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PubMed2006

Evaluation of a model for Escherichia coli O157:H7 colonization in streptomycin-treated adult cattle.

OBJECTIVE: To develop a repeatable model for studying colonization with streptomycin-resistant Escherichia coli O157:H7 in adult cattle. ANIMALS: 5 adult mixed-breed beef cattle. PROCEDURES: Cattle were surgically cannulated in the duodenum, treated daily with streptomycin (33 mg/kg) via the duodenal cannula prior to and during experimental colonizations, and colonized with 10(10) CFUs of streptomycin-resistant E coli O157:H7 via the duodenal cannula. Colonization of rectal mucus and shedding in feces were monitored. Antimicrobials were administered to eliminate the colonizing strain so that 5 repeated colonization experiments could be performed. A comprehensive analysis of colonization was performed at necropsy. RESULTS: Streptomycin treatment resulted in improved experimental colonization variables, compared with untreated controls, during initiation (days 2 to 6) and early maintenance (days 7 to 12) of colonization. Elimination of the colonizing strain followed by 5 repeated colonizations in the same animals indicated the repeatability of the protocol. Positive results of bacteriologic culture of feces 7 and 12 days after colonization were obtained in 100% and 84% of samples, respectively, across all animals and trials. At necropsy, highest magnitude recovery was in terminal rectal mucus. CONCLUSIONS AND CLINICAL RELEVANCE: The model was highly repeatable and novel with respect to streptomycin treatment, use of duodenal cannulas, and repeated colonizations of the same animals. Its use in adult cattle, from which most bovine-derived food originates, is critical to the study of preharvest food safety. The findings have implications for understanding intermittency of shedding in the field and for proposed vaccine-based interventions.

Animals↗
PubMed2000

K-ras point mutation is associated with enhancement by deoxycholic acid of colon carcinogenesis induced by azoxymethane, but not with its attenuation by all-trans-retinoic acid.

The effects of deoxycholic acid (DCA) with and without all-trans-retinoic acid (ATRA) on the incidence of colon tumors induced by azoxymethane, the incidence of K-ras point mutation in colon tumors and the labeling index of colon mucosa were investigated in male Wistar rats. Rats received 5 weekly injections of 7.4 mg/kg body weight of azoxymethane. From the start of the experiment, all rats in 3 groups also received chow pellets containing 0.3% DCA with and without s.c. injections of 0.75 or 1.5 mg/kg body weight of ATRA every other day until the end of week 45. Oral administration of DCA significantly increased the incidence of colon tumors in week 45. Concomitant use of DCA and ATRA at either dose significantly attenuated the enhancement by DCA of colon tumorigenesis. Administration of DCA significantly increased the incidence of K-ras point mutation in colon tumors and the labeling index in the colon mucosa. Combined administration of DCA and ATRA significantly reduced the labeling index of colon mucosa, which was increased by DCA, but did not affect the incidence of K-ras point mutation in colon tumors. These findings suggest that DCA enhances development of colon tumors and that this enhancement is attenuated by ATRA. A possible mechanism of this enhancement is induction of K-ras point mutation. However, decreased cell proliferation in the colon mucosa may be closely related to the attenuation of DCA-enhanced colon tumorigenesis, but not suppression of K-ras point mutation.

Administration, Oral↗
PubMed1989

Colonic complications of severe acute pancreatitis.

Colonic complications are rare in acute pancreatitis. Over the last 9 years at St. Mary's Hospital, London, UK, we have managed severe acute pancreatitis by intensive supportive therapy followed by sub-total pancreatic resection and/or debridement in those who fail to improve. Of the 22 patients who have undergone this form of surgery, nine were found to have colonic involvement in the form of either necrosis or perforation. In addition, one patient presenting at West Middlesex University Hospital, Isleworth, UK, had severe acute pancreatitis and almost total colonic necrosis as an unexpected finding at emergency laparotomy. These ten patients comprised seven men and three women of median age 59 years and with a median of four Ranson criteria. In seven patients, colonic involvement was discovered at the time of pancreatic surgery or laparotomy for pancreatitis and in the remainder it presented between 1 and 3 weeks later as either a faecal fistula (n = 2) or persistent abdominal sepsis (n = 1). The ascending colon was involved in one patient, the splenic flexure and descending colon in one, the transverse colon in three, the splenic flexure alone in four, and one patient had almost total colonic involvement. All patients underwent resection of the involved colon and exteriorization with either a proximal colostomy (n = 7) or ileostomy (n = 3) and a distal mucous fistula. Pathological examination of the resected colons revealed a spectrum of changes from pericolitis through to ischaemic necrosis suggesting at least two possible mechanisms. Six patients died from overwhelming sepsis between 1 day and 4 weeks (median 11 days) after colonic resection. Severe acute pancreatitis must be recognized as a cause of colonic ischaemia and necrosis; this complication is associated with a very poor prognosis despite surgical intervention.

