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At least 19 recordsLinked to original sources
PubMed1981

Colon epithelium. IV. Human colon carcinogenesis. Changes in human colon mucosa adjacent to and remote from carcinomas of the colon.

To verify the popular belief that the mucosa of the colon remote from a carcinoma is normal, in a retrospective study colon mucosae from 30 patients were studied; 15 patients had colon carcinoma and the other 15 patients without any obvious tumor in their colons served as controls. All the patients having colon carcinoma showed definite abnormalities in the mucosa remote from the tumor. None of the 15 control patients showed such morphologic changes in the mucosal sections sampled at random. The mucous changes observed were: dilatation and distortion of the crypts with flattening of the lining cells, overcrowding of crypts with mucous cells and basophilic cells, lining of the crypt with eosinophilic surface epithelial cells, and focal cellular stratification in the crypts. These abnormalities were also consistently observed in the transitional mucosa adjacent to the tumor in all of the 15 patients with colon cancer. Histochemical studies for the detection of epithelial acidic mucosubstances showed that sialomucin predominated in the colon mucosa harboring a carcinoma irrespective of the location of the tumor, whereas colon mucosa from otherwise normal individuals and patients with noncarcinomatous diseases showed a predominance of sulfomucin. Therefore, mucosa of the colon harboring a carcinoma was conclusively demonstrated to be morphologically and histochemically abnormal. The significance of these abnormalities and their possible role in the de novo histogenesis of colon carcinoma are discussed.

Adenocarcinoma↗
PubMedDate not supplied

OVX1 and CEA in patients with colon carcinoma, colon polyps and benign colon disorders.

The OVX1 tumor marker promises to complement CA125 for detection of early stage ovarian carcinoma. OVX1 has also been shown to be elevated in colon cancer patients. This study is designed to assess serum OVX1 levels in patients with specific stages of colon cancer, colon polyps or other GI disorders. Serum OVX1 and CEA were measured by radioimmunoassay or enzyme immunoassay for 206 patients at the time of colonoscopy or staging for colon carcinoma. In patients with stage I, II, III, or IV colon carcinoma, serum OVX1 was positive in 37%, 48%, 74% and 63%, respectively. Fifty-three percent of patients with colon polyps had elevated OVX1 levels, while OVX1 levels were positive in only 7% of healthy controls. If both OVX1 and CEA were considered, at least one of these markers was elevated in 36%, 60%, 79% or 89% of patients with stage I, II, III or IV colon carcinoma, respectively. The majority of patients with inflammatory bowel disease or diverticulosis also had elevated OVX1 levels. Both markers were positive in 27% of patients with colon carcinoma, and not in any patients with a normal colonoscopy or with a diagnosis of diverticulosis or hemorrhoids. In conclusion, serum OVX1 improves the sensitivity of CEA for detecting colon polyps and colon cancer; however, the use of OVX1 in this setting is hindered by its elevation in non-malignant colonic processes.

Antigens, Tumor-Associated, Carbohydrate↗
PubMed1995

Epidermal growth factor expression in human colon and colon carcinomas: anti-sense epidermal growth factor receptor RNA down-regulates the proliferation of human colon cancer cells.

Human colon cancer cell lines express epidermal growth factor (EGF) mRNA, secrete EGF and may respond to it via the cell-surface EGF receptor (EGFR). Expression of these molecules in human colon and colon tumor, however, is not clear. Reverse transcription-polymerase chain reaction (RT-PCR) analyses of RNA prepared from paired normal human colon and colon tumor samples from 12 individuals followed by Southern blotting analyses of the RT-PCR products revealed a major fragment of 527 bp and a minor fragment of 404 bp that hybridized to a human EGF cDNA probe under stringent conditions. Identical results were obtained from 8 human colon cancer cell lines. Cloning and sequencing of PCR products confirmed that both fragments were from the human EGF gene; the 527-bp fragment corresponded exactly to nucleotides 2,891 to 3,417 of the human EGF mRNA reported by others. A deletion of 123 nucleotides (nucleotides 3,172 to 3,294) was found in the 404-bp fragment. Immunohistochemical studies using cyostat sections of human colon specimens showed that EGF was expressed in the human colon and that expression was restricted to the epithelial colonic crypt cells and epithelium-derived cancer cells. Since EGF and EGF-related molecules are potent mitogens that mediated their effect through the EGFR, we also determined the efficacy of anti-sense EGFR RNA in circumventing the EGFR-related pathway of proliferation. Expression of anti-sense EGFR RNA, by transfection with an inducible anti-sense EGFR expression vector, down-regulated cell-surface EGFR expression and proliferation of these cells and their ability to grow in soft agar. Anti-sense EGFR RNA was found to be an anti-proliferative agent in both relatively non-aggressive and highly aggressive human colon cancer cells.

