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PubMed1999

Differential expression of prostaglandin endoperoxide H synthase-2 and formation of activated beta-catenin-LEF-1 transcription complex in mouse colonic epithelial cells contrasting in Apc.

Mutations in Apc underlie the intestinal lesions in familial adenomatous polyposis and are found in >85% of sporadic colon cancers. They are frequently associated with overexpression of prostaglandin endoperoxide H synthase-2 (PGHS-2) in colonic adenomas. It has been suggested that Apc mutations are linked mechanistically to increased PGHS-2 expression by elevated nuclear accumulation of beta-catenin-Tcf-LEF transcription complex. In the present study, we show that PGHS-2 is differentially expressed in mouse colonic epithelial cells with distinct Apc status. Cells with a mutated Apc expressed markedly higher levels of PGHS-2 mRNA and protein and produced significantly more prostaglandin E2 than cells with normal Apc. Using electrophoretic mobility shift assays, we demonstrate that DNA-beta-catenin-LEF-1 complex formation is differentially induced in these two cell lines in an Apc-dependent manner. Our data indicate that the differential induction of beta-catenin-LEF-1 complex correlates closely with differential expression of PGHS-2. These findings support the hypothesis that the differential expression of PGHS-2 is mediated through the proposed beta-catenin/Tcf-LEF signaling pathway.

Alleles↗
PubMed1987

The pouch as an alternative to permanent ileostomy.

Restorative proctocolectomy has become a realistic alternative to construction of a permanent stoma for patients with ulcerative colitis and familial polyposis coli. The operation restores intestinal continuity but continent patients have to open their bowels 4-5 times during the day, and over half have to rise at night to defaecate. The potential complications are considerable, but their frequency decreases with experience with the operation. This article reviews the place and results of ileoanal pouch anastomosis.

Adult↗
PubMed1986

[New observations in a case of Cronkhite-Canada syndrome].

We report about a 76 years old patient with Cronkhite-Canada syndrome. The diagnosis has been found with the following clinical symptoms: diarrhea, anorexia, alopecia, and onychotrophia. Laboratory values: severe hypoproteinemia (total serum protein 4.3 g/dl, albumin 2.4 g/dl); endoscopical and radiological findings: a generalized polyposis which involved the whole intestine except the oesophagus. As far as we saw in our literature-overview of 55 patients with Cronkhite-Canada syndrome, this patient had for the first time a carcinoma of the urinary bladder and a Bricker operation 17 years before the onset of his disease. Further we remarked a lack in the resorption of the enterally administered thyroidal hormones. The progress was fatal despite a parenteral hyperalimentation and a treatment with antibiotics and glucocorticoids.

Aged↗
PubMed2002

Wnt signaling regulates expression of the receptor tyrosine kinase met in colorectal cancer.

Overexpression of the receptor tyrosine kinase Met is an early event in the colorectal adenoma-carcinoma sequence. This suggests a link with disruption of adenomatous polyposis coli-controlled regulation of beta-catenin/T-cell factor (TCF)-mediated transcriptional activation, which is crucial in initiating tumorigenesis. Indeed, in intestinal biopsies from patients with familial adenomatous polyposis, we find Met already overexpressed in dysplastic aberrant crypt foci, the earliest neoplastic lesions of colorectal cancer (CRC). Moreover, in CRC cells, induction of dominant-negative TCF proteins and the consequent abrogation of beta-catenin/TCF-mediated transcriptional activation lead to a strong down-regulation of Met expression. Our results indicate that Met expression is part of a genetic program controlled by the Wnt pathway and suggest a role for Met in controlling the turnover and differentiation of intestinal epithelium.

Adenoma↗
PubMed2004

Adenomatous polyposis coli truncation mutations in 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-induced intestinal tumours of multiple intestinal neoplasia mice.

