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At least 361 records · Page 20Linked to original sources
PubMed1999

Coordinate regulation of cyclooxygenase-2 and TGF-beta1 in replication error-positive colon cancer and azoxymethane-induced rat colonic tumors.

Evidence is accumulating which indicates that cyclooxygenase-2 (COX-2) is involved in the pathogenesis of colorectal cancer. We evaluated the expression of COX-2 in replication error-positive (RER) colon cancers, colon cancers metastatic to liver and azoxymethane (AOM)-induced rat colonic tumors. Immunohistochemistry showed that COX-2 was low to undetectable in normal human mucosa, but abundant in the RER adenocarcinomas we examined. COX-2 immunoreactivity in metastatic colon cancers was less abundant, but clearly detectable. In the colon of AOM-treated rats, COX-2 protein was not detectable in normal mucosa, but present in most of the epithelial cells comprising the tumors. The TGF-beta1 staining pattern in these human and rat tumors was similar to that observed for COX-2. The role of TGF-beta in RER adenocarcinomas is complex because of the increased mutation rate of TGF-beta type II receptors. Northern analysis showed abundant TGF-beta1 mRNA in AOM-induced tumors, but not in paired mucosa. TGF-beta1 induced the expression of COX-2 mRNA and protein in intestinal epithelial cells (IEC-6). Chronic TGF-beta1 treatment caused a TGF-beta-dependent overexpression of COX-2 in rat intestinal epithelial cells (RIE-1). TGF-beta1 may regulate COX-2 expression during the colonic adenoma to carcinoma sequence.

Animals↗
PubMed2003

Azoxymethane-induced beta-catenin-accumulated crypts in colonic mucosa of rodents as an intermediate biomarker for colon carcinogenesis.

It is now well established that bile acids act as colon tumor promoters. However, a previous study provided conflicting data showing that dietary exposure of cholic acid (CHA), a primary bile acid, inhibits the carcinogen-induced formation of aberrant crypt foci (ACF), possible preneoplastic lesions, in colonic mucosa of rodents. Recently we found beta-catenin-accumulated crypts (BCAC) in colonic mucosa of rats initiated with azoxymethane (AOM) and provided evidence that BCAC might be preneoplastic lesions independent from ACF. In the present study, we investigated the modifying effects of dietary CHA on the formation of BCAC as well as ACF in male F344 rats after exposure to AOM to determine if the differences in the effect of CHA on these lesions could account for this discrepancy. The results indicate that administration of CHA (0.5%) in the diet during the post-initiation phase significantly reduced the total number, multiplicity and size of ACF (P < 0.00001) in AOM-exposed colonic mucosa as reported previously. The number of ACF even with >4 aberrant crypts/focus was also decreased significantly (P < 0.0002), suggesting that the large ACF are little resistant to continuous feeding of 0.5% CHA diet. Interestingly, the dietary CHA significantly enhanced both the multiplicity (P < 0.002) and size (P < 0.00001), but not the incidence, of AOM-induced BCAC when compared with the control diet group. Importantly, the number of large BCAC with >6 crypts/lesion was increased significantly by the dietary CHA (P < 0.003). Our results support the concept that BCAC are precursors of colon tumors and indicate the usefulness of BCAC as intermediate biomarkers for colon carcinogenesis, although the methodology for their detection requires further improvement.

Animals↗
PubMed1990

Effects of sodium sulfate on fecal pH and proliferation of colonic mucosa in patients at high risk for colon cancer.

High fecal pH level has been suggested as a risk factor for colorectal cancer. We previously demonstrated that, although sodium sulfate did not affect the proliferation rate of colonic mucosa, as indicated by thymidine-labeling index, it did lower fecal pH in subjects at average risk for colon cancer. In the current study, we evaluated the effects of sodium sulfate on fecal pH and proliferation of colonic mucosa in subjects at high risk for colon cancer. Fifty-seven patients who had had colonic polyps removed were randomly assigned to two groups to receive either sodium sulfate (27 patients) or a placebo (25 patients) at a mean dose of 4 g/day for 14 days. Age, sex, height, and weight were comparable in both groups. Before intervention, levels of fecal pH were similar in the two groups, but after intervention, fecal pH was reduced only in the sodium sulfate group (mean decrease, 0.3 U; P less than .01). Thymidine-labeling index (number of labeled cells per number of cells counted) was similar in the two groups prior to intervention and did not change significantly after intervention (mean increase, 0.9%; P = .35). Regression analysis revealed no correlation between the change in labeling index and the change in fecal pH. We conclude that high fecal pH level is only indirectly associated with the development of colon cancer and, therefore, may be a secondary, rather than a primary, measure of cancer risk.

