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

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

Although colorectal cancer (CRC), complicating ulcerative colitis and Crohn's disease, only accounts for 1-2% of all cases of CRC in the general population, it is considered a serious complication of the disease and accounts for approximately 15% of all deaths in inflammatory bowel disease (IBD) patients. The magnitude of the risk was found to differ, even in population-based studies. Recent figures suggest that the risk of colon cancer for people with IBD increases by 0.5-1.0% yearly, 8-10 years after diagnosis. The magnitude of CRC risk increases with early age at IBD diagnosis, longer duration of symptoms, and extent of the disease, with pancolitis having a more severe inflammation burden and risk of the dysplasia-carcinoma cascade. Considering the chronic nature of the disease, it is remarkable that there is such a low incidence of CRC in some of the population-based studies, and possible explanations have to be investigated. One possible cancer-protective factor could be treatment with 5-aminosalicylic acid preparations (5-ASAs). Adenocarcinoma of the small bowel is extremely rare, compared with adenocarcinoma of the large bowel. Although only few small bowel cancers have been reported in Crohn's disease, the number was significantly increased in relation to the expected number.
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PMID:Review article: the incidence and prevalence of colorectal cancer in inflammatory bowel disease. 1295 Apr 13

The Board of Editors of Gastroenterology identified 6 topics in basic gastroenterology research in which exciting advancements have been made during the past year. These topics are (1) NOD2 variants in Crohn's disease, (2) Heliobacter pylori and CagA and VacA pathogenesis, (3) beta-catenin function in normal colonic epithelia and colon cancer, (4) DNA methylation in colonic cancer, (5) the HCV replicon, and (6) the use of small interfering RNA in somatic cell genetics. Basic research in gastroenterology has been characterized during the past year by the rapid translation from fundamental research into pathophysiological systems. New technological advances are being applied to difficult areas of gastrointestinal research. Well-defined patient populations are critical to extend the knowledge derived from the human genome to gastrointestinal diseases.
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PMID:Gastrointestinal basic science 2002-2003: the year in review. 1501 26

Colon carcinoma arising in inflammatory bowel disease often exhibits aggressive behavior compared to sporadic carcinomas. The rationale for the different biological behaviors of these two groups of tumors is not fully understood. In this study, we have examined carcinomas arising in inflammatory bowel disease (IBD) and sporadic carcinomas (SCA) for molecular differences that may provide clues for the behavioral disparity of these tumors. Thirty-eight colon carcinomas (12 from ulcerative colitis, 5 from Crohn's disease, and 21 SCA) were analyzed by immunohistochemistry for cell adhesion molecules (E-cadherin, beta-catenin, CD44), cell cycle regulatory proteins (cyclin D1, p27, p21), mismatch repair proteins (hMLH1, hMSH2), cyclooxygenase-2 and DPC4. Carcinomas arising in IBD showed significant decrease in expression of cell adhesion molecules, the cell cycle inhibitor protein, p21, and increased expression of cyclooxygenase-2 compared to sporadic carcinomas. No differences were observed in the expression of cell cycle regulatory proteins p27, cyclin D1, DPC4 and mismatch repair proteins between these two groups of tumors. Decreased expression of p21 as well as adhesion molecules may provide increased impetus for the aggressive behavior of tumors arising in inflammatory bowel disease.
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PMID:Comparative analysis of cell adhesion molecules, cell cycle regulatory proteins, mismatch repair genes, cyclooxygenase-2, and DPC4 in carcinomas arising in inflammatory bowel disease and sporadic colon cancer. 1506 31

