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)

Interleukin-8 (IL-8) is a potent cytokine for recruitment and activation of neutrophils. To visualize its distribution in the intestinal mucosa and to understand better its possible role in the induction and promotion of inflammatory bowel disease, expression of the IL-8 gene was analyzed in resected bowel segments of 14 patients with active Crohn's disease or ulcerative colitis. In situ hybridization with IL-8 anti-sense RNA probes revealed strong and specific signals in the histologically affected mucosa. The number of cells expressing IL-8 gene correlated with the histological grade of active inflammation. In accordance with the characteristic histological signs of active disease, IL-8-expressing cells were diffusely distributed over the entire affected mucosa in patients with ulcerative colitis, whereas in patients with Crohn's disease, IL-8-expressing cells showed a focal distribution pattern. Cells expressing IL-8 were mainly located at the base of ulcers, in inflammatory exudates on mucosal surfaces, in crypt abscesses, and at the border of fistulae. Analysis of semi-serial sections pointed to macrophages, neutrophils, and epithelial cells as possible sources of this cytokine in active inflammatory bowel disease. We consistently failed to detect IL-8 messenger RNA in the mucosa of uninvolved bowel segments and in normal-appearing control mucosa of patients with colon cancer. In contrast, tissue specimens from two patients with acute appendicitis displayed IL-8-expressing cells in the mucosa. These results support the notion that IL-8 plays and important but nonspecific role in the pathogenesis of inflammatory bowel disease and that the production of IL-8 messenger RNA is restricted to areas with histological signs of inflammatory activity and mucosal destruction.
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PMID:Expression of interleukin-8 gene in inflammatory bowel disease is related to the histological grade of active inflammation. 817 48

Chronic diarrhea is defined as the passage of more than 200 g of stool per day for more than three weeks. This condition may result from decreased absorption of gastrointestinal contents or increased fluid secretion into the bowel. Although chronic diarrhea can have many etiologies, irritable bowel syndrome, lactose intolerance, dietary factors, inflammatory bowel disease and colon cancer are the causes most frequently encountered in primary care practice. An orderly work-up, beginning with a complete history an a thorough physical examination, is essential. Whenever possible, treatment should be directed at the underlying cause of the diarrheal condition. If the diarrhea persists and the etiology remains obscure, administration of opiates or bile-sequestering agents often is helpful in alleviating symptoms. New approaches to decreasing secretions, such as the use of clonidine therapy, are being studied.
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PMID:Chronic diarrhea: evaluation and treatment. 824 77

Intestinal involvement of endometriosis requiring treatment is 5%, but only 0.7% needs intestinal resection. The authors report two cases of colic endometriosis and illustrate problems in diagnosis and management of this disease. Usually intestinal endometriosis takes the form of asymptomatic superficial serosal implants, encountered incidentally at laparotomy for other diseases, but it can also result in obstruction and occasionally bleeding. Any premenopausal woman with episodic bowel symptoms associated with gynecologic complaints should be suspected of endometriosis of the colon. Diagnosis can be suspected by double-contrast enema examination and colonoscopy with biopsy, although neither is likely to establish the diagnosis with certainty. In fact there are no radiologic or diagnostic imaging findings that are specific for endometriosis and unequivocal diagnosis requires microscopic examination. Differential diagnosis includes primary carcinoma of the colon and other benign diseases (pelvic inflammatory disease, diverticulitis, inflammatory bowel disease, pelvic abscess, polyps, etc.). The treatment of patients with uncomplicated, but symptomatic gastrointestinal endometriosis depends on the age of the patient and her childbearing attitude. Resection of the affected bowel should be done in patient with pain, bleeding, changes in bowel habits and intestinal obstruction and it is necessary to avoid neglecting a malignant tumor. Total abdominal hysterectomy and bilateral oophorectomy is the treatment of choice in the perimenopausal and menopausal women. In symptomatic women desiring children the only resection of involved colon may be appropriate treatment. In these subjects hormonal therapy can be useful.
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PMID:[Endometriosis of the large intestine. A report of 2 clinical cases]. 825 7