Adult↗
PubMed2005

Effect of polyethylene glycol electrolyte balanced solution on patients with acute colonic pseudo obstruction after resolution of colonic dilation: a prospective, randomised, placebo controlled trial.

BACKGROUND AND AIMS: Conservative therapy for patients with acute colonic pseudo obstruction (Ogilvie's syndrome) may be successful initially but relapses are common. The aim of the present study was to evaluate the effect of polyethylene glycol (PEG) electrolyte balanced solution on the relapse rate of the syndrome after initial resolution with neostigmine or endoscopic decompression. PATIENTS AND METHODS: The study was performed on 30 consecutive patients who presented with abdominal distension and radiographic evidence of colonic dilation, with a caecal diameter > or = 10 cm, that resolved conservatively. Patients then were randomised to receive daily 29.5 g of PEG (n = 15) or similar placebo (n = 15). Patients were monitored daily for a seven day period for stool and flatus evacuations, and colonic diameter on abdominal radiographs. Administration of the test solutions and assessment of patient symptoms and x rays were performed in a blinded fashion. A caecal diameter > or = 8 cm with a concomitant > or =10% increase after initial successful therapeutic intervention was considered as a relapse and these patients, after a second therapeutic intervention, were eligible to receive open label PEG. RESULTS: Twenty five patients received neostigmine as the initial therapeutic intervention which resulted in resolution of colonic dilation in 88% of cases. Eight patients had successful endoscopic decompression. Five (33.3%) patients in the placebo group had recurrent caecal dilation compared with none in the PEG group (p = 0.04). Therapy with PEG resulted in a significant increase in stool and flatus evacuations (p = 0.001 and 0.032, respectively) as well as in a significant decrease in the diameter of caecum, ascending and transverse colon, and abdominal circumference (p = 0.017, 0.018, 0.014, and 0.008, respectively). CONCLUSIONS: Administration of PEG in patients with Ogilvie's syndrome after initial resolution of colonic dilation may increase the sustained response rate after initial therapeutic intervention.

Acute Disease↗
PubMed1999

Interleukin 1 and interleukin 1beta converting enzyme (caspase 1) expression in the human colonic epithelial barrier. Caspase 1 downregulation in colon cancer.

BACKGROUND: Interleukin (IL) 1beta converting enzyme (now known as caspase 1) is able to process pro-IL-1beta into its active form and is involved in proapoptotic signalling. AIMS: To characterise IL-1 and caspase 1 expression in human colonic epithelial cells. METHODS: Intracellular IL-1 content (IL-1alpha and IL-1beta) was measured by ELISA in freshly isolated human normal colonocytes. Caspase 1 expression was determined both at the mRNA level using in situ hybridisation and reverse transcription polymerase chain reaction, and at the protein level by immunoblotting experiments using antibodies specific for the proform of caspase 1 and for its cleavage forms. RESULTS: Low amounts of IL-1beta were found in nearly all preparations (92%), and IL-1alpha was detected in only 45% of human colonocyte preparations. The normal colonic epithelium strongly expressed caspase 1, both at the mRNA level and at the protein level in its latent form. In contrast, caspase 1 was not expressed in colon cancer (primary colonic adenocarcinomas and cancer cell lines). CONCLUSIONS: The demonstration that the human colonic epithelial barrier is able to express caspase 1 and its substrate IL-1beta reinforces the concept that, under certain conditions, the epithelium could trigger an inflammatory reaction. In addition, the finding that caspase 1 was downregulated in colonic adenocarcinomas supports the concept that disrupted apoptosis pathways may be involved in tumour formation and/or may confer resistance to treatment.

