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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cumulative risk of developing colon cancer in patients with ulcerative colitis has been stated to increase 10%-20% for every decade of duration of disease after 10 yr. We reviewed the clinical course of 673 patients with inflammatory bowel disease restricted to the colon who were seen by the authors since 1955. A subset of 258 patients with a diagnosis of ulcerative colitis established before 1970 and followed by the authors was studied by both the classical life table and a generalized approach to estimate the risk of colorectal carcinoma. Only nine instances of colorectal carcinoma occurred. Using the former method and eliminating 3 patients referred with known colorectal carcinoma, the actuarial risk for developing this complication for all patients, regardless of extent of disease, was computed to be only 6.6% at 26 yr and 11.4% at 32 yr following the onset of ulcerative colitis. The cumulative probability of colorectal carcinoma among patients with universal colitis at 26 yr was 19.7% by the generalized method and 11.6% using the standard life table. The generalized approach consistently gave higher risk estimates due to a smaller number of patients in the denominator of the risk calculation. Using an alternative method, we calculated cancer risk from the date first seen for patients with universal extent and a history of greater than or equal to 10 yr of disease (means = 17.4 yr). The magnitude of the resulting colorectal carcinoma risk was even less than previously reported in hospitalized patients. This method is more suited for colorectal carcinoma risk assessment of a large series of ulcerative colitis patients seen in private practice and the results should modify the fear of cancer development in these patients.
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PMID:Assessment of colorectal cancer risk in patients with ulcerative colitis: experience from a private practice. 685 58

We isolated lymphocytes from the lamina propria of colon from 19 patients with inflammatory bowel disease, colon cancer, and certain benign conditions to determine: (1) if these lymphocytes could mediate mitogen-induced (MICC) and spontaneous cell-mediated cytotoxicity (SCMC), and (2) if there were any differences in cytotoxic effectiveness which could relate to the underlying disease. We found that lamina propria lymphocytes functioned well in MICC reactions with phytohaemagglutinin, but not concanavalin A as the inducing mitogen (specific lysis 28 5% vs 5 3%). Lamina propria lymphocytes did not mediate SCMC (specific lysis 0.3%). Neither the presence of inflammation not the underlying disease of the patient influenced the cytotoxic activity. Peripheral blood lymphocytes from normal subjects and patients performed well in MICC assay with both phytohaemagglutinin and concanvalin A as the inducing mitogen and were equally effective in SCMC reactions.
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PMID:Human colonic mononuclear cells: studies of cytotoxic function. 697 35

Two hundred and twenty seven patients had multiple follow-up total colonoscopies after initial endoscopic polypectomy. All adenomas were removed at the initial examination ('clean colon') in those patients who had no history of colon cancer, inflammatory bowel disease or polyposis coli; when re-endoscoped within one year 56% of them were found to have further adenomas. Nine percent had adenomas over 10 mm diameter which are presumed to have been missed during the index colonoscopy. Patients with single or multiple adenomas had an equal likelihood of being found to have further lesions on a one-year follow-up colonoscopy. With an apparent chance of missing a significant-size polyp at colonoscopy of at least 10% we recommend that all patients have a follow-up colonoscopy within one year after polypectomy. 133 Patients in whom no adenomas were found at the one year colonoscopy ('negative colonoscopy') were followed up. The incidence of new adenomas occurring within four years of 'negative colonoscopy' was 35% for those with a single adenoma at the index examination and twice as high for patients with multiple adenomas. If no polyp is found at one year, we recommend that interval follow-up colonoscopies should be performed every two years if more than one adenoma was removed during the initial examination, and every three years if only one was removed.
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PMID:Surveillance intervals after colonoscopic polypectomy. 707 64

The etiology and the pathogenesis of the chronic inflammatory bowel diseases known as Crohn's disease and ulcerative colitis have not been defined. Therefore, in this study the main emphasis was placed on description of the pathologic anatomy. Disturbed blood supply and vascular disorders have been discussed as etiopathogenetic factors. The results in the literature are frequently contradictory. For this reason, the vascular system of the colon in Crohn's disease and ulcerative colitis was systematically examined by means of various morphological methods in this study. Microvascular corrosion casting and translucent specimens were taken from operative specimens taken from 12 patients with Crohn's disease and 8 with ulcerative colitis. For comparison, tumor-free parts of 6 colon cancer specimens were examined. The evaluation was done by scanning electron- and/or stereoscopic microscopy. In the presence of chronic inflammatory bowel disease dilatation of the submucosal veins, caliber differences in the tunica muscularis and rarefaction of the penetrating blood vessels were found. In summary, an impairment of the blood flow in the tunica muscularis can be postulated. For the first time, the resulting venous stasis has been described, in contrast to the previously described disturbed arterial blood supply.
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PMID:[Angio-architecture of the colon in Crohn disease and ulcerative colitis. Light microscopy and scanning electron microscopy studies with reference to the morphology of the healthy large intestine]. 750 Jul 95