Acute Disease↗
PubMed1994

Monoamine oxidase B inhibitor enhances experimental carcinogenesis in rat colon induced by azoxymethane.

The effects of prolonged administration of the monoamine oxidase (MAO)-A inhibitor N-methyl-N-propargyl-3-(2,4-dichlorophenoxy)propylamine (clorgyline) and the MAO-B inhibitor N-methyl-N-2-propynyl-benzylamine (pargyline) on the incidence, number and histology of colon tumors induced by azoxymethane (AOM), and on the norepinephrine (NE) concentration in the colon wall and the labeling index of colon mucosa were investigated in Wistar rats. Rats were treated s.c. with 7.4 mg/kg body weight of AOM once a week for 10 weeks, and also s.c. with 5 mg/kg body weight of clorgyline or 50 mg/kg body weight of pargyline in 0.9% NaCl until the end of the experiment. Treatment with pargyline significantly increased the incidence of colon tumors in week 35. However, it did not influence the histological appearance of the colon tumors or the histological types and depth of involvement of colon adenocarcinomas. Furthermore, it significantly increased the NE concentration in the colon wall and the labeling index of the colon mucosa during and after AOM-treatment. In contrast, clorgyline had no influence on the development or histological appearance of colon tumors. These findings indicate that the MAO-B inhibitor, but not the MAO-A inhibitor, enhanced colon carcinogenesis, and that its effect may be related to its effect in increasing the NE concentration in the colon wall and subsequently increasing the proliferation of colon epithelial cells.

Animals↗
PubMed2004

Effects of adlay on azoxymethane-induced colon carcinogenesis in rats.

Adlay (Coix lachryma-jobi L. var. ma-yuen Stapf) is a grass crop used in traditional Chinese medicine and as a nutritious food. It has been reported that adlay has anti-inflammatory and anti-tumor activity. Cyclooxygenase-2 (COX-2) is an inducible enzyme functionally related to both inflammation and colon carcinogenesis and is the target of many chemopreventive agents. This study investigated the effect of adlay on colon carcinogenesis and COX-2 expression. In a short-term experiment, male F344 rats were fed diets containing different doses of dehulled adlay and received the colon-specific carcinogen, azoxymethane (AOM), by intraperitoneal injection. All rats were killed after 5 weeks of feeding, and the colons were examined for the preneoplastic lesion, aberrant crypt foci (ACF). Dietary dehulled adlay at levels of 10%, 20%, or 40% significantly reduced the numbers of ACF and aberrant crypts. Dehulled adlay reduced the number of ACF of different sizes but did not affect the crypt multiplicity. Most ACF were found in the middle and distal colons; dehulled adlay significantly suppressed the formation of ACF in the middle colon. In a long-term experiment, male F344 rats were fed diets containing different doses of dehulled adlay and injected with AOM. All rats were killed after 52 weeks of feeding, and colons were examined for tumors and COX-2 protein expression. The results indicated that dehulled adlay did not inhibit colon tumors in spite of a slight suppressing effect in the proximal colon. Rats fed diets containing 20% dehulled adlay had less COX-2 protein expression in both proximal and distal colon tumors. The inconsistent effects between COX-2 protein expression and tumor outcome may be due to regional differences in the colon and the malignancy of the tumors. These findings suggest that dehulled adlay suppresses early events in colon carcinogenesis but not the formation of tumors.

Animals↗
PubMed2005

Sporadic colonic hamartomas in adults: a retrospective study.

BACKGROUND: Colonic hamartomas are uncommon in adults. The aims of this study were to determine (1) the prevalence of colonic hamartomas in an adult population undergoing colonoscopy and (2) the clinical, endoscopic, and histologic features of colonic hamartomas in adult patients. METHODS: A pathology database identified 19 adult patients of 12,707 patients with colonic hamartomas in the 11-year study period from January 1992 to October 2002. An endoscopic computer database provided information about the number of colonoscopies performed and the presence or the absence of colonic polyp(s) in study patients. Charts of patients with colonic hamartomas were reviewed, and clinical and demographic data were collated. RESULTS: Nineteen patients were found to have colonic hamartomas. The mean age of these patients was 55 years, with an age distribution ranging from 25 to 81 years. The prevalence of colonic hamartomas in this study population was 0.15%. The prevalence of hamartomas in patients with colon polyps at index colonoscopy was 0.073%. Colonic hamartomas were more common in men than in women. The indication for colonoscopy for the majority (68%) of patients was hematochezia or the presence of occult blood in the stool. Three fourths of the polyps were greater than 1 cm in diameter, and 89% were pedunculated. Two thirds of the hamartomatous polyps were localized to the rectosigmoid region. Endoscopic characteristics of hamartomas were indistinguishable from adenomas. CONCLUSIONS: Colonic hamartomas in adults are rare. They tend to be single, pedunculated, and localized predominantly in the rectosigmoid region. Endoscopic resection of colonic hamartomas was successful in all patients.