The heterocyclic amine 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) induces intestinal tumours in C57BL/6J-multiple intestinal neoplasia (Min)/+ mice. The main mechanism for PhIP-induced tumour induction in Min/+ mice is loss of the wild-type adenomatous polyposis coli (Apc) allele, i.e. loss of heterozygosity (LOH). In this study, single injections of either 10, 17.5 or 25 mg/kg PhIP on days 3-6 after birth all increased the mean number of small intestinal tumours two to three-fold, from 37.7 in controls to 124.8 in the PhIP-treated Min/+ mice. In total, we analysed 292 small intestinal tumours and 253 of these had LOH. The frequency of LOH in the Apc gene was 88, 93, 83 and 84% in tumours of 0, 10, 17.5 and 25 mg/kg PhIP-treated mice, respectively. Therefore, these lower doses of PhIP did not reduce the frequency of LOH, as found in our previous study with a single injection of 50 mg/kg PhIP (Mutat. Res. 1-2 (2002) 157). In the second part of this study, we wanted to characterise Apc truncation mutations from tumour samples apparently retaining the Apc wild-type allele from this and two previous experiments with PhIP-exposed Min/+ mice. In the first half of exon 15 in Apc, we verified 25 mutations from 804 tumour samples of PhIP-treated mice. Of these were 60% G-->T transversions, and 16% G deletions, indicating that these are the predominant types of PhIP-induced truncation mutations in the Apc gene in Min/+ mice. Most of the mutations were located between codon 989 and 1156 corresponding to the first part of the beta-catenin binding region. We also identified two Apc truncation mutations from 606 spontaneously formed intestinal tumours from untreated Min/+ mice, one C-->T transition and one T insertion, which were different from those induced by PhIP.

Animals↗
PubMedDate not supplied

[The diagnosis and surgical treatment of intestinal amebiasis].

Ninety-one patients with intestinal amebiasis (IA) were studied. All had been long suffering from IA due to the fact that it had not been diagnosed in time. Indications for emergency surgery were profuse hemorrhage, perforation of amebic ulcers, gangrene, and toxic dilatation of the large intestine. Planned operations were made in pseudopolyposis, strictures of the large intestine. Surgical treatment was performed along with specific therapy. Seven patients died due to late diagnosis, ineffective therapy and profound systemic and regional changes caused by these factors. It is necessary to differentiate ulcerative colitis, polyposis, and tumors of the large intestine with IA.

Adolescent↗
PubMed2001

Intestinal tumours induced by the food carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine in multiple intestinal neoplasia mice have truncation mutations as well as loss of the wild-type Apc(+) allele.

C57BL/6J-Min/+ (multiple intestinal neoplasia) is a murine model for familial adenomatous polyposis (FAP), where the mice are heterozygous for a nonsense Apc(Min) (adenomatous polyposis coli) mutation, and therefore develop numerous spontaneous adenomas in the small intestine and colon. Neonatal exposure of Min/+ mice to the food carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) (eight subcutaneous injections of 25 or 50 mg/kg PhIP to pups or 50 mg/kg PhIP to lactating dams) markedly increased (2--9-fold) the number of intestinal tumours, especially in the small intestine. We examined whether the Apc gene was affected in small intestinal and colonic tumours induced by PhIP. In spontaneous tumours formed in these mice, the main mechanism for tumour induction is loss of the wild-type Apc(+) allele, i.e. loss of heterozygosity (LOH). Also in the PhIP-induced tumours, this is a major mechanism, since large fractions of PhIP-induced tumours had LOH in APC: However, mechanisms other than LOH must also prevail, since a lower frequency of LOH was found in the small intestinal tumours from male mice exposed to PhIP either via breast milk (65%) or by direct injection (68%), compared with the untreated controls (92%). Tumours that had retained the wild-type Apc(+) allele were further analysed for presence of truncated Apc proteins with in vitro synthesized protein (IVSP) assay. Truncated Apc proteins, indicating truncation mutations in exon 15 of the Apc gene, were detected in 20% (8 of 40) of the tumours not showing LOH from the small intestine after PhIP exposure, all in segment 2 (codons 686--1217). Seventeen percent (2 of 12) of the colonic tumours had a truncated Apc protein in segment 3 (codons 1099--1693). Importantly, no truncated proteins were detected in tumours from unexposed mice with apparently retained wild-type Apc(+) allele. These results show that PhIP induces intestinal tumours in the Min/+ mice both by causing LOH and truncation mutations in the wild-type Apc(+) allele.

Adenoma↗
PubMed1993

Minute adenomas of the depressed type in familial adenomatous polyposis of the colon. A pathway to ordinary polypoid adenomas.