The clinical course of 37 patients who underwent 46 liver transplantations for primary (n = 33) and secondary (n = 4) sclerosing cholangitis was reviewed. The median follow-up was 37 months. The patient and graft survivals for patients with primary sclerosing cholangitis at 1, 2, and 5 years were 96.9%, 91.6%, 87.9%, and 83.1%, 74.2%, 65.2%, respectively. In the patients with primary sclerosing cholangitis (PSC), prior surgery except for simple cholecystectomy was associated with significantly greater operative time and blood loss. No cholangiocarcinoma was identified at the time of transplantation. Human leukocyte antigen typing for PSC patients was heavily weighed toward B8 (58.8%) compared with control (11.8%). Sixty-two percent of patients with PSC also had inflammatory bowel disease. Moderate or severe rejection requiring OKT3, "rescue therapy" with FK506, or retransplantation was relatively higher in patients with inflammatory bowel disease (70%) versus patients without inflammatory bowel disease (36.4%) and a matched control group (37.5%). Progressive inflammatory bowel disease was seen in 6 of 19 patients, with 3 developing cancer and a dysplasia. Two patients in the entire group died of sepsis and 3 of colon cancer (2 recurrent and 1 primary). These data demonstrate that excellent survival results can be achieved in this group of patients. Rejection is frequent and often severe and steroid refractory. Colon cancer represents the most frequent cause of death in PSC patients after liver transplantation and demands constant attention.
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PMID:Liver transplantation for sclerosing cholangitis. 763 12

Approximately 60% of sera from ulcerative colitis (UC) patients contains Igs reactive with neutrophil components, raising the question of the origin of these anti-neutrophil cytoplasmic Abs (ANCA). Our assertion that ANCA is a marker for a mucosal disease-related immune response predicts the existence of ANCA producing B cell clones in the lamina propria lymphocyte (LPL) fraction of UC patients. This hypothesis was tested by examining 12-day culture supernatants of LPL ANCA expression. LPL were isolated from surgically removed mucosa from patients with UC, Crohn's disease (CD), and diverticulitis. Normal mucosa was obtained from accident victims or normal margins of colon cancer resections. Supernatants were assayed by a fixed neutrophil ELISA. The ANCA staining pattern of supernatants expressing ANCA, as determined by ELISA, was assessed by indirect immunofluorescent staining of alcohol-fixed neutrophils. ANCA was found in 70% of culture supernatants from UC LPL fractions. In contrast, only approximately 11% of supernatants from CD and diverticulitis/normal (noninflammatory bowel disease (IBD)) LPL displayed ANCA binding. A perinuclear (pANCA) staining pattern was obtained with 70% of ANCA-expressing UC LPL supernatants, whereas ANCA-expressing CD and non-IBD LPL supernatants displayed a cytoplasmic reaction. PBL and mesenteric lymph node lymphocytes lacked spontaneous pANCA production, and pANCA production from PBL was not inducible. These findings indicate the existence of pANCA-producing B cell clones in mucosal lesions of UC patients and support our hypothesis that pANCA production is a consequence of a mucosal immune response specific to UC.
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PMID:Perinuclear anti-neutrophil cytoplasmic antibodies are spontaneously produced by mucosal B cells of ulcerative colitis patients. 767 39

Increased binding of the lectin peanut agglutinin is a common feature in epithelial malignancy and hyperplasia. This may have considerable functional importance in the intestine by allowing interaction between the epithelium and mitogenic lectins of dietary or microbial origin. Peanut agglutinin binds the disaccharide Thomsen-Friedenreich (TF, T or core 1) blood group antigen, Gal beta (1-3) GalNAc alpha-, but is not totally specific for this site. Consequently, there has been controversy about the presence of this structure in colon cancer; studies with anti-TF monoclonal antibodies have failed to detect it. We have examined the presence of TF antigen in colonic mucus glycoprotein (mucin) using endo-alpha-N-acetylgalactosaminidase (O-Glycanase), which specifically catalyzes the hydrolysis of TF antigen from glycoconjugates. Samples of adenocarcinoma, inflammatory bowel disease (ulcerative colitis), and normal mucin were treated with O-glycanase, the liberated disaccharide was separated from the glycoprotein and analyzed using dual CarboPac PA-100 column high performance anion-exchange chromatography coupled with pulsed amperometric detection. O-Glycanase treatment released increased amounts of TF antigen from both colonic adenocarcinoma (8.0 +/- 3.9 ng/micrograms protein, n = 11; P < 0.0001 ANOVA) and ulcerative colitis mucin (3.3 +/- 0.3 ng/micrograms protein, n = 5; P = 0.04) compared with mucin samples from histologically normal mucosa distant from carcinoma (1.5 +/- 1.1 ng/micrograms protein, n = 9). However, after mild acid treatment to remove sialic acids and fucose, releasable TF antigen was increased in all nine of these histologically normal mucin samples (5.5 +/- 2.6 ng/micrograms protein, P < 0.0002). We conclude that TF antigen is an oncofetal antigen which is expressed in colon cancer, but is concealed by further glycosylation (sialylation and/or fucosylation) in the normal colonic mucosa.
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PMID:Direct demonstration of increased expression of Thomsen-Friedenreich (TF) antigen in colonic adenocarcinoma and ulcerative colitis mucin and its concealment in normal mucin. 786 Jul 40

