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Query: UMLS:C0009402 (colorectal cancer)
 53,228 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

People at average risk for colorectal cancer (asymptomatic, age > or = 45 years, no risk factors) are offered fecal occult blood testing each year and sigmoidoscopy every five years. In case of a positive fecal occult blood test, examination of the whole colon by colonoscopy should be performed. Colorectal cancer risk is significantly lowered by endoscopic polypectomy in patients with adenomas. After complete removal of adenomatous polyps a control colonoscopy is advised three years after the initial examination. People with a positive family history of colorectal cancer or adenomatous polyps, of inherited polyposis syndromes, of a hereditary non-polyposis colorectal cancer, after polypectomy, after resection of colorectal cancer and with inflammatory bowel disease possess an increased risk for the development of colorectal cancer. Surveillance recommendations in these cases are detailed. In order to increase the cost-benefit ratio in surveillance after curative resection of colorectal cancer the frequency of the surveillance procedures can be reduced. In patients with total or extensive ulcerative colitis colonoscopy with multiple biopsies should be performed after a disease duration of eight to ten years, further recommendations depend on the histopathologic results.
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PMID:[Prevention and early detection of colorectal carcinoma by endoscopic examinations]. 965 8

Patients with ulcerative colitis have an increased risk for developing colon cancer compared to the general population. The risk is related to the extension of the disease and its duration. This risk is the same for Crohn's colitis patients of equal extension and duration. By chemoprevention we mean the use of specific natural or synthetic chemical agents to reverse, suppress or prevent progression to invasive cancer. The chemopreventive agents for colon cancer are either of natural origin (vitamins, minerals, food constituents) or synthetic chemicals (difluoromethyl ornithine) and pharmaceutical agents (aspirin, oltipraz). Apart from folate, no other agent has so far been used in vivo for the prevention of colon cancer in long-standing inflammatory bowel disease. The use of folate was, however, not primarily intended to prevent cancer but to enhance folate absorption in ulcerative colitis. From retrospective studies, within the framework of cancer surveillance programmes, it became evident that folate supplementation may play a positive role as a chemopreventive agent against colorectal cancer in patients with long-standing, extensive ulcerative colitis. There is also evidence suggesting that folate supplementation may contribute to regulation of rectal cell proliferation in ulcerative colitis patients. There is a real need for multicentre, randomized, prospective clinical studies in order to evaluate the promising role of folate in preventing colorectal cancer in patients with long-standing inflammatory bowel disease.
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PMID:Chemoprevention of colorectal cancer in inflammatory bowel disease? A potential role for folate. 978 43

The clinical course and prognosis of ulcerative colitis was studied in a group of 413 Greek patients. The study lasted for 16 years and follow-up was achieved in 95% of the patients. Both sexes were almost equally affected, mainly between the ages of 40-49. Most of the patients lived in cities and had high educational levels. Familial clustering for inflammatory bowel disease was found in 2.7% of the patients. In most of them the disease was confined to the rectosigmoid area or left bowel and was of mild to moderate severity. The disease course included exacerbations--mainly of mild to moderate severity--and remissions. Mortality was absent during first attack, and it was generally low at the completion of the study. Excluding deaths caused by colorectal cancer, most of the deaths were unrelated to the ulcerative colitis itself. Unusual combinations of ulcerative colitis with other diseases, including diseases of autoimmune origin, were noted. There were no differences between men and women in the various clinicoepidemiologic parameters or in the course of the disease. Surgery was performed in 16.7% of patients, whereas surgery at first attack was required in 0.5%. In comparison with the nonoperated group, patients who were operated on were significantly younger at the time of onset of symptoms and had significantly more extensive disease. Factors prognostic of severe attacks and colectomy were extensive disease, young age at onset, and severe recurrences. Evolution to cancer was observed in 1.45%, whereas extraintestinal cancers also appeared in 1.5%. At the completion of the follow-up period, 5.8% of the patients were dead, 16% had only one attack, 2.7% experienced continuous symptoms, whereas in 58.8% of them, the disease course included exacerbations and remissions. On the basis of the outcome of severe attacks and the more favorable short-term prognosis, it could be argued that ulcerative colitis in Greece runs a milder course compared with that of other developed countries in Western Europe and North America.
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PMID:Ulcerative colitis in Greece: clinicoepidemiological data, course, and prognostic factors in 413 consecutive patients. 980 46