BACKGROUND: It has been thought that colorectal adenomas are polypoid from their beginning. Although depressed adenomas have been described, they have been considered an unusual form and have not been studied systemically. METHOD: More than 5000 colorectal adenomas in 24 resected large intestines of patients with familial adenomatous polyposis were examined by dissecting microscopic study. These adenomas were classified by their surface appearance as depressed, flat, or polypoid type. The frequencies and sizes of the three types were determined. RESULTS: In addition to ordinary polypoid adenomas, many adenomas of the depressed type were found. Of the 5287 adenomas detected, 635 (12.0%) were depressed, 967 (18.3%) were flat, and 3685 (69.7%) were polypoid. Depressed adenomas constituted approximately 15% of all adenomas smaller than 1.5 mm diameter. However, they were rare in those of 1.5-2.0 mm diameter and were not found among those of more than 2.0 mm in diameter. CONCLUSION: These findings suggest that some ordinary polypoid adenomas originate from minute depressed adenomas.

Adenoma↗
PubMed1984

The spectrum of polyposis.

Familial polyposis is a systemic defect of growth regulation. Extracolonic expressions are common and serious, about equal in risk to carcinoma of the large intestine. Periodic surveillance of the upper gastrointestinal tract is particularly important. More intensive surveillance of the large intestine may lead to better results in patients with polyposis who have carcinoma of the large intestine develop.

Abdominal Neoplasms↗
PubMed2002

Prostaglandin E(2) protects intestinal tumors from nonsteroidal anti-inflammatory drug-induced regression in Apc(Min/+) mice.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are antitumorigenic in humans as well as in animal models of intestinal neoplasia, such as the adenomatous polyposis coli (Min/+) (Apc(Min/+)) mouse. NSAIDs inhibit cyclooxygenase (COX) isozymes, which are responsible for the committed step in prostaglandin biosynthesis, and this has been considered the primary mechanism by which NSAIDs exert their antitumorigenic effects. However, mounting evidence suggests the existence of COX-independent mechanisms. In the present study, we attempted to clarify this issue by treating Apc(Min/+) mice bearing established tumors with NSAIDs (piroxicam and sulindac, 0.5 and 0.6 mg/mouse/day, respectively) for 6 days and concomitantly bypassing COX inhibition by treatment with the E prostaglandin (EP) receptor agonists 16,16-dimethyl-prostaglandin E(2) (PGE(2)) and 17-phenyl-trinor-PGE(2) (10 microg each, three times daily) administered via gavage and/or i.p. routes. Treatment with piroxicam and sulindac resulted in 95% and 52% fewer tumors, respectively, and a higher ratio of apoptosis:mitosis in tumors from sulindac-treated mice as compared with controls. These effects were attenuated by concomitant EP receptor agonist treatment, suggesting PGE(2) is important in the maintenance of tumor integrity. Immunological sequestration of PGE(2) with an anti-PGE(2) monoclonal antibody likewise resulted in 33% fewer tumors in Apc(Min/+) mice relative to untreated controls, additionally substantiating a role for PGE(2) in tumorigenesis. The EP receptor subtype EP1 mediates the effects of PGE(2) by increasing intracellular calcium levels ([Ca(2+)](i)), whereas antagonism of EP1 has been shown to attenuate tumorigenesis in Apc(Min/+) mice. We demonstrate that [Ca(2+)](i) is significantly elevated in tumors of Apc(Min/+) mice relative to the adjacent normal-appearing mucosa. Furthermore, treatment with piroxicam results in significantly lower [Ca(2+)](i) in tumors, and this effect is attenuated by concomitant treatment with the EP1/EP3 receptor agonist 17-phenyl-trinor-PGE(2). Overall, our results suggest that NSAIDs exert their antitumorigenic effects, in part, via interference with PGE(2) biosynthesis, and these effects may be mediated through changes in intracellular calcium levels.

16,16-Dimethylprostaglandin E2↗
PubMed2000

Cortisol producing adrenal adenoma--a new manifestation of Gardner's syndrome.