Adult↗
PubMed2004

Mechanisms involved in carbachol-induced Ca(2+) sensitization of contractile elements in rat proximal and distal colon.

1. Mechanisms involved in Ca(2+) sensitization of contractile elements induced by the activation of muscarinic receptors in membrane-permeabilized preparations of the rat proximal and distal colon were studied. 2. In alpha-toxin-permeabilized preparations from the rat proximal and distal colon, Ca(2+) induced a rapid phasic and subsequent tonic component. After Ca(2+)-induced contraction reached a plateau, guanosine 5'-triphosphate (GTP) and carbachol (CCh) in the presence of GTP further contracted preparations of both the proximal and distal colon (Ca(2+) sensitization). Y-27632, a rho-kinase inhibitor, inhibited GTP plus CCh-induced Ca(2+) sensitization more significantly in the proximal colon than in the distal colon. 3. Y-27632 at 10 microm had no effect on Ca(2+)-induced contraction or slightly inhibited phorbol-12,13-dibutyrate-induced Ca(2+) sensitization in either proximal or distal colon. Chelerythrine, a protein kinase C inhibitor, inhibited GTP plus CCh-induced Ca(2+) sensitization in the distal colon, but not in the proximal colon. The component of Ca(2+) sensitization that persisted after the chelerythrine treatment was completely inhibited by Y-27632. 4. In beta-escin-permeabilized preparations of the proximal colon, C3 exoenzyme completely inhibited GTP plus CCh-induced Ca(2+) sensitization, but PKC(19-31) did not. In the distal colon, C3 exoenzyme abolished GTP-induced Ca(2+) sensitization. It inhibited CCh-induced sensitization by 50 % and the remaining component was inhibited by PKC(19-31). 5. These results suggest that both protein kinase C and rho pathways in parallel mediate the Ca(2+) sensitization coupled to activation of muscarinic receptors in the rat distal colon, whereas the rho pathway alone mediates this action in the proximal colon.

ADP Ribose Transferases↗
PubMed2001

Increased levels of insulin-like growth factor binding protein-2 in sera and tumours from patients with colonic neoplasia with and without acromegaly.

OBJECTIVE: Patients with acromegaly are at increased risk of developing colorectal carcinoma and premalignant tubulovillous adenoma. The pathogenesis of these neoplasms could involve a stimulatory effect of serum growth factors on colonic epithelial cell proliferation. The aim of this study was to evaluate changes in (1) serum IGF-I, IGF-II, IGFBP-3 and IGFBP-2 and (2) changes in local expression of IGFBPs and p53 in colonic epithelium in patients with colonic neoplasia with and without acromegaly. DESIGN: A cross-sectional retrospective study was performed. Fasting serum samples were obtained at the time of colonoscopy for patients with acromegaly and at the time of surgery for patients with colonic neoplasia without acromegaly. MEASUREMENTS: Serum IGF-I, IGF-II, IGFBP-2 and IGFBP-3 were measured using specific immunoassays. Tissue expression of IGFBP-2, IGFBP-3 and p53 status were determined by immunohistochemistry. PATIENTS: Group 1: 26 age- and sex-matched control subjects (range 40-69 years); group 2: 18 patients with acromegaly without colonic neoplasia (range 39-68 years); group 3: 18 patients with acromegaly and colonic neoplasia (range 41-74 years, 11 = adenoma, seven = carcinoma); group 4: 19 patients with colonic neoplasia without endocrine disease (range 43-91 years, four = adenoma, 15 = carcinoma). Immunohistochemical staining of colonic biopsies was performed for IGFBP-2, IGFBP-3 and p53 in groups 3 and 4. RESULTS: Mean serum IGF-I and IGFBP-3 levels were significantly elevated in group 2 (371 +/- 131 microg/l and 6.5 +/- 1.8 mg/l, respectively) and group 3 (379 +/- 174 microg/l and 5.8 +/- 1.6 mg/l, respectively), and significantly reduced in group 4 (103 +/- 36 microg/l and 2.4 +/- 1 mg/l) compared to controls (165 +/- 40 microg/l and 4.7 +/- 1 mg/l; P < 0.0001, P < 0.001, respectively). However, median serum IGFBP-2 levels were significantly elevated in group 3 (P < 0.01) and group 4 (P < 0.0001). Immunostaining for IGFBP-2 showed strong areas of immunoreactivity in the cytoplasm of malignant colonic epithelium compared to benign epithelium. IGFBP-3 immunostaining showed strong areas of immunoreactivity in the cytoplasm and in the nucleus of malignant and benign colonic epithelium compared to the normal epithelium. Nuclear staining for p53 was observed in three patients from group 3 (two carcinoma, one adenoma) and four patients from group 4 (all carcinoma). CONCLUSION: Our results describe changes in IGFBP-2 expression in colonic neoplasia in patients with and without acromegaly, which suggest that this binding protein may regulate local bioavailability of IGF, which in turn could modulate colonic cell proliferation and/or differentiation.

