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PubMed1998

Stimulation of epithelial cell proliferation of isolated distal colon of rats by continuous colonic infusion of ammonia or short-chain fatty acids is nonadditive.

Dietary fibers accelerate colonic epithelial cell proliferation at least in part by modulating bacterial metabolism in the large intestine. Ammonia and short-chain fatty acids (SCFA) are major metabolites of hindgut bacteria and are believed to affect epithelial cell kinetics of the colon. However, the effect of luminal ammonia itself and the possible interaction of ammonia with SCFA on colonic epithelial cell proliferation have not yet been studied. The colon of rats was surgically isolated and continuously administered infusates with saline, ammonia, SCFA or both into the isolated colon for 7 d in a two-way factorial design. On d 7, vincrystine sulfate was administered intravenously to cause metaphase arrest. The activity of epithelial cell proliferation in the distal colon was estimated by using a stathmokinetic method and by histologic examination. The crypt size was significantly larger in rats given infusates containing SCFA than in rats given infusates without SCFA. Infusion of ammonia or SCFA significantly stimulated colonic epithelial cell proliferation compared with the saline infusion. Infusion of both ammonia and SCFA resulted in accumulated mitoses per crypt that did not differ from the other three infusions although the value tended to be lower than when SCFA alone were infused. Thus, stimulation of epithelial cell proliferation by ammonia and SCFA is not additive, and the interaction between them should be considered when the effects of dietary fibers on gut epithelial proliferation are investigated.

Ammonia↗
PubMed2000

Biomarkers of human colonic cell growth are influenced differently by a history of colonic neoplasia and the consumption of acarbose.

The nutritional effects of butyrate on the colonic mucosa and studies of transformed cells suggest that butyrate has anti-colon cancer effects. If butyrate has antineoplastic effects, mucosal growth contrasts between normal subjects and those with a history of colonic neoplasia would parallel changes in growth characteristics caused by butyrate in a colon neoplasia population. To test this hypothesis, rectal biopsies from a survey of colonoscopy patients (n = 50) with and without a history of colonic neoplasia (controls) were compared. Similarly, rectal biopsies were compared from subjects (n = 44) with a colon neoplasia history in an acarbose-placebo crossover trial. Control subjects in the colonoscopy survey had higher bromodeoxyuridine (BrdU) uptake than subjects with a history of neoplasia (P = 0.05). The control subjects also had a higher correlation of BrdU and Ki-67 labeling (P = 0.003). Both findings were paralleled by acarbose use. Acarbose augmented BrdU uptake (P = 0.0001) and improved the correlation of BrdU and Ki-67 labeling (P = 0.013). Acarbose also augmented fecal butyrate (P = 0.0001), which was positively correlated with Ki-67 labeling (P = 0.003). p52 antigen had an earlier pattern of crypt distribution in subjects with a history of colon neoplasia but was not affected by acarbose use. Lewis-Y antigen was expressed earlier in the crypt with acarbose but had similar expression in the colonoscopy survey groups. The use of acarbose to enhance fecal butyrate concentration produced mucosal changes paralleling the findings in control subjects as opposed to those with neoplasia, supporting the concept of an antineoplastic role for butyrate.

Acarbose↗
PubMed2005

Expression profiling of colon cancer cell lines and colon biopsies: towards a screening system for potential cancer-preventive compounds.

Interest in mechanisms of colon cancer prevention by food compounds is strong and research in this area is often performed with cultured colon cancer cells. In order to assess utility for screening of potential cancer-preventive (food) compounds, expression profiles of 14 human cell lines derived from colonic tissue were measured using cDNA microarrays with 4000 genes and compared with expression profiles in biopsies of human colon tumours and normal tissue. Differences and similarities in the gene expression profiles of the cell lines were analysed by clustering and principal component analysis (PCA). Cytoskeleton genes and immune response genes are two functional classes of genes that contributed to the differences between the cell lines. A subset of 72 colon cancer-specific genes was identified by comparing expression profiles in human colon biopsies of tumour tissue and normal tissue. A separation of the cell lines based on the tumour stage of the original adenocarcinoma was observed after PCA of expression data of the subset of colon cancer-specific genes in the cell lines. The results of this study may be useful in the ongoing research into mechanisms of cancer prevention by dietary components.