Adult↗
PubMed2006

Resection of asynchronous quadruple advanced colonic carcinomas followed by reconstruction with ileal interposition between the transverse colon and rectum.

We report an extremely rare case of resectable asynchronous quadruple advanced colonic carcinomas. Successful reconstruction was performed after resection with an ileal interposition between the remaining colon and rectum, and the patient recovered bowel function. Resections of the four colonic lesions in three operations allowed us to leave a portion of the large bowel and to thereby preserve the rectum and a portion of the transverse colon. After resection of the third and fourth cancer lesions, we reconstructed the large bowel with ileal segment interposition between the residual transverse colon and rectum, leaving a 15-cm-long segment portion of the transverse colon. This surgical procedure is an option for reconstruction after left-sided colectomy.

Adenocarcinoma↗
PubMed2000

Caveolin-1 levels are down-regulated in human colon tumors, and ectopic expression of caveolin-1 in colon carcinoma cell lines reduces cell tumorigenicity.

Caveolin-1 expression and function were investigated in human colon cancer. Low levels of caveolin-1 mRNA and protein were detected in several colon carcinoma cell lines. Moreover, caveolin-1 protein levels were significantly reduced in human tumor epithelial mucosa (3.6 +/- 1.4-fold) when compared with normal colon mucosa for a majority (10 of 15) of the patients characterized. To directly assess the role of caveolin-1 in tumor development, caveolin-1 was reexpressed in the HT29 and DLD1 colon carcinoma cells, and the resulting HT29-cav-1 or DLD1-cav-1 cells were tested for tumorigenicity in nude mice. In most experiments, tumor formation was either blocked or retarded for HT29-cav-1 cells (10 of 13 mice) and DLD1-cav-1 cells (5 of 7 mice), as compared with both mock-transfected and parental HT29 or DLD1 cells. Interestingly, basal caveolin-1 levels were significantly reduced in HT29-cav-1 and DLD1-cav-1 cells isolated from tumors. Likewise, endogenous caveolin-1 mRNA and protein levels were found to be reduced in NIH-3T3 cells recovered from tumors after injection into nude mice. Thus, reexpression of caveolin-1 in colon carcinoma lines reduced the probability of tumor formation in vivo, and when tumors did develop from either HT29-cav-1, DLD1-cav-1, or NIH-3T3 cells, lower basal levels of caveolin-1 were detected. Finally, evidence was obtained indicating that initial caveolin-1 down-regulation in colon cancer cells need not be an entirely irreversible process because cell survival on selection for either drug resistance or increased metastatic potential correlated with increased caveolin-1 expression levels.

3T3 Cells↗
PubMedDate not supplied

Autografting colonic adenocarcinomas into the colonic submucosa in rats.

After inducing colonic tumors in 47 rats by weekly subcutaneous injections of 1,2-dimethylhydrazine, all rats were laparotomized and tumors were autotransplanted to tumor-free areas of the transverse colon. True autotransplants were considered to be tumors occurring in the grafted areas, which were covered by normal colonic mucosa. The frequency of auto-grafted tumors was 35.5%. In a previous work, a low incidence of 1,2-dimethylhydrazine-induced tumors was found in the transverse colon of the rat. The present results suggest that the failure of tumor growth in the transverse colon may be unrelated to an intrinsic natural "resistance" of that segment of the colon to tumor growth.

1,2-Dimethylhydrazine↗
PubMedDate not supplied

Implantation of colon cancer cells on intact and damaged colon mucosa and serosa: an experimental study in the rat.

The ability of malignant colon cancer cells to implant on intact and damaged colonic mucosa and serosa was tested in a series of experiments using male WAG rats. The mucosa was damaged in an "acute" way by multiple biopsies and in a "chronic" way by means of a chemically induced colitis. The creation of an anastomosis provoked both mucosal and serosal damages. CC531 colon cancer cells injected intraluminally as an enema implanted at the serosal side of an anastomosis without invading the mucosa in 66% of the rats. An intact colon mucosa is 100% resistant to the implantation of viable CC531 cells. In contrast, tumour growth was noticed in 100% of the rats when the malignant cells were sprayed over the intact colon serosa at laparotomy. Mucosal damage by biopsies in the presence of viable colon cancer cells resulted in mucosal implantation and intraluminal tumour growth in one out of thirty rats. No tumour growth was observed when the CC531 cells were instilled on one week old mucosal ulcerations resulting from a chemical induced colitis.