Acromegaly↗
PubMed2004

Protein kinase CbetaII regulates its own expression in rat intestinal epithelial cells and the colonic epithelium in vivo.

Protein kinase C betaII (PKCbetaII) is induced early during colon carcinogenesis. Transgenic mice expressing elevated PKCbetaII in the colonic epithelium (transgenic PKCbetaII mice) exhibit hyperproliferation and enhanced colon carcinogenesis. Here we demonstrate that nullizygous PKCbeta (PKCbetaKO) mice are highly resistant to azoxymethane (AOM)-induced preneoplastic lesions, aberrant crypt foci. However, reexpression of PKCbetaII in the colon of PKCbetaKO mice by transgenesis restores susceptibility to AOM-induced colon carcinogenesis. Expression of human PKCbetaII in rat intestinal epithelial (RIE) cells induces expression of endogenous rat PKCbetaII mRNA and protein. Induction of PKCbetaII is dependent upon catalytically active PKCbetaII and does not appear to involve changes in alternative splicing of the PKCbeta gene. Two human PKCbeta promoter constructs are activated by expression of PKCbetaII in RIE cells. Both PKCbeta promoter activity and PKCbetaII mRNA levels are inhibited by the MEK1 and -2 inhibitor U0126, but not the Cox-2 inhibitor celecoxib in RIE/PKCbetaII cells. PKCbeta promoter activity correlates directly with expression of endogenous PKCbetaII mRNA and protein in HT29 and HCT116 human colon cancer cell lines. PKCbeta promoter activity and PKCbetaII mRNA expression in HCT116 cells are inhibited by the selective PKCbeta inhibitor LY317615 and by U0126, demonstrating autoregulation of PKCbetaII expression. Transgenic PKCbetaII mice exhibit specific induction of endogenous PKCbetaII, but not its splice variant PKCbetaI, in the colonic epithelium in vivo. Taken together, our results demonstrate that 1) expression of PKCbetaII in the colonic epithelium is both necessary and sufficient to confer susceptibility to AOM-induced colon carcinogenesis in transgenic mice, 2) PKCbetaII regulates its own expression in RIE and human colon cancer cells in vitro and in the colonic epithelium in vivo, and 3) PKCbetaII autoregulation is mediated through a MEK-dependent signaling pathway in RIE/PKCbetaII and HCT116 colon cancer cells.

Animals↗
PubMed1998

Insulin-like growth factor-I and II receptor expression in rat colon mucosa are affected by dietary lipid intake.

Epidemiologic data and animal models have demonstrated a correlation between dietary fat composition and colon cancer risk. We have previously found that dietary fat alters cell proliferation in rat colon, which may influence the risk of colon cancer. Growth factors, including insulin-like growth factor (IGF) I and II, regulate the cell cycle in most mammalian tissues. Hence, we measured IGF-I and IGF-II receptor expression in colonocytes from Sprague-Dawley rats fed diets containing either beef tallow (BT) or corn oil (CO) at 12, 30 or 37% of energy for 4 wk. Quantitative reverse transcriptase polymerase chain reaction (RT-PCR) using an internal standard was used to examine the relative expression of both IGF-I and II receptor mRNA in three sections of the colon. The IGF-I receptor protein was also measured by Western immunoblot. In the distal colon, IGF-I receptor gene expression and protein increased significantly as the percentage of CO increased. In both proximal and middle colon, an increased percentage of BT resulted in significantly increased IGF-II receptor expression. In the proximal colon, IGF-II receptor expression decreased with increasing CO concentration, whereas in the middle colon, rats fed 37% CO had significantly higher IGF-II receptor expression than rats fed 12 or 30% CO. IGF-II receptor gene expression in proximal colon decreased with increased fat quantity, independently of fat source, whereas in the middle colon, increased fat quantity resulted in increased IGF-II receptor expression. Thus IGF-I and IGF-II receptor mRNA and IGF-I receptor protein level in colon mucosa were significantly altered by dietary fat source and quantity, thereby suggesting a potential influence of dietary fat on the endocrine regulation of colon cell mitogenesis.

