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Results for “Intestinal Polyposis”

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At least 1,387 records · Page 77Linked to original sources
PubMed1984

A clinical and histopathological study of gastric polyps in familial polyposis coli.

Fundic gland area gastric polyps in familial polyposis coli (FPC) were compared with those in non-familial polyposis coli clinicopathologically to elucidate their histogenetic and biological characteristics. Some differences were observed in age, sex, and radiological and endoscopical features. Although the polyps were similar histologically, they showed an apparent histochemical difference between the two groups in periodic borohydride technique/potassium hydroxide/periodic acid-Schiff stain which demonstrates O-acylated sialic acid. The superficial and foveolar epithelium of the polyps was positive in 10 of 12 familial polyposis coli cases, while the epithelium was positive in only one of 13 non-familial polyposis coli cases with the same staining. These results suggest differences between the two groups in the degree of epithelial intestinal metaplasia. The presence of gastric polyps with O-acylated sialic acid therefore indicates the necessity of examination of the colorectum.

Adolescent↗
PubMed1996

Operations for familial adenomatous polyposis.

The purpose of this article is to discuss the advantages and disadvantages of surgical procedures designed to eliminate the risk of colorectal cancer, the surgical treatment of extracolonic polyps, and the management of desmoid tumors.

Adenomatous Polyposis Coli↗
PubMed1998

[Effect of proctocolectomy on fluid balance--comparison of conventional ileostomy, ileorectal anastomosis and ileoanal pouch operation].

Total colectomy for ulcerative colitis (UC) and familiar adenomatous polyposis coli (FAP) is mainly performed as an ileoanal Pouch procedure (IAP). Alternatives are ileorectal anastomosis (IRA) and conventional proctocolectomy with Brooke ileostomy (CPS). The different surgical techniques may influence the excretion of water and electrolytes in stool and urine and may lead to a higher risk for urolithiasis. We investigated patients (12 IAP, 12 IRA and 8 CPS) several years after surgery and compared them to twelve normal controls. Total fecal and urinary output was collected at two consecutive days. Volume and electrolytes were determined in stool and urine. The risk for urinary stone formation was calculated by nomograms. Fecal volume and sodium (Na+) excretion was increased in all therapy groups compared to controls. IAP and IRA had significant less stool volume and Na+ excretion compared to CPS. Augmented fecal Na+ excretion was compensated by reduction of renal output after colectomy compared to controls. There were no significant differences in the daily urine volume between any groups. There was no urolithiasis in any groups. The nomograms showed a risk for all groups and controls to develop urinary stones.

Adenomatous Polyposis Coli↗
PubMed2006

Hyperplastic polyposis and cancer of the colon with gastrinoma of the duodenum.

BACKGROUND: A 64-year-old woman presented to the emergency room with a 3-month history of intermittent abdominal cramps, accompanied by nausea, vomiting, anorexia, and decreased bowel movements consistent with a partial intestinal obstruction. She had a 12-year history of peptic ulcers, which had been treated with histamine-2 blockers. INVESTIGATIONS: Physical examination, abdominal X-ray, abdominal CT scan, colonoscopy and assessment of gastrin levels. DIAGNOSIS: Duodenal neuroendocrine neoplasm showing gastrin expression and stage III (T3N2M0), poorly differentiated adenocarcinoma of the cecum arising from hyperplastic polyposis. MANAGEMENT: Right-sided hemicolectomy with ileocolonic anastomosis, duodenal resection, leucovorin and 5-fluorouracil chemotherapy, annual colonoscopic surveillance, and polypectomy.

Adenocarcinoma↗
PubMedDate not supplied

[Complex estimation of proliferative activity of epithelial cells of the large intestine damaged by polyps and cancer].

Peculiarities of mitotic regime and expression of proliferating cell nuclear antigen were investigated in 18 polyps and 35 cases of colorectal cancer. Direct relationship between spectrum and degree of manifestation of proliferative activity, level of morphological malignant tumors and accumulation of oncopathology in the patient pedigrees was established.

Adenomatous Polyposis Coli↗
PubMed2004

Myh deficiency enhances intestinal tumorigenesis in multiple intestinal neoplasia (ApcMin/+) mice.

