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PubMed1992

DNA adducts detected by 32P-postlabelling, in the intestine of rats given bile from patients with familial adenomatous polyposis and from unaffected controls.

Duodenal adenomas are common in patients with familial adenomatous polyposis (FAP) and cluster around the papilla, suggesting the involvement of bile in their development. Using 32P-postlabelling we determined levels of DNA adducts in the small bowel and colon of rats treated with bile from FAP and control patients. We found a significantly higher level of adducts in the small bowel of rats treated with FAP gallbladder bile compared with control gallbladder bile (P = 0.0034). This result supports the hypothesis that bile plays a role in the development of neoplasia in the foregut of FAP patients.

Adenomatous Polyposis Coli↗
PubMed1989

HLA typing intestinohepatic schistosomiasis.

Patients with simple and/or complicated intestinal bilharziasis and normal controls were chosen for CBC, complete urine and stool analysis, liver function tests, liver biopsy, sigmoidoscopy and rectal biopsy. HLA typing was done by microcytotoxicity test. A statistically significant increased frequency of HLA-B8 antigen was present in with or without polyposis and with or without hepatosplenomegaly, as compared to controls (P less than 0.01). Also HLA-B8 showed a statistically significant increased frequency in those with or without polyposis and with hepatosplenomegaly and without polyposis (P less than 0.05). The HLA-A25 and A26 showed a significant increased frequency among all groups (P less than 0.05). HLA-A1, A9, B18 were variable in frequency among all groups. It was concluded that patients with bilharzial hepatosplenomegaly specially with intestinal polyposis have a high frequency of HLA-B8.

Adolescent↗
PubMed1998

The sulfide metabolite of sulindac prevents tumors and restores enterocyte apoptosis in a murine model of familial adenomatous polyposis.

Sulindac, a non-steroidal anti-inflammatory drug (NSAID), is effective in treating intestinal adenomas in humans with Familial Adenomatous Polyposis (FAP) and in preventing intestinal tumors in the C57Bl/6J-Min+ (Min) mouse, an animal model of FAP. Sulindac is a prodrug metabolized by the liver and intestinal flora to a sulfone, which has no anti-inflammatory activity, and a sulfide, which is the active anti-inflammatory metabolite. In this study, we determined which of these metabolites is responsible for the anti-tumor effect of sulindac in Min mice. Min mice were treated with either sulindac sulfone or sulindac sulfide (0.5 +/- 0.1 mg/day). Min mice and homozygous C57Bl/6J-(+/+) normal litter-mates lacking the Apc mutation (+/+) were used as controls. At 110 days of age, all mice were euthanized and their intestinal tracts examined. Control Min mice had 33.2 +/- 6.6 tumors per mouse compared to 0.6 +/- 0.3 tumors for sulindac sulfide-treated Min mice (P < 0.001) and 21.9 +/- 4.5 tumors per mouse for sulindac sulfone-treated Min mice (P > 0.05). Decreased enterocyte apoptosis was observed in Min control mice and Min mice treated with sulindac sulfone. Sulindac sulfide restored to normal the level of apoptosis in the mucosa of Min animals and decreased levels of PGE2 in the small intestine of treated Min animals by 59% (P < 0.001). These data suggest that the anti-tumor effect of sulindac in Apc-deficient animals is mediated by the sulfide metabolite and correlates with suppression of tissue prostaglandin synthesis.

Adenomatous Polyposis Coli↗
PubMed2004

The role of video capsule endoscopy in the diagnosis of digestive diseases: a review of current possibilities.

Video capsule endoscopy represents a significant advance in the investigation of intestinal diseases. The performance of the procedure and indications are reviewed here in order to establish guidelines for its use, in accordance with current knowledge from the published literature. Capsule endoscopy is performed in patients who have fasted for 12 h, but who are allowed to drink 2 h after and to eat 4 h after ingesting the capsule. Software features highlighting suspected blood and allowing simultaneous viewing of two images reduce the time required to review the findings, as well as improving the diagnostic yield. Pacemakers and other electrical medical devices are no longer a contraindication to the procedure. Indications that have been validated include obscure digestive bleeding, intestinal lesions related to nonsteroidal anti-inflammatory drugs, and familial polyposis. Capsule endoscopy frequently detects intestinal lesions in patients with Crohn's disease and could become the first-choice examination in patients with suspected Crohn's disease after conventional endoscopic investigations. Other indications currently under evaluation include celiac disease, pediatric indications, and examination of other parts of the gastrointestinal tract.

