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

The gastrointestinal tract (GIT) is a major source of extrapineal melatonin. In some animals, tissue concentrations of melatonin in the GIT surpass blood levels by 10-100 times and the digestive tract contributes significantly to melatonin concentrations in the peripheral blood, particularly during the day. Some melatonin found in the GIT may originate from the pineal gland, as the organs of the digestive system contain binding sites, which in some species exhibit circadian variation. Unlike the production of pineal melatonin, which is under the photoperiodic control, release of GI melatonin seems to be related to periodicity of food intake. Melatonin and melatonin binding sites were localized in all GI tissues of mammalian and avian embryos. Postnatally, melatonin was localized in the GIT of newborn mice and rats. Phylogenetically, melatonin and melatonin binding sites were detected in GIT of numerous mammals, birds and lower vertebrates. Melatonin is probably produced in the serotonin-rich enterochromaffin cells (EC) of the GI mucosa and can be released into the portal vein postprandially. In addition, melatonin can act as an autocrine or a paracrine hormone affecting the function of GI epithelium, lymphatic tissues of the immune system and the smooth muscles of the digestive tube. Finally, melatonin may act as a luminal hormone, synchronizing the sequential digestive processes. Higher peripheral and tissue levels of melatonin were observed not only after food intake but also after a long-term food deprivation. Such melatonin release may have a direct effect on the various GI tissues but may also act indirectly via the CNS; such action might be mediated by sympathetic or parasympathetic nerves. Melatonin can protect GI mucosa from ulceration by its antioxidant action, stimulation of the immune system and by fostering microcirculation and epithelial regeneration. Melatonin may reduce the secretion of pepsin and the hydrochloric acid and influence the activity of the myoelectric complexes of the gut via its action in the CNS. Tissue or blood levels of melatonin may serve as a marker of GI lesions or tumors. Clinically, melatonin has a potential for a prevention or treatment of colorectal cancer, ulcerative colitis, irritable bowel syndrome, children colic and diarrhea.
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PMID:Localization, physiological significance and possible clinical implication of gastrointestinal melatonin. 1172 Oct 91

Ulcerative colitis and colonic Crohn's disease (together known as inflammatory bowel disease or IBD) are both associated with increased risk for colorectal cancer. Although it is customary to emphasize differences in the biology of IBD-associated and sporadic colon cancer, we believe these are far outweighed by the similarities. These similarities suggest that they might have similar pathogenic mechanisms. Because the normal colon is arguably in a continual state of low-grade inflammation in response to its microbial flora, it is reasonable to speculate that both IBD-associated and sporadic colon cancer might be the consequence of bacteria-induced inflammation.
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PMID:Inflammation and colorectal cancer: IBD-associated and sporadic cancer compared. 1179 61

The definition of 'irritable bowel syndrome' (IBS) as given by the Dutch College of General Practitioners' standard may be too broad to define IBS. Coeliac disease should be added to the differential diagnosis of IBS. Attention should be given to subjects with an increased familial risk of colorectal cancer. Based on the results of thorough investigations, the role of disturbed motility, visceral hyperalgesia, modified cerebrovisceral perception, induction by infectious diseases and contributing psychological factors should be recognised as pathophysiologically relevant for IBS. When treating patients, making a positive diagnosis of IBS, explaining possible pathophysiological factors and exploring contributing factors is much more important than simply giving reassurance. Medical therapy is of limited value, but may relieve symptoms in selected patients.
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PMID:[The Dutch College of General Practitioners' 'Irritable bowel syndrome' standard; reaction from the field of gastroenterology]. 1219 34

With the heterogeneous clinical presentation of IBD, endoscopy plays an integral role in the initial diagnosis of ulcerative colitis and Crohn's disease. Although radiographic tests often are supplemental in the work-up of IBD, colonoscopy with biopsy is the test of choice if IBD is suspected and is more sensitive than radiographic tests. Endoscopic features can be helpful in differentiating ulcerative colitis and Crohn's disease. Currently the only mode for detecting dysplasia and stratifying the risk of developing colorectal cancer is through complete colonoscopy with multiple biopsy specimens. Complications of IBD can be managed effectively with endoscopic therapy. The role of endoscopic ultrasound and future developments in endoscopic therapy need to be defined by future studies.
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PMID:Endoscopy in inflammatory bowel disease. 1212 27