The relation between inflammatory bowel disease (IBD) and colorectal cancer (CRC) is not clearly defined. Some investigators suggest that patients with extensive colitis have a genetic predisposition to CRC and that long-standing inflammation is not of primary importance in the promotion of cancer. We have assessed any increased risk of colon cancer in the relatives of IBD patients. We studied the prevalence of malignancy in the relatives of 251 IBD patients [198 ulcerative colitis (UC); 53 Crohn's disease of the colon (CDC)] and 251 orthopedic patients (ORTHO) as controls. In all patients (UC, CDC) as well as in controls (ORTHO) the prevalence of colon, extracolic digestive and extradigestive malignant tumors in the first-degree relatives was evaluated. We found no significant difference in the number of colorectal tumors or of tumors of any other kind in the diverse group of relatives of patients with IBD and ORTHO patients. Our data do not point to the existence of hereditary factors linking UC or CDC to CRC.
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PMID:Prevalence and relative risk of malignancy in relatives of inflammatory bowel disease patients and control subjects. 980 47

Circulating tumour cells play a central role in the metastatic process, but little is known about the relationship between this cellular subpopulation and the development of secondary disease. This study was aimed at assessing the presence of colonic cells in peripheral blood of patients with colorectal cancer in different evolutionary stages, by means of reverse transcriptase polymerase chain reaction (RT-PCR) targeted to carcinoembryonic antigen (CEA) mRNA. In vitro sensitivity was established in a recovery experiment by preparing serial colorectal cancer cell dilutions. Thereafter, 95 colorectal cancer patients and a control group including healthy subjects (n=11), patients with other gastrointestinal neoplasms (n=11) or inflammatory bowel disease (n=9) were analysed. Specific cDNA primers for CEA transcripts were used to apply RT-PCR to peripheral blood samples. Tumour cells were detected down to five cells per 10 ml blood, thus indicating a sensitivity limit of approximately one tumour cell per 10(7) white blood cells. CEA mRNA expression was detected in 39 out of 95 colorectal cancer patients (41.1%), there being a significant correlation with the presence of distant metastases at inclusion. None of the healthy volunteers and only 1 of 11 patients (9.1%) with other gastrointestinal neoplasms had detectable CEA mRNA in peripheral blood. By contrast, CEA mRNA was detected in five of the nine patients (55.6%) with inflammatory bowel disease. These results confirm that it is feasible to amplify CEA mRNA in the peripheral blood, its presence being almost certainly derived from circulating malignant cells in colorectal cancer patients. However, CEA mRNA detectable in blood of patients with inflammatory bowel disease suggests the presence of circulating non-neoplastic colonic epithelial cells.
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PMID:Detection of colonic cells in peripheral blood of colorectal cancer patients by means of reverse transcriptase and polymerase chain reaction. 982 81

The pleiotropic cytokine leukemia inhibitory factor (LIF) possesses proinflammatory properties in common with tumor necrosis factor (TNF-alpha), interleukine (IL) -1 and -6, such as the induction of acute phase protein synthesis. LIF may have chemotactic activity through the induction of IL-8 production. LIF is produced by normal and tumoral cells and appears to facilitate in vivo rat colon carcinoma cells growth. Inflammatory bowel diseases, ulcerative colitis (UC) in particular, are histologically characterized by the infiltration of the colonic mucosa with activated neutrophils, macrophages and lymphocytes. Cytokines with their inflammatory as well as their regulatory activities may play a role in the perpetuation and possibly the initiation of inflammation in this disease and its local and/or systemic complications. Moreover, colorectal cancer is a late well identified complication in patients with long standing inflammatory bowel disease, UC in particular. Taken together, these results suggest that LIF could be involved in tumorigenic and/or metastatic processes of colorectal cells in UC patients. The aims of the present study was to quantify and to compare the colonic and systemic productions of LIF in UC patients. We showed for the first time in patients with UC, a high local production of LIF well correlated with IL-8 production. We also analyzed the effect of LIF on a human colon carcinoma cell line HT29. We demonstrated that LIF stimulated HT29 cell growth in a dose dependent-manner. These results suggest that LIF may play a critical role in the susceptibility of colonic host cells to tumor growth in patients with UC.
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PMID:Leukemia inhibitory factor involvement in human ulcerative colitis and its potential role in malignant course. 988 4

