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PubMed2004

Juvenile polyposis with macrocephaly and mental retardation (? Ruvalcava-Myhre-Smith syndrome)--a case report.

A male child aged one and a half years with a history of rectal bleeding, on examination was found to have severe degree of anaemia with grade -III protein-energy-malnutrition and pneumonia. Colonoscopy revealed features of colonic polyposis. An upper gastro-intestinal endoscopy showed a duodenal polyp while barium meal follow-through did not reveal any polyps in the small intestine. Total colectomy and ileo-rectal anastomosis was done. Following histopathological study, the diagnosis of Juvenile polyposis syndrome was made, a very rare entity and is known to lead to adenocarcinoma of the gastrointestinal tract. In addition the child was found to have macrocephaly and mental retardation. The rarity and importance of the diagnosis of juvenile polyposis syndrome associated with macrocephaly and mental retardation (?Ruvalcava-Myhre-Smith syndrome) prompted the documentation of this case.

Adenomatous Polyposis Coli↗
PubMed2005

Isolated crypts form spheres prior to full intestinal differentiation when grown as xenografts: an in vivo model for the study of intestinal differentiation and crypt neogenesis, and for the abnormal crypt architecture of juvenile polyposis coli.

We describe a model system in which single crypts, isolated from newborn rats, were embedded in a type I collagen gel and subcutaneously grafted to the flanks of nude mice, whereupon they underwent full intestinal morphogenesis. Small fragments of small intestine and colon were incubated with the divalent cation chelator EDTA, resulting in the release of crypts and villi. Released crypts were then suspended sparsely in type I collagen gel. Segments of gel containing a single crypt were grafted subcutaneously into a nude mouse. Grafts were harvested at weekly intervals. By 2 days, the mouth of the crypts had joined to seal the crypt and, within 1 week, the structure ballooned to form a spherical cystic structure lined by flattened epithelial cells showing no evidence of cytodifferentiation. After 2 weeks, host stromal cells had invaded the collagen and settled around this spherical crypt. At points where stromal cells appeared in contact with the crypt, the epithelium exhibited a more columnar phenotype. By 4 weeks, the 'crypt sphere' was surrounded by stroma expressing alpha-smooth muscle actin and, at this time, multiple buds appeared that gave rise to new crypts. By 5 weeks, villi had formed and cell lineages associated with the small intestine and colon were present; the original single crypt had transformed into a functional intestinal unit. Therefore, we have shown that a single crypt has the potential to grow, give rise to other crypts and dependent structures such as villi. This model has considerable potential for use in gene transfer experiments in the study of intestinal differentiation, and for the analysis of crypt neogenesis via crypt fission. Moreover, the appearances showed a close resemblance to those seen in juvenile polyposis syndrome (JPS), where the budding and fission of single crypts isolated by stromal overgrowth offers an alternative explanation for the histogenesis of JPS.

Adenomatous Polyposis Coli↗
PubMed2003

Polyamines as modifiers of genetic risk factors in human intestinal cancers.

Polyamines are downstream mediators of genetic risk factors in human intestinal cancers. The adenomatous polyposis coli (APC) tumour-suppressor gene, which is mutated in essentially all human colon cancers, regulates the expression of several e-box transcription factors. These factors, in turn, regulate the transcription of ornithine decarboxylase (ODC), the first enzyme in polyamine synthesis. The Kirsten ras ( K-ras ) oncogene regulates the expression of several genes, including suppressing the expression of peroxisomal proliferator-activated receptor gamma (PPARgamma). This PPAR, in turn, activates the expression of the spermidine/spermine-N(1)-acetyltransferase (SSAT), the first enzyme in polyamine catabolism. The non-steroidal anti-inflammatory drug (NSAID) sulindac induces the transcription of SSAT via activation of PPARgamma. Inactivation of the APC tumour-suppressor gene, and the activation of K-ras, have a combined effect on increasing tissue polyamine contents due to increased synthesis and decreased catabolism of the polyamines. Pharmacological strategies for suppressing ODC (e.g. the enzyme-activated inhibitor alpha-difluoromethylornithine) and activating SSAT (e.g. NSAIDs) are potent inhibitors of intestinal carcinogenesis in rodent models. Clinical trials combining these classes of agent in humans with risk factors for colon cancer are in progress.

Antineoplastic Agents↗
PubMed1999

Intestinal tumorigenesis in the Apc1638N mouse treated with aspirin and resistant starch for up to 5 months.