Anastomosis, Surgical↗
PubMed1993

Transcription of carcinoembryonic antigen in normal colon and colon carcinoma. In situ hybridization study and implication for a new in vivo functional model.

Recently carcinoembryonic antigen (CEA) has been functionally identified in vitro as a cell adhesion protein. Identification of its function in vivo requires knowing how CEA mRNA is transcribed in intact tissues. For this purpose, 16 cases of colon adenocarcinomas and autologous normal colon were studied by quantitative in situ hybridization for the expression of CEA mRNA. Normal colonic crypts displayed an upward gradient of mRNA expression. In colon carcinoma, tumor cells at the deep invading front of the tumor contain 2.6 times more CEA mRNA than tumor cells near the luminal surface. Immunoelectron microscopy showed intercellular CEA. In normal colon and colonic carcinoma, changes in CEA mRNA were paralleled by similar gradients in CEA protein, consistent with a transcriptional regulation of CEA expression. A new in vivo model of CEA function is presented to account for this overexpression of CEA occurring at sites characterized by changes in cell adhesion. The model requires that secreted CEA inhibits cell adhesion mediated by cell-bound CEA.

Aged↗
PubMed2000

Decreased expression of CD44, alpha-catenin, and deleted colon carcinoma and altered expression of beta-catenin in ulcerative colitis-associated dysplasia and carcinoma, as compared with sporadic colon neoplasms.

BACKGROUND: To clarify the cell adhesion status in ulcerative colitis (UC)-associated colon neoplasm, expression of cell adhesion molecules were investigated and compared with that of sporadic colon neoplasm. METHODS: A total of 14 low grade dysplasias, 16 high grade dysplasias, and 8 adenocarcinomas associated with UC and 17 sporadic adenomas with mild to moderate dysplasia, 22 adenomas with severe dysplasia, and 15 invasive adenocarcinomas were immunohistochemically examined using monoclonal antibodies against CD44, E-cadherin, alpha- and beta-catenin, and deleted colon carcinoma (DCC). RESULTS: CD44, especially its standard form, and DCC expression was stronger in the sporadic colon neoplasms than in the UC-associated lesions. Although E-cadherin did not show significant differences between the two cases, alpha-catenin was more expressed in sporadic colon adenomas with severe dysplasia and carcinomas than in their UC-associated counterparts. Membranous beta-catenin staining was stronger in UC-associated neoplasms, whereas sporadic lesions had greater cytoplasmic and nuclear expression. CONCLUSIONS: The differences in cell adhesion molecule expression suggests that UC-associated and sporadic colon neoplasms arise from different pathways of tumorigenesis.

Cadherins↗
PubMed2004

Colon cancer specific nuclear matrix protein alterations in human colonic adenomatous polyps.

Most colon cancers arise within preexisting adenomatous polyps or adenomas. The slow evolution from the non-invasive premalignant lesion, the adenomatous polyp, to invasive cancer supports a strategy of early detection. Recently, we identified unique nuclear matrix proteins (NMPs) specific for colon cancer (CC2, CC3, CC4, CC5). Most of the NMPs identified are common to all cell types, but several identified NMPs are tissue and cell line specific. The objective of this study is to describe and characterize the NMP profile of premalignant adenomatous colon polyps. Specifically when in the adenoma-carcinoma sequence four specific colon cancer NMPs, previously described, appear. Using two-dimensional (2-D) gel analysis 20 colon polyps (one juvenile polyp, six tubular adenoma (TA), seven tubulovillous adenoma (TVA), six TVA with focal high-grade dysplasia (HGD), were analyzed for the presence of four (CC2, CC3, CC4, CC5) specific NMPs. CC2 was not seen in any of the premalignant polyps. CC5 was present in only two premalignant TVA with HGD and in one TA. CC3 and CC4 were present in most adenomas. None of the NMPs were seen in the juvenile polyp, which is not considered to be a precursor of colon cancer. CC2 and CC5 are NMPs expressed at the junction of an advanced adenoma and invasive colorectal cancer. CC3 and CC4 are expressed earlier in the evolution of adenomatous polyps. Development of an assay to these proteins may serve as a new method for early detection of colorectal cancer.

