Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Delayed neutrophil apoptosis is a feature of persistent acute inflammation. Neutrophil-mediated damage has been shown to be associated with the development of inflammatory bowel disease (IBD). Persistence of these cells both at the colonic site and circulation may further contribute to IBD. The aims of this study were to determine whether neutrophils isolated from IBD patients delay apoptosis and to investigate possible mechanisms involved in this delay. We studied 20 patients with IBD, 13 with Crohn's disease, and 7 with ulcerative colitis, all of whom were undergoing intestinal resection for symptomatic disease. Seventeen patients undergoing elective resection of colon cancer acted as operative controls. Systemic, mesenteric arterial, and mesenteric venous blood was harvested. Neutrophils isolated from patients with IBD showed decreased spontaneous apoptosis compared to cancer patients. Mesenteric venous serum of IBD patients contributed to this delay, which contained higher concentrations of interleukin-8 (IL-8). Pro-caspase 3 expression was also reduced in IBD neutrophils, which may contribute to decreased spontaneous and Fas antibody-induced apoptosis. Neutrophil apoptosis may be altered in Crohn's disease and ulcerative colitis through release of anti-apoptotic cytokines and altered caspase expression. The alterations in cell death mechanisms may lead to persistence of the inflammatory response associated with IBD.
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PMID:Neutrophil apoptosis is delayed in patients with inflammatory bowel disease. 1080 10

This is a review of some of the most important growing points in the specialties of gastroenterology and hepatology. It does not aim to be completely comprehensive but to pick out major areas of importance to examination candidates and doctors without special experience in the field. Topics covered include: upper gastrointestinal haemorrhage; Barrett's oesophagus; carcinoma of the oesophagus; achalasia; Helicobacter pylori; duodenal ulcer prevention; coeliac disease; dermatitis herpetiformis; Crohn's disease; small bowel overgrowth; ulcerative colitis; carcinoma of the large bowel; obesity; endoscope sterilisation; gall stones; liver transplantation; autoimmune liver disease; viral hepatitis; metabolic liver diseases; and pancreatic insufficiency.
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PMID:Advances in gastroenterology and hepatology. 1082 44

The first case of cancer in inflammatory bowel disease (IBD) was reported at The Mount Sinai Hospital in 1925 in a patient with ulcerative colitis (UC). In 1956, carcinoma of the jejunum was described in a patient with regional enteritis (Crohn's disease [CD]). IBD cancers are preceded by dysplasia, and the relative risk increases with duration of the IBD. CD cancers are more proximally distributed than are UC cancers. Both tend to occur at the site of the overt disease and both develop at earlier ages (47 UC, 50 CD) than in the de novo colorectal cancer (70 years). The absolute cumulative colon cancer frequencies (8% UC, 7% CD) are identical after 20 years, emphasizing the importance of regular surveillance in both types of IBD. Moreover, the increased risk of colon cancer exists in patients with CD even when CD is confined to the small bowel, and patients with IBD have increased risks of developing extraintestinal and reticuloendothelial tumors in both CD and UC, as well as ano-vulval and malignant melanoma in CD. Colitic colorectal cancers are often diffuse, extensive, multiple and right-sided with insidious presentation. The prognosis is no worse after operation than that of de novo colon cancer. Most small bowel cancers in CD are adenocarcinomas, rather than sarcomas, and present at a younger age, more diffusely and more distally than de novo cancers, usually making them undiagnosable at a curable early stage; indeed, two-thirds present with intestinal obstruction. Strictures of the colon are common in patients with IBD, and they have a 10-fold risk for colon cancer, 30-fold for UC, and 6-fold for CD. The risk increases with disease duration. The indications for surgery are absolute, relative and incidental, and the procedures include segmental resection, total proctocolectomy, subtotal colectomy and palliative procedures.
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PMID:Cancer in inflammatory bowel disease. 1082 8