Adenocarcinoma↗
PubMed2006

Neural gastrointestinal electrical stimulation enhances colonic motility in a chronic canine model of delayed colonic transit.

Neural gastrointestinal electrical stimulation (NGES) induces sequential contractions and enhances emptying in acute canine gastric and colonic models. This study was set to determine (i) the effect of NGES in a chronic canine model of delayed colonic transit and (ii) possible mechanism of action. Four pairs of electrodes were implanted in the distal colon of nine mongrel dogs. Delayed colonic transit was induced by diphenoxylate/atropine and alosetron. Transit was fluoroscopically determined by the rate of evacuation of radiopaque markers, and was tested twice in each dog, in random order, on and off stimulation. Two stimulation sequences, separated by 1 min, were delivered twice a day via exteriorized electrodes. Colonic manometry during stimulation was performed before and after intravenous (i.v.) injection of 1 mg of atropine. Complete evacuation of all markers was significantly shortened by NGES, from 4 days to 2 days, interquartile range 3-4 days vs 2-3 days, respectively, P = 0.016. NGES induced strong sequential contractions that were significantly diminished by atropine: 190.0 +/- 14.0 mmHg vs 48.7 +/- 19.4 mmHg, respectively (P < 0.001). NGES induces strong sequential colonic contractions and significantly accelerates movement of content in a canine model of delayed colonic transit. The effect is atropine sensitive.

Animals↗
PubMed2001

Prolonged multi-point recording of colonic manometry in the unprepared human colon: providing insight into potentially relevant pressure wave parameters.

OBJECTIVES: To determine the feasibility of and derive normative data for prolonged, 24-h, multipoint, closely spaced, water perfused manometry of the unprepared human colon. METHODS: In 14 healthy volunteers, 24-h recordings were made using a water perfused, balloon-tipped, 17 lumen catheter which was passed pernasally and positioned so that 16 recording sites spanned the colon at 7.5 cm intervals from cecum to rectum. The area under the pressure curve and propagating pressure wave parameters were quantified for the 16 regions. High amplitude propagating sequences were defined as were rectal motor complexes. RESULTS: Nasocolonic recording was well tolerated and achievable. Propagation sequences, including high amplitude propagating sequences, originated in the cecum (0.32 +/- 0.05/h) more frequently than in other regions and the extent of propagation correlated significantly with proximity of the site of sequence origin to the cecum (p < 0.001). Propagation velocity of propagating sequences was greater than high amplitude propagating sequences (p = 0.0002) and region-dependent, unlike high amplitude propagating sequences (p < 0.01). The frequency of propagating sequences did not increase after the meal, but frequency of high amplitude propagating sequences was increased significantly by the meal (p < 0.01). Rectal motor complexes were seen throughout the colon with no apparent periodicity. CONCLUSIONS: Prolonged, multipoint, perfusion manometry of the unprepared colon provides improved spatial resolution of colonic motor patterns and confirms the diurnal and regional variations in propagating pressure waves detected in the prepared colon. The study demonstrates differences between high amplitude propagating sequences and propagating sequence parameters that may have functional significance; and also, that the rectal motor complex is a ubiquitous pan colonic motor pattern.

Adult↗
PubMed2005

Citrobacter rodentium lifA/efa1 is essential for colonic colonization and crypt cell hyperplasia in vivo.