Adenocarcinoma↗
PubMed1983

The distribution of acidic coomassie blue-stained proteins from uninvolved human liver, hepatoma, normal colon, primary colon cancer, and colon metastases to the liver, determined by two-dimensional protein electrophoresis.

The distribution of Coomassie blue-stained proteins from uninvolved regions of 4 human livers, from 1 hepatocellular carcinoma, and from 4 samples each of uninvolved colon, primary adenocarcinoma of the colon, and colon cancer metastatic to the liver was analyzed by two-dimensional protein electrophoresis. From a comparison of acidic proteins between pI 3.5 and 6.5, we conclude (1) that the majority (66 of 82) of denoted acidic proteins from 4 normal liver samples were represented in the hepatocellular carcinoma. Fifty-one of 58 proteins denoted in the 4 colon samples were detected in each of the 4 primary colon cancers; (2) that the "normograms" of proteins from normal colon and normal liver differed in many details, and their dissimilar patterns identified the source of the sample; (3) that hepatoma and primary adenocarcinoma of the colon were easily distinguished by their distribution of proteins; (4) that colon cancer metastatic to the liver contained a majority (50/58) of acidic proteins enumerated in primary colon cancer. These results indicate that uninvolved liver and colon and their primary or secondary cancers can be identified by their distribution of electrophoresed acidic proteins.

Adenocarcinoma↗
PubMed1988

[Colonic response to the meal of the right colon, the left colon, the rectosigmoid and the rectosigmoidal junction in digestive functional disorders].

The aim of this work was to answer the two following questions: 1) is there any difference between the right colonic, the left colonic, and the rectosigmoid motility? 2) does the rectosigmoid junction (radiological and endoscopic entity) exhibit a specific motility pattern? Colonic motility was assessed by electromyography. We used an intraluminal probe supporting 15 groups of 3 ring electrodes. Inside the probe a lead pellet was placed opposite each electrode. The probe was inserted through the colon by colonoscopy. A visual analysis of the signal was performed and we distinguished: Long Spike Bursts (LSB) activity (propagating in oral or aboral direction or not propagating) from Short Spike Bursts (SSB) activity as previously described. Twenty patients suffering from the irritable bowel syndrome included in a subgroup defined as abdominal pain, were studied, and two groups were defined as follows: the tip of the probe was positioned in the caecum in 9: group "Right colon" patients. An electrode was specifically located on the rectosigmoid junction in 15: group "Junction" patients. In the "Right colon" group, the postprandial increase of LSB activity in the rectosigmoid lasted longer than in the right and left colons. During the postprandial period, the right colon exhibited a lower LSB activity than the rectosigmoid (p less than 0.01). After the meal LSB activity propagating in aboral direction was increased in the right colon while it was inhibited in the rectosigmoid. LSB activity propagating in the oral direction was increased both in the right colon and rectosigmoid after the meal. In the "Junction" group, we observed a specific myoelectrical activity at the rectosigmoid junction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Oestrogen inactivation in the colon: analysis of the expression and regulation of 17beta-hydroxysteroid dehydrogenase isozymes in normal colon and colonic cancer.