The human GNAI2 gene coding for G protein, Galphai2, is located on chromosome 3p21 in proximity to the region where an inflammatory bowel disease (IBD) locus has been suggested. Galphai2-deficient mice develop a lethal diffuse colitis that resembles human ulcerative colitis (UC) and frequently progresses to colon adenocarcinoma. Furthermore, the human GNAI2 gene is subject to point mutations at certain positions, including three at codon 179, all of which have been reported in human endocrine tumors. In order to evaluate the possible involvement of this gene in IBD pathogenesis, we have examined GNAI2 codon 179 sequences in 28 familial IBD patients, including 13 UC, 15 Crohn's disease (CD), and 7 patients with colon cancer/dysplasia, from 12 multiplex IBD families. The wildtype codon 179, CGC for arginine, plus the first G of the codon 180 engender a sequence recognizable by the enzyme BstUI. Mutations, therefore, can result in the abrogation of BstUI digestion of polymerase chain reaction (PCR) products containing the codon 179. Using the PCR-restriction fragment length polymorphism technique, all 28 IBD patients, including those with colon cancer, and 14 non-IBD family members show a BstUI-cleavable PCR-banding pattern indicating the presence of wildtype codon 179. We conclude that, in the familial IBD and colon cancer/dysplasia patients studied, there is no detectable mutation in the codon 179 of the GNAI2 gene.
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PMID:Absence of GNAI2 codon 179 oncogene mutations in inflammatory bowel disease. 1083 69

Increased cytoplasmic beta-catenin levels and the associated nuclear beta-catenin/T-cell factor (Tcf)-lymphoid enhancer factor (LEF) complex formation have been frequently found in colon cancer. In this context, overproduction of nitric oxide (NO) attributable to inflammatory stimuli in diseases such as ulcerative colitis and Crohn's disease may-contribute to colonic carcinogenesis. Therefore, we examined the modulation by NO of cytoplasmic beta-catenin levels and the formation of the nuclear beta-catenin/LEF-1 DNA binding complex in conditionally immortalized mouse colonic epithelial cells that differed in adenomatous polyposis coli (Apc) genotype, namely young adult mouse colon (YAMC; Apc+/+) and immortal mouse colon epithelium (IMCE; ApcMin/+). Unlike most colon cancer cell lines, this pair of cell lines has either nondetectable or low basal level of beta-catenin when they are cultured under nonpermissive and nonproliferative conditions. Using electrophoretic mobility shift assays, we found that NO-releasing agents (E)-methyl-2-[(E)-hydroxyimino]-5-nitro-6-methoxy-3-hexeneamide and S-nitroso-N-acetylpenicillamine greatly enhanced the formation of beta-catenin/LEF-1 DNA binding complex in a concentration- and time-dependent fashion in YAMC and IMCE cells. Significantly, IMCE cells showed a markedly greater amount of nuclear beta-catenin/LEF-1 DNA binding complex in response to NO. Super shift by anti-beta-catenin antibody confirmed the presence of beta-catenin in the complex. Western blot analysis of the soluble cytoplasmic fractions demonstrated that these NO donors caused differential accumulation of cytoplasmic beta-catenin in YAMC and IMCE. In conclusion, this study indicates that the defective beta-catenin degradation machinery attributable to ApcMin/+ mutation in IMCE cells not only affects basal levels but also contributes to NO-induced dysregulation of cytoplasmic beta-catenin and nuclear beta-catenin/LEF-1 DNA binding complex formation.
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PMID:Differential formation of beta-catenin/lymphoid enhancer factor-1 DNA binding complex induced by nitric oxide in mouse colonic epithelial cells differing in adenomatous polyposis coli (Apc) genotype. 1091 42

It is well known that patients with long-standing inflammatory bowel disease (IBD), ulcerative colitis (UC) or Crohn's disease(CD) are at increased risk for developing colorectal cancer (CC). Before adenocarcinoma develops, the intestinal epithelium progress through a premalignant phase of dysplasia, which can be identified via mucosal biopsy and routine tissue histology. Surveillance colonoscopy and prophylactic colectomy for dysplasia or asymptomatic cancer is advised as a method of reducing cancer-related mortality. Many physicians suggests that surveillance for extensive colitis should begin after 8 to 10 years of disease, and surveillance for left-sided colitis should begin after 15-20 years. Colonoscopy is recommended with frequent biopsies, at least every 10 cm in all four quadrants, and with biopsy of any suspicious lesion. The emerging field of colon cancer genetics has identified several important tumor markers that have potential to improve sensitivity for detection of early neoplasia.
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PMID:[Premalignant and malignant changes in idiopathic inflammatory bowel disease]. 1095 65