Previously, we have identified a large gene (lifA, for lymphocyte inhibitory factor A) in enteropathogenic Escherichia coli (EPEC) encoding a protein termed lymphostatin that suppresses cytokine expression in vitro. This protein also functions as an adhesion factor for enterohemorrhagic E. coli (EHEC) and Shiga toxin-producing E. coli and is alternatively known as efa1 (EHEC factor for adherence 1). The lifA/efa1 gene is also present in Citrobacter rodentium, an enteric pathogen that causes a disease termed transmissible murine colonic hyperplasia (TMCH), which induces colitis and massive crypt cell proliferation, in mice. To determine if lifA/efa1 is required for C. rodentium-induced colonic pathology in vivo, three in-frame mutations were generated, disrupting the glycosyltransferase (GlM12) and protease (PrMC31) motifs and a domain in between that does not encode any known activity (EID3). In contrast to infection with wild-type C. rodentium, that with any of the lifA/efa1 mutant strains did not induce weight loss or TMCH. Enteric infection with motif mutants GlM12 and PrM31 resulted in significantly reduced colonization counts during the entire 20-day course of infection. In contrast, EID3 was indistinguishable from the wild type during the initial colonic colonization, but cleared rapidly after day 8 of the infection. The colonic epithelium of all infected mice displayed increased epithelial regeneration. However, significantly increased regeneration was observed by day 20 only in mice infected with the wild-type in comparison to those infected with lifA/efa1 mutant EID3. In summary, lifA/efa1 is a critical gene outside the locus for enterocyte effacement that regulates bacterial colonization, crypt cell proliferation, and epithelial cell regeneration.

Animals↗
PubMed2004

Enteric neurones modulate the colonic permeability response to luminal bile acids in rat colon in vivo.

BACKGROUND: The mechanisms behind microscopic colitis and exacerbations of ulcerative colitis are incompletely understood. It seems highly likely that both luminal antigens and bile are involved. The aim of this study was to test the hypothesis that bile acids increase colonic mucosal permeability by activating enteric neurones. METHOD: The effect of 4 mM deoxycholic acid (DCA) on the appearance rate of intravenously administered (3)H-mannitol and (14)C-urea into the lumen of the proximal and distal rat colon was measured in vivo and expressed as clearance. The nerve blocking agents atropine and hexamethonium were given intravenously, and lidocaine was applied onto the serosal surface of the colon, before and after DCA exposure RESULTS: DCA markedly increased clearance of the permeability probes into the lumen in both colonic segments and also the ratio of mannitol/urea clearance, particularly in the distal colon. Pretreatment with atropine, hexamethonium, and lidocaine significantly inhibited the increase in clearance by approximately 65-80% but did not affect the clearance ratio. In the distal colon, the inhibitory effect of lidocaine was not statistically significant. Also, administration of atropine and hexamethonium after DCA exposure significantly inhibited the DCA effect on clearance of the probes. CONCLUSION: The results suggest that in vivo, the permeability increase induced by a moderate concentration of bile acid is to a large extent mediated by a neural mechanism involving muscarinic and nicotinic receptors. This mechanism may be a link between the central nervous system and colonic mucosal barrier function, and may be a new target for treatment.

Animals↗
PubMed1991

Colonic fermentation of dietary fibre to short chain fatty acids in patients with adenomatous polyps and colonic cancer.

Short chain (C2-C6) fatty acids are produced in the colon through bacterial fermentation of mainly dietary fibre. Butyrate (C4) possesses antineoplastic effects on human colon carcinoma cells, and epidemiological studies indicate that high fibre diets may reduce the incidence of colorectal cancer. The role of dietary fibre during colorectal carcinogenesis might therefore be related to its fermentation to butyrate. Faecal concentrations of total short chain fatty acids and concentrations and ratios of the individual C2-C6 fatty acids did not differ between 16 healthy controls, 17 patients with colonic adenomas, and 17 patients with colonic cancer. Comparison of the molar production velocities (mmol/l.hour) of total and individual short chain fatty acids from glucose, ispagula, wheat bran, and albumin in six and 24 hour faecal incubations showed no differences. The ratio of butyrate production to total short chain fatty acid production from fibre, however, was reduced in patients with colonic cancer and adenomas compared with healthy controls (ispagula, six hours: 6.4, 7.6, and 11.5% respectively, p = 0.005 and 24 hour: 9.1, 9.9, and 15.4%, p = 0.002; wheat bran, six hours: 9.9, 10.2, and 14.7% respectively, p = 0.06 and 24 hours: 15.1, 16.8, and 21.0%, p = 0.01). It may be that the low ratios of colonic butyrate formation combined with low fibre diets increase the risk of colonic neoplasia.

