PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Intestinal Polyps”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources
PubMed1989

Mesenteric fibromatosis in Gardner's syndrome.

Gardner's syndrome, first described in the 1950s, is a composite clinical entity characterized by intestinal polyps, osteomas, fibromas, and epidermal cysts. A case of mesenteric fibromatosis in Gardner's syndrome is presented. Whereas most of the literature on this subject stresses the significance of the intestinal polyposis and its premalignant potential, in this paper the serious significance of the intraabdominal fibromas is stressed. This case demonstrates an unusual complication of erosion of this tumor into the small intestine, resulting in multiple intestinal fistulae with abscess formation. Surgical management of this problem necessitated resection of the fibroma and involved small intestine. A review of the literature is presented.

Adult↗
PubMed2000

Expression analysis of the group IIA secretory phospholipase A(2) in mice with differential susceptibility to azoxymethane-induced colon tumorigenesis.

The murine non-pancreatic secretory phospholipase A(2) (sPLA(2)) has been proposed as a tumor modifier of multiple intestinal neoplasia (Min). A genetic polymorphism in the mouse gene that causes a disruption in exon 3 results in loss of functional protein. Mouse strains with a disrupted sPLA(2) gene are susceptible to the Min phenotype and develop numerous intestinal polyps, whereas mice with normal sPLA(2) develop only a limited number of polyps. The following study was undertaken to test the hypothesis that sPLA(2) plays an equivalent role in murine susceptibility to the colon carcinogen azoxymethane (AOM). sPLA(2) status was confirmed by sequencing in mice that are highly susceptible (A/J), susceptible (SWR/J) and resistant (AKR/J) to AOM-induced tumorigenesis. Constitutive expression of sPLA(2) mRNA was compared in small intestine and colon of untreated mice using semi-quantitative RT-PCR. Whereas mRNA expression was nearly absent in A/J mice, AKR/J mice exhibited extensive expression throughout the intestine. Despite the wild-type sPLA(2) gene, colonic mRNA expression in SWR/J mice was significantly lower relative to AKR/J. Immunohistochemical analysis of sPLA(2) protein confirmed the mRNA data. The effect of AOM on colonic sPLA(2) expression was also examined. Twenty-four weeks after the last of six weekly injections of AOM (10 mg/kg i.p.), RT-PCR analysis of distal colons revealed a significant increase in mRNA in normal-appearing epithelium and tumor tissue from AOM-treated mice relative to controls. However, there was no corresponding increase in protein expression in A/J mice. The absence of sPLA(2) expression within control colons of tumor-susceptible A/J mice together with low expression in SWR/J colons is consistent with its potential role as an intestinal tumor modifier, but the carcinogen-induced increase in expression raises doubts as to the significance of sPLA(2) in inhibiting carcinogenesis.

Animals↗
PubMedDate not supplied

Small-intestinal involvement in familial polyposis diagnosed by operative intestinal fiberscopy: report of four cases.

Operative intestinal fiberscopy, in which the duodenal fiberscope was introduced during laparotomy for colectomy in familial polyposis via the enterotomy opening, permitted the demonstration of small intestinal polyps in six of seven consecutive cases. Four of the six patients had adenomatous polyps in the proximal jejunum, including one patient with the concomitant presence of ileal adenomas. Polyposis due to lymphoid hyperplasia in the terminal ileum was found in three patients. Preoperative upper gastrointestinal surveys revealed adenomas in the duodenums of all seven patients, adenomas in the gastric antrum in three, and multiple hamartomas in the gastric corpus in two. Thus, in familial polyposis or Gardner's syndrome, more or less the entire gastrointestinal tract seems to be involved and the term "gastrointestinal polyposis" seems to describe these conditions.

Adenoma↗
PubMed1994

Ganglioneuromas of the gastrointestinal tract. Relation to Von Recklinghausen disease and other multiple tumor syndromes.

We studied 43 patients with ganglioneuromas of the gastrointestinal tract accessioned at the Armed Forces Institute of Pathology (AFIP) from 1940 to 1990 in order to determine their relation to von Recklinghausen's disease and other multiple tumor syndromes. They fell into three groups: polypoid ganglioneuroma (28 patients); ganglioneuromatous polyposis (7 patients); and diffuse ganglioneuromatosis (8 patients). Follow-up (1-24 years, average 8 years) for 16 of 28 patients with polypoid ganglioneuroma showed that none of these patients developed von Recklinghausen's disease or evidence or multiple tumor syndromes. Three of seven patients with ganglioneuromatous polyposis were alive and well but were reported to have multiple cutaneous lipomas and one reported a family history of multiple intestinal polyps. For seven of eight patients, diffuse ganglioneuromatosis was associated with other tumors, namely multiple endocrine neoplasia type IIb, multiple ganglioneuromas and neurofibromas limited to the gastrointestinal tract, von Recklinghausen's disease and neurogenic sarcoma. We conclude that the solitary polypoid ganglioneuroma of the gastrointestinal tract is not associated with the subsequent development of von Recklinghausen's disease or multiple endocrine neoplasia. All three forms of gastrointestinal ganglioneuromatous disease appear to be largely centered in the colon and rectum, unlike neurofibromas and neurofibromatosis, which, in our experience, occur more commonly in the small intestine and stomach.

Adult↗
PubMed1999

Germline and somatic mutations of the STK11/LKB1 Peutz-Jeghers gene in pancreatic and biliary cancers.

Peutz-Jeghers syndrome (PJS) is an autosomal-dominant disorder characterized by hamartomatous polyps in the gastrointestinal tract and by pigmented macules of the lips, buccal mucosa, and digits. Less appreciated is the fact that PJS also predisposes patients to an increased risk of gastrointestinal cancer, and pancreatic cancer has been reported in many PJS patients. It was recently shown that germline mutations of the STK11/LKB1 gene are responsible for PJS. We investigated the role of STK11/LKB1 in the development of pancreatic and biliary cancer in patients with and without the PJS. In a PJS patient having a germline splice site mutation in the STK11/LKB1 gene, sequencing analysis of an intestinal polyp and pancreatic cancer from this patient revealed loss of the wild-type allele of the STK11/LKB1 gene in the cancer. Inactivation of STK11/LKB1, by homozygous deletions or somatic sequence mutations coupled with loss of heterozygosity, was also demonstrated in 4-6% of 127 sporadic pancreatic and biliary adenocarcinomas. Our results demonstrate that germline and somatic genetic alterations of the STK11/LKB1 gene may play a causal role in carcinogenesis and that the same gene contributes to the development of both sporadic and familial forms of cancer.

AMP-Activated Protein Kinase Kinases↗