Epidemiological data suggest that oestrogen contributes to the aetiology of colonic cancer. Furthermore, recent studies have suggested that local hormone metabolism may play a key role in determining colonic responsiveness to oestrogen. To further clarify this mechanism we have characterized the expression and regulation of isozymes of 17beta-hydroxysteroid dehydrogenase (17beta-HSD) in vitro and in situ. Immunohistochemistry was used to confirm expression of the type 2 and 4 isozymes of 17beta-HSD (17beta-HSD2 and 4) in normal colonic epithelial cells. Parallel studies suggested that both isozymes were abnormally expressed in colonic tumours and this was confirmed by Western blot analyses. Abnormal expression of 17beta-HSD2 and 4 proteins was also observed in Caco-2, HT-29 and SW620 colonic cancer cell lines, although the overall pattern of oestrogen metabolism in these cells was similar to that seen in primary colonic mucosal tissue. The predominant activity (conversion of oestradiol to oestrone) was highest in Caco-2>SW620>HT-29, which correlated inversely with the rate of proliferation of the cell lines. Regulatory studies using SW620 cells indicated that the most potent stimulator of oestradiol to oestrone inactivation was the antiproliferative agent 1,25-dihydroxyvitamin D3 (1,25D3), whilst oestradiol itself inhibited 17beta-HSD activity. Both oestradiol and 1,25D3 decreased mRNA for 17beta-HSD2 and 4. Data indicate that the high capacity for inactivation of oestrogens in the colon is associated with the presence of 17beta-HSD2 and 4 in epithelial cells. Abnormal expression of both isozymes in colonic cancer cells and the stimulation of oestrogen inactivation by the antiproliferative agent 1,25D3 highlights a possible role for 17beta-HSD isozymes as modulators of colonic cell proliferation.

17-Hydroxysteroid Dehydrogenases↗
PubMed2001

Nuclear localization of beta-catenin and plakoglobin in primary and metastatic human colonic carcinomas, colonic adenomas, and normal colon.

Beta-catenin is a cytoskeleton-associated signaling molecule shown to be elevated in various carcinomas but mostly in colon cancer owing to its impaired degradation. In contrast, its close homologue plakoglobin was shown to suppress the tumorigenicity of certain tumor cells. In the present study, we have used a semiquantitative immunohistochemical approach to evaluate the extent of nuclear localization of beta-catenin in human colonic adenocarcinomas and adenomas and compared it to the distribution of plakoglobin in the same tissues. We show that beta-catenin accumulates in the nuclei of the epithelium of primary and metastatic colonic adenocarcinoma as well as in colonic adenomas. In contrast, nuclear plakoglobin levels in these tissues were low, even compared to those found in epithelial cells of normal colon. These results support the view that the increase in beta-catenin levels in colon cancer cells occurs early in the tumorigenic process, leading to its nuclear localization, not only in invasive adenocarcinoma, but also in colonic adenoma with mild dysplasia.

Adenocarcinoma↗
PubMed1998

GABA content and GAD activity in colon tumors taken from patients with colon cancer or from xenografted human colon cancer cells growing as s.c. tumors in athymic nu/nu mice.

A significantly high GABA level and GAD activity was found in human colon cancer tissue as compared with normal macroscopically unchanged human colon wall taken from the same patients. Similarly in athymic nu/nu mice transplanted with human colon adenocarcinoma cells established in in vitro culture (line CX-2) the high level of GABA accompanied by high GAD activity was found in subcutaneously growing tumors as compared with the unchanged colon wall and unchanged skin tissue from the same tumor bearing mice. Interestingly, the level of GAD activity in the macroscopically unchanged colon tissue of mice transplanted with tumor cells were increased in comparison with normal colon of healthy control mice. For the skin, only GAD activity was higher in the material coming from tumor bearing mice than in the material from normal control mice, whereas GABA level was even lower in the skin of tumor inoculated mice compared with control group. An increase in GABA level and in GAD activity can perhaps reflect a local immune response to the neoplastic process. The observed direction of GABA metabolism in tumor of the colon indicates a possibility to interfere in this process using the agonists of the GABA-ergic system.

Adenocarcinoma↗
PubMed1984

Chemical and histochemical studies of normal and diseased human gastrointestinal tract. I. A comparison between histologically normal colon, colonic tumours, ulcerative colitis and diverticular disease of the colon.

