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At least 271 records · Page 15Linked to original sources
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↗
PubMed2003

The cohesin SMC3 is a target the for beta-catenin/TCF4 transactivation pathway.

The structural maintenance of chromosome protein SMC3 is a component of the cohesin complex that mediates sister chromatid cohesion and segregation in prokaryotes and eukaryotes. It is also present extracellularly in the form of a chondroitin sulfate proteoglycan known as bamacan. We have found previously that SMC3 expression is elevated in a large fraction of human colon carcinomas. The additional finding that the protein is significantly increased in the intestinal polyps of ApcMin/+ mice has led us to hypothesize that SMC3 expression is linked to activation of the APC/beta-catenin/TCF4 pathway. The immunohistochemical analysis of colon adenocarcinomas from clinical specimens revealed that beta-catenin and SMC3 antigens co-localize with maximal stain intensity within the transformed areas. Cloning and sequencing of 1578 bp of the human SMC3 promoter unveiled the presence of seven putative consensus sequences for beta-catenin/TCF4 binding, two of which are conserved in the mouse Smc3 promoter. Transient transfection experiments in HCT116 and SW480 human colon carcinoma cells using deletion and mutated promoter constructs in luciferase reporter vectors confirmed that the putative sites, the first located at -48 bp and the second located at -701 bp, are susceptible to beta-catenin/TCF4 transactivation. Co-transfection with a beta-catenin expression vector enhanced the promoter activity whereas E-cadherin had the opposite effect. Binding of beta-catenin/TCF4 complexes from SW480 nuclear extracts to these sequences was confirmed by electrophoretic shift and supershift mobility assays. Altogether these results are consistent with the idea that the beta-catenin/TCF4 transactivation pathway contributes to SMC3 overexpression in intestinal tumorigenesis.

Animals↗
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↗
PubMed2002

Sonographic diagnosis of multiple small-bowel intussusceptions in Peutz-Jeghers syndrome: a case report.

Peutz-Jeghers syndrome (PJS) is a rare, though well-described, hereditary polyposis syndrome associated with mucocutaneous pigmentation that typically presents in the second decade of life with complications related to intestinal polyps. We present two cases of teenaged girls presenting with small-bowel intussusceptions within a 3-month period. Sonographic examinations readily revealed small-bowel intussusceptions with secondary small-bowel obstruction. In both the symptoms were less severe than one would expect given the underlying pathology found at subsequent surgery. Sonographic imaging with pathologic correlation is provided.

Child↗
PubMed2001

Absence of post-translational aspartyl beta-hydroxylation of epidermal growth factor domains in mice leads to developmental defects and an increased incidence of intestinal neoplasia.

The BAH genomic locus encodes three distinct proteins: junctin, humbug, and BAH. All three proteins share common exons, but differ significantly based upon the use of alternative terminal exons. The biological roles of BAH and humbug and their functional relationship to junctin remain unclear. To evaluate the role of BAH in vivo, the catalytic domain of BAH was specifically targeted such that the coding regions of junctin and humbug remained undisturbed. BAH null mice lack measurable BAH protein in several tissues, lack aspartyl beta-hydroxylase activity in liver preparations, and exhibit no hydroxylation of the epidermal growth factor (EGF) domain of clotting Factor X. In addition to reduced fertility in females, BAH null mice display several developmental defects including syndactyly, facial dysmorphology, and a mild defect in hard palate formation. The developmental defects present in BAH null mice are similar to defects observed in knock-outs and hypomorphs of the Notch ligand Serrate-2. In this work, beta-hydroxylation of Asp residues in EGF domains is demonstrated for a soluble form of a Notch ligand, human Jagged-1. These results along with recent reports that another post-translational modification of EGF domains in Notch gene family members (glycosylation by Fringe) alters Notch pathway signaling, lends credence to the suggestion that aspartyl beta-hydroxylation may represent another post-translational modification of EGF domains that can modulate Notch pathway signaling. Previous work has demonstrated increased levels of BAH in certain tumor tissues and a role for BAH in tumorigenesis has been proposed. The role of hydroxylase in tumor formation was tested directly by crossing BAH KO mice with an intestinal tumor model, APCmin mice. Surprisingly, BAH null/APCmin mice show a statistically significant increase in both intestinal polyp size and number when compared with BAH wild-type/APCmin controls. These results suggest that, in contrast to expectations, loss of BAH catalytic activity may promote tumor formation.

Amino Acid Sequence↗
PubMed1996

Suppression of intestinal polyposis in Apc delta716 knockout mice by inhibition of cyclooxygenase 2 (COX-2).

Two cyclooxygenase isozymes catalyze conversion of arachidonic acid to prostaglandin H2: constitutive COX-1 and inducible COX-2. To assess the role of COX-2 in colorectal tumorigenisis, we determined the effects of COX-2 gene (Ptgs2) knockouts and a novel COX-2 inhibitor on Apc delta716 knockout mice, a model of human familial adenomatous polyposis. A Ptgs2 null mutation reduced the number and size of the intestinal polyps dramatically. Furthermore, treating Apc delta716 mice with a novel COX-2 inhibitor reduced the polyp number more significantly than with sulindac, which inhibits both isoenzymes. These results provide direct genetic evidence that COX-2 plays a key role in tumorigenesis and indicate that COX-2-selective inhibitors can be a novel class of therapeutic agents for colorectal polyposis and cancer.

Adenomatous Polyposis Coli↗
PubMed1979

Desmoid tumors and mesenteric fibromatosis in Gardner's syndrome: report of kindred 109.

Kindred 109, from which Gardner's syndrome was first described, now has 224 members, 28 of whom have inherited the syndrome. Among the group of 28, desmoid tumors or mesenteric fibromatosis or both have developed in eight (29%). In four patients, the fibrous dysplasia appeared to originate in postsurgical abdominal incisional scars; in two of these cases, the mesenteric involvement resulted in death. In one patient, the process was present in the mesentery at the original operation. In three patients, the fibrous dysplastic lesions were extraincisional, with no known trauma associated with their occurrence.

Abdominal Muscles↗
PubMed1977

Diet and metabolism: large-bowel cancer.

Epidemiological data demonstrate that colon cancer incidence is associated mainly with high dietary fat consumption. Studies in metabolic epidemiology indicate that high fat intake influences both the amount and type of bile acids and neutral sterols and intestinal microflora acting on these compounds which may contain tumorigenic activity for the colon. This is compatible with the results of studies comparing populations with high or low risk for the colon cancer and patients with colon cancer.

Bacteria↗