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PubMed2006

Genetic and nutritional deficiencies in folate metabolism influence tumorigenicity in Apcmin/+ mice.

Epidemiological studies indicate that adequate dietary folate is protective against colon cancer, although mechanisms remain largely elusive. We investigated the effects of genetic disruptions of folate transport and metabolism and of dietary folate deficiency in a mouse model of colon cancer, the Apc(min/+) mouse. Apc(min/+) mice with heterozygous knockout of the gene for reduced folate carrier 1 (Rfc1(+/-)) developed significantly fewer adenomas compared to Rfc1(+/+)Apc(min/+) mice [30.3+/-4.6 vs. 60.4+/-9.4 on a control diet (CD) and 42.6+/-4.4 vs. 55.8+/-7.6 on a folate-deficient diet, respectively]. Rfc1(+/-)Apc(min/+) mice also carried a lower tumor load, an indicator of tumor size as well as of tumor number. In contrast, there were no differences in adenoma formation between Apc(min/+) mice carrying a knockout allele for methionine synthase (Mtr(+/-)), an enzyme that catalyzes folate-dependent homocysteine remethylation, and Mtr(+/+)Apc(min/+) mice. However, in both Mtr groups of mice, dietary folate deficiency significantly increased adenoma number (from 32.3+/-3.8 on a CD to 48.1+/-4.2 on a folate-deficient diet), increased plasma homocysteine, decreased global DNA methylation in preneoplastic intestines and increased apoptosis in tissues. There were no genotype-associated differences in these parameters in the Rfc1 group, suggesting that the protection conferred by Rfc1 deficiency is carried out through a different mechanism. In conclusion, genetic and nutritional disturbances in folate metabolism can have distinct influences on tumorigenesis in Apc(min/+) mice; altered levels of homocysteine, global DNA methylation and apoptosis may contribute mechanistically to dietary influence.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed2002

Therapeutic utility of aspirin in the ApcMin/+ murine model of colon carcinogenesis.

BACKGROUND: In recent years it has become evident that nonsteroidal anti-inflammatory drugs, in particular aspirin represent a potential class of cancer chemotherapeutic agents. Despite the wealth of knowledge gained from epidemiological, clinical and animal studies, the effectiveness of aspirin to treat established gastrointestinal cancer has not been determined. The present study examines the ability of aspirin to treat established polyposis in Min/+ mice. METHODS: Min/+ mice with established polyposis were treated orally once daily from 12-16 weeks of age with either drug vehicle or aspirin (25 mg/kg). Upon completion of treatment, the number, location and size of intestinal tumours was determined. Additional variables examined were the number of apoptotic cells within tumours and COX activity. RESULTS: Administration of aspirin for 4 weeks to Min/+ mice produce no effect on tumour number compared to vehicle-treated Min/+ mice (65 +/- 8 vs. 63 +/- 9, respectively). In addition, aspirin had no effect on tumour size or location. However, aspirin treatment produced a greater than 2-fold (p<0.05) increase in the number of apoptotic positive cells within tumours and significantly decreased hepatic PGE2 content. CONCLUSIONS: Aspirin was found to have no effect on tumour number and size when administered to Min/+ mice with established polyposis. The findings in the present study call in to question the utility of aspirin as a stand-alone treatment for established GI cancer. However, aspirin's ability to significantly promote apoptosis may render it suitable for use in combinatorial chemotherapy.

Adenomatous Polyposis Coli↗
PubMed1975

Epidermoid cysts, polyposis coli and Gardner's syndrome.

One hundred and ninety-six members of 15 families with Gardner's syndrome were investigated to determine the type of skin cyst that is part of this syndrome. These were shown to be epidermoid cysts and not pilar cysts or steatocystoma multiplex. They were solitary or multiple and seldom large and disfiguring. The skin cysts often occurred before the intestinal polyps were detectable. The presence of epidermoid cysts in children should be an indication for sigmoidoscopy when the child reaches the age of 14 years, and at 3-yearly intervals thereafter up to the age of 30 years, whether or not there is a family history of polyposis coli. At present it is not possible to say if Gardner's syndrome is the same as, or different from, familial polyposis. Until all patients with colonic polyps have a full clinical examination, looking for skin cysts and osteomas, X-rays of the skull and long bones to detect osteomas and dental X-rays for abnormalities of the teeth this question will remain unanswered.

Adolescent↗
PubMed1987

[Proctocolectomy with direct ileoanastomosis and superimposed small intestine pouch].

Our experiences with 26 patients show that total proctocolectomy with direct ileoanal pouch anastomosis and without maintenance of the rectal muscle cuff proves to be an excellent method for secure and lasting treatment of UC and ACR as well as of manifest cancer. The advantage of this method is the maintenance of normal continence function at a lower operative risk and few postoperative complications. Contraindication for this operative approach is still Crohn' disease. Furthermore the indication is limited by primary dysfunction of the anal sphincter.