Contraindications↗
PubMed1996

Frequency and histological appearance of adenomas in multiple intestinal neoplasia mice are unaffected by severe combined immunodeficiency (scid) mutation.

Well-characterized murine mutations are powerful analytical tools for the genetic analysis of tumorigenesis. We crossed the multiple intestinal neoplasia (Min) allele of adenomatous polyposis coli (Apc), which produces a profound pre-disposition to intestinal neoplasia, with the severe combined immunodeficiency (scid) mutation, which causes defective double-strand DNA repair and severe immunodeficiency, on the common C57BL/6J genetic background to assay for any combined effect on intestinal tumorigenesis. Several phenotypic traits were exacerbated in an apparently additive manner in the double mutant mice, including reduced immunoglobulin levels, reduced body weight and increased morbidity. However, quantitation and histological evaluation of polyp phenotype indicated that these mutations did not interact to affect either polyp frequency or progression. Thus, neither genome instability nor lack of immunosurveillance conferred by scid contributes to intestinal polyps in this model.

Adenomatous Polyposis Coli↗
PubMed1997

Adenocarcinoma arising in "J" pouch after total proctocolectomy for familial polyposis coli.

A patient of familial adenomatous polyposis (FAP) without extra intestinal lesions is presented. The patient underwent a proctocolectomy with J pouch ileal reservoir with an ileoanal anastomosis. The clinical course was further complicated by an adenocarcinoma developing in the J pouch. This was excised totally and a terminal illeostomy was constructed. The aim of doing a prophylactic proctocolectomy in familial polyposis coli is to prevent a malignancy developing and to restore function with an illeoanal pouch. However polyps can occur in the gastric, duodenal and intestinal mucosa, which can lead to malignancy. Greater awareness and close follow up is needed even after prophylactic proctocolectomy.

Adenocarcinoma↗
PubMed2003

Lymphodepletion in the ApcMin/+ mouse model of intestinal tumorigenesis.

Germ line mutations in the Adenomatous polyposis coli tumor suppressor gene cause a hereditary form of intestinal tumorigenesis in both mice and man. Here we show that in Apc(Min/+) mice, which carry a heterozygous germ line mutation at codon 850 of Apc, there is progressive loss of immature and mature thymocytes from approximately 80 days of age with complete regression of the thymus by 120 days. In addition, Apc(Min/+) mice show parallel depletion of splenic natural killer (NK) cells, immature B cells, and B progenitor cells in bone marrow due to complete loss of interleukin 7 (IL-7)-dependent B-cell progenitors. Using bone marrow transplantation experiments into wild-type recipients, we have shown that the capacity of transplanted Apc(Min/+) bone marrow cells for T- and B-cell development appears normal. In contrast, although the Apc(Min/+) bone marrow microenvironment supported short-term reconstitution with wild-type bone marrow, Apc(Min/+) animals that received transplants subsequently underwent lymphodepletion. Fibroblast colony-forming unit (CFU-F) colony assays revealed a significant reduction in colony-forming mesenchymal progenitor cells in the bone marrow of Apc(Min/+) mice compared with wild-type animals prior to the onset of lymphodepletion. This suggests that an altered bone marrow microenvironment may account for the selective lymphocyte depletion observed in this model of familial adenomatous polyposis.

Adenomatous Polyposis Coli↗
PubMed2001

Variability in the severity of colonic disease in familial adenomatous polyposis results from differences in tumour initiation rather than progression and depends relatively little on patient age.

