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Results for “Intestinal Polyposis”

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At least 163 records · Page 9Linked to original sources
PubMed2006

Cancer chemoprevention of intestinal polyposis in ApcMin/+ mice by sulforaphane, a natural product derived from cruciferous vegetable.

Sulforaphane (SFN) is an isothiocyanate that is present abundantly in widely consumed cruciferous vegetables and has a particularly high content in broccoli and cauliflower. It has been shown to be an effective inhibitor of some carcinogen-induced cancers in rodents. Here, we investigated the chemopreventive efficacy of SFN in the ApcMin/+ mouse model. ApcMin/+ mice were fed with diet supplemented with two different dose levels of SFN (300 and 600 p.p.m.) for 3 weeks. Our results clearly demonstrated that ApcMin/+ mice fed with SFN-supplemented diet developed significantly less and smaller polyps with higher apoptotic and lower proliferative indices in their small intestine, in a SFN dose-dependent manner. In addition, immunohistochemical (IHC) staining of the adenomas indicated that SFN significantly suppressed the expression of phosphorylated c-Jun N-terminal kinase (p-JNK), phosphorylated extracellular signal-regulated kinases (p-ERK) and phosphorylated-Akt (p-Akt), which were found to be highly expressed in the adenomas of ApcMin/+ mice. In contrast, expression of two important biomarkers of the Wnt signaling pathway, beta-catenin and cyclin-D1 was unaffected by SFN treatment. Measurement of SFN and its metabolite SFN-GSH in the small intestine using LC-MS indicates that the concentrations between 3 and 30 nmol/g are required to prevent, or retard adenoma formation in the gastrointestinal tract of ApcMin/+ mice.

Adenoma↗
PubMed1977

[Problems with therapy of familial intestinal polyposis (author's transl)].

This study describes a family with gastrointestinal adenomatous polyposis. One member had symptoms of Peutz-Jeghers disease with histologically typical polyps besides those of the adenomatous type. In cases of clinical gastrointestinal polyposis the exact histologic diagnosis of an endoscopic sample is mandatory. The benign e.g. non adenomatous, finding compels one to auxiously care for those patients and to prophylactically examine all members of the patients family, while adenomatosis implies prophylactic surgery. The indications are discussed.

Adenoma↗
PubMed1979

[Intestinal polyposis (author's transl)].

Recto-colonic polyposis is typical of pre-malignant lesions. Recognition and the application of appropriate treatment offer true prophylaxis against recto-colonic carcinoma in sufferers. Careful study should be made of other family members, the only way in which latent forms may be discovered before the stage of malignant change.

Colonic Neoplasms↗
PubMed1983

Medical aspects of hereditary intestinal polyposis.

Extracolonic manifestations are often associated with familial polyposis coli, but the cysts and osteomas may be few and inconspicuous. Abnormal fibrous reactions may also occur and may be a cause of death. These manifestations act as "external markers" for the later appearances of adenomas. In any family, some individuals may manifest some extracolonic manifestations and other individuals may not. Other abnormalities, usually neoplastic, described in familial polyposis coli families, are probably fortuitous occurrences, but medulloblastoma has been found relatively frequently. Turcot's syndrome, described in a unique family, should be used more restrictively. Diagnosis depends on histology showing adenomas, but no particular number is required in an afflicted family member. Total reliance on sigmoidoscopy alone is potentially hazardous as the descending colon may be affected initially. Inherent problems regarding "isolated cases" are outlined.

Adenoma↗
PubMed1994

Common bile duct obstruction related to intestinal polyposis in a child with Peutz-Jeghers syndrome.

Peutz-Jeghers syndrome is characterized by hamartomatous polyposis of the small and large bowel and mucocutaneous pigmentation. The authors describe a 9-year-old girl with small bowel obstruction related to duodenal intussusception caused by polyposis in the fourth portion of the duodenum. Operative reduction of the intussusception and excision of the polyps were performed, at which time the pancreas appeared to have mild pancreatitis. A liver biopsy specimen showed mild portal fibrosis and ductal proliferation. The patient did well postoperatively, but later presented with symptoms consistent with biliary obstruction. Percutaneous transhepatic cholangiography showed pancreatic and biliary duct dilatation as well as obstruction of the common bile duct, which extended into the left upper quadrant. Exploration showed ampullary obstruction several centimeters proximal to the line of resection. Sphincteroplasty was performed. The postoperative course was uncomplicated. The authors conclude that Peutz-Jeghers syndrome with polyps in the duodenum can markedly distort duodenal and ductal anatomy and can lead to ampullary obstruction.

Child↗
PubMed1984

[Co-existence of fibrous bone dysplasia and familial intestinal polyposis].

The aetiology of fibrous bone dysplasia is unknown. Combinations with endocrine and non-endocrine diseases are recognised. The co-existence of polyostotic fibrous dysplasia with Peutz-Jeghers syndrome has not been previously described. A patient is now reported who had both these diseases. They have in common a benign proliferative tendency in various organs, but the common denominator is unknown. The basic relationship between the conditions requires further observation and study.

Adult↗
PubMed2000

Gastrin is a target of the beta-catenin/TCF-4 growth-signaling pathway in a model of intestinal polyposis.

Mutations in the adenomatous polyposis coli (APC) tumor suppressor gene occur in most colorectal cancers and lead to activation of beta-catenin. Whereas several downstream targets of beta-catenin have been identified (c-myc, cyclin D1, PPARdelta), the precise functional significance of many of these targets has not been examined directly using genetic approaches. Previous studies have shown that the gene encoding the hormone gastrin is activated during colon cancer progression and the less-processed forms of gastrin are important colonic trophic factors. We show here that the gastrin gene is a downstream target of the beta-catenin/TCF-4 signaling pathway and that cotransfection of a constitutively active beta-catenin expression construct causes a threefold increase in gastrin promoter activity. APC(min-/+) mice overexpressing one of the alternatively processed forms of gastrin, glycine-extended gastrin, show a significant increase in polyp number. Gastrin-deficient APC(min-/+) mice, conversely, showed a marked decrease in polyp number and a significantly decreased polyp proliferation rate. Activation of gastrin by beta-catenin may therefore represent an early event in colorectal tumorigenesis and may contribute significantly toward neoplastic progression. The identification of gastrin as a functionally relevant downstream target of the beta-catenin signaling pathway provides a new target for therapeutic modalities in the treatment of colorectal cancer.

Adenomatous Polyposis Coli↗
PubMed1987

Nonfamilial intestinal polyposis and brain tumor in a 5-year-old girl.

A 5-year-old girl with glioblastoma multiforme and simultaneous adenocarcinoma in one of multiple colonic polyps is the youngest reported case of Turcot's syndrome. A literature survey and a classification based on family pedigree and pattern of inheritance are proposed.

Adenocarcinoma↗