Adenomatous Polyposis Coli↗
PubMed1998

The intestinal epithelium and its neoplasms: genetic, cellular and tissue interactions.

The Min (multiple intestinal neoplasia) strain of the laboratory mouse and its derivatives permit the fundamental study of factors that regulate the transition between normal and neoplastic growth. A gene of central importance in mediating these alternative patterns of growth is Apc, the mouse homologue of the human adenomatous polyposis coli (APC) gene. When adenomas form in the Min mouse, both copies of the Apc gene must be inactivated. One copy is mutated by the nonsense Apc allele carried in heterozygous form in this strain. The other copy can be silenced by any of several mechanisms. These range from loss of the homologue bearing the wild-type Apc allele; to interstitial deletions surrounding the wild-type allele; to intragenic mutation, including nonsense alleles; and finally, to a reduction in expression of the locus, perhaps owing to mutation in a regulatory locus. Each of these proposed mechanisms may constitute a two-hit genetic process as initially posited by Knudson; however, apparently the two hits could involve either a single locus or two loci. The kinetic order for the transition to adenoma may be still higher than two, if polyclonal adenomas require stronger interactions than passive fusion. The severity of the intestinal neoplastic phenotype of the Min mouse is strongly dependent upon loci other than Apc. One of these, Mom1, has now been rigorously identified at the molecular level as encoding an active resistance conferred by a secretory phospholipase. Mom1 acts locally within a crypt lineage, not systemically. Within the crypt lineage, however, its action seems to be non-autonomous: when tumours arise in Mom1 heterozygotes, the active resistance allele is maintained in the tumour (MOH or maintenance of heterozygosity). Indeed, the secretory phospholipase is synthesized by post-mitotic Paneth cells, not by the proliferative cells that presumably generate the tumour. An analysis of autonomy of modifier gene action in chimeric mice deserves detailed attention both to the number of genetic factors for which an animal is chimeric and to the clonal structure of the tissue in question. Beyond Mom1, other loci can strongly modify the severity of the Min phenotype. An emergent challenge is to find ways to identify the full set of genes that interact with the intestinal cancer predisposition of the Min mouse strain. With such a set, one can then work, using contemporary mouse genetics, to identify the molecular, cellular and organismal strategies that integrate their functions. Finally, with appropriately phenotyped human families, one can investigate by a candidate approach which modifying factors influence the epidemiology of human colon cancer. Even if a candidate modifier does not explain any of the genetic epidemiology of colon cancer in human populations, modifier activities discovered by mouse genetics provide candidates for chemopreventive and/or therapeutic modalities in the human.

Adenoma↗
PubMed1999

[Congenital hypertrophy of retinal pigment epithelium: a marker in familial adenomatous polyposis].

PURPOSE: Familial adenomatous polyposis (FAP) is an inherited autosomal dominant disorder with marked propensity for malignant transformation. The potential for congenital hypertrophy of retinal pigment epithelium (CHRPE) as a phenotypic marker for this disease is recognized. MATERIAL AND METHODS: We report our investigations in 11 families with familial adenomatous polyposis. CHRPE characteristics were described and the relations between genotype and phenotype and those between CHRPE and severity of FAP are discussed. DISCUSSION: All members of the family should undergo retinal examination at the earliest age possible. The results give an indication of the severity of the intestinal disease and allow an approximate localization of the mutation in the coding sequence, leading to a more rapid genetic analysis.

Adenomatous Polyposis Coli↗
PubMed1991

[Peutz-Jeghers syndrome (mucocutaneous melanosis associated with gastrointestinal polyposis). Presentation of 5 cases presenting in the same family].

Five brothers suffering from Peutz-Jeghers syndrome with freckles in the skin of the face and mucous membrane of the oral cavity, and intestinal polyps are reported. These patients have not been traditionally considered of being at risk. The current opinion is that patients with this disorder can develop malignancies in the gastrointestinal tract, and tumors in other organs.

Adolescent↗
PubMed2006

Molecular characterization of the bacteria adherent to human colorectal mucosa.

