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Results for “Intestinal Polyposis”

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At least 487 records · Page 27Linked to original sources
PubMed2000

E-cadherin and adenomatous polyposis coli mutations are synergistic in intestinal tumor initiation in mice.

BACKGROUND & AIMS: Inactivation of the adenomatous polyposis coli (APC) gene is observed at early stages of intestinal tumor formation, whereas loss of E-cadherin is usually associated with tumor progression. Because both proteins compete for the binding to beta-catenin, an essential component of the Wnt signaling pathway, reduction of E-cadherin levels in an Apc mouse model could influence both tumor initiation and progression. In addition, loss or haploinsufficiency of E-cadherin may affect tumorigenesis by altering its cell-adhesive and associated functions. METHODS: Apc1638N mice were bred with animals carrying a targeted E-cadherin knockout mutation. RESULTS: Double heterozygous animals showed a significant 9-fold and 5-fold increase of intestinal and gastric tumor numbers, respectively, compared with Apc1638N animals. The intestinal tumors of both groups showed no significant differences in grading and staging. Loss of heterozygosity analysis at the Apc and E-cadherin loci in both intestinal and gastric Apc(+/1638N)/E-cad(+/-) tumors revealed loss of the wild-type Apc allele in most cases, whereas the wild-type E-cadherin allele was always retained. This was supported by a positive, although reduced, staining for E-cadherin of intestinal tumor sections. CONCLUSIONS: Introduction of the E-cadherin mutation in Apc1638N animals enhances Apc-driven tumor initiation without clearly affecting tumor progression.

Adenomatous Polyposis Coli Protein↗
PubMed1999

[Current approaches to the diagnosis and treatment of pilots with combined polyposis of the stomach and large intestine].

Findings of diagnostics and treatment of 198 pilots suffering from combined polyposis in the stomach and large intestine are presented. Different therapeutic tactics should be chosen for these patients. Annual dynamic evaluation should be made in case of a benign course and without an upward tendency, whereas diagnosed villus polyps, villus-tubular adenoma with the second or third phase of dysplasia, adenomatous polyps with regional 2nd or 3d phase dysplasia will require early polypectomy to be followed by yearly dynamic endoscopy. The proposed tactics is angled at early diagnostics of stomach and large intestine cancers. This tactics allows considerable prolongation of the flight career of pilots with the diagnosis of combined polypous lesions.

Adult↗
PubMed2003

Gastrointestinal polyposis syndromes.

Numerous polyposis syndromes involve the gastrointestinal (GI) tract, including both non-hereditary and hereditary types. Causative genes are now known for the seven major syndromes. Genetic and clinicopathologic features are reviewed here and cancer predisposition is emphasized. Genetic testing is available for the GI polyposis syndromes, and can be accessed through GeneTests-GeneClinics on the Internet at http://www.genetests.org/. The website is available at no cost and is a publicly funded medical genetics resource for health care providers and researchers.

Adenomatous Polyposis Coli↗
PubMed2005

Double-balloon endoscopy.

PURPOSE OF REVIEW: Our strategy for small intestinal diseases has dramatically been brushed up with a novel technique, double-balloon endoscopy, which exhibits extremely better insertability and maneuverability compared with conventional methods. Double-balloon endoscopy has a potential to change radically the approach for the small intestinal diseases in the future. In this article, the publications on double-balloon endoscope will be reviewed. RECENT FINDINGS: A double-balloon endoscope can be inserted into deeper portions of the small intestine via both oral and anal approaches, and allows endoscopic observation as well as treatment for the entire small intestine without general anesthesia. Reports have been made on this method's safety and low frequency of complication: it is very useful for diagnosis and treatment of small intestinal diseases, including small intestinal bleeding, small intestinal tumor, stenosis of small intestine, and polyposis syndrome. SUMMARY: The development of double-balloon endoscopy enabled observation and treatment in the entire small intestine. The double-balloon endoscopy has a potential to be a standard of enteroscopy by replacing conventional push enteroscopy and intraoperative enteroscopy. In the near future, the double-balloon endoscopy, together with the capsule endoscopy, will be essential modalities for the management of small intestinal diseases.

Endoscopy, Gastrointestinal↗
PubMed2004

Ursodeoxycholate/Sulindac combination treatment effectively prevents intestinal adenomas in a mouse model of polyposis.

BACKGROUND & AIMS: Preclinical studies in animal models, human epidemiological data, and clinical trials in patients with adenomatous polyposis have consistently indicated that sulindac and other nonsteroidal antiinflammatory drugs or cyclooxygenase inhibitors have the greatest potential efficacy among current candidates for colon tumor chemopreventive agents. However, at highly effective doses they all have some risk of toxicity, and their therapeutic profile might be improved by use at lower, more tolerable doses, in combination with a second agent acting via other mechanisms. METHODS: Sulindac was tested in combination with ursodeoxycholic acid (ursodiol), a naturally occurring 7-B-epimer of the bile component chenodeoxycholic acid, for prevention of adenomas in the Min mouse model of adenomatous polyposis. RESULTS: Ursodeoxycholic acid caused a dose-dependent decrease in the number of intestinal tumors. Unlike sulindac and other nonsteroidal anti-inflammatory drugs, which are quite beneficial in the distal intestine but are somewhat less effective in the proximal small intestine (especially the clinically important periampullary duodenum), ursodeoxycholate had equal efficacy throughout the entire intestine, both proximal and distal. Combined treatment with low-dose sulindac was less toxic, with normal weight gain and fewer gastrointestinal ulcerations than high-dose sulindac. Combined treatment with sulindac and ursodeoxycholate was more effective than either agent alone for the prevention of tumors throughout the entire intestine. CONCLUSIONS: These experiments provide the first evidence that ursodeoxycholic acid is effective for preventing adenomas in an animal model. Cyclooxygenase inhibition, when combined with this naturally occurring bile component, may become a promising approach for colon cancer prevention.