INTRODUCTION: As large scale genetic analysis becomes increasingly efficient, attention is turning to problems arising from inaccurate measurement of the phenotype. We have investigated the underlying basis of variation in disease severity in the large intestine of familial adenomatous polyposis (FAP) patients. The development of objective and reproducible measures may have future use in genetic studies, such as analysis of modifier genes. METHODS: We examined the ratio of adenomas to crypts from microscopic slides taken from all parts of the colon of 44 resected FAP specimens. These findings were compared with a carefully reported macroscopic polyp count. Age dependency of adenoma counts (in the period around colectomy) was also analysed. RESULTS: The adenoma:crypt ratio strongly correlated with reported macroscopic polyp count (r=0.82, p<0.001) with no significant residual variation. Polyp density measured using the adenoma: crypt ratio did not vary significantly within an individual colon. Apparent visible variation in polyp density within any colon was not found at the microscopic level. There was no detectable age related increase in macroscopic adenoma count between siblings over the age range at which colectomies were performed. DISCUSSION: The severity of colonic polyposis in FAP can be determined accurately by counting the adenoma:crypt ratio in sections derived from stored tissue blocks. Variation between patients-dependent on APC genotype and, probably, modifier genes-is manifest at both the microscopic and macroscopic levels. Thus variation in disease severity is more likely to result from different rates of tumour initiation than from differences in progression of microadenomas to macroscopic tumours. The absence of a detectable relationship between adenoma number and age (over the range studied) suggests that most tumours may be initiated relatively early in the patient's life, perhaps at a time of particular susceptibility.

Adenomatous Polyposis Coli↗
PubMed1995

Diagnosis and therapy of hereditary polyposis syndromes.

The hereditary polyposis syndromes include the adenomatous polyposis syndromes (familial adenomatous polyposis and Gardner syndrome, and Turcot syndrome) and the hamartomatous polyposis syndromes (Peutz-Jeghers syndrome, juvenile polyposis, and Cowden's disease). The adenomatous polyposis syndromes are characterized by numerous adenomatous polyps throughout the entire colon and a spectrum of extracolonic manifestations; they invariably progress to colorectal cancer without appropriate intervention. The hamartomatous polyposis syndromes are characterized by diffuse intestinal or colonic hamartomatous polyps, such as juvenile polyps. Although hamartomatous polyps have virtually no malignant potential, the hamartomatous polyposis syndromes are associated with increased risk of cancer, both within and outside the small intestine and the colon. Diagnosis of symptomatic polyposis is by colonoscopy, but in presymptomatic screening of familial adenomatous polyposis, genetic testing can be effective, and it is becoming increasingly available though research laboratories. Management involves treatment of affected individuals, counseling of patients and their families, screening of at-risk individuals, and surveillance of affected patients for extracolonic cancers. Treatment of adenomatous polyposis is primarily colectomy during the second or third decade. For the hamartomatous polyposis syndromes, surveillance for early cancers and their excision remain the only practical, although not totally satisfactory, approaches.

Adenomatous Polyposis Coli↗
PubMed2001

Early phase of intestinal mantle cell lymphoma: a report of two cases associated with advanced colonic adenocarcinoma.

Intestinal mantle cell lymphoma characteristically produces multiple polyps, a finding reported as multiple lymphomatous polyposis. The early stages of intestinal mantle cell lymphoma before polyp formation and the pattern of initial lymph node invasion, however, have not been described. We recently encountered two cases of intestinal mantle cell lymphoma in their early development found incidentally associated with advanced colonic adenocarcinoma. We present herein the clinical, histopathological, immunohistochemical, and molecular genetic features of these two cases. In one case, a single polypoid mass was found with invasion limited to mucosa and submucosa of the terminal ileum and without lymph node compromise. In the second case, there were multiple mucosal aggregates of neoplastic cells without formation of polyps. Regional lymph nodes in the latter case showed either partial or complete involvement by lymphoma. In both cases, immunohistochemistry (CD20+, CD5+, cyclin D1+, CD10-, and CD23-), and demonstration of clonal immunoglobulin heavy chain and bcl-1 gene rearrangements by PCR analysis confirmed the diagnosis of mantle cell lymphoma.