INTRODUCTION: Familial adenomatous polyposis (FAP) is an autosomal dominant disorder which typically presents with colorectal cancer in early adult life secondary to extensive adenomatous polyps of the colon. Gardner's syndrome is a variant of FAP in which desmoid tumors, osteomas and pigmented retinal lesions occur together with intestinal manifestations. The APC gene (adenomatous polyposis coli) at 5q21 is a tumor suppressor gene which is mutant in FAP. PATIENT: A 36 year old woman presented with a history of polyposis ventriculi, ovarian desmoid cysts, and disseminated desmoid tumors. Her familial history was unremarkable. On admission she complained weight gain, secondary amenorrhea, and episodes of hypertension followed by paroxysmal headache. RESULTS: Elevated urinary free cortisol (878 microg/24h), suppressed basal ACTH (< 5 pg/ml) and insuppressible serum cortisol after low dose dexamethasone (189 ng/ml) revealed adrenal Cushing's syndrome. Abdominal NMR showed an adrenal mass two centimeter in diameter with inhomogeneous contrast enhancement. Unilateral adrenalectomy was performed and an adrenal adenoma was diagnosed by histological criteria. For mutational detection DNA from peripheral blood leucocytes was extracted. A protein truncation test was performed, which revealed a termination mutation between codon 1099 and 1623 of the APC gene. Direct sequencing showed a point mutation in exon 15 of the APC gene at position 1542 (CAG --> TAG). This region is known to be altered in patients with extraintestinal manifestation of FAP. CONCLUSION: In patients with Gardner's syndrome adrenal tumors leading to hormonal excess should be considered. Whether mutations in the APC gene have implications in sporadic adrenal tumorigenesis needs to be proven.

Adenoma↗
PubMed2003

[Intestinal ganglioneuromatosis diagnosed in adult patients].

AIM: Intestinal ganglioneuromatosis is essentially described in children and rarely in adults. The purpose of this study was to evaluate the clinical pathological patterns of intestinal ganglioneuromatosis diagnosed in adult patients. MATERIALS AND METHODS: Ten patients were included in this study (6 men, 4 woman; mean age=55.4 years). The diagnosis was established from ileocolorectal biopsies (n=5) or from a surgical specimen (n=5). An immunohistochemical study was performed with antibodies directed against S100 protein, synaptophysin, PGP9.5, neurofilament, tau protein, c-Kit and c-Ret. Clinical symptoms, endoscopic data and outcome were retrospectively reviewed. RESULTS: The diagnosis of intestinal ganglioneuromatosis was established solely on the basis of the microscopic examination in all 10 cases. Three patients presented with acute occlusion. The endoscopic examination showed unusual spasticity of the colon or colectasia in 5 cases, raspberry-like polyps in 2 cases and finger-like polyps in 3 cases. Ganglioneuromatosis was characterized by diffuse Schwann cell hyperplasia expressing S100 protein in close contact to nerve fibers expressing neurofilament, tau protein, synaptophysin, PGP9.5 and to ganglion cells expressing c-Ret. There was no hyperplasia of interstitial cells of Cajal. Intestinal ganglioneuromatosis was localized in the mucosa in 9 cases and extended through the entire intestinal wall in 1 case. The finger-like polyps corresponded to ganglioneuromatosis, while the raspberry-like polyps corresponded to adenomas. Two patients had von Recklinghausen's disease, 1 had multiple endocrine neoplasia type 2B and 1 had Cowden's disease. Intestinal ganglioneuromatosis was associated with nonfamilial adenomatous polyposis in 2 patients and colonic adenocarcinoma in 1 patient. The patients with finger-like polyps had no associated disease. CONCLUSION: Intestinal ganglioneuromatosis in adults is distinctive from that in children. In adults, intestinal ganglioneuromatosis is always a microscopic diagnosis although finger-like polyps observed at colonoscopy may be suggestive. Gastroenterologists must be aware of the higher risk of occlusion and intestinal neoplasia.

Adult↗
PubMedDate not supplied

Intestinal adenomas of Min-mice lack enterochromaffin cells, and have increased lysozyme production in non-Paneth cells.

BACKGROUND: Adenomatous polyposis coli (APC) are important in maintaining normal epithelial mucosa. Intestinal tissues with mutations in Apc have disturbed cell proliferation, differentiation and migration. Paneth and enterochromaffin cells were studied in the intestine and intestinal adenomas from Min-mice with heterozygote and homozygote mutations in Apc, respectively. MATERIALS AND METHODS: The presence of Paneth and enterochromaffin cells in normal intestine and adenomas from Min-mice was studied in sections stained with lysozyme/PAS and connexin32. RESULTS: Min-mice intestinal adenomas had an increased number of lysozyme-producing Paneth/goblet and non-Paneth cells and a reduced number of enterochromaffin cells. The large intestine had a significantly higher number of enterochromaffin cells than the small intestine and more were seen in the large intestine of Min- compared with wt-mice. CONCLUSION: Altered cell differentiation in adenomas might be caused by different response to Wnt-signalling, while an increased number of enterochromaffin cells in the large intestine is rather an effect of a heterozygous Apc(Min) mutation.