Although ulcerative colitis and Crohn's disease are relatively uncommon disorders, most primary care practices include a number of individuals with these diagnoses. Much of the initial evaluation and long-term care of these patients is managed or coordinated by their primary care physicians. A familiarity with current principles of diagnosis and treatment is essential. Ulcerative colitis and Crohn's disease are related, immunologically mediated disorders of unknown cause. Both are characterized by chronic relapsing courses, frequent need for surgical intervention, and increased colorectal cancer risk. Significant differences are seen between these two inflammatory bowel disease syndromes, in their histopathologic features, clinical manifestations, and response to treatment. This review focuses on the colorectal manifestations of inflammatory bowel disease, emphasizing clinical presentation, approach to diagnosis, medical and surgical management, and long-term prognosis.
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PMID:Inflammatory bowel disease. 992 99

Collagenous colitis is a recently described form of chronic inflammatory bowel disease. Other inflammatory bowel disorders are associated with increased risk of colorectal and extracolonic malignancies, but this has not been evaluated in collagenous colitis. Colorectal and extracolonic malignancies were identified in 117 patients with collagenous colitis from the Johns Hopkins Registry. The incidence rates of identified tumors, overall incidence rate of tumors, and overall mortality were then compared with general population through person year analysis with adjustment for population. No cases of colorectal cancer were found in collagenous colitis patients during a mean follow-up period of 7.0 years (range 2-12 years) after the diagnosis of colitis. Two patients developed colorectal cancer prior to the diagnosis of colitis, but no increase in life-time relative risk of colorectal cancer was found (relative risk 0.52; 95% confidence limits 0.05-1.5). An increased relative risk of lung cancer in women (relative risk 3.7; 95% confidence limits 1.0-9.6; p = 0.048) was noted. The relative risk of overall malignancy and overall mortality was not different than the general population. In collagenous colitis patients the life-time relative risk of colorectal cancer and the relative risk after the diagnosis of colitis with a mean observation period of 7 years was not increased. An increase in relative risk of lung cancer in women with collagenous colitis argues for further investigation of the role of smoking and other factors in this disorder.
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PMID:Cancer risk in collagenous colitis. 1002 48

Colorectal carcinoma is a leading cause of death in the United States. Risk factors include genetic predisposition, diet, obesity, and inflammatory bowel disease. Early detection and chemoprevention can lead to a lower death rate. Future developments will include sensitive and specific large-scale screening.
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PMID:Colorectal carcinoma: etiology, diagnosis, and screening. 1020 Sep 6

Recent experimental and epidemiological evidence suggests that nonsteroidal anti-inflammatory drugs (NSAIDs) are effective in the prevention of colorectal cancer. However, the toxicity associated with the long-term use of most classical NSAIDs has limited their usefulness for the purpose of cancer chemoprevention. Inflammatory bowel disease (IBD) patients, in particular, are sensitive to the adverse side effects of NSAIDs, and these patients also have an increased risk for the development of intestinal cancer. 5-Aminosalicylic acid (5-ASA) is an anti-inflammatory drug commonly used in the treatment of IBD and may provide protection against the development of colorectal cancer in these patients. To directly evaluate the ability of 5-ASA to suppress intestinal tumors, we studied several formulations of 5-ASA (free acid, sulfasalazine, and Pentasa) at multiple oral dosage levels [500, 2400, 4800, and 9600 parts/million (ppm)] in the adenomatous polyposis coli (Apc) mouse model of multiple intestinal neoplasia (Min). Although the ApcMin mouse is not a model of colitis-associated neoplasia, it is, nonetheless, a useful model for assessing the ability of anti-inflammatory agents to prevent tumor formation in a genetically preinitiated population of cells. We used a study design in which drug was provided ad libitum through the diet beginning at the time of weaning (28 days of age) until 100 days of age. We included 200 ppm of piroxicam and 160 ppm of sulindac as positive controls, and the negative control was AIN-93G diet alone. Treatment with either piroxicam or sulindac produced statistically significant reductions in intestinal tumor multiplicity (95% and 83% reductions in tumor number, respectively; P < 0.001 versus controls). By contrast, none of the 5-ASA drug formulations or dosage levels produced consistent dose-progressive changes in polyp number, distribution, or size, despite high luminal and serum concentrations of 5-ASA and its primary metabolite N-acetyl-5-ASA. Thus, 5-ASA does not seem to possess direct chemosuppressive activity against the development of nascent intestinal adenomas in the ApcMin mouse. However, because intestinal tumor development in the ApcMin mouse is driven by a germline mutation in the Apc gene rather than by chronic inflammation, we caution that these findings do not definitively exclude the possibility that 5-ASA may exert a chemopreventive effect in human IBD patients.
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PMID:Evaluation of 5-aminosalicylic acid (5-ASA) for cancer chemoprevention: lack of efficacy against nascent adenomatous polyps in the Apc(Min) mouse. 1021 22


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