Adenocarcinoma↗
PubMed2000

Identification and quantification of aberrant crypt foci in the colon of Min mice--a murine model of familial adenomatous polyposis.

Min mice are heterozygous for a nonsense mutation in the murine adenomatous polyposis coli (APC) gene and spontaneously develop multiple intestinal neoplasms similar to the familial adenomatous polyposis (FAP) syndrome in humans. Aberrant crypt foci (ACF) are assumed to be preneoplastic lesions in both murine and human colon carcinogenesis and have been observed in FAP patients. Light microscopic examination of the colonic mucosa of 42 Min mice did not show even a single 'classical' ACF on the basis of previously defined criteria, specifying that they are elevated above the surrounding mucosa. However, in Min mice we discovered aberrant crypt foci of a different type, which we denoted ACF(Min). In contrast to the classical type, ACF(Min) were not elevated above the surrounding mucosa, their detection was totally dependent on methylene blue staining and transillumination, and they could not be identified with scanning electron microscopy. Histopathologic examination of ACF(Min) showed dysplastic crypts, similar to those found in larger lesions--that is, microadenomas in the Min mouse. The number of ACF(Min) increased up to the age of 6 weeks and then seemed to remain at a constant level of approximately four per colon. In conclusion, by transillumination of whole-mount preparations stained with methylene blue, we have identified and quantified small microscopic lesions that may be precursors of colonic adenomas in Min mice.

Adenomatous Polyposis Coli↗
PubMed2002

[COX inhibitor, suppression of polyposis, and chemoprevention].

Early experiments using carcinogen-induced rat intestinal tumor models demonstrated the inhibitory effects of non-steroidal anti-inflammatory drugs (NSAIDs) on intestinal tumorigenesis. Furthermore, epidemiological studies and clinical trials for familial adenomatous polyposis (FAP) patients supported the possibility that NSAIDs can be used as chemopreventive agents. The major target molecules of NSAIDs are cyclooxygenases (COX), which catalyze the rate-limiting step of prostaglandin biosynthesis. Two isoenzymes of COX have been identified: COX-1 and COX-2. Whereas COX-1 is expressed constitutively in most tissues and responsible for tissue homeostasis, COX-2 is inducible and plays an important role in inflammation and tumorigenesis. A genetic study using compound mutant mice of COX-2-/- and Apc delta 716, a model for human familial adenomatous polyposis (FAP), directly demonstrated that induction of COX-2 is critical for intestinal polyp formation. Numerous studies have also demonstrated that COX-2-selective inhibitors suppress intestinal polyp formation in Apc gene-mutant mice and xenografted cancer cell growths. In addition, stimulation of angiogenesis is one of the major effects by COX-2 expression that is induced in the polyp stromal cells. These data from animal model studies should be helpful in understanding the in vivo mechanism(s) of tumor suppression by NSAIDs or COX-2 inhibitors. Here, we review the animal studies that reported the suppression of intestinal tumor growths by NSAIDs or COX-2 inhibitors.

Adenomatous Polyposis Coli↗
PubMed2003

Effects of a glycogen synthase kinase-3 inhibitor, lithium, in adenomatous polyposis coli mutant mice.

Glycogen synthase kinase-3 (GSK-3) is an intermediary enzyme in various cellular pathways, and has been implicated in the pathophysiology and treatment of numerous diseases, including Alzheimer's disease, diabetes, and bipolar disorder. There is therefore in developing potent, selective GSK-3 inhibitors for the treatment of these devastating illnesses. A concern, however, is that the Wnt-signaling pathway-of which GSK-3 is an important intermediary molecule-has been implicated in many human cancers. It is thus of considerable importance to determine if GSK-3 inhibitors have tumorigenic potential in systems predisposed to developing tumors by virtue of mutations of the Wnt-signaling pathway. We therefore investigated the effects of a GSK-3 inhibitor, lithium, in a murine model predisposed to the formation of tumors due to activation of the Wnt pathway-the adenomatous polyposis coli (APC) multiple intestinal neoplasia (min) mouse. We found that 60 days of lithium treatment did not produce a significant increase in the number of tumors in these genetically predisposed mice. Lithium treatment resulted in a modest overall increase in the tumor size. The APC (min) mouse has previously been shown to be a robust indicator of tumorigenesis, with large increases in tumor number observed in response to a variety of agents; thus, our results suggest that lithium-and perhaps other inhibitors of GSK-3-pose a low risk for the development of cancers of the Wnt pathway. These results are consistent with the available epidemiological evidence that long-term lithium therapy does not increase cancer morbidity or mortality, but rather is associated with reduced overall mortality in bipolar disorder.