The risk of cancer in IBD is real and is a cause of anxiety and concern among patients and practitioners. Current modalities for detecting dysplasia in IBD are crude and insensitive and subject to observer and sampling bias. This evidence-based review confirms a significant increased risk for colorectal cancer among patients with pancolonic UC and, to a lesser extent, in patients with left-sided disease. Risk increases with longer duration of disease; early age at diagnosis; coexisting PSC; and, perhaps, a family history of colorectal cancer. Physicians must pay greater attention to the manner in which they implement surveillance colonoscopies, including paying heed to the location and number of biopsy specimens required to maximize the benefit. With respect to CD, the evidence suggests that patients with extensive colonic involvement of long duration carry a similar risk of colorectal cancer to patients with UC and should be considered candidates for surveillance colonoscopy.
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PMID:Cancer in inflammatory bowel disease. An evidence-based analysis and guide for physicians and patients. 1212 35

The gastrointestinal tract of vertebrate species is a rich source of extrapineal melatonin. The concentration of melatonin in the gastrointestinal tissues surpasses blood levels by 10-100 times and there is at least 400x more melatonin in the gastrointestinal tract than in the pineal gland. The gastrointestinal tract contributes significantly to circulating concentrations of melatonin, especially during the daytime and melatonin may serve as an endocrine, paracrine, or autocrine hormone influencing the regeneration and function of epithelium, enhancing the immune system of the gut, and reducing the tone of gastrointestinal muscles. As binding sites for melatonin exhibit circadian variation in various species, it has been hypothesized that some melatonin found in the gastrointestinal tract might be of pineal origin. Unlike the photoperiodically regulated production of melatonin in the pineal, the release of gastrointestinal melatonin seems to be related to the periodicity of food intake. Phylogenetically, melatonin and its binding sites were detected in the gastrointestinal tract of lower vertebrates, birds, and mammals. Melatonin was found also in large quantities in the embryonic tissue of the mammalian and avian gastrointestinal tract. Food intake and, paradoxically, also longterm food deprivation resulted in an increase of tissue and plasma concentrations of melatonin. Melatonin release may have a direct effect on many gastrointestinal tissues but may also well influence the digestive tract indirectly, via the central nervous system and the sympathetic and parasympathetic nerves. Melatonin prevents ulcerations of gastrointestinal mucosa by an antioxidant action, reduction of secretion of hydrochloric acid, stimulation of the immune system, fostering epithelial regeneration, and increasing microcirculation. Because of its unique properties, melatonin could be considered for prevention or treatment of colorectal cancer, ulcerative colitis, gastric ulcers, irritable bowel syndrome, and childhood colic.
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PMID:Gastrointestinal melatonin: localization, function, and clinical relevance. 1239 7

Colorectal cancer is an important, and often dreaded, consequence of long-standing UC and Crohn's colitis. Surveillance colonoscopy, despite its limitations, is beneficial for detecting earlier stage cancers and, probably, mortality reduction. Agents such as anti-inflammatory medications, folic acid, and ursodeoxycholic acid show promise for chemoprevention in this disease. Future research will help to define better the natural history of dysplasia in IBD, and to determine how molecular approaches may be integrated into surveillance programs to reduce CRC risk.
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PMID:Cancer prevention in patients with inflammatory bowel disease. 1248 82

The assessment of inflammatory activity in intestinal disease in man can be done using a variety of different techniques, from measurement of conventional noninvasive acute-phase inflammatory markers in plasma (C-reactive protein and the erythrocyte sedimentation rate) to the direct assessment of disease activity by intestinal biopsy. However, most of these techniques have significant limitations when it comes to assessing functional components of the disease that relate to activity and prognosis. Here we briefly review the value of a novel emerging intestinal function test, fecal calprotectin. Single stool assay of neutrophil-specific proteins (calprotectin, lactoferrin) give the same quantitative data on intestinal inflammation as the 4-day fecal excretion of indium-111-labeled white cells. Elevated levels of fecal calprotectin have been demonstrated in patients with NSAID-induced enteropathy and have been used in the diagnosis of colorectal cancer. Fecal calprotectin is increased in over 95% of patients with inflammatory bowel disease (IBD) and correlates with clinical disease activity. It reliably differentiates between patients with IBD and irritable bowel syndrome (IBS). More importantly, at a given fecal calprotectin concentration in patients with quiescent IBD, the test has a specificity and sensitivity in excess of 85% in predicting clinical relapse of disease. This suggests that relapse of IBD is closely related to the degree of intestinal inflammation and suggests that targeted treatment at an asymptomatic stage of the disease may be indicated. (c) 2001 Prous Science. All rights reserved.
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PMID:Fecal calprotectin as an index of intestinal inflammation. 1278 1