Animals↗
PubMed1992

Inverse modulation of steady-state messenger RNA levels of two non-integrin laminin-binding proteins in human colon carcinoma.

BACKGROUND: Interactions between cells and the basement membrane glycoprotein laminin are altered during colon cancer progression. Colon carcinoma and normal mucosa cells express a variety of laminin-binding proteins, including the 67-kd laminin receptor (67 LR) and a 31-kd human laminin-binding protein (HLBP31) homologous to the 31-kd human IgE-binding protein/galactoside-binding lectin. PURPOSE: To investigate whether various laminin-binding proteins are differentially expressed in human colon carcinoma, we studied messenger RNA (mRNA) levels of the 67 LR and HLBP31 in matched tumor and adjacent normal mucosa samples from a series of 21 patients. METHODS: Total cellular RNA from tumor and normal mucosa was isolated and analyzed by Northern and slot blot hybridization. In addition, HLBP31 protein levels were assessed by the immunoblot technique. Quantitative laminin affinity chromatography was also used to measure the synthesis of HLBP31 protein in five human cancer cell lines. RESULTS: The steady-state mRNA level of HLBP31 was downregulated (i.e., decreased) in 18 of 21 human colon carcinomas compared with the level in their corresponding normal colonic mucosa. On average, the level of HLBP31 mRNA was decreased 50% +/- 30% (+/- SD) in the colon cancers. The mean ratio of colon cancer HLBP31 mRNA to adjacent normal mucosa HLBP31 mRNA was twofold lower in primary tumors of patients with metastases (0.3 +/- 0.2 SD) than in primary tumors of patients free of metastatic lesions (0.6 +/- 0.2 SD). The differences between the two groups of patients were statistically significant (P less than .05, Wilcoxon-Mann-Whitney test). We have previously shown that the ratio of colon cancer 67 LR mRNA to corresponding normal mucosa 67 LR mRNA was increased in the same patient population. When the two ratios (ratio of cancer to normal HLBP31 mRNA and ratio of cancer to normal 67 LR mRNA) were compared, HLBP31 mRNA/67 LR mRNA was significantly lower (P less than .05) in primary tumors with metastases (mean +/- SD, 0.3 +/- 0.2) than in primary cancers without metastases (mean +/- SD, 0.7 +/- 0.5). The steady-state level of HLBP31 mRNA was directly correlated with the amount of HLBP31 protein in both colon tissue samples and human cancer cell lines. CONCLUSION: HLBP31 mRNA expression in colon cancer tissues is modulated inversely to that of 67 LR mRNA expression. The down-regulation of HLBP31 appears to be associated with the metastatic capabilities of colon cancer cells. IMPLICATIONS: Prospective studies on a large cohort should determine if the systematic detection of HLBP31 and 67 LR protein and/or mRNA can be a valuable adjunct in the prognostic evaluation of primary colon cancers.

Amino Acid Sequence↗
PubMed1991

Effect of oltipraz [5-(2-pyrazinyl)-4-methyl-1,2-dithiol-3-thione] on azoxymethane-induced biochemical changes related to early colon carcinogenesis in male F344 rats.

Epidemiologic studies suggest that the consumption of cruciferous vegetables is associated with a reduced risk for several types of cancer including cancer of colon. Experimental studies indicate that dithiolthiones, naturally occurring substances in cruciferous vegetables, possess anticarcinogenic properties. 5-(2-Pyrazinyl)-4-methyl-1,2-dithiol-3-thione (oltipraz), a substituted dithiolthione, has been tested for its chemopreventive activity. We studied the effect of dietary oltipraz on liver and colonic mucosal enzymes and DNA adducts to evaluate the modulating role of this agent during the early period of azoxymethane (AOM)-induced carcinogenesis. At 6 weeks of age, groups of animals were fed the AIN-76A diet containing 0 and 300 ppm oltipraz. At 8 weeks of age, all of the animals except vehicle-treated animals were administered a subcutaneous injection of AOM (15 mg/kg body wt/week for 2 weeks). Animals intended for vehicle treatment were administered normal saline subcutaneously. Fifteen hours after the second AOM injection, six animals each from control oltipraz diet groups were sacrificed and liver and colonic mucosa from each animal were used for DNA adduct analysis. Animals intended for liver and colonic mucosal glutathione S-transferase, tyrosine specific protein kinase (TPK), and ornithine decarboxylase (ODC) enzyme assays were killed 5 days after the second AOM or saline injection. The results of this study indicated that dietary oltipraz significantly increased liver (P less than 0.001) and colonic mucosal (P greater than 0.05) weights, but had no effect on body weights (P greater than 0.05). In saline-treated animals, feeding of oltipraz significantly increased the cytosolic glutathione S-transferase (P less than 0.001) and ODC (P less than 0.05) activities in the liver and colon when compared with those fed the control diet. Although our unpublished results indicate an inhibitory role of oltipraz when fed during the initiation and postinitiation phases of intestinal carcinogenesis, the increased ODC activity may indicate a possible role of oltipraz in colon tumor promotion. Additional studies are indicated to test the antitumor properties of oltipraz administered during the postinitiation phases. AOM treatment significantly increased the TPK (P less than 0.0001) and ODC (P less than 0.01) activities in the liver and colon of animals fed the control diet. Dietary oltipraz significantly suppressed the AOM-induced TPK (P less than 0.001) activities in liver and colon and ODC (P less than 0.01) activity of colon. Analysis of nucleic acid bases, O6-methylguanine, and 7-methylguanine revealed that dietary oltipraz significantly (P less than 0.05) inhibited the AOM-induced adduct species. These results suggest that dietary oltipraz enhances the colonic and liver glutathione S-transferase activity and reduced the formation of DNA adducts. In addition, dietary oltipraz modulates liver and colonic ODC and TPK activities that have been shown to play a role in tumor promotion.