Adenomatous Polyps↗
PubMed1986

Hereditary gastrointestinal polyposis syndromes.

Hereditary gastrointestinal polyposis syndromes can be divided into adenomatous and hamartomatous types. Familial adenomatous polyposis coli (FAPC) is the prototype adenomatous polyposis syndrome and is defined by the autosomal dominant transmission of multiple (more than 100) colorectal adenomas. Virtually all affected patients develop colorectal carcinoma if untreated. Adenomas may develop also in the stomach and small bowel in FAPC patients, but the incidence of carcinoma in these sites is low. A variety of extracolonic manifestations has been reported in FAPC, with the name Gardner's syndrome applied to kindreds with osteomas of the skull and mandible, multiple epidermal cysts, and other skin and soft-tissue lesions. In Turcot's syndrome, brain tumors are present. The distinction between Gardner's and Turcot's syndromes and classical FAPC has become blurred because of marked overlap between them; some authorities consider them to be varying manifestations of a single genetic defect. The hamartomatous polyposes include Peutz-Jeghers syndrome, familial juvenile polyposis, Cowden's disease, intestinal ganglioneuromatosis, and the Ruvalcaba-Myrhe-Smith syndrome. The incidence of gastrointestinal cancer in patients with Peutz-Jeghers syndrome and familial juvenile polyposis exceeds that in the normal population, but is relatively low. In Cowden's disease, the gastrointestinal tract may be the site of multiple hamartomas, but there is no associated increase in the incidence of gastrointestinal cancers; instead, there is an increased incidence of carcinoma of the breast and thyroid. Intestinal ganglioneuromatosis occurs in von Recklinghausen's disease, in association with multiple endocrine neoplasia, type 2b, or as an isolated abnormality. Patients with ganglioneuromatosis do not appear to have an increased risk of developing gastrointestinal cancer. Ruvalcaba-Myrhe-Smith syndrome comprises macrocephaly, mental deficiency, an unusual craniofacial appearance, hamartomatous intestinal polyposis, and pigmented macules on the penis. No increased risk of developing cancer has been identified in the few reported cases.

Adenomatous Polyposis Coli↗
PubMed1999

The molecular basis and clinical aspects of Peutz-Jeghers syndrome.

Peutz-Jeghers syndrome (PJS) is a classic, but not widely known hereditary trait [1, 2]. Its clinical hallmarks are intestinal hamartomatous polyposis and melanin pigmentation of the skin and mucous membranes. In addition, PJS predisposes to cancer [3, 4]. The most common malignancies are small intestinal, colorectal, stomach and pancreatic adenocarcinomas. Other cancer types that probably occur in excess in PJS families include breast and uterine cervical cancer, as well as testicular and ovarian sex cord tumors. The relative risk of cancer may be as high as 18 times that of the general population, and the cancer patients' prognosis is reduced. Recently, the predisposing locus was mapped to 19p13.3 using a novel method [5]. Subsequently, the causative gene was shown to be LKB1 (a.k.a. STK11), a serine/threonine kinase of unknown function [6]. Although preliminary reports seem to suggest a minor role for LKB1 in sporadic tumorigenesis [7-12], further investigations are needed.

AMP-Activated Protein Kinase Kinases↗
PubMed1998

Chemoprevention of spontaneous intestinal adenomas in the adenomatous polyposis coli Min mouse model with aspirin.

BACKGROUND & AIMS: Colorectal cancer is a significant source of morbidity and mortality in the United States and other Western countries. Epidemiological and experimental data indicate that regular use of aspirin reduces colon cancer risk. This study was designed to determine if aspirin would significantly inhibit gastrointestinal tumor formation in a mouse model of familial adenomatous polyposis. METHODS: Six-week-old male and female C57BL/6J +/+ (control) and C57BL/6J ApcMin/+ (Min) mice were fed either a control AIN-76A diet or one supplemented with 250 or 500 parts per million (ppm) aspirin (n = 6 per group) for 7 weeks. RESULTS: All of the Min mice, but no control mice, developed gastrointestinal tumors. Aspirin significantly reduced tumor multiplicity (number of tumors per mouse) in the small intestine, but not the colon, from an average of 35.8 tumors per mouse (control diet) to 16 and 18.5 tumors per mouse with 250 and 500 ppm aspirin, respectively. Total tumor load (sum of tumor diameters per mouse) was also significantly reduced, from 93.2 mm in total diameter to 40. 4 and 45.0 mm with 250 and 500 ppm aspirin, respectively. Results were not significantly different because of sex or aspirin dose. CONCLUSIONS: High doses of aspirin are effective chemopreventive agents in a mouse model of spontaneous intestinal tumor formation.

Adenoma↗