Protooncogenes are cell cycle-related genes that are involved in cell growth of proliferation. Alterations in the level of expression of these genes, or expression of aberrant gene productions, have been observed in tumors and precancerous conditions. To determine if expression of these genes is altered in patients with inflammatory bowel disease (IBD) --who are at risk for development of colon cancer--we assayed transcripts of 15 protooncogenes in colonic epithelial cells of IBD patients and controls. Nine of these genes (H-ras, c-myc, c-fos, c-jun, junB, N-myc, c-abl, c-yes, and p53) were expressed in epithelial cells, whereas two (RB1 and N-ras) were not. expression of four other genes (c-src, K-ras, c-raf, and c-myb) was observed, but the intensity of these bands was too low for densitometric analysis. The steady-state levels of transcripts of H-ras and five nuclear protooncogenes (c-myc, c-fos, c-jun, junB, and N-myc) were lower in epithelial cells from involved or uninvolved IBD samples than in normal epithelial cells from either sporadic colon cancer or diverticulitis patients. The level of c-fos mRNA was two- to threefold higher in involved than in uninvolved areas of the colons of two ulcerative colitis (UC) patients, but not in one Crohn's disease (CD) patient. Message abundance of c-abl transcripts was two- to threefold lower in UC epithelial cells than in either the CD or control samples. The steady-state level of c-yes-encoded mRNA was considerably higher in IBD patients resected for colon cancer than in patients resected for active chronic IBD or in controls. The level of p53 message was constant in these samples. Increased levels of c-fos mRNA in involved UC relative to uninvolved UC may be related to the disease process. Decreased expression of c-abl transcript in UC may be a diagnostic marker for UC and may be related to the rate of cell turnover in these diseases. Enhanced expression of c-yes in IBD patients with tumors compared to active chronic IBD and controls suggests that expression of this gene may be a marker for development of colon cancer in IBD.
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PMID:Expression of protooncogene-encoded mRNA by colonic epithelial cells in inflammatory bowel disease. 867 85

Peripheral blood monocytes are recruited to the inflamed mucosa of inflammatory bowel disease but the specific chemotactic signals responsible for their attraction are not known. Monocyte chemoattractant protein-1 (MCP-1) is a chemokine with potent monocyte attracting and activating properties and the aim of this study was to examine its expression and production in inflammatory bowel disease. In situ hybridization demonstrated mRNA for MCP-1 in macrophages, some of which had been recently recruited from the circulation as demonstrated by their co-expression of the monocyte marker CD 14, as well as in smooth muscle and endothelial cells in inflamed mucosa. Immunohistochemical studies showed a corresponding distribution of MCP-1 protein production by macrophages, smooth muscle, and endothelial cells. By contrast minimal MCP-1 mRNA expression and protein were found in histologically normal mucosa. Macrophages isolated from surgically resected inflammatory bowel disease colons and examined by Northern analysis expressed MCP-1 mRNA significantly more frequently (15/24 vs. 0/19, P< 0.0001) than macrophages from histologically normal mucosa from colon cancer resections. Blood monocytes stimulated by lipopolysaccharide and treated with hydrocortisone, 5-aminosalicylic acid, or cyclosporin A showed reduced MCP-1 expression and production in the presence of these agents. This study demonstrates increased expression of MCP-1 mRNA and protein and cells of origin of MCP-1 in inflamed intestinal mucosa. Together with the demonstrated influence of therapeutic agents on monocyte MCP-1 production the findings suggest a role for MCP-1 in monocyte attraction to the mucosal lesion of inflammatory bowel disease.
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PMID:Enhanced expression and production of monocyte chemoattractant protein-1 in inflammatory bowel disease mucosa. 869 Oct 64

Renewal of the gastrointestinal (GI) epithelium fulfills the normal functions of maintaining the integrity of the mucosa, repairing mucosal injury, and replenishing the specialized cells of the epithelium. Alterations in epithelial renewal also are intimately involved in transformation of the epithelium to benign and malignant neoplasms. Certain abnormalities in epithelial proliferation, including an increase in the rate of proliferation and expansion of proliferating cells beyond the normal zone of proliferation, are closely linked to the predisposition for and frank development of GI cancer. These abnormalities are common to all human premalignant conditions studied, including Barrett's epithelium, chronic gastritis, inflammatory bowel disease, and colon polyps; they also occur in experimental carcinogenesis. The same proliferative abnormalities have also been observed in some relatives of patients with colon neoplasms who themselves do not have any colon polyps or cancer. Several agents, including calcium, vitamins A, C, and E, and omega-3 fatty acids, have been shown to reverse the abnormal proliferation under some laboratory and clinical conditions. Moreover, some nonsteroidal anti-inflammatory drugs appear to decrease the size of colon polyps in familial polyposis and to reduce the risk for colon cancer in the general population. We await further clinical trials that will indicate whether such ordinary supplements as calcium, vitamins, fish oil, or aspirin have a role in the treatment of patients with premalignant conditions of the gastrointestinal tract.
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PMID:A review of gastrointestinal epithelial renewal and its relevance to the development of adenocarcinomas of the gastrointestinal tract. 877 83