Animals↗
PubMed1998

Apolipoprotein A-I reverse transcriptase-polymerase chain reaction analysis for detection of hematogenous colon cancer dissemination.

Detection of systemic tumor dissemination in colon carcinoma patients might be important for selection of appropriate treatment modalities. It has been previously shown that Apolipoprotein A-I (Apo A-I) is expressed in human intestinal epithelial cells, and in some human colon carcinoma cell lines. We examined the expression of Apo A-I mRNA in 14 human primary colon carcinomas by Northern blot and/or reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. An Apo A-I specific transcript was found in up to 70% of the colon carcinomas. We developed an RT-PCR assay for Apo A-I transcripts, to identify circulating carcinoma cells in the peripheral blood of colon cancer patients. The Apo A-I RT-PCR assay was optimized using limiting dilution of an Apo A-I positive cancer cell line mixed with peripheral blood from healthy donor. In this system, up to 10 colon carcinoma cells were detected in 5 ml of peripheral blood. We examined Apo A-I mRNA expression in peripheral blood samples from 4 healthy donors, 20 colon carcinoma patients, and 11 individuals with tumor disease other than colon cancer. No Apo A-I mRNA was detected in the healthy donors and in the patients without colon cancer. Two out of 10 patients with metastatic colon carcinoma were positive by this assay, whereas Apo A-I mRNA was not found in any of the blood samples from the 10 radically resected colon carcinoma patients. These data suggest that Apo A-I RT-PCR assay is a highly specific and sensitive assay, although a low number of advanced colon carcinoma patients was found to be positive.

Apolipoprotein A-I↗
PubMed2002

Chemopreventive properties of a selective inducible nitric oxide synthase inhibitor in colon carcinogenesis, administered alone or in combination with celecoxib, a selective cyclooxygenase-2 inhibitor.

The inducible isoforms of nitric oxide synthase (iNOS) and cyclooxygenase (COX-2) are overexpressed in colonic tumors of humans, as well as in colon tumors that develop in rats after the administration of the colon-specific carcinogen, azoxymethane (AOM). iNOS may regulate COX-2 production of proinflammatory prostaglandins, which are known to play a key role in colon tumor development. Experiments were designed to assess the potential chemopreventive properties of highly selective iNOS inhibitors, administered individually and in combination with a selective COX-2 inhibitor, on the development of AOM-induced colonic aberrant crypt foci (ACF). F344 rats were fed experimental diets containing one of the following: 0, 10, 30, or 100 parts/million (ppm) of the selective iNOS inhibitor L-N(6)-(1-iminoethyl)lysine tetrazole-amide (SC-51); 1800 ppm of the less potent, selective iNOS inhibitor aminoguanidine (AG); 500 ppm of the COX-2 inhibitor celecoxib; 320 ppm of the nonsteroidal anti-inflammatory sulindac (positive control); or 30 ppm of SC-51 with 500 ppm of celecoxib, and 100 ppm of SC-51 with 500 ppm of celecoxib. One and 2 weeks later, rats received s.c. injections of AOM at a dose of 15 mg/kg of body weight. At 17 weeks of age, all rats were sacrificed. Colons were evaluated for ACF, and colonic mucosae were assayed for COX and NOS isoform enzyme activities. Samples of venous blood, collected at various time points, were analyzed for these agents. SC-51, administered alone, demonstrated dose-dependent inhibition of the incidence of colonic ACF. The highest doses of SC-51 (100 ppm) and AG (1800 ppm) significantly suppressed the incidence of colonic ACF (P < 0.01 and < 0.001, respectively) and crypt multiplicity in terms of numbers of aberrant crypts/focus (P < 0.0001). Importantly, the combination of either low or high effective doses of SC-51 (30 or 100 ppm) and celecoxib (500 ppm) suppressed AOM-induced colonic ACF formation (P < 0.05 and < 0.001, respectively) and reduced multiplicity of four or more aberrant crypts/focus (P < 0.0001) to a greater extent than did these agents administered individually. As expected, sulindac inhibited colonic ACF formation (P < 0.001) and reduced the multiplicity of four or more aberrant crypts (P < 0.0001) to approximately 45%. The enzymatic activities of COX-2 and iNOS were significantly induced in the AOM-treated animals, and administration of the iNOS inhibitors, SC-51 and AG, significantly inhibited the activities of both iNOS and COX-2 in the colonic mucosa. The combined administration of SC-51 and celecoxib inhibited the COX-2 activity to a greater extent than did either of these agents administered alone. These findings support the hypothesis that selective iNOS inhibitors may have chemopreventive properties and that coadministration with a selective COX-2 inhibitor may have additional chemopreventive potential.