Chemical and histochemical methods were used to compare the epithelial glycoproteins from formalin-fixed surgical specimens of normal human large intestine, colonic tumours, ulcerative colitis and diverticular disease. All the epithelial glycoproteins contained fucose, galactose, glucosamine, galactosamine and, in addition, sialic acids both with and without O-acyl substituents in the side chain and/or at position C4. The glycoproteins of the normal ascending and descending colons differed significantly with respect to the percentage of the sialic acids released following digestion of the de-O-acylated glycoprotein with Vibrio cholera neuraminidase and to the molar fucose-sialic acid ratio. Statistical analysis of the chemical data showed that (a) compared to normal, the sialic acids of the tumour and ulcerative colitis glycoproteins from the descending colon were significantly less substituted in the side chain and at position C4; (b) the O-acetyl substitution pattern of the sialic acids of the ulcerative colitis glycoproteins from the ascending colon and the quantitative composition of the carbohydrate prosthetic groups of the ulcerative colitis glycoproteins from both ascending and descending colons differed from normal; (c) it was not always possible to distinguish between the ulcerative colitis and tumour glycoproteins on the basis of the O-acetyl substitution pattern of their sialic acids; and (d), there were minor differences between normal glycoproteins and those from cases of diverticular disease.

Colitis, Ulcerative↗
PubMed1981

Squamous cell carcinoma arising in a duplication of the colon: case report and literature review of squamous cell carcinoma of the colon and of malignancy complicating colonic duplication.

A case of squamous cell carcinoma arising in a duplication of the colon is reported, and the literature of squamous cell carcinoma of the colon and of malignancy complicating duplications of the colon is reviewed. This is the 23rd case of "pure" squamous cell carcinoma of the colon to be reported, and the second reported as arising in a duplication of the colon. Several possible mechanisms for the development of a squamous cell carcinoma in the colon are discussed.

Carcinoma, Squamous Cell↗
PubMed2000

Melatonin and colon carcinogenesis. III. Effect of melatonin on proliferative activity and apoptosis in colon mucosa and colon tumors induced by 1,2-dimethylhydrazine in rats.

Forty-eight two-month-old outbred female LIO rats were injected weekly with a single dose of 1,2-dimethylhydrazine (DMH; 21 mg/kg of body weight) administered s.c. for 15 consecutive weeks. From the day of the 1st injection of the carcinogen the part of rats were given five days a week during the night time (from 18.00 h to 08.00 h) melatonin dissolved in tap water, 20 mg/l. 10 rats were treated similarly with solvents and served as control. The experiment was terminated 6 months after the first injection of the carcinogen. Colon tumors (mainly adenocarcinomas) developed in a hundred percent of rats exposed both to DMH or to DMH plus melatonin. However, descending colon carcinomas were observed in 65 % of rats exposed to DMH plus melatonin against 100% in those exposed to DMH alone (p < 0.01). The multiplicity of colon tumors was also reduced in rats under the influence of melatonin. This effect is correlated with the significant inhibitory effect of the pineal hormone on mitotic index and with stimulating effect of melatonin on the relative number of apoptotic cells (TUNEL-method) in colon tumors. Long-term treatment with melatonin was followed also by the decrease in the area of lymphoid infiltrates in the colon mucosa of tumor-bearing rats.

1,2-Dimethylhydrazine↗
PubMed1979

Studies on the pathogenesis of swine dysentery. I. Characterization of the lesions in colons and colonic segments inoculated with pure cultures or colonic content containing Treponema hyodysenteriae.

Swine dysentery was induced in pigs and in ligated colonic segments by inoculation of pure cultures of, or colonic contents containing, Treponema hyodysenteriae. The mildest changes, best seen in ligated segments 48 or 72 hours after inoculation, were congestion and leucocytic margination in mucosal capillaries and depletion of mucigen from goblet cells lining the base of the crypts of Lieberkühn. Superficial mucosal necrosis and crypt cell hyperplasia were later changes. Perfusion studies with India ink did not demonstrate occlusive mucosal ischemia in acute swine dysentery. Mucosa with lesions of swine dysentery contained at least 10(5) colony forming units of T. hyodysenteriae per gram. Mucosa without lesions had 10(5) or fewer T. hyodysenteriae per gram. Segments with acute swine dysentery were distended with clear mucoid fluid with electrolyte composition indicative of net colonic secretion. No increase in the concentration of volatile fatty acids was detected in content from intact colons or colonic segments with lesions of acute swine dysentery.