Several matrix metalloproteinases (MMPs) have been implicated in intestinal inflammation, mucosal wound healing, and cancer progression. The purpose of this study was to examine the cellular location and putative function of MMP-19, MMP-26 (matrilysin-2), and MMP-28 (epilysin), in normal, inflammatory, and malignant conditions of the intestine. Peroperative tissue specimens from patients with ulcerative colitis (UC) (n = 16) and archival tissue samples of ischemic colitis (n = 9), Crohn's disease (n = 7), UC (n = 8), colon cancer (n = 20), and healthy intestine (n = 5) were examined using immunohistochemical analyses with polyclonal antibodies. Unlike many classical MMPs, MMP-19, MMP-26, and MMP-28 were all expressed in normal intestine. In inflammatory bowel disease (IBD), MMP- 19 was expressed in nonmigrating enterocytes and shedding epithelium. MMP-26 was detected in migrating enterocytes, unlike MMP-28. In colon carcinomas, MMP-19 and MMP-28 expression was downregulated in tumor epithelium. Staining for MMP-26 revealed a meshwork-like pattern between cancer islets, which was absent from most dedifferentiated areas. Our results suggest that MMP-19 is involved in epithelial proliferation and MMP-26 in enterocyte migration, while MMP-28 expression is not associated with inflammatory and destructive changes seen in IBD. In contrast to many previously characterized MMPs, MMP-19 and MMP-28 are downregulated during malignant transformation of the colon and may play a prominent role in tissue homeostasis.
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PMID:Differential expression of three matrix metalloproteinases, MMP-19, MMP-26, and MMP-28, in normal and inflamed intestine and colon cancer. 1518 74

Breast, prostate, and lung cancer have been successfully detected with 99mTc bombesin (99mTc-leu13-BN1), the radiopharmaceutical that our group developed from synthesis to diagnostic trials. Overexpression of bombesin receptors (BNRs) in colon cancer is well known: the aim of this study was to assess whether or not colon cancer can be detected with a 99mTc-leu13-BN1 scan. Thirteen (13) patients, 7 of whom with known rectal cancer and 6 scheduled to undergo endoscopic removal of polyps for suspicion of colon cancer, were studied with a 99mTc-leu13-BN1 scan. Dynamic, single photon emission computed tomography, and whole-body scans were performed within 1 hour, before discharge of radioactivity from the liver into the duodenum. Sixteen (16) of 17 colorectal cancer locations were detected with a 99mTc-leu13-BN1 scan with 94.1% sensitivity. Six (6) lesions were benign: 1 Crohn's disease, 1 polyp with mild dysplasia, 4 polyps with simple hyperplasia; 99mTc-leu13-BN1 scans were positive in two nontumoral lesions, Crohn's disease, and mild dysplasia and true negative in 4: specificity was 67%. Of the 7 patients with known rectal cancer, 5, who underwent operations instead of radiation therapy, showed lymph-node invasion on 99mTc-leu13-BN1 scans. Operations confirmed the scintigraphic staging. 99mTc-leu13-BN1 is taken up by colon cancer. Scans are sensitive, although scarcely specific. 99mTc-leu13-BN1 allows for node-invasion detection.
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PMID:Detection of colon cancer with 99mTc-labeled bombesin derivative (99mTc-leu13-BN1). 1518 5

Patients with ulcerative colitis and Crohn's disease are at increased risk for developing colorectal cancer. To date, no known genetic basis has been identified to explain colorectal cancer predisposition in these inflammatory bowel diseases. Instead, it is assumed that chronic inflammation is what causes cancer. This is supported by the fact that colon cancer risk increases with longer duration of colitis, greater anatomic extent of colitis, the concomitant presence of other inflammatory manifestations such as primary sclerosing cholangitis, and the fact that certain drugs used to treat inflammation, such as 5-aminosalicylates and steroids, may prevent the development of colorectal cancer. The major carcinogenic pathways that lead to sporadic colorectal cancer, namely chromosomal instability, microsatellite instability, and hypermethylation, also occur in colitis-associated colorectal cancers. Unlike normal colonic mucosa, however, inflamed colonic mucosa demonstrates abnormalities in these molecular pathways even before any histological evidence of dysplasia or cancer. Whereas the reasons for this are unknown, oxidative stress likely plays a role. Reactive oxygen and nitrogen species produced by inflammatory cells can interact with key genes involved in carcinogenic pathways such as p53, DNA mismatch repair genes, and even DNA base excision-repair genes. Other factors such as NF-kappaB and cyclooxygenases may also contribute. Administering agents that cause colitis in healthy rodents or genetically engineered cancer-prone mice accelerates the development of colorectal cancer. Mice genetically prone to inflammatory bowel disease also develop colorectal cancer especially in the presence of bacterial colonization. These observations offer compelling support for the role of inflammation in colon carcinogenesis.
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PMID:Inflammation and cancer IV. Colorectal cancer in inflammatory bowel disease: the role of inflammation. 1519 58