Animals↗
PubMed2003

[Expression of P27 protein and cyclin E in colon cancer].

BACKGROUND & OBJECTIVE: P27 protein and cyclin E were negative cell cycle regulators. Until the present, the influence of P27 protein and cyclin E on progression of colon cancer was unclear. The aim of this study was to observe the expression features of P27 protein and cyclin E in the tissues of colon neoplasms, and to investigate the relationship between colon neoplasms and tumor special growth factor (TSGF). METHODS: Sixty-nine cases of samples included 23 normal tissues, 28 colon polyps (13 inflammatory polyps and 15 adenomatous polyps), and 18 colon carcinomas. The location and expression of P27 protein and cyclin E were determined using immunohistochemical method in all samples. These samples were diagnosed using formal pathological techniques simultaneously; the relationship between colon neoplasms and TSGF was also investigated. RESULTS: The positive signal of P27 and cyclin E was found mainly in the cytoplasm and extracellular matrix of normal colon tissues, inflammatory polyps, and adenomatous polyps. Less amount of positive expression product of P27 protein and cyclin E was observed in colon carcinoma cells; and the positive signal was only located in the cytoplasm of gland-like cells. The content of TSGF in colon carcinoma tissues was significantly higher than that in normal tissues (117.3+/-57.02 versus 64.16+/-27.5,P< 0.01), but there was no significant difference between colon carcinoma tissues and inflammatory polyp tissues (117.3+/-57.02 versus 92.5+/-47.9,P >0.05). CONCLUSION: P27 protein and cyclin E participate in the adjustment process of colon neoplasm occurrence and progression. The reduced expression of P27 protein and cyclin E may indicate the possibility of colon carcinoma.

Adult↗
PubMedDate not supplied

[Indications for temporary diversions and for primary resections in emergency colon surgery].

The authors make a critical analysis of indications for temporary derivations, and for "d'emblée" resection in the emergency surgery of the colon. This study is based on a series of 267 cases where emergency surgery was necessary for various conditions of the colon. All were operated in the I-st Clinic of Surgery from Craiova. The authors stress the inefficiency of cecostomy for the solution of occlusions due to neoplasms of the colon, and list the present indications of this type of temporary derivation, which include: protection of a colo-colonic anastomosis, and the solution of perforations (diastatic, traumatic) of the caecum. Supratumoral anus is considered as the choice solution for cancers of the left colon complicated by occlusion. Latero-lateral ileo-transverse anastomosis is considered as a temporary derivation, and is indicated in tumours of the right colon also complicated by occlusion. In cases of emergency the authors practice colonic resections by necessity, but they also perform colonic exeresis with relative indications. In cases of colonic resections by necessity the problem is mainly the opportunity of recovery of the digestive transit. Emergency colectomies with relative indications concern colonic cancer, or volvulus of the colon, and particular conditions are necessary for their performance. The authors consider the protection of colo-colonic, or recto-colic anastomoses as useful.

Anastomosis, Surgical↗
PubMed1987

Oncofetal expression of Lex carbohydrate antigens in human colonic adenocarcinomas. Regulation through type 2 core chain synthesis rather than fucosylation.