The Apc1638N mouse model, which carries a targeted mutant allele within the adenomatous polyposis (Apc) gene and develops intestinal tumours spontaneously, predominantly in the small bowel, was used to investigate the effects of two potential chemopreventive agents, aspirin and alpha-amylase resistant starch (RS). Heterozygous Apc+/Apc1638N mice were fed semi-purified diets rich in animal fat, animal proteins and sucrose and low in dietary fibre (Western style diets) from approximately 6 weeks up to 6 months of age. Two of the diets contained aspirin (300 mg/kg diet) and two RS (1:1 mixture of raw potato starch: Hylon VII at 200 g/kg diet) in a 2 x 2 factorial design. A fifth treatment group were fed a conventional rodent chow diet. The mice fed the Western style diets became almost three times as fat as the chow-fed mice but this did not affect tumour yield. Treatment with RS resulted in significantly more intestinal tumours whereas aspirin alone had no effect. However, there was a significant aspirin x RS interaction, which suggests that aspirin could prevent the small intestine tumour-enhancing effects of RS in this Apc-driven tumorigenesis model. The possibility that large amounts of purified forms of resistant starch may have adverse effects within the small bowel is a novel observation that requires further investigation since greater intakes of starchy foods (and of RS) are being encouraged as a public health measure in compensation for reduced dietary fat intake. However, it remains possible that any increased risk is restricted to carriers of germline mutations in APC.

Adenocarcinoma↗
PubMed1990

Occult radiopaque jaw lesions in familial adenomatous polyposis.

Osteomatous jaw lesions have been reported to occur in connection with familial adenomatous polyposis (FAP) of the intestines. The disease is fatal if not treated. The aim of this investigation was to study the occurrence of bone jaw lesions in Swedish families, where some family members have developed FAP, in order to evaluate if these bone changes may be regarded as clinical markers of the disease. 132 individuals from ten families with FAP and a matched control group of 250 individuals were examined. Osteomatous lesions were diagnosed in 24 per cent in the FAP families and in 2 per cent in the controls. Individuals with verified FAP showed an increased occurrens of jaw lesions. Also in family members without verified FAP, first-degree relatives and other relatives, showed a significant higher incidence of osteomatous jaw lesions compared to the controls. Our results suggest that osteomatous jaw lesions in families with FAP are of predictive significance.

Adenomatous Polyposis Coli↗
PubMed2005

Studying the consequences of immediate loss of gene function in the intestine: APC.

The use of mouse models to study neoplasia is proving particularly powerful in dissecting the mechanisms underlying disease initiation and progression. However, the majority of these models have been somewhat limited in studying the very early effects of loss of gene function, as tumour initiation relies upon either constitutive loss of gene function or spontaneous somatic loss of function. We have therefore adopted a strategy of using an inducible Cre-lox-based system to analyse the effects of loss of gene function, the use of which is reviewed here for the intestinal tumour suppressor APC (adenomatous polyposis coli). Using this approach, we have conditionally and synchronously inactivated APC in virtually all the epithelial cells of the adult murine small intestine. After 5 days following induction of Cre-mediated recombination, mice show grossly altered crypt/villus architecture. Deficiency in APC perturbs migration, alters the normal programme of differentiation and results in increased proliferation and apoptosis. Microarray analysis reveals the transcriptome to be significantly altered; reflecting both gross phenotypic changes and changes in transcriptional activation. These findings demonstrate that APC is indeed the critical determinant of cell fate in the intestinal epithelium, explaining its role as the cellular 'gatekeeper' in preventing neoplasia.

Adenomatous Polyposis Coli↗
PubMed2005

[Oral and maxillofacial manifestations of familial adenomatosis polyposis. Gardner's syndrome].

Patients suffering from familial adenomatosis polyposis develop multiple pre-malignant gastrointestinal polyps and are at high risk of developing colon cancer. In addition extra-intestinal manifestations are observed frequently. The combination of extra-intestinal manifestations and familial adenomatosis polyposis is named Gardner's syndrome. An early diagnosis of this disease is important because it could mean a better prognosis for the patient. This review describes the oral and maxillofacial symptoms of FAP, and its potential implications for dental treatment.

Abnormalities, Multiple↗
PubMed2000

Localization of cyclooxygenase-2 in human sporadic colorectal adenomas.

A putative target for the anti-colorectal cancer action of nonsteroidal anti-inflammatory drugs is the inducible isoform of cyclooxygenase (COX), COX-2. COX-2 is expressed within intestinal adenomas in murine polyposis models, but expression has been poorly characterized in human colorectal neoplasms. Therefore, we investigated the localization of the COX-2 protein in human sporadic colorectal adenomas. Immunohistochemistry for COX-2 and CD68 (a tissue macrophage marker) was performed on formalin-fixed, paraffin-embedded (n = 52) and frozen, acetone-fixed (n = 6) sections of human sporadic colorectal adenomas. Forty of 52 (77%) formalin-fixed adenomas expressed immunoreactive COX-2. COX-2 was localized to superficial interstitial macrophages in 39 cases (75%) and to deep interstitial macrophages in 9 cases (17%). COX-2 staining of dysplastic epithelial cells was observed in 15 cases (29%). A logistic regression analysis identified the adenoma site (P = 0.012) and histological type (P = 0.001) as independent predictors of superficial macrophage COX-2 expression. There was no relationship between the number of macrophages within an adenoma and macrophage COX-2 expression. These results indicate that COX-2 is expressed predominantly by interstitial macrophages within human sporadic colorectal adenomas. If COX-2 does indeed play a role in the early stages of colorectal carcinogenesis in man, these data suggest COX-2-mediated paracrine signaling between the macrophages and epithelial cells within adenomas.