A case of a 38 year-old male patient, from Lima, with a three-year period illness, characterized by abdominal pain, diarrhea, ponderal weight loss and fever is showed. He is examined by colonoscopy, with endoscopic diagnosis of colon cancer and undergoes surgery. The histopathological diagnosis was severe acute and chronic ulcerative ileocolitis, suggesting Crohn disease. A month later he again showed abdominal pain, diarrhea and fever, so a new colonoscopy is performed revealing multiple ileum ulcers and in the anastomotic area. The biopsy revealed an acute and chronic inflammatory process. The colon radiography showed a filling defect and irregularity in the cecum, and the upper endoscopy revealed esophageal ulcers. In addition, a number of analyses were carried out, such as: coproculture, HIV, and VK on sputum and feces, as well as CEA dosage, resulting all of them negative. The thorax radiography was also normal.He was diagnosed with Crohn's disease and was treated with mesalacin. Evolution was fast, showing weight gain, which allowed the discharge of the patient from the hospital seven (7) days later. The anatomical pathology never did confirm the final diagnosis, which brings us to the question:Are the granulomas always necessary for the final diagnosis of Crohn's disease?
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PMID:[Are granulomas necessary for the final diagnosis of Crohn disease?]. 1524 96

Acute diverticulitis of the cecum and ascending colon, also called right-sided diverticulitis, represents a relatively rare disorder in the western hemisphere. Pseudodiverticula and, less frequently, solitary congenital diverticula are regarded as the underlying causes of acute diverticulitis. We report the helical CT findings in four patients with acute right-sided colonic diverticulitis. The CT was performed with a collimation of 8 mm, a pitch of 1.5 and an increment of 8 mm, and with variable administration of intravenous, oral and rectal contrast material. In two of the four patients, the acute diverticulitis was detected in the cecum and ascending colon, respectively. In two patients, the diagnosis could be confirmed during surgery and subsequent histologic examination of the resected specimen. On the initial CT studies, acute diverticulitis was correctly diagnosed in two patients and suspected in one patient without identifying an inflamed diverticulum. In one patient, the offending diverticulum in the ascending colon caused an inflammatory pseudotumor at the level of the ileocecal region. This process was initially mistaken as Crohn's disease. The CT diagnosis of a right-sided colonic diverticulitis is based on an inflamed diverticulum in the center of pericolic inflammatory changes and a preserved wall enhancement (target sign). Other CT findings, such as fatty pericolic infiltration and colon wall thickening, are rather non-specific and can also be found in a number of different ileocolic disorders, especially in colon cancer. In selected cases, the diagnosis can only be established by follow up CT after the pericolic infiltration has markedly subsided and an offending diverticulum has emerged.
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PMID:[Computed tomography (CT) of acute diverticulitis of the cecum and ascending colon]. 1534 60

A 68-year-old Japanese man with a history of linitis plastica carcinoma of the stomach and subsequent gastrectomy 8 years previously presented with lower abdominal pain. Radiological and endoscopic examinations showed multiple submucosal nodular lesions similar to Crohn's disease in the ileocecal area. A firm diagnosis could not be made after initial multiple biopsies. Finally, a submucosal biopsy revealed adenocarcinoma. The ileocecal lesion was diagnosed as a recurrence because of the histological findings, which included mucosal preservation, a similarity with the histologic type of stomach carcinoma, and atypical immunoreactivity for primary colon carcinoma; the lesion was negative for both cytokeratin 7 and cytokeratin 20. In cases where metastatic carcinoma of the colon is suspected, we recommend early consideration of a submucosal biopsy.
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PMID:Metastatic carcinoma of the colon similar to Crohn's disease: a case report. 1555 60


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