AIMS: To study large intestinal mucosal bacterial communities by Denaturing Gradient Gel Electrophoresis (DGGE) profiling and sequencing of 16S rRNA gene polymerase chain reaction (PCR) products amplified from DNA extracted from colorectal biopsies taken from healthy individuals. The specific aims were to determine how similar the mucosa-associated bacterial communities are within and between individuals and also to characterize the phylogenetic origin of isolated DGGE bands. METHODS AND RESULTS: Human colorectal biopsies were taken at routine colonoscopy from 33 patients with normal looking mucosa. The DNA was extracted directly from single biopsies and the bacterial 16S rDNA PCR amplified. The PCR products were profiled using DGGE to generate a fingerprint of the dominant members of the bacterial community associated with the biopsy. The reproducibility of this method was high (>98%). Washed and unwashed biopsies gave similar DGGE banding patterns (Median Similarity Coefficient - MSC 96%, InterQuartile Range - IQR 3.0%, n = 5). Adjacent biopsies sampled from the same patient using different forceps gave similar DGGE profiles (MSC 94%, n = 2). Two colorectal biopsies sampled at locations 2-5 cm apart, from each of 18 patients, resulted in very similar profiles (MSC 100%, IQR 2.8%). Biopsies sampled from different locations within the large intestine of the same patient also gave similar DGGE profiles (MSC 98% IQR 3.3%n = 6). Although all patients (n = 33) gave different DGGE profiles, some similarity (c. 34%) was observed between profiles obtained from 15 patients arbitrarily selected. 35 DGGE bands were excised and sequenced. Many were found to be most closely related to uncultured bacterial sequence entries in the Genbank database. Others belonged to typical gut bacterial genera including Bacteroides, Ruminococcus, Faecalibacterium and Clostridium. CONCLUSIONS: Bacterial communities adherent to colorectal mucosa within a normal patient show little variation; in contrast, mucosal bacterial communities sampled from different patients with normal colorectal mucosa show a high degree of variation. SIGNIFICANCE AND IMPACT OF THE STUDY: This research demonstrates that DGGE profiling of 16S rRNA gene PCR products amplified from DNA extracted directly from mucosal samples offers fresh insight into the bacterial communities that are adherent to colorectal mucosa. These findings are important with respect to further studies on the gastrointestinal tract in health and disease.

Adenomatous Polyposis Coli↗
PubMedDate not supplied

Acellular dermal matrix provides a good option for abdominal wall closure following small bowel transplantation: a case report.

Following small bowel transplantation (SBTx), approximating the midline abdominal fascia can be problematic in patients with severely retracted abdominal cavities. We first report the use of acellular dermal matrix (ADM) for abdominal closure following living related SBTx. A 44-year-old woman with ultra-short gut syndrome secondary to multiple bowel resections received a 160-cm segmental intestinal graft from her daughter. The graft ileocolic vessels were anastomosed end to side to the inferior vena cava and distal aorta. A terminal ileostomy was fashioned because the patient had previous panproctocolectomy. The graft perfused well, and the laparotomy was primarily closed. On postoperative day 1, the patient required surgical exploration for evacuation of hematoma. Due to graft edema in a significantly retracted abdominal cavity, a 12x7 cm fascia defect was evident. Leaving the abdomen open or using a mesh was not entertained as options due to the high risk of infections. Primary closure under tension would also jeopardize the transplant, increasing the risk of thrombosis. The fascia defect was closed using a segment of ADM. The patient did well and went home on the postoperative day 11. At 2-year follow-up she is well and on oral diet without fascia defect or incisional hernia. This is the first report of the use of ADM for abdominal closure in patients receiving a SBTx. ADM is considered safe when used in contaminated sites and can allow primary closure of difficult wounds often seen in SBTx patients.

Adenomatous Polyposis Coli↗
PubMed1996

[Involvement of the large intestine in neurofibromatosis type 1].

This report presents the cases of two female patients aged 54 and 57 years, both with colon involvement of type 1 neurofibromatosis. The first woman had a polypoid neuronal hyperplasia containing small Wagner-Meissner corpuscles, which had allowed identification of the neuronal nature of the lesion in a small mucosal biopsy specimen taken previously. The second patient had an idiopathic megacolon of the sigmoid, which had to be extirpated because of acute obstruction and ileus. Morphological examination revealed a typical plexiform neurofibroma of the bowel wall and neuronal hyperplasia of the colonic mucosa and submucosa, which had obviously caused disordered gut mobility leading to functional stenosis and extreme dilatation of prestenotic bowel parts. Gastrointestinal neurofibromatosis is rare and is characterized morphologically by neuronal hyperplasia of the mucosa and submucosa, sometimes containing small aggregates of ganglion cells by which it can easily be identified. However, in the majority of cases the increase of proliferating mucosal nerve fibres can only be confirmed by S-100 protein immunostaining. Furthermore, solitary, multiple and plexiform neurofibromas are found, but only the last, which arises from mesenteric or subserosal nerves, is virtually pathognomonic for neurofibromatosis. Gastrointestinal neurofibromas are usually late manifestations of the disease, but in exceptional cases they can be the initial sign of neurofibromatosis in patients who have no external stigmata that arouse suspicion. The occurrence of gastrointestinal neurofibromas should therefore lead to a careful search for other features of NF-1 in the affected patients and in their families.

Adenomatous Polyposis Coli↗
PubMed1998

Infrequent somatic mutation of the adenomatous polyposis coli gene in aberrant crypt foci of human colon tissue.