Animals↗
PubMed1981

Colon epithelium. III. In vitro studies of colon carcinogenesis in Fischer 344 rats. N-methyl-N'-nitro-N-nitrosoguanidine-induced changes in colon epithelium in explant culture.

Colon explants from the inbred F344 rat descending colon pretreated in vivo with azoxymethane and maintained in explant culture were exposed to the carcinogen N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). One week after the MNNG treatment, the colon crypts showed marked crowding, hypercellularity, and stratification of cells. Nine weeks after the treatment, the explants showed epithelial papillary projections on the surface epithelium and within the crypts, in addition to hypercellularity and stratification. The control untreated explants maintained a single layer of epithelium during the entire culture period. Ultrastructurally, the treated cells showed an unusual concentration of free polysomes and thin and thick filaments, multiple and bizarre nucleoli, nuclear indentations and pseudoinclusions, and intracellular lumina. Sulfomucin was the predominant component in the control untreated explants as well as in the normal descending colons of rats and humans. One week after treatment the crypts of the carcinogen-treated explants showed an increase in sialomucin, and by 9 weeks after treatment, they showed mostly sialomucin. These features, compared and correlated with those of the parallel in vivo animal model as well as with human material, lend additional support to de novo histogenesis of colon carcinoma.

Animals↗
PubMed1995

Systemic and colonic venous plasma eicosanoid and endotoxin concentrations, and colonic venous serum tumor necrosis factor and interleukin-6 activities in horses during low-flow ischemia and reperfusion of the large colon.

Twenty-four horses were randomly allocated to 3 groups. Horses were anesthetized, subjected to a ventral midline celiotomy, and the large colon was exteriorized and instrumented. Group-1 horses served as sham-operated controls. Group-2 horses were subjected to 6 hours of low-flow colonic arterial ischemia, and group-3 horses were subjected to 3 hours of ischemia and 3 hours of reperfusion. Baseline (BL) samples were collected, then low-flow ischemia was induced by reducing ventral colonic arterial blood flow to 20% of BL. All horses were monitored for 6 hours after BL data were collected. Blood samples were collected from the colonic vein and main pulmonary artery (systemic venous [SV]) for measurement of plasma endotoxin, 6-keto prostaglandin F1 alpha (6-kPG), thromboxane B2 (TXB2), and prostaglandin E2 (PGE2) concentrations. Tumor necrosis factor and interleukin-6 activities were measured in colonic venous (CV) serum samples. Data were analyzed, using two-way ANOVA, and post-hoc comparisons were made, using Dunnett's and Tukey's tests. Statistical significance was set at P < 0.05. Endotoxin was not detected in CV or SV plasma at any time. There was no detectable tumor necrosis factor or interleukin-6 activity in CV samples at any time. There were no differences at BL among groups for CV or SV 6-kPG, PGE2, or TXB2 concentrations, nor were there any changes across time in group-1 horses.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1993

[Effects of intra-operative colonic irrigation on colonic flora in patients with intestinal obstruction caused by left colonic carcinomas].

We studied the effects of intra-operative colonic irrigation on intestinal bacteria in patients with carcinomatous obstruction of the left colon. The results showed: The floral volume of aerobes and anaerobes in colonic content and mucosa in obstructive patients increased significantly (P < 0.01), but it was reduced obviously by intra-operative colonic irrigation (P < 0.01), reaching the level of that as in the nonobstructive patients who received oral antibiotics and mechanical intestinal preparation.

Colon↗
PubMed1999

[Pancreatic and colonic simultaneous or successive resections of tumors in both organs, duodenum infiltrating colon carcinoma and pancreas tail carcinoma invading left colon. Report 10 cases].