Adenoma↗
PubMed1989

Skin tags are not a risk factor for colorectal polyps.

To ascertain whether acrochordons (simple skin tags) are associated with a higher risk for colon polyps, we prospectively studied 218 male and female patients, age 40 or older without history of colon cancer, polyps, ulcerative colitis, familial polyposis, or recent lower intestinal symptoms. Each patient was assessed for the presence of skin tags. A screening flexible sigmoidoscopy was then performed without knowledge of the dermatologic findings. All polypoid lesions were recorded, and patients with polyps greater than or equal to 3 mm in diameter underwent full colonoscopy and polypectomy. Twenty patients (9.2%) had documented adenomatous polyps on colonoscopy. Nineteen other patients had hyperplastic polyps and mamillations. There was no significant difference in the prevalence of polypoid lesions in those with skin tags compared with those without skin tags, either analyzed as group totals or stratified by age, sex, or type of polyp. We conclude that skin tags are not associated with a higher than usual risk for colonic polyps and should not be used as a marker for more intensive screening.

Adult↗
PubMed2005

Peutz-Jeghers syndrome. A case report.

Peutz-Jeghers syndrome (PJS) is an unusual hamartomatous polyposis of the gastro intestinal (GI) tract, with pigmentation around lips and macules on the buccal mucosa. The case of a 10-year-old girl who presented with intussusception is reported. A polyp was found to be the cause of an invagination. Histologically it was a hamartoma. PJS is a rare syndrome inherited in an autosomal dominant pattern. Most patients have recurrent episodes of polyp induced bowel intussusception which requires repeated laparotomies. In addition, these patients have an increased risk of malignant disease in gastrointestinal and also non-gastrointestinal sites. To prevent cancer and short bowel syndrome, aggressive screening is recommended. Upper and lower endoscopy should be performed every two years from 10 years of age. Extra-intestinal surveillance for cancers, including abdominal and pelvic ultrasound, as well as testicular and breast examinations once yearly should be introduced in the second decade of life.

Abdominal Pain↗
PubMed1991

[Colectomy with resection of the rectal mucosa and formation of the ileo-rectal anastomosis as an alternative of permanent ileostomy].

A new method for surgical management of patients with diffuse polyposis of the large intestine is described. It was applied in 22 patients with total involvement of all parts of the large intestine in polyps. The essence of the suggested operation consists in preservation of the rectum after its demucosation and the formation of a cecal++-ileorectal anastomosis at the level of the pelvic peritoneum. The operative techniques are described. Experience in various types of intestinal anastomoses with a demucosated rectum as well as the techniques of the most optimal anastomosis are analysed. Retrospective analysis of the results of treatment allowed the authors to conclude that in inclusion of demucosated rectum into the intestinal passage its reservoir and accumulative function is maintained. Follow-up of the patients showed that small intestinal type mucosa regenerates in the rectum after mucosectomy in one third of patients and colonic-type mucosa in the remaining patients. It is pointed out that recurrent growth of polyps in the rectum after adequate demucosation was not encountered.

Adolescent↗
PubMed1990

[Gardner's syndrome: report of a case].

Gardner's syndrome consists of multiple polyposis of the large intestine and soft and hard tissue tumors. The syndrome should be considered in case of supernumerary teeth, odontomas, osteoma and soft tissue tumors. These findings often precede colonic involvement. Careful attention should be directed towards the family history. The importance of this syndrome lies in the great tendency of the polyps to become malignant. Dentist and oral surgeon play an important role in the early detection of this syndrome and thus prevention of malignant degeneration of the intestinal polyps.

Adolescent↗
PubMedDate not supplied

[Stomach polyps. Clinical and therapeutic considerations].

The main clinical and therapeutic problems of gastric polyps are examined on the basis of 7 personal cases and the literature on the subject. 5 of the cases were adenomatous polyps proper, one of them in malignant degeneration and associated with polyposis of the large intestine. In 2 other cases, the histopathological picture revealed Peutz-Jeghers type hamartomatosis polyps confined to the gastric region without the typical cutaneo-mucous stigmata or familial character. Classification of polyps must allow not only for aetiopathogenetic or clinical criteria but for histopathological and histogenetic criteria also. A clear-cut distinction must be made between adenomatous polyps, of definite malignant potential, and pseudoneoplastic polypoid lesions that are essentially benign. The main diagnostic techniques available to handle a symptomatology that is often oligosymptomatic and aspecific, or associated with complications (such as ulcers, haemorrhage, stenosis or, not least, malignant transformation) are reviewed and stress laid on the importance of endoscopy prior to histopathological study which is of value only if carried out on a totally removed polypous lesion. The guidelines for indicating and selecting the radial surgical technique are presented.

Adult↗