Adenomatous Polyposis Coli↗
PubMed2005

A prospective trial comparing wireless capsule endoscopy and barium contrast series for small-bowel surveillance in hereditary GI polyposis syndromes.

BACKGROUND: Capsule endoscopy has demonstrated its clinical utility in the evaluation of the small bowel, and, accordingly, it has been suggested that it could be useful for the identification of small-intestinal polyps in patients with polyposis syndromes. The objective was to establish the effectiveness of wireless capsule endoscopy for detecting small-bowel polyps in patients with hereditary GI polyposis syndromes in comparison with barium contrast series. METHODS: Consecutive patients with GI polyposis syndromes were included. Small-bowel follow-through series and capsule endoscopy were performed within 1 week, in a blind fashion. The number and the location of polyps were analyzed. RESULTS: Twenty-four patients with familial adenomatous polyposis (n = 20) or Peutz-Jeghers syndrome (n = 4) were included. Capsule endoscopy detected small-bowel polyps in 7 of 24 patients (29%), whereas a barium contrast study identified small-intestinal polyps in only 3 of these 7 patients. In the 4 remaining patients, all of them with familial adenomatous polyposis, polyps detected by the capsule but missed in radiographic series were located at either ileum (2 patients), jejunum (1), or duodenum (1). No procedure-related complication was observed in any patient. CONCLUSIONS: Wireless capsule endoscopy is a highly accurate technique for the detection of small-bowel polyps in patients with hereditary GI polyposis syndromes, and it represents a valuable alternative to barium contrast series in the surveillance of patients with Peutz-Jeghers syndrome.

Administration, Rectal↗
PubMed1985

Villous polyposis of the ileum: report of a case.

Villous adenomas occur only rarely in the small intestine and are often associated with malignant changes. Multiple villous adenomas of the small intestine are usually seen only in patients with familial polyposis coli. This is a report of a patient with multiple villous adenomas of the ileum associated with a carcinoma of the cecum which originated from a villous adenoma near the ileocecal valve. There was no evidence of other colonic polyps and no history of familial polyposis coli. It appears that polyposis of the small intestine is a rare clinical entity which cannot often be diagnosed due to difficulty in visualizing this area.

Adenoma↗
PubMed1995

[Budd-Chiari syndrome in children: case report].

This work aims at describing a particular case of Budd-Chiari syndrome in a ten-year-old girl. In our patient, the subjective and objective features of this disease, which is already rare during childhood, are associated with a well-assessed polyposis in the blind intestine (intestinum caecum). In our opinion, a possible connection between these two pathological events, a connection unheard of in the literature so far, is an interesting issue to be dealt with in this case report. The follow-up of our patient took place at the Pediatric Hospital of the University of Rome "La Sapienza" and lasted an overall period of 6 months. The girl was hospitalized twice and she underwent a large number of radiological and laboratory tests. The therapy consisted only of medical treatment and support measures. Liver transplant is regarded as the only chance to obtain a full recovery, but it has not yet been performed on our patient. It is by comparing those researches carried out on similar cases with the outcome of our personal study, that we come to the conclusion that, as for our patient, the Budd-Chiari syndrome can be classified as an idiopathic syndrome. Moreover, the fact that this syndrome and the polyposis of caecum occur at the same time in a patient can probably be considered as a coincidence.

Budd-Chiari Syndrome↗