine cyclic monophosphate on cell proliferation in the epithelium of the jejunal crypts, the colonic crypts and in colonic carcinomata of rat.

1. Cell proliferation in the jejunal crypts, the colonic crypts and in dimethylhydrazine (DMH)-induced adenocarcinomata of rat colon was measured using a stathmokinetic technique. 2. Dibutryl cyclic adneosine monophosphate (dibutyryl cAMP) was found to inhibit cell proliferation in colonic crypts and in colonic adenocarcinomata. 3. Dibutryl cAMP at very high doses was found to inhibit jejunal crypt cell proliferation but at lower doses was found to accelerate jejunal crypt cell proliferation. 4. Neither bilateral adrenalectomy nor chemical sympathectomy was found to abolish the ability of dibutryl cAMP to stimulate jejunal crypt cell proliferation. 5. The present results are difficult to interpret in terms of known hormonal influences on cell proliferation in the tissues examined and of established actions, of these hormones on cyclic nucleotide metabolism in other tissues.

Adrenalectomy↗
PubMed1982

In situ analysis of the inflammatory cell infiltrates in colon carcinomas and in the normal colon wall.

Inflammatory cells (lymphocytes, plasma cells, macrophages, mast cells and polymorphonucleated cells) forming infiltrates in the stroma of ten colon carcinomas were analysed in situ and compared with the cells of the normal colon wall. The cancer stroma contained a larger proportion of lymphocytes, while the number of IgA-containing plasma cells was markedly reduced compared to the normal colon mucosa from the resection edge. In both tissues the number of macrophages was much higher than the study of H & E stained routine preparations would suggest. The peritumoural cell infiltrates consisted of 47% lymphocytes, 19% plasma cells, 15% macrophages (including monocytes) and 5% granulated mast cells, while 15% of all inflammatory cells were polymorphonucleated (PMN). Necrotic areas of the tumours were dominated by a larger number of PMN and macrophages. Compared to the normal colon wall, the significant differences in cell composition and the accumulation of mononuclear cells (MC) at the cancer borders indicate that populations of cells are selectively attracted to the tumour site, although the factors responsible for the local cell reaction in cancer are still unknown.

Adenocarcinoma↗
PubMed1991

Quantification of acid mucins in the descending colon of rats having simultaneously growing colonic tumors.

The acid mucins contained in goblet cells of the descending colon of 34 male Sprague-Dawley rats were histochemically labeled by Alcian blue pH 2.5 and quantified in an image analyzer (Cortex Controller). Twenty-two of these 34 rats were treated with 1,2-dimethylhydrazine (DMH) suspended in EDTA solution as a stabilizing agent and the remaining 12 rats with EDTA only. Of the 22 DMH-treated rats, 11 had concomitantly an adenocarcinoma elsewhere in the colon and the remaining 11 rats had no colonic tumors despite DMH treatment. The results indicated that Alcian blue-positive areas occupied 34.5% of the mucosa of the descending colon in tumor-bearing rats, and 35.2% in non-tumor-bearing DMH-treated rats. For EDTA-treated rats the percentage of mucosa occupied by Alcian blue-positive cells was 48.1%. The difference between DMH-treated rats (with or without tumors) and EDTA-treated rats was significant (p less than 0.001). These results suggest that the decrease of Alcian blue areas is related to the protracted treatment with DMH. Whether the decrease in acid mucins is induced by the carcinogen per se or whether it represents a true biochemical premalignant change at the cytoplasmic level remains to be elucidated.

1,2-Dimethylhydrazine↗
PubMed1970

Factors controlling colonic motility: colonic pressures and transit after meals in patients with total gastrectomy, pernicious anaemia or duodenal ulcer.

The motor responses of the proximal colon, sigmoid, and rectum to the ingestion of a standard meal have been compared in patients with total gastrectomy, pernicious anaemia, or duodenal ulcer. Colonic pressure activity increased during and after food in all the patients, but this was only once associated with propulsive activity. The results suggest that the postprandial pressure activity in the sigmoid colon is greater after total gastrectomy than in the other two groups. It is concluded that entry of food into the upper small intestine is the most important factor in initiating the colonic pressure response to food, since this response does not require the presence of the stomach, acid, antral gastrin, or of vagal innervation.

Adult↗