Ulcerative colitis and Crohn's disease (together known as Inflammatory Bowel Disease or IBD) are both associated with increased risk for colorectal cancer. Although it is conventional to emphasise differences between IBD-associated and sporadic colon cancer, such as a lower rate of Adenomatosis Polyposis Coli mutations and earlier p53 mutations, IBD-associated cancer has a similar dysplasia-cancer sequence to sporadic colon cancer, similar frequencies of major chromosomal abnormalities and of microsatellite instability and similar glycosylation changes. This suggests that IBD-associated colon cancer and sporadic colon cancer might have similar pathogenic mechanisms. Because the normal colon is arguably in a continual state of low-grade inflammation in response to its microbial flora, it is reasonable to suggest that both IBD-associated and sporadic colon cancer may be the consequence of bacteria-induced inflammation. We have speculated that the glycosylation changes might result in recruitment to the mucosa of bacterial and dietary lectins that might otherwise pass harmlessly though the gut lumen. These could then lead to increased inflammation and/or proliferation and thence to ulceration or cancer. The glycosylation changes include increased expression of onco-fetal carbohydrates, such as the galactose-terminated Thomsen-Friedenreich antigen (Gal beta1,3GalNAc alpha-), increased sialylation of terminal structures and reduced sulphation. These changes cannot readily be explained by alterations in glycosyltransferase activity but similar changes can be induced in vitro by alkalinisation of the Golgi lumen. Consequences of these changes may be relevant not only for cell-surface glycoconjugates but also for intracellular glycoconjugates.
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PMID:Altered glycosylation in inflammatory bowel disease: a possible role in cancer development. 1282 Jul 18

Due to the development of more effective medications, those infected with HIV are living longer. Consequently, more tumors and infections have been added to the AIDS-defining criteria in the last decade. Our aim was to review the occurrence and clinical course of colorectal (CR) malignancies in HIV infected/AIDS patients from a single institution. A retrospective review of HIV/AIDS patients with colorectal malignant tumors was undertaken. We included adult patients, with ELISA and Western blot test positive for HIV, and primary malignant tumors located in the colon or rectum. Malignant neoplasms of the anus were excluded for the purposes of this study. Twelve patients (9 males and 3 females), mean age 41 years, were identified with the following neoplasm: 6 adenocarcinomas (ACA), 5 non-Hodgkin lymphomas (NHL), and 1 small-cell carcinoma. Intravenous drug abuse was the main risk factor for HIV. No patient had identified risk factors for colorectal neoplasm. Five out of six patients with ACA had metastatic disease at the time of diagnosis. One patient with stage II ACA developed early liver metastases after colonic resection. Seven out of 12 patients underwent surgery. Six (85.7%) of these sustained postoperative complications, primarily wound infection. The overall survival in our series was dismal, averaging 20 months. For NHL average survival was 29 months, and 12 months for CR-ACA. This is the largest series of cases of colorectal cancer in the HIV/AIDS patient population published in the English language and the largest number of colorectal ACA reported in this unique population. Early in our experience, tumors frequently found in immunoincompetent patients were detected (NHL). More recently, we have only treated patients with colorectal ACA; none of them had no risk factors for colorectal cancer (family history, IBD, FAP, HNPCC). These patients developed tumors at earlier ages and were diagnosed at an advanced stage. Therefore, these tumors may be associated with the grade of immunosuppression induced during the course of the HIV infection and with a tumorigenic effect of the HIV on the colonic epithelium. Consequently, a high index of suspicion when evaluating chronic abdominal complaints in such patients is warranted. The use of the new antiretroviral therapy regimens should be further evaluated to know its impact in the survival.
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PMID:Colorectal malignancies in HIV-positive patients. 1462 61


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