BACKGROUND: The authors examined somatic mutations of the adenomatous polyposis coli (APC) gene in 84 human aberrant crypt foci (ACF) to determine whether APC gene mutations were involved in the histologic progression of ACF. METHODS: Mutation cluster regions of the APC gene were subjected to polymerase chain reaction single-strand conformation polymorphism analysis and direct sequencing. RESULTS: Four kinds of deletion were detected in the mutation cluster regions of APC gene in five ACF. APC mutation was detected in 1 of 18 ACF with Stage I abnormalities (6%). Four of 10 adenomatous ACF (40%) harbored the mutation. There were no mutations in 56 hyperplastic ACF. CONCLUSIONS: These results suggest that APC mutations may be involved initially in only a limited number of adenomas in ACF.

Adenomatous Polyposis Coli↗
PubMed1982

Familial juvenile colonic polyposis with associated colon cancer.

A mother and son were found to have multiple juvenile polyps of the colon; later a metastatic adenocarcinoma of the large bowel developed in the mother. In both patients, histologic examination of the polyps did not reveal adenomas, but some of the juvenile polyps contained adenomatous-like elements. Because of the mother's history of colon cancer and the adenomatous features in some of the son's juvenile polyps, he underwent an elective subtotal colectomy. This family may represent a phenotype variation with features of both the juvenile and adenomatous polyposis syndromes and the presence of dysplasia of the glandular epithelium could be a marker of potential malignancy in patients with juvenile polyposis coli.

Adenocarcinoma↗
PubMed1990

Incidence of dysplasia in the anorectal mucosa in patients having restorative proctocolectomy.

The incidence of dysplasia in the mucosal strippings from the anorectal stump was studied in 132 patients treated by restorative proctocolectomy with ileal reservoir for ulcerative colitis and familial adenomatosis. The anorectal mucosa was stripped from the level of division of the gut tube to the dentate line. Of 118 patients with ulcerative colitis, 12 (10.2 per cent) had dysplasia in some part of the large bowel. Mucosal strippings were examined histologically in 118 cases, of which only three (2.5 per cent) showed dysplasia. There was a correlation between dysplasia and the presence of carcinoma and the duration of the disease in the operative specimen of colon and rectum and also in the anorectal mucosal specimen although the number of patients with carcinoma (eight cases) in this analysis was small. All 14 patients with familial adenomatous polyposis showed large bowel mucosal dysplasia in the operative specimen which was severe in six cases. Anorectal mucosal strippings were examined in these patients and 12 showed dysplasia which was severe in three.

Adenomatous Polyposis Coli↗
PubMed1996

Pouch-related fistula following restorative proctocolectomy.

Prognostic factors and outcome of pouch-related fistula were analysed from a series of 21 patients, 20 of whom had an ileal J pouch manually anastomosed to the dentate line following mucosectomy. Fistula occurred more often after pouch formation for ulcerative colitis than for familial adenomatous polyposis. In 6 patients the fistula occurred more than 5 months after closure of the diverting loop ileostomy. The origin of the leak was the anastomosis in 14 patients, the vertical staple line in two and the end of the efferent limb in five. Nine forms of treatment were utilized and these were successful in 11 patients and unsuccessful in ten including three pouch excisions. Adverse prognostic factors were late fistula, the presence of an enterocutaneous or a pouch-vaginal fistula track, and diagnosed or suspected Crohn's disease. Resolution of the fistula followed none of six diverting loop ileostomies performed alone, three of 33 attempted drainage procedures, four of ten direct closures, and four of five repeat ileal pouch-anal anastomoses. It is concluded that an aggressive therapeutic approach using repeat ileal pouch-anal anastomosis increases the success rate.

Adenomatous Polyposis Coli↗
PubMed1995

Duodenal adenomatosis in familial adenomatous polyposis. DAF Project Group.

In order to evaluate the prevalence of duodenal adenomas in familial adenomatous polyposis (FAP) and the risk of carcinoma development, a multicenter study was initiated in Denmark, Finland, Holland, Norway and Sweden, which have national polyposis registers with an almost complete registration. Patients aged 20 years or more are being examined with biennial gastroduodenoscopy during 1990-2000. Multiple duodenal biopsies are examined by one pathologist from each country, and the endoscopic and histological criteria of Spigelman have been adopted. At the end of August 1992, 312 patients with a median age of 37 years (range 20-86) had completed their first endoscopy. The duodenum was examined in 310 patients, of whom 199 (64%) had duodenal adenomas. Twenty-two patients (11% of all patients with duodenal adenomas) had no endoscopically visible polyps. One patient had an asymptomatic adenocarcinoma. The Spigelman stage worsened significantly (P < 0.05) with time from the diagnosis of FAP, which may suggest an increasing risk of carcinoma by time.

Adenomatous Polyposis Coli↗