Since January 1995, Valtrac biofragmentary ring for compressive anastomosis of the colon has been employed in Croatia. This study comprises experience in four Croatian hospitals in which 244 anastomoses of the colon with Valtrac biofragmentary ring were performed in the four-year period (1995-1998). The average age of the patients was 64.7 years. One hundred and eighty-seven of them (76.64%) were operated for colon cancer, 15 (6.1%) for Crohn's disease, eight (3.3%) for rectal cancer, and 34 for other diseases. One hundred and nineteen anastomoses were made between small intestine and colon, and 125 end-to-end of the colon. Valtrac BAR 28 mm in diameter was most frequently used (41.8%), and 34 mm in diameter least often (8.6%). Sixteen patients had complications related to anastomosis. One had obstruction which required repeated surgery, and 15 (6.15%) dehiscence of the anastomosis, of which 12 were reoperated. In the postoperative course six patients (2.46%) died due to the sequelae of dehiscence. Compressive anastomoses with Valtrac biofragmentary ring should be considered equal to manual and stapler methods when choosing the technique of colon anastomosis.
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PMID:[Anastomosis of the colon using the Valtrac biofragmentable ring]. 1104 May 36

SPARC is a glycoprotein of the extracellular matrix that exhibits a number of biological functions such as disruption of cell adhesion and modulation of matrix metalloprotease expression. These properties, in concert with the expression of the molecule during development, repair, and neoplastic progression, suggest that SPARC has an important role in remodeling in a variety of tissues. However, the role of SPARC in the intestine is unclear since the development expression and tissular origin of SPARC in this organ appears to be species-dependent. As a first step to investigate the function of SPARC in the tissues of the intestine, we have analyzed its expression at the protein and mRNA levels in the human fetal and adult small intestinal and colonic mucosa as well as in intestinal cell models. Our results show that SPARC expression is differentially regulated during development and along the length of the human intestine. In the colon, SPARC was predominantly found at the epithelial-mesenchymal interface at the fetal stage, below detection levels in the normal adult, but re-expressed in the stroma of colonic tumors. In the small intestine, low levels of SPARC expression were observed at an early stage of morphogenesis (between 9 and 11 weeks) but expression was not detected at subsequent developmental stages nor was it induced in the mucosa of Crohn's disease. While SPARC appeared to be produced mainly by mesenchymal and stromal cells in the intact intestine it was not detected in colon cancer cells. Taken together, these results indicate that SPARC is subject to an onco-fetal pattern of expression in the stroma of the colonic mucosa while its expression is much more restricted in the small intestine, suggesting a differential involvement of this molecule in the extracellular matrix remodeling occurring along the length of the developing and diseased human intestinal mucosa.
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PMID:Expression of SPARC/osteonectin/BM4O in the human gut: predominance in the stroma of the remodeling distal intestine. 1125 29

Colorectal carcinoma rarely affects children and has a dismal prognosis with 5-year survival rates as low as 2.5%-7% despite apparently radical surgery. Here we report the case of an adenocarcinoma of the sigmoid colon in a 15-year-old girl preceded by uncertain abdominal complaints of 5 years' duration. Pathological work-up revealed a tumour with lymph node metastases (pT3NI). Immunohistochemical evidence of p53 overexpression by the tumour cells raised the suspicion of an underlying Li-Fraumeni syndrome. In addition, there were aphthoid ulceration, fissuration of the non-tumorous mucosa, along with a mixed transmural infiltrate composed of macrophages, eosinophils, and non-typical giant cells, which were compatible with simultaneous Crohn's disease. Anamnestic data concerning the occurrence of idiopathic inflammatory bowel disease or colorectal carcinoma in the patient's relatives were non-contributory. The present results suggest a possible relationship between Crohn's disease and colon cancer due to the defective p53 gene product.
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PMID:Adenocarcinoma of the colon developing on the basis of Crohn's disease in childhood. 1127 78

The most common form of hereditary CRC is hereditary non-polyposis colorectal cancer (HNPCC), several mutator genes have been identified in this syndrome. The molecular genetic discoveries are providing news insights into the pathogenesis of CRC. The CRC in Lynch syndrome shows microsatellite instability and it also shows a special histology now referred to as an undifferentiated medullary or solid cribriform carcinoma. This histology is uncommon in various populations. In addition CRC in HNPCC shows an excess of mucoid features as well as peritumoral lymphocyte infiltration and Crohn-like reaction. It is very important to make a diagnosis based on the natural history features of a particular cancer syndrome in combination with a well orchestrated family history. We report the case of a 44 year old man with colon cancer and adenomatous polyps, without family history of adenomatous polyps but with familial antecedent of colon cancer in his father, with a suspicion of Lynch syndrome.
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PMID:[Hereditary familial non polypoid colorectal cancer]. 1137 Jan 76


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