The cotton top tamarin is a unique model of human ulcerative colitis. This disease is clinically and histologically similar. It is also complicated in some cases by colon cancer. The cotton top tamarin provides an appropriate animal model for assessing new treatments in inflammatory bowel disease.
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PMID:Cytokines in the cotton top tamarin model of human ulcerative colitis. 889

Ursodeoxycholate (UDCA) has anti-inflammatory and chemoprotective effects in animal models of inflammatory bowel disease and colon cancer. Because overproduction of nitric oxide (NO) by the inducible isoform of NO synthase (iNOS) is implicated in the pathogenesis of these conditions, we investigated the ability of UDCA to inhibit NO production in transformed human intestinal epithelial (DLD-1) cells. Nitrite/nitrate production was measured by the Griess reaction, enzymatic activity of iNOS was assessed by conversion of L-arginine to L-citrulline, and protein and mRNA were measured by Western and Northern blotting. Dose-dependent inhibition of interleukin-1 beta- and interferon-gamma-stimulated nitrite/nitrate production was observed when cells were preincubated for 6 h with UDCA (0-800 microM), and a substantial inhibition (81 +/- 3.2%) was seen at 500 microM. In cytokine-stimulated cells, UDCA reduced iNOS mRNA, protein, and enzyme activity without exerting cytotoxicity. UDCA had a minimal direct inhibitory effect on iNOS enzyme activity. UDCA pretreatment also reduced the expression of iNOS in the colonic epithelium of rats treated with bacterial lipopolysaccharide. Thus UDCA inhibits the induction of epithelial iNOS in vitro and in vivo, and this effect may contribute to the anti-inflammatory and chemoprotective actions of UDCA.
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PMID:Ursodeoxycholate inhibits induction of NOS in human intestinal epithelial cells and in vivo. 925 19

Colon cancer occurring in patients with Lynch Syndrome and in Inflammatory Bowel Disease (IBD) share many features. There is some evidence to support the assumption that multiple genetic factors play an important role in the pathogenesis of idiopathic IBD and Lynch Syndrome. In our previous study, providing detailed medical, genetic and pathologic findings on 202 hereditary non polyposis colorectal cancer (HNPCC) relatives we found in the colonic mucosa features indicating an IBD though all the screened subjects of the family denied symptoms of IBD. Some studies have reported that the rate of undetected IBD ranges from 27 to 38%. Finally, a member of this family, considered not at risk for cancer by genetic analysis results, developed a clinically manifested IBD. The morphological aspects of the disease were not discussed in our previous study. It is possible that many members of this family inherit a major gene giving liability to the disease and are carriers of a subclinical form of IBD with a minimal morphological marker which becomes manifest in some members when other factors intervene. A possible genetic model linking the two diseases can be suggested: IBD needs two major genes for susceptibility (s) and clinical development (D). Both can be present in IBD and Lynch Syndrome, but in the latter a third gene plays a suppressor role on the development gene (D). In conclusion, we hypothesize that the IBD developing gene may be considered as protective against HNPCC, and this condition may result in a selective genetic advantage.
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PMID:HNPCC-Lynch syndrome and idiopathic inflammatory bowel disease. A hypothesis on sharing of genes. 925 95

With the objective of exploring the association between breakfast and minor anal complaints, an age, sex and pregnancy matched case-control study was carried out in the out-patient clinics at Birmingham Heartlands Hospital. Patients were selected after personal interviews using a structured questionnaire in out-patient clinics. Information on age, sex, occupation and breakfast habits, as well as on haemorrhoids and anal fissure, was obtained. Patients who had haemorrhoids or anal fissure were placed in the case group; the remainder were controls. Any patient with diverticulosis, inflammatory bowel disease, colon cancer or bowel resection for any reason was excluded from the study. The main outcome measures were the odds of developing haemorrhoids or fissure in patients who did not eat breakfast. The results are based on 47 cases that were age, sex and pregnancy matched. Of the case group, 36% did not eat breakfast, compared with 11% in the control group. The analysis demonstrated a 7.5-fold increase in the odds of suffering from haemorrhoids or anal fissures in matched subjects who did not eat breakfast, with a very high level of significance (P = 0.0036). This indicates that there is a very strong association between failure to eat breakfast and haemorrhoids or anal fissure. It is anticipated that educating the public to eat breakfast would lead to a long-term fall in the incidence of anal complaints, in the attendant morbidity for the patients and in the cost to the health service.
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PMID:The effect of breakfast on minor anal complaints: a matched case-control study. 935 68


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