Adenomatous Polyps↗
PubMed1993

Rare frequency of activation of the Ki-ras gene in rat colon tumors induced by heterocyclic amines: possible alternative mechanisms of human colon carcinogenesis.

Heterocyclic amines present in cooked foods are known to produce colon tumors in F344 rats at a high incidence, indicating the possibility of involvement of ras gene activation in colon carcinogenesis in rats as in humans. We examined mutations at codons 12, 13, and 61 of the Ki-ras, Ha-ras, and N-ras genes by polymerase chain reaction--direct sequencing in seven colon tumors in F344 rats induced by 2-amino-6-methyldipyrido-[1,2-a:3',2'-d]imidazole (Glu-P-1), 11 induced by 2-amino-3-methylimidazo[4,5-f]quinoline, and nine induced by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine. A Ki-ras gene mutation (G-->T at the second position in codon 12) was found in one Glu-P-1-induced colon adenocarcinoma. None of the other 26 tumors had mutations in any of these three ras family genes. These results indicate that in rats, colon carcinogenesis induced by heterocyclic amines may be induced by alterations of other oncogenes or tumor suppressor genes. We think this experimental system using carcinogens to which humans are exposed is a good model for studying alterations of other genes in human colon tumors in which no Ki-ras alterations are observed.

Adenocarcinoma↗
PubMed1995

Expression of phospholipases gamma 1, beta 1, and delta 1 in primary human colon carcinomas and colon carcinoma cell lines.

The levels of expression of phosphoinositide-specific phospholipase Cs (PLCs) were examined in a series of primary human colon carcinomas and in eight colon carcinoma cell lines by using monoclonal antibodies and cDNA probes for PLC gamma 1, PLC beta 1, and PLC delta 1. Western and northern blot analyses of PLC gamma 1 revealed elevated expression of this isozyme at both the protein and mRNA levels in most tumors when compared with paired adjacent normal mucosa samples (in 11 of 13 pairs in the western blots and 8 of 9 pairs in the northern blots). On the other hand, decreased levels of the PLC delta 1 protein were seen in most colon carcinomas (12 of 13 paired samples). The levels of PLC beta 1 protein were too low to detect possible differences between the carcinoma and normal mucosa samples. Relatively high expression of PLC gamma 1 was found in almost all of the eight human colon carcinoma cell lines at both the protein and mRNA levels. Only weak expression of PLC beta 1 was detected in these cell lines, by both western and northern blot analyses, and PLC delta 1 protein was not detected in any of the carcinoma cell lines. These findings provide evidence that colon carcinomas display altered expression of individual isoforms of PLCs and suggest that increased expression of PLC gamma 1 may play an important role in colon carcinogenesis.

Adult↗
PubMed1994

The occurrence of colon cancer in patients with known premalignant colonic mucosal diseases.

Both ulcerative colitis and familial polyposis are colonic mucosal diseases which are known to predispose to colon cancer. While colonoscopy is an accurate modality used in screening and surveillance for patients with these two diseases, patients continue to present with colon cancer with these known premalignant diseases. This study was conducted to ascertain why patients with known premalignant disease still develop life-threatening colon cancer and to assess the clinical profile and prognosis of patients with known ulcerative colitis (UC) and familial polyposis coli (FPC) who subsequently develop colon cancer. Total colectomy, mucosal proctectomy, and ileoanal pullthrough was performed on 367 patients with UC and FPC between January 1982 and March 1993 at our institution. Of these, 15 had invasive adenocarcinoma of the colon (4.1%) in addition to the primary disease. These 15 patients were studied in detail. The average duration of disease from diagnosis to definitive treatment of cancer was 17 years. Thirteen of the patients in this series had UC (87%), while only 2 had FPC (13%). Colonoscopy was used to make the diagnosis in 11 patients (73%), while the diagnosis was made only at the time of surgery in 3 (20%). Nine of the patients presented with a Dukes' B2 cancer or worse, representing 60% of the series. A high percentage had synchronous invasive cancers in this series--6 patients (40%). Despite the relatively high percentage of advanced cancers in this series, at a mean follow-up of 47.1 months, 14 of the 15 patients are still living. One patient has known recurrent disease while 1 has an elevated CEA with no other evidence of recurrence.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1995

Prospective evaluation of laparoscopic colon resection versus open colon resection for adenocarcinoma. A multicenter study.