Monoallelic APC and biallelic MYH (homolog of Escherichia coli mutY) germ-line mutations are independently associated with a strong predisposition to colorectal adenomas and carcinoma in humans. Whereas mice heterozygous for mutant Apc develop intestinal tumors, mice homozygous for mutant Myh do not show increased tumor susceptibility. We analyzed the phenotype of Apc(Min/+)/Myh(-/-) mice and found that they developed significantly more adenomas in the small intestine than did Apc(Min/+)/Myh(+/+) or Apc(Min/+)/Myh(+/-) mice (median 231 versus 151 versus 152). In the large bowel, Apc(Min/+)/Myh(-/-) mice showed significant increases in the number of aberrant crypt foci. In addition, Apc(Min/+)/Myh(-/-) mice developed an increased number of mammary tumors. Molecular analyses suggested that at least 19% of intestinal tumors from Apc(Min/+)/Myh(-/-) mice had acquired intragenic Apc mutations rather than allelic loss. Consistent with a defect in base excision repair, three intragenic Apc mutations in polyps without allelic loss from Apc(Min/+)/Myh(-/-) mice were shown to be G:C to T:A transversions which resulted in termination codons; no such mutations were found in polyps from Apc(Min/+)/Myh(+/+) or Apc(Min/+)/Myh(+/-) mice. Tumors from Apc(Min/+)/Myh(+/-) mice harbored neither somatic mutations nor allelic loss at Myh. Thus, homozygous, but not heterozygous, Myh deficiency enhanced intestinal tumorigenesis in Apc(Min/+) mice. The excess small-bowel adenomas in Apc(Min/+)/Myh(-/-) mice, therefore, appear to be a model of MYH-associated polyposis in humans.

Adenoma↗
PubMed2003

Regional response leading to tumorigenesis after sulindac in small and large intestine of mice with Apc mutations.

Sulindac and other NSAIDs have been widely studied as potential chemopreventive agents for colon cancer. Short-term studies have shown adenomatous polyps to regress in patients with familial adenomatous polyposis (FAP). In this study the effect of sulindac on cancer as an endpoint was evaluated in ApcMin mice, a preclinical model of FAP with an Apc mutation in codon 850 that leads to gastrointestinal adenomas and carcinomas. Three groups of mice were studied all of which were fed AIN-76A diet: one group was fed AIN-76A diet alone, a second group received sulindac 200 p.p.m. premixed in the diet and a third group received sulindac 180 p.p.m. added in drinking water. ApcMin mice were killed 9 weeks after feeding was initiated. Mice receiving sulindac developed fewer tumors in the intestine overall; the major decrease in tumor development after sulindac was seen in the small intestine regardless of route of administration. In the large intestine, however, sulindac significantly increased the incidence, multiplicity and volume of tumors in the colon of ApcMin mice, a regional response to sulindac differing from previous reports. Quantitative measurements of apoptosis, Bax and Bcl-xL protein expression in the ApcMin mice revealed the ratio of Bax/Bcl-xL expression and apoptosis increased in the small intestine but decreased in the cecum, consistent with the regional tumorigenesis observed after sulindac. These findings thus suggest involvement of Bax and apoptosis in tumors developing after sulindac treatment in this mouse model.

Animals↗
PubMed2002

Microadenomatous lesions involving loss of Apc heterozygosity in the colon of adult Apc(Min/+) mice.

Mutations in the human adenomatous polyposis coli (APC) gene are causative for familial adenomatous polyposis (FAP), a rare condition in which numerous colonic polyps arise during puberty and, if left untreated, lead to colon cancer. Mouse model for human FAP, Apc(Min/+) mouse, contains a truncating mutation in the Apc gene and spontaneously develops intestinal adenomas. However, the distribution of tumors along the intestine found in Apc(Min/+) mice is different from that in human FAP. A majority of intestinal polyps in the Apc(Min/+) mice is known to be located in the small intestine but rarely detected in the colon. We report here that adult Apc(Min/+) mice develop dozens of microadenomatous lesions in the colon (>20 lesions/colon). Surprisingly, the vast majority of such adenomatous lesions consisting of colonic crypts were <300 microm in their greatest dimension, whereas lesions in the small intestine showed various sizes. The allelic loss analysis revealed that these adenomatous crypts in the colon have already lost the remaining allele of Apc. Such findings suggest that, in contrast to tumorigenesis in the small intestine, loss of heterozygosity of the Apc gene is not sufficient for tumor development in the colon of Apc(Min/+) mice. Our results may give an account for the low incidence of colonic tumors in Apc(Min/+) mice.

Adenomatous Polyposis Coli↗