A link between inflammation of the colon in inflammatory bowel disease (IBD) and the increased risk of colon cancer in ulcerative colitis (UC) may be provided by growth factor receptor genes. Their expression may be altered in response to growth factors present in the mucosa, and this, in turn, may induce further genetic changes, linked to carcinogenesis, in the cells of the colonic epithelium. To test this hypothesis, we assayed steady-state levels of eight growth factor receptor mRNAs in colonic epithelial cells of IBD patients and controls. Four of these genes (EGF-R, IGFI-R, CSF1-R, and PDGF-R-beta) were expressed in epithelial cells, whereas four (erbB-2, erbB-3, NGF-R, and met) were not. The level of the former in involved or uninvolved IBD was considerably lower than in normal epithelial cells from either sporadic colon cancer or diverticulitis patients. In contrast, expression was much higher in IBD patients with colon tumors than in active chronic IBD. The level of PDGF-R-beta mRNA was two- to fourfold higher in involved than in uninvolved areas of the colons of two UC patients, but not in one Crohn's disease patient. Message abundance of its ligand, PDGF-beta, however, was the same in paired UC samples. The pattern of expression of PDGF-beta and cripto was identical to that of EGF-R, whereas the level of mRNA of amphiregulin was the same in active chronic IBD and IBD patients with tumors. A fourth growth factor, Kfgf, was not expressed. Increased levels of PDGF-R-beta mRNA in involved UC relative to uninvolved UC may be related to the disease process in UC. Decreased expression of growth factor- and growth factor receptor-encoded mRNA in active chronic IBD may be related to the disease process, or it may be an effect of steroid therapy undergone by these patients. Enhanced expression of these genes in IBD patients with tumors compared to those without tumors suggests that this may be a marker for development of colon cancer in IBD.
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PMID:Expression of growth factor receptor-encoded mRNA by colonic epithelial cells is altered in inflammatory bowel disease. 789 32

Inflammatory bowel disease, in particular ulcerative colitis, is characterized by localization of leukocytes in close proximity to the colonic epithelium, which may be mediated by the expression of intercellular adhesion molecules (ICAM-1; CD 54). We previously reported the presence of an organ-specific M(r) 40K colonic protein that acts as an autoantigen in ulcerative colitis and is present on the surface of colonic epithelial cells and also in DLD-1 colon cancer cells. Using the colon tumor cell line DLD-1 and flow cytometry, ICAM-1 antibody binding by untreated cultured DLD-1 cells was similar to background antibody binding (mean channel number, MCN = 9.77 +/- 2.13). Interferon-gamma (100 U) induced a 1-2 log increase in anti-ICAM-1 antibody binding from as early as 12 hr after exposure up to 72 hr and a moderate increase (up to about 100%) in the binding of anti-M(r) 40K antibody. Additional studies showed that anti-ICAM-1 and anti-M(r) 40K antibodies bound to DLD-1 cells regardless of the presence of the other antibody. Taken together, the present observations suggest that the epitopes of ICAM-1 and M(r) 40K molecules are coexpressed by colonic epithelial cells, regardless of the presence of the other molecule. Furthermore, lymphocytes in the colonic mucosa that are activated to produce interferon-gamma may upregulate the expression of both of these molecules.
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PMID:Amplified expression of intercellular adhesion molecule-1 (ICAM-1) and M(r) 40K protein by DLD-1 colon tumor cells by interferon-gamma. 809 38

The thickness of adherent mucus gel on the surface of colonic mucosa was measured in surgically resected specimens from 46 'control' patients most of whom had carcinoma of the colon; 12 were from right colon, 17 left colon, and 21 from rectum. In addition specimens were examined from 17 patients with ulcerative colitis and 15 patients with Crohn's disease. In controls a continuous layer of mucus was readily seen on specially prepared sections viewed by phase contrast illumination. Mean values for right and left colon and rectum were 107 (48), 134 (68), and 155 (54) microns respectively with a significant difference between right colon and rectum (p = 0.015). Values in ulcerative colitis showed greater variation and in those areas with acute inflammation mucosa was denuded of the mucus layer. In contrast, values for Crohn's disease were normal or greater than normal in thickness--right colon 190 (83) microns compared with 107 48 microns, p = 0.0093. A series of validation experiments are described for the method used to measure mucus thickness. The possible role of mucus in the pathogenesis of inflammatory bowel disease is discussed.
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PMID:Thickness of adherent mucus gel on colonic mucosa in humans and its relevance to colitis. 815 Mar 46


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