Adenoma↗
PubMed1995

Resection-induced colonic adaptation is augmented by IGF-I and associated with upregulation of colonic IGF-I mRNA.

The effects of exogenous insulin-like growth factor-I (IGF-I) on colonic adaptation were examined in male Sprague-Dawley rats (n = 60, 225-275 mg) after either a 60% small bowel and cecal resection (RX) or mid-small bowel transection with reanastomosis (TX). Animals received a 7-day treatment with either IGF-I (2.4 mg.kg-1.day-1) or vehicle (V; 0.1 mol/l acetic acid). Body weight decreased significantly after resection (-25.6 +/- 4.0 g; P < 0.05 vs. TX/V). IGF-I treatment significantly reduced weight loss after resection (-12.4 +/- 3.8 g; P < 0.01 vs. RX/V) and induced significant weight gain after transection (15.6 +/- 4.0 g; P < 0.05 vs. TX/V). Plasma IGF-I decreased with resection (526 +/- 41 TX/V vs. 344 +/- 17 ng/ml RX/V; P < 0.01). IGF-I treatment significantly increased plasma IGF-I levels (805 +/- 100 ng/ml TX/IGF, 677 +/- 56 ng/ml RX/IGF). After resection, IGF-I treatment significantly increased colonic mucosal weight, DNA, protein content, and crypt depth when compared with resection alone (P < 0.05). Colonic water absorption, measured by an in vivo [3H]polyethylene glycol assay, was significantly increased by IGF-I treatment in resected animals (399 +/- 23 RX/IGF vs. 306 +/- 32 microliter.cm-1.h-1 RX/V; P < 0.05). Resection resulted in increased steady-state colonic IGF-I mRNA (182% of TX/V; P < 0.01) without significantly affecting IGF-I receptor mRNA expression. Regulation of IGF binding protein (BP)-3 and -4 was discoordinate, with IGFBP-3 mRNA tending to decrease with resection (67% of TX/V; P is not significant) and IGFBP-4 increasing significantly (191% of TX/V; P < 0.05). An important role for IGF-I in colonic adaptation after massive intestinal resection is indicated by 1) significantly enhanced colonic mucosal growth and water absorption with IGF-I treatment and 2) postresection upregulation of colonic IGF-I mRNA and alteration of IGFBP-3 and IGFBP-4 mRNA expression.

Adaptation, Physiological↗
PubMed2006

The cost-effectiveness of colonic stenting as a bridge to curative surgery in patients with acute left-sided malignant colonic obstruction: a Canadian perspective.

BACKGROUND: Over the past several years, colonic stenting has been advocated as an alternative to the traditional surgical approach for relieving acute malignant left-sided colonic obstruction. The aim of the present study was to determine the most cost-effective strategy in a Canadian setting. patients and METHODS: A decision analytical model was developed to compare three competing strategies: CS - emergent colonic stenting followed by elective resective surgery and reanastomosis; RS - emergent resective surgery followed by creation of either a diverting colostomy or primary reanastomosis; and DC - emergent diverting colostomy followed by elective resective surgery and reanastomosis. The costs were estimated from the perspective of the Manitoba provincial health plan. RESULTS: The use of CS resulted in fewer total operative procedures per patient (mean CS 1.03, RS 1.32, DC 1.9), lower mortality rate (CS 5%, RS 11%, DC 13%) and lower likelihood of requiring a permanent stoma (CS 7%, RS 14%, DC 14%). CS is slightly more expensive than DC, but less costly than RS (DC 11,851 dollars, CS 13,164 dollars, RS 13,820 dollars). The incremental cost-effectiveness ratio associated with the use of CS versus DC is 1,415 dollars to prevent a temporary stoma, 1,516 dollars to prevent an additional operation and 15,734 dollars to prevent an additional death. CONCLUSIONS: Colonic stenting for patients with acute colonic obstruction secondary to a resectable colonic tumour is comparable in cost with surgical options, and reduces the likelihood of requiring both temporary and permanent stomas. Colonic stenting should be offered as the initial therapeutic modality for Canadian colorectal cancer patients presenting with acute obstruction as a bridge to definitive RS.