Adenomatous Polyposis Coli↗
PubMed1996

Ultrastructural changes in the small intestinal epithelium after total resection of the colon.

UNLABELLED: The aim of the study was to analyze ultrastructural changes in the mucosa of the small intestine after total resection of the colon in 29 patients (familial polyposis in 21, ulcerative colitis in 8). We studied specimens of the small intestinal mucosa obtained from ano- and rectoscopy. The specimens were routinely processed for transmission electron microscopy. Early after the operation (up to 4-5 months) we observed marked structural disorders of the mucosal epithelium and regenerative cell atypia (dysplasia-like changes). At 6 months after the operation we found rapidly progressing normalization of the epithelial mucosa and its mimicking the epithelium of the colon: increased amount of mucous cells, formation of vacuolized cells, almost complete atrophy of microvilli on the surface of enterocytes, increase of the intercellular space (retention space). Foci with dysplasia features were quite numerous in group I, in contrast to group II where they were sporadic. CONCLUSION: the epithelium of small intestinal mucosa has the ability of convergence towards the epithelium of colon.

Adenomatous Polyposis Coli↗
PubMed2004

[Familial adenomatous polyposis with extracolonic manifestations--case report].

The familial adenomatous polyposis syndrome is an autosomal dominant inherited disease characterized by progressive development of multiple adenomatous polyps throughout the colon and rectum. Due to the malignant potential of adenomatous polyps, colorectal cancer develops in 100% of cases, approximately 10-15 years after the onset of symptoms. Extracolonic manifestations of the disease including adenomatous polyps of the stomach, duodenum, small intestine and periampullatory region are rare. The etiology of the disease is germline mutation at the site of tumor suppressor gene located on chromosomes 5q21-22. A case is described of a 48-year-old man hospitalized at the Department of Abdominal Surgery, Sveti Duh General Hospital in Zagreb for the treatment of familial adenomatous polyposis syndrome. For some time the patient reported occasional abdominal pain, frequent stools and diarrhea with blood, anemia and body weight loss. Laboratory, radiology and endoscopy examinations verified multiple adenomatous polyps of the colon and rectum, also with polyps of the stomach, duodenum and jejunum. Histopathology confirmed the polyps to show moderately poorly differentiated cylindric epithelium and moderate to severe dysplasia. Radical surgery was required, so proctocolectomy with Brook ileostomy was performed. The postoperative recovery and wound healing were normal. The patient was discharged twelve days of the surgery for home care. Oncologic treatment was suggested. Verified extracolonic manifestations of the disease require periodical endoscopic follow up and possible treatment.

Adenomatous Polyposis Coli↗
PubMed1986

Solitary hamartomatous polyp of the duodenum in the absence of familial polyposis.

A large hamartomatous polyp of the Peutz-Jegher type was discovered in the distal duodenum by endoscopy in a patient with occult gastrointestinal bleeding. There were no other polyps in the gastrointestinal tract and the patient lacked any stigmata associated with the familial polyposis syndromes. This is the second well-documented case of an isolated hamartomatous polyp of the Peutz-Jegher type in the small intestine occurring in the absence of familial polyposis.

Adenomatous Polyposis Coli↗
PubMed1975

Hereditary polypoid diseases of the gastrointestinal tract: a working classification.

Almost all published cases of hereditary intestinal polypoid diseases can be meaningfully classified into a relatively few distinct syndromes including familial polyposis of the colon, Peutz-Jeghers syndrome, and juvenile polyposis. Familial polyposis is characterized by the development of numerous adenomatous polyps of the colon and subsequent development of colorectal carcinoma in nearly all patients. Extracolonic manifestations are common but do not influence the premalignant nature of this syndrome. Peutz-Jeghers syndrome is identifiable by a combination of circumoral melanin pigmentation and hamartomatous polyps. These polypoid lesions have an unusually wide distribution and may occur in the respiratory, gastrointestinal, or genitourinary tract. There is a small but definite increased incidence of gastrointestinal cancer in these patients. Juvenile polyposis presents a more variable spectrum. In one form there is extensive intestinal involvement leading to diarrhea, inanition, and increased susceptibility to infection. Another form is limited to the colon and easily confused with familial polyposis. With the third form, there is involvement of the stomach, intestines, and colon, which makes it easily mistaken for the Peutz-Jeghers syndrome.

Adult↗