Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009402 (colorectal cancer)
 53,228 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Macroscopic examination of large intestinal resection specimens by the surgical pathologist provides important diagnostic and prognostic information. This review summarises current recommended protocols and evidence based guidelines for gross description, dissection, and histological block selection in both neoplastic and non-neoplastic colorectal disease. Specific lesions discussed include colorectal cancer, polypectomies and polyposis syndromes, and inflammatory bowel disease. Microscopic examination is briefly described, with emphasis on certain pitfalls that might be encountered in routine practice. A section covering special techniques for the investigation of occult bleeding is included.
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PMID:ACP Best practice no 159. Examination of large intestine resection specimens. 1088 15

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

Patients with inflammatory bowel disease (IBD) have long been known to be at increased risk of development of colorectal cancer; however, there are many nuances to cancer prevention strategies in IBD that remain unresolved. During the past year, two publications reported on the resection of otherwise typical adenoma-like masses by means of polypectomy, after which these patients were followed with continued endoscopic surveillance, rather than pursuing colectomy. Another concern in IBD is whether there is an increase in the number of other cancers, in particular lymphomas. One issue regarding lymphoma risk is whether immunomodulatory drug use predisposes to this cancer. One study of a large group of 6-mercaptopurine users did not suggest an increased risk for patients with IBD using this drug. There are a variety of nonintestinal problems that patients with IBD may confront. Osteopenia has received considerable attention in the past decade. This year, data have been published that quantify for the first time the risk of fractures in patients with IBD based on population, and these data were compared with a matched control group from the same population. Data on the further exploration of the issue of osteopenia in pediatric IBD have also been reported, as have some of the only studies of therapy for osteopenia in IBD. These and data on other extraintestinal manifestations of IBD have all emerged in the past year.
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PMID:Neoplastic and other complications of inflammatory bowel disease. 1107 46

As an animal model for human inflammatory bowel disease and colorectal cancer, the cotton-top tamarin remains controversial. Demonstration of antigenic similarity to the human would enhance its validity. Using colonic extracts and washings, we compared binding of seven monoclonal antibodies reactive with bowel and cancer antigens in both tamarins and humans with inflammatory bowel disease. Additionally, telomerase activity was tested for. Expression of a mucin antigen specific to human cancer was increased in tamarin colonic washings as well as aminoproteoglycans and EGFR in tamarin extracts, as compared to those of humans with inflammatory bowel disease (P < 0.005). An adenoma-associated antigen and k-ras p21 protein were negative in the tamarin. A trend to greater telomerase activity exists in tamarins. The antigenic similarity validates this model for human inflammatory bowel disease and colorectal cancer. A trend to increased telomerase activity in tamarins is consistent with the greater predisposition to cancer in these animals.
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PMID:Gastrointestinal tract antigenic profile of cotton-top tamarin, Saguinus oedipus, is similar to that of humans with inflammatory bowel disease. 1125 47

The pathogenesis of inflammatory bowel disease (IBD) continues to be explored, with the emphasis on genetically determined host immune dysregulation as it applies to interactions with luminal bacteria. The role of endoscopic ultrasound in the evaluation of IBD continues to be studied. Recent advances in the evaluation of enterocutaneous fistulas have been made through the use of hydrogen peroxide to enhance definition of the fistula course and characteristics of the neighboring bowel, as evaluated by transabdominal ultrasound. Refinements have been made in the use and interpretation of the results of surveillance colonoscopy for detection of colorectal cancer and dysplasia in IBD, but a consistent approach still needs to be applied by individual practitioners. New data exist on the usefulness of methotrexate for maintenance of remission, while a lack of efficacy has been demonstrated for mesalamine in the prevention of postoperative recurrence. The role of anti-tumor necrosis factor (TNF) antibody therapy in the treatment of IBD continues to be investigated.
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PMID:Inflammatory bowel disease. 1127 16

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

Interleukin-10-deficient mice develop colitis and colorectal cancer similar to the inflammatory bowel disease associated cancer in humans. The aim of this study was to identify possible mutations of oncogenes and tumour suppressor genes involved in tumorigenesis in Interleukin-10 (IL-10)-deficient mice. Twenty colon carcinomas from IL-10-deficient mice were screened for mutations in the K-ras and p53 genes by 'cold' single-strand-conformation polymorphism. Immunohistochemical staining was performed to detect mutations in the proteins P53, APC and MSH2, and the transforming growth factor beta type II receptor. Microsatellite instability was analysed at eight chromosomal loci and plasma levels of transforming growth factor beta1 (TGF-beta1) were also measured. At 9 weeks, 14% of the animals developed colorectal cancer, and at 10-31 weeks the incidence of carcinoma was 65%. No mutations were detected in the analysed oncogene and tumour suppressor genes. Plasma TGF-beta1 levels in IL-10-deficient mice 10-31 weeks old were higher than in wild-type littermates e.g. 45.7 +/- 4.6 ng/ml versus 19.8 +/- 4.5 ng/ml (P<0.01). No alterations in K-ras, p53, APC: and Msh2 genes suggests that other genes are involved in the development of these tumours. Elevated TGF-beta1 plasma levels correspond to the high incidence of dysplasia and cancer. Normal expression of the TGF-beta II receptors hints at genetic alterations in other members of the TGF-beta receptor signal transduction pathway.
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PMID:Interleukin-10-deficient mice and inflammatory bowel disease associated cancer development. 1128 4