Aged↗
PubMed1991

Pyloric antrum gastrin cell hyperplasia after jejunum or colon transposition: effects of jejunal or colonic mucosa on G cells.

Jejunal or colonic segments are currently used as esophageal substitutes after resection of intractable peptic stenoses. The present study was carried out in order to investigate the effects of the jejunal or colonic mucosa on antral gastrin (G) cells. Colonic or jejunal patches with intact vascular supply were sutured to the pyloric antrum or the higher portion of the gastric body in 40 rats. Ten further animals were used as controls. Three to 4 months after surgery, the serum gastrin levels were weekly determined in fasted (24 h) and freely fed rats using radioimmunoassay. The pyloric antrum was then removed, and the G cell density was assessed with an immunoperoxidase method. Transposal of the colonic mucosa to the antrum increased G cell density and basal serum gastrin levels, while grafting of the jejunal mucosa did not. G cell proliferation proved to be dependent on the topographic location of the colonic patch with respect to the pyloric antrum. Serum gastrin values in freely fed rats tended to be greater in the colon-to-antrum transposition group than in the other experimental groups, but the difference was not significant. In conclusion, variations between the properties of the jejunal and colonic mucosa would include their uneven effects on antral G cells.

Animals↗
PubMedDate not supplied

Detection of hTERT mRNA in colonic brush specimens as an adjunct to cytopathologic diagnosis of colonic adenocarcinoma.

OBJECTIVE: To investigate the role of reverse transcriptase polymerase chain reaction (RT-PCR) in determining telomerase catalytic subunit (hTERT) mRNA to assist with the diagnosis of colonic adenocarcinoma (CCA) in colonic brush cytology specimens. STUDY DESIGN: Twenty-seven colonic brushes of CCA were obtained. Initial cytologic diagnoses included CCA, suspicious for CCA (SFC), atypical (ATY) and unsatisfactory. The cytologic specimens were reviewed. A homogeneous RT-PCR assay for hTERT mRNA was performed on 27 colonic brushes of CCA and 24 controls (10 negative brushes, 6 resected CCA and 8 benign colonic mucosa from resected specimens). A RT-PCR assay for beta 2-microglobulin was used as an internal control for mRNA quality. RESULTS: On review, the initial cytopathologic diagnosis of CCA was confirmed in all 7 cases. In addition, 7 of 19 initially interpreted as SFC and ATY seemed to demonstrate unequivocal cytomorphologic features of malignancy. Telomerase mRNA was more often expressed in CCA than in negative controls in both brush (30%) and resected specimens (57%) (P < .05). Seven cases with hTERT mRNA expression were initially diagnosed as CCA (three), SFC (three) and ATY (one). CONCLUSION: CCA may be underdiagnosed in brush cytopathology. The expression of hTERT mRNA may be determined by RT-PCR in brush specimens and may eventually prove to be a useful diagnostic adjunct in the interpretation of inconclusive cases of CCA. Sparse cellularity in brush specimens may result in a relatively low rate of hTERT detection in colonic brushes of CCA; inflammatory changes may contribute to a higher-than-expected rate of hTERT expression in benign colonic epithelium.

Adenocarcinoma↗
PubMed2000

Chemoprevention of colon cancer carcinogenesis by balsalazide: inhibition of azoxymethane-induced aberrant crypt formation in the rat colon and intestinal tumor formation in the B6-Min/+ mouse.