The mechanism of expression of a series of glycolipid antigens carrying the Lex determinant structure, Gal beta 1----4[Fuc alpha 1----3]GlcNAc beta 1----, and characterized by oncofetal expression in fetal colon and colonic adenocarcinomas has been studied in human fetal and adult proximal colon tissue. Results presented from TLC immunostain analysis of neutral glycolipids isolated from normal adult colonic mucosa have indicated the presence of only barely detectable quantities of both an Lex-active glycolipid that co-migrated with III3V3Fuc2nLc6 and its precursor nLc6. These structures were found in large quantities in glycolipid fractions from human adenocarcinoma tumors and human small cell lung carcinoma NCI-H69 cells. In contrast, type 1 chain-based Lea antigen structures were found in both normal mucosa and adenocarcinomas. Analysis of gangliosides of normal colonic mucosa by TLC immunostain indicated the presence of a series of type 2 chain-based gangliosides; however, sialyl-Lex was not detected. The ability of normal colonic mucosa to synthesize type 2 chain core structures was demonstrated by the presence of a beta 1----4 galactosyltransferase activity with Lc3 as an acceptor in an amount equivalent to 60-65% of the total galactosyltransferase activity. An alpha 1----3 fucosyltransferase was also found to be expressed in significant quantity in adult colonic mucosa. Kinetic studies indicated that this is most probably the alpha 1----3/4 fucosyltransferase suggested to be a product of the Lewis gene (Le). Thus, although normal adult colonic mucosa contained the enzymes to synthesize Lex and sialyl-Lex structures, these antigens were not found. Tissue immunofluorescence studies indicated that type 2 chain precursors and the alpha 1----3/4 fucosyltransferase were found in different cell populations in adult proximal colonic mucosa. However, both type 2 chain core structures and their fucosylated derivatives were found to be associated with epithelial cells of fetal colon. These results indicate that oncofetal expression of Lex antigens in fetal colonic epithelium and in adenocarcinomas but not in normal adult mucosa is due to the retrogenetic expression of type 2 chain precursors which are not found in normal adult colonic epithelial cells.

Adenocarcinoma↗
PubMed1993

Inhibitory effect of caffeic acid esters on azoxymethane-induced biochemical changes and aberrant crypt foci formation in rat colon.

Previous work from this laboratory established that caffeic acid esters, present in the propolis of honey bee hives, are potent inhibitors of human colon tumor cell growth, suggesting that these compounds may possess antitumor activity against colon carcinogenesis. The present study was designed to investigate (a) the inhibitory effects of methyl caffeate (MC) and phenylethyl caffeate (PEC) on azoxymethane (AOM)-induced ornithine decarboxylase (ODC), tyrosine protein kinase (TPK), and arachidonic acid metabolism in liver and colonic mucosa of male F344 rats, (b) the effects of caffeic acid, MC, PEC, phenylethyl-3-methylcaffeate (PEMC), and phenylethyl dimethylcaffeate (PEDMC) on in vitro arachidonic acid metabolism in liver and colonic mucosa, and (c) the effects of PEC, PEMC, and PEDMC on AOM-induced aberrant crypt foci (ACF) formation in the colon of F344 rats. At 5 weeks of age, groups of animals were fed diets containing 600 ppm MC or PEC (biochemical study) or 500 ppm PEC, PEMC, or PEDMC (ACF study). Two weeks later, all animals except the vehicle-treated groups were given s.c. injections of AOM, once weekly for 2 weeks. The animals intended for the biochemical study were sacrificed 5 days later and colonic mucosa and liver were analyzed for ODC, TPK, lipoxygenase, and cyclooxygenase metabolites. The animals intended for the ACF study were sacrificed 9 weeks later and analyzed for ACF in the colon. The results indicate that the PEC diet significantly inhibited AOM-induced ODC (P < 0.05) and TPK (P < 0.001) activities in liver and colon. The PEC diet significantly (P < 0.001) suppressed the AOM-induced lipoxygenase metabolites 8(S)- and 12(S)-hydroxyeicosatetraenoic acid (HETE). The animals fed the MC diet exhibited a moderate inhibitory effect on ODC and 5(S)-, 8(S)-, 12(S)-, and 15(S)-HETEs and a significant (P < 0.001) effect on colonic TPK activity. However, the MC and PEC diets showed no significant inhibitory effects on cyclooxygenase metabolism. In an in vitro study, caffeic acid and MC showed inhibitory effects on HETE formation only at a 100 microM concentration, whereas PEC, PEMC, and PEDMC suppressed in vitro HETE formation in a dose-dependent manner. AOM-induced colonic ACF were significantly inhibited in the animals fed PEC (55%), PEMC (82%), or PEDMC (81%). The results of the present study indicate that PEC, PEMC, and PEDMC, present in honey, inhibit AOM-induced colonic preneoplastic lesions, ODC, TPK, and lipoxygenase activity, which are relevant to colon carcinogenesis.

Animals↗