The diagnostic value of pyruvate-kinase type tumor M2 (Tumor M2-PK) has been investigated in different tumors, and showed interesting results in cases of renal cancer, pancreatic cancer, lung cancer and some cases of gastric cancer. In this study we investigated EDTA-plasma of 68 patients with gastrointestinal cancer, 22 patients with inflammatory bowel disease (IBD) and 60 healthy controls. Sensitivity of Tumor M2-PK was 70.6% for all GI-tumors, that of CA19-9 was 55.4% and that of CEA was 53.3%. In pancreatic cancer CA19-9 showed the best sensitivity. In oesophageal/gastric cancer Tumor M2-PK was most sensitive and in colorectal cancer CEA and Tumor M2-PK showed the best results. The specificity of Tumor M2-PK was 90-96, 7%. In IBD some individuals showed elevated Tumor M2-PK levels but there was no correlation to CRP or to the clinical activity score. The results indicated that Tumor M2-PK might be a valuable marker in gastrointestinal cancer.
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PMID:Tumor M2-pyruvate kinase: a promising tumor marker in the diagnosis of gastro-intestinal cancer. 1132 48

Some earlier studies have indicated that patients with inflammatory bowel disease, especially those with long-standing and extensive ulcerative colitis, have an increased risk of colorectal cancer. Moreover, others in tertiary care centres have suggested that patients with Crohn's disease also have a higher risk of colorectal cancer. Canadian data on colorectal cancer in Crohn's disease appear to be limited. For this investigation, a single clinician database of 877 patients with Crohn's disease was used. Altogether, there were six patients with colorectal cancer (ie, overall rate of 0.7%). All of these patients were men with an initial diagnosis of Crohn's disease established at a mean age of approximately 28 years, with either ileocolonic disease or colonic disease alone, but not with ileal disease alone. Although there was a predominance of women in the overall study population (ie, 56.1%), no women developed colorectal cancer. The clinical behaviour of Crohn's disease was classified as nonstricturing in all six patients with colorectal cancer, but in two patients, Crohn's disease was complicated by a perirectal abscess or a fistula. All cancers were located in the rectum and were diagnosed 30 years, 22 years, seven years, 18 years, 20 years and 40 years after Crohn's disease was initially diagnosed. In three patients, the cancer was detected in a residual rectal stump after a partial colon resection at least 10 years earlier. In five patients, localized extension of disease through the serosa, nodal or distant metastases (ie, liver, lung) was found at the time of cancer diagnosis; two patients have since died. The present study confirms that Crohn's disease involving the colon may be a possible risk factor for the development of colorectal cancer, at least in younger men, but, in this study, not in women. However, part of this increased risk in men may have been related to the presence of a rectal stump, rather than to Crohn's disease per se.
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PMID:Colorectal cancer complicating Crohn's disease. 1133 24

Colorectal cancer (CRC) occurs with an increased incidence in individuals with chronic inflammatory bowel disease (IBD) of the colon. Recent data suggest that a family history of colorectal cancer is an independent risk factor for CRC in IBD, an observation that implies that genetic factors are relevant to the development of CRC in this context. Among the genetic defects associated with CRC, the APC I1307K mutation has been detected nearly exclusively in individuals of Ashkenazi Jewish (AJ) origin, occurring in 6%-7% of the AJ general population and in 10%-28% of AJ with a either a personal or family history of CRC or adenomatous polyps. These findings, together with the increased incidence of IBD in AJ, prompted the current analysis of the contribution of the APC I1307K variant of CRC in AJ IBD patients. APC I1307K carrier frequencies were determined in 306 AJ individuals affected with IBD and 308 of their unaffected relatives ascertained from a family collection obtained for the identification of IBD susceptibility genes. Prevalence of the I1307K variant was not significantly different among individuals with IBD, Crohn's disease, ulcerative colitis, and unaffected relatives (6.9%, 7.6%, 4.7%, and 6.2%, respectively), and the mutation was detected in only one of five IBD-affected individuals with a diagnosis of CRC. These results reveal that IBD patients of AJ origin carry the APC I1307K variant at the same rate as individuals within the general AJ population. Lack of an increased APC I1307K carrier rate suggests that this mutation does not account for the increased CRC susceptibility associated with IBD.
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PMID:Carrier rate of APC I1307K is not increased in inflammatory bowel disease patients of Ashkenazi Jewish origin. 1135 31


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