Non-steroidal anti-inflammatory drugs (NSAIDs) including aspirin have been shown to suppress colon carcinogenesis and in some cases reduce the size of colorectal polyps. Balsalazide disodium (BSZ) is a colon-specific prodrug of the salicylate, 5-aminosalicylic acid. The aim of the present study was to test the chemopreventive activity of BSZ in two established animal models of colon tumorigenesis, azoxymethane-induced aberrant crypt formation in the rat and intestinal tumor formation in the B6-Min/+ mouse. Aberrant crypt foci (ACF) were induced in Fischer 344 rats via 2 subcutaneous injections of azoxymethane (20 mg/kg). BSZ was supplied in the drinking water for 8 weeks and ACF quantitated. B6-Min/+ mice were treated from 55 days of age for 90 days and intestinal tumors scored for number, size and location. BSZ treatment of AOM-injected rats reduced ACF formation in a dose-dependent manner by 60% with the greatest effect observed on ACF with 4 or more crypts. In B6-Min/+ mice a dose-dependent reduction of intestinal tumor number was observed which reached 80% in the distal small intestine and colon. A preliminary mechanistic study in cultured human colon cancer cells showed that both BSZ and 5-ASA inhibited colon cancer cell proliferation in vitro. However, 5-ASA but not BSZ produced changes consistent with the induction of apoptosis. BSZ produces a dose-dependent chemopreventive effect on colon carcinogenesis. A possible mechanism is consistent with the inhibition of cellular proliferation and the induction of apoptosis.

Aminosalicylic Acids↗
PubMed1991

Induced adenocarcinoma of the ascending colon on LE and Wistar/Shhi rats and virus like particles in the serum of colon cancer carrying WF rats.

Intraperitoneal injection of the serum of colon cancer carrying WF rats induced, within two months, colon carcinomas in the ascending colon of LE and Wistar/Shi rats when they were given it during their suckling. We had also induced colon carcinomas in the ascending colon of ACI rats by the same methods. Therefore, it is supported that this serum derived from colon cancer carrying WF rats must have some transmissible agent in itself. In addition, we ultracentrifuged the serum of cancer carrying WF rats and we found, in the sediment, numerous round or oval virus like corpuscles by electron microscopy studies. Negatively stained corpuscles by phosphotungstic acid staining clearly revealed fine spike appearance on their surface. We believe that these virus like corpuscles are the etiological agent for the transmissible colon carcinoma of WF rat strain.

Adenocarcinoma↗
PubMed2004

[Altered colonic transit in TNBS-induced experimental colitis in guinea pig and distribution of nitric oxide synthase in the colonic wall].

BACKGROUND/AIMS: Inflammation-induced alterations in smooth muscle contractility may be due to the effects on smooth muscle itself, neurotransmitters or enteric nerves. In dextran sulfate sodium-induced colitic rat, the delay in colonic transit was caused by decreased activity and production of neuronal nitric oxide synthase (nNOS) in the myenteric plexus of the distal colon. The aim of this study was to investigate the relationship between the delay in colonic transit and the distribution of inducible NOS (iNOS) and nNOS immunoreactive cells in the myenteric plexus of trinitrobenzene sulfonic acid (TNBS)-induced colitic guinea pig. METHODS: Sacrificed and their colonic tissues of forty-five TNBS-induced colitic guinea pigs were used to measure the colonic transit, and analyzed by immunohistochemistry. RESULTS: Colonic transit was delayed significantly at 3, 7 and 14 days after administration of TNBS. In control, nNOS immunoreactivity was present in the mucosa, submucosa, lamina propria, and ganglion cells of the myenteric plexus, while after TNBS treatment, reduced nNOS cells were found. However, the number of nNOS ganglion cells in the myenteric plexus was similar to those seen in controls. After administration of TNBS, iNOS immunoreactivity was increased in the mucosa and submucosa, but the number of iNOS positive ganglion cells in the myenteric plexus was not changed compared to control. CONCLUSIONS: It is suggested that in TNBS-induced guinea pig colitis, delayed colonic transit is not associated with the expression of nNOS nor iNOS in the myenteric plexus.

Animals↗
PubMed2005

Indole-3-carbinol inhibits the growth of human colon carcinoma cells but enhances the tumor multiplicity and volume of azoxymethane-induced rat colon carcinogenesis.