Two patients with cancer of the right colon fistulized in duodenum underwent simultaneous right hemicolectomies and cephalic duodenopancreatectomies. There were no important post-operative complications and they are both alive eleven and ten years after surgery. In another case a piece of duodenum adherent to colon was resected and the duodenum was transversally sutured, segments IV and V of the liver were also resected because of a infiltration. The patient is well more than three years after surgery. Another similar patient who underwent resection of a part of the duodenum during a right hemicolectomy due to adenocarcinoma, developed the head of the pancreas ten months later which was resected by means of a cephalic duodenopancreatectomy. He survived the second operation for three years and a half and died with carcinomatosis. A fourth female patient who had been referred due to jaundice caused by cephalopancreatic cancer was reoperated two months later with resection of the tumor Seven months after duodenopancreatectomy she underwent another operation for resection of a bleeding cancer of the rectum by means of anterior resection. She survived for four and a half years. Cancers of body and tail of the pancreas sometimes invade the left colon and make necessary resection in the same operation. This happened in four other cases. In two of them it was necessary to resect stomach and the first jejunal loop. Respective survivals were of two years and nine months in two cases, others are 4111 alive more than two years after surgery. But the fourth case, who had an acinar carcinoma, died a month later with en hepatic metastasis which grew rapidly. The opposite happened to the tenth patient because colon cancer invaded pancreas and stomach, that were partially resected. The patient is alive two and a half years later.

Adult↗
PubMed1984

The effect of relative bowel rest on healing of colonic anastomoses. Breaking strength and collagen in the colonic wall following left colon resection and anastomosis in the rat.

The breaking strength of anastomoses in the left colon in the early phase of healing was studied in rats fed low residue diet (Biosorbin MCT) and the results were compared to those from rats fed standard laboratory diet. Further, eventual correlation between mechanical strength development and collagen content in the colonic wall around the anastomosis was evaluated. The anastomotic strength with sutures in place decreased by approximately 30% of the immediate postoperative value during the first two days in both groups of animals. There was no correlation between changes in anastomotic strength and collagen content at that time. After the second day there was a gradual increase of anastomotic strength, reaching the strength at day 0 after 7 days. The regain of strength was mainly due to collagen deposition in the anastomosis. Despite more collagen deposition in animals on standard laboratory diet the anastomoses had comparable strength development in the two groups. It was concluded that low residue diet does not impair the suture holding capacity or the anastomotic strength. Instead there was some evidence for a more uncomplicated healing when the bowel content was diminished.

Animals↗
PubMed1996

Molecular nature of colon tumors in hereditary nonpolyposis colon cancer, familial polyposis, and sporadic colon cancer.

BACKGROUND & AIMS: Microsatellite instability (replication error [RER]) is a characteristic of tumors in hereditary nonpolyposis colon cancer (HNPCC), but the mechanism of HNPCC carcinogenesis is not yet understood. To clarify the nature of HNPCC tumors, RER and genetic changes were compared between HNPCC and non-HNPCC tumors. METHODS: RER and genetic changes were analyzed in 21 HNPCC, 389 familial adenomatous polyposis, and 206 sporadic tumors using polymerase chain reaction, single-strand conformation polymorphism, sequencing, and Southern hybridization. RESULTS. in HNPCC, 95% tumors at all stages showed RER positivity (altered loci, 4.3 of 5). In familial adenomatous polyposis and sporadic tumors, RER positivity (1.7 of 5) was 3% in adenoma and intramucosal carcinoma, 13%-24% in invasive carcinoma, and 35% in carcinoma metastasized to liver. Fifty percent of RER-positive HNPCC tumors had both germline and somatic mutations of hMSH2 or hMLH1 gene, whereas 6% of RER-positive non-HNPCC had somatic mutation. APC, p53, and K-ras-2 mutations and loss of heterozygosity of tumor-suppressor genes were significantly less frequent (P = 0.03 to 0.0006) but transforming growth factor beta type II receptor mutation was significantly more frequent (P = 0.000001) in HNPCC than in non-HNPCC. CONCLUSIONS: RER positivity occurs from an early stage of carcinogenesis in HNPCC but in later stages in non-HNPCC. Most HNPCC tumors may develop through different genetic changes from those in the adenoma-carcinoma sequence, although a certain percentage develops through APC mutation.

Adaptor Proteins, Signal Transducing↗