Laparoscopic colon resection (LCR) has been performed in the United States sine 1990. This procedure has been accepted by many as a reasonable alternative for nonmalignant, colonic, surgical disease, but the laparoscopic approach remains controversial for curative treatment of carcinoma. In this paper, the results of a nonrandomized series of two large experiences of laparoscopic colon resections were performed and followed for 3 1/2 years in a prospective fashion against an equal number of patients who underwent open resection. The setting was several large metropolitan hospitals in San Antonio, Texas. Over 194 patients were involved in this study. Each patient once diagnosed with resectable colonic cancer was allowed to choose their own procedure, laparoscopic or open colon resection, either of which was performed by the authors. Factors considered include age, sex, body habitus, stage of cancer, margins of resection, numbers of lymph nodes retrieved, hospitalization time, and follow-up period. Observations at this time indicate the following: (1) LCR allows for resection comparable to the classical approach, (2) equal numbers of mesenteric lymph nodes can be retrieved, (3) adequacy of margins of resection can be accurately determined by colonoscopy during LCR, and (4) brief follow-up periods show comparable survival and disease-free intervals. It is the conclusion of the authors that with proper training LCR will come to be recognized as a safe, effective surgical option for treatment of selected patients with colon cancer.

Adenocarcinoma↗
PubMed1996

Fucosyltransferase III and sialyl-Le(x) expression correlate in cultured colon carcinoma cells but not in colon carcinoma tissue.

The potential contribution of fucosyltransferases to the overexpression of sialyl-Le(x) antigen was investigated in the colon carcinoma cell line HT-29 and in human colon carcinoma tissue. In HT-29 cells as well as in normal or malignant colonic tissues Fuc-TIII, Fuc-TIV, Fuc-TVI but not Fuc-TV nor Fuc-TVII were detectable after RT-PCR. Sodium butyrate treatment of HT-29 cells increased (to about 200%) and DMSO treatment decreased (to about 20%) the expression of sialyl-Le(x). This modulation of sialyl-Le(x) was concomitant with the analogous increase/decrease of mRNA of Fuc-TIII but not Fuc-TIV. Fuc-TVI was not detectable by Northern blotting in HT-29 cells. In six human colon carcinomas which exhibited strong overexpression of sialyl-Le(x), the expression of Fuc-TIII-mRNA was the same or lower than in the corresponding normal colonic tissue. Thus Fuc-TIII expression may be affecting the expression of the sialyl-Le(x) moiety in HT-29 cells but not in human colon carcinoma tissue.

Antibodies, Monoclonal↗
PubMed1992

Histological reactivity of a monoclonal antibody against rat colon cancer cells on human and rat normal gut and colonic tumours.

A monoclonal antibody, F11C, was raised against rat colon cancer cells. Its immunoreactivity on normal human and rat gut as well as human and rat colonic tumours was studied by the avidin-biotin-peroxidase complex technique. In both normal rat and human gastrointestinal tract, F11C stained surface epithelial cells from the fundus to distal colon, mainly as supranuclear vesicles. These vesicles appeared to be part of the Golgi apparatus on electron microscopy with immunogold labelling. Twenty primary rat colon tumours and 28 of 43 human colon tumours were also stained, with a heterogeneous pattern but much more strongly than the normal colonic mucosa. Biochemical purification suggested that in rat tumours F11C epitope was carried by a high molecular weight glycoprotein. Absorption experiments with synthetic oligosaccharides showed that F11C monoclonal antibody reacted with blood group A-related oligosaccharides. Nevertheless, F11C reactivity on human tissues was not related to the individual ABO or Lewis phenotype.

1,2-Dimethylhydrazine↗