Indole-3-carbinol (I3C) is a naturally occurring phytochemical which exerts a broad range of biological activities. The purpose of this study was to examine the effects of I3C on colon carcinogenesis, cell proliferation, cell-cycle progression and apoptosis, and on the levels of expression of several cell-cycle control molecules. We used a long-term rat model by using azoxymethane (AOM) to induce tumors (adenomas and adenocarcinomas) in the colon. In the present study, we found that after AOM injection, the treatment of male F344 rats with 0.01 and 0.05% I3C caused a significant increase in the tumor multiplicity of adenocarcinomas by 2.2- (P<0.05 for 0.01% I3C) and 2.1-fold (P<0.0002 for 0.05% I3C) respectively, when compared to the control rats. In addition, the tumor multiplicity of adenoma plus adenocarcinoma and the volume of adenocarcinoma were also increased by 2.0- (P<0.00001) and 2.1-fold (P<0.05) respectively, compared to the control. I3C significantly increased the proliferating cell nuclear antigen labeling index (PCNA LI) (P<0.008) and decreased the apoptotic index (P<0.05) of the colon adenocarcinoma. In contrast, in HCT 116 and HT29 human colon carcinoma cells, I3C inhibited growth and induced G1-phase cell-cycle arrest and apoptosis. Furthermore, I3C caused approximately a 2- to 4-fold increase in the cellular levels of p27KIP1 and p21CIP1 mRNA. These results suggest that I3C inhibits the growth of human colon carcinoma cells, at least in part, by inducing p27KIP1 and p21CIP1-mediated G1 cell-cycle arrest but dietary I3C promotes AOM-induced rat colon carcinogenesis by inhibiting the apoptosis of colon tumors. Therefore, the present study may provide further evidence for the ambivalent modulatory activity of I3C and this information may be useful when including I3C in cancer chemoprevention and/or extensive clinical therapy trials.

Adenocarcinoma↗
PubMed1991

Suppression of experimental lung colonization of a metastatic variant of murine colon adenocarcinoma 26 by a monoclonal antibody 8F11 inhibiting tumor cell-induced platelet aggregation.

We have previously established and characterized two monoclonal antibodies, 8F11 and 20A11, that recognize an Mr 44,000 membrane glycoprotein of metastatic murine colon 26 cells. Both monoclonal antibodies inhibit platelet aggregation induced by the tumor cells in vitro. In this report, the inhibitory effect of 8F11 on lung colonization of i.v.-inoculated tumor cells was examined. The i.v. administration of 8F11 suppressed lung colonization of NL-17, a highly metastatic variant of colon 26. Inhibition of NL-17 lung colonization by 8F11 was dose dependent with a maximum of 80% inhibition at a dose of 800 micrograms 8F11/mouse. 8F11 did not inhibit metastases at doses lower than 100 micrograms/mouse. Inhibition of pulmonary metastases by 8F11 was greatest when the antibody was administered 2 h before tumor inoculation. The effect was diminished when the antibody was given 2 h after tumor inoculation. The pulmonary retention of i.v.-inoculated radiolabeled NL-17 cells was decreased by 8F11. F(ab')2 fragments of 8F11 also effectively inhibited lung colonization by NL-17 cells, suggesting that mechanisms unrelated to immune-mediated destruction are involved. These results indicate that the monoclonal antibody 8F11 suppresses the lung colonization of NL-17 cells by interfering with the initial arrest of tumor cells in the lung vasculature through the inhibition of tumor cell-platelet interaction.

Adenocarcinoma↗
PubMed1986

Comparison of right colon, left colon, and rectal carcinoma.

Three hundred fifteen cases of adenocarcinoma were analyzed for differences between lesions in the right colon, left colon, and rectum for the period 1978 to 1983. The right colon cancers accounted for 1/3 of the cases and were associated with a higher incidence of anemia. The incidence of obstruction was the same between the right and left colon but lower for the rectal lesions. Left colon and rectal cancers had a higher incidence of gross bleeding than right colon cancers, but all had a high rate of occult blood in the stool. The Duke stage of the lesions, which was similar throughout the colon and rectum, is a reliable prognostic indicator.

Adult↗