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PubMed1997

A fish oil derived concentrate enriched in eicosapentaenoic and docosahexaenoic acid as ethyl ester suppresses the formation and growth of intestinal polyps in the Min mouse.

We examined whether the n-3 polyunsaturated fatty acid ethyl ester enriched fish oil K85 (54.4% of eicosapentaenoic acid and 30.3% of docosahexaenoic acid as ethyl esters) could inhibit the intestinal tumorigenesis in Min mice, a murine model of familial adenomatous polyposis (FAP). Min mice that are heterozygous for a nonsense mutation in the Apc gene, develop spontaneously multiple intestinal neoplasms, primarily in the small intestine. K85 was dissolved in corn oil (vehicle) and mixed into the AIN-76A diet. The total oil content (K85 + corn oil) was 12% in all diets. The various experimental diets contained 0 (vehicle control), 0.4, 1.25 or 2.5% of K85. In the small intestine, the mean number of tumors/mouse was 105 +/- 18 (SEM) in control males and 70 +/- 11 in control females. Dietary K85 treatment reduced the number of small intestinal tumors: in males, the maximum reduction was 66% (P = 0.002) with 0.4% of K85; and in females, the maximum reduction was 48% (P = 0.043) with 2.5% of K85, but the inhibition was only slightly increased from 0.4% to 2.5% of K85. The mean tumor diameter was 1.33 +/- 0.08 mm in control males and 1.06 +/- 0.08 in control females, and the diameter ranged from <0.1 mm (monocryptal adenomas) to 4 mm. The small intestinal tumor diameter was reduced by K85 in a dose-dependent manner: in males, with a maximum reduction of 26% (r = -0.64, P = 0.004); and in females, with a maximum reduction of 38% (r = -0.61, P < 0.004). In the large intestine, the mean number of tumors/mouse was 1.0 +/- 0.5 in males and 0.8 +/- 0.2 in females. Although K85 treatment tended to reduce the number and diameter of the large intestinal tumors, these effects did not reach statistical significance. Aberrant crypt foci not elevated from the flat mucosa (ACF(Min)) occurring in the colon of Min mice were also scored. The mean number of ACF(Min)/colon (3.8 +/- 0.9) and the crypt multiplicity (1.49 +/- 0.28) in females were reduced by 73% (P = 0.03) and 60% (P = 0.048) with 2.5% of K85, respectively, whereas no significant effect could be observed in the males.

Adenomatous Polyposis Coli↗
PubMed1978

A family of Gardner's syndrome with report of an autopsy case.

A family with Gardner's syndrome including one autopsy case is reported. A 22 year-old man had multiple polyposis of the colon and the small intestine, epidermal cysts, soft part tumor of the abdominal skin and osteomas in the calvarium and rib, and died of a carcinoma in the transverse colon and embolism of the brain. Histologically, all polyps were diagnosed as adenomatous polyp. The greater their diameter, the higher the tendency of atypism was observed. However, the polyps around the cancer were few, small, and with low atypism, and we could not obtain evidence showing direct transformation of adenomatous polyps into carcinoma. His two elder brothers had multiple polyposis of the colon, epidermal cysts and osteomas in the calvarium or mandibular bone, but are still alive.

Adult↗
PubMed1997

Mutations of the Ki-ras, p53 and APC genes in adenocarcinomas of the human small intestine.

In contrast to the origins of colorectal carcinomas, the mechanisms of carcinogenesis in the small intestine remain unclear. We therefore analyzed the mutational status of the Ki-ras, p53, and adenomatous polyposis coli (APC) genes in primary carcinomas of the small intestine and compared the mutation patterns with those established for colorectal cancers. DNA was extracted from 15 formalin-fixed, paraffin-embedded lesions. Codons 12, 13 and 61 of the Ki-ras gene, exons 5-8 of the p53 gene, and codons 1268-1569, which contain the mutation cluster region (MCR) of the APC gene, were amplified by means of PCR, subcloned and sequenced. Mutations of the Ki-ras and p53 genes were observed in 8 (53.3%) and 4 lesions (26.7%), respectively. The mutational frequency of the Ki-ras gene in the present series of small intestinal carcinomas was similar, while that of the p53 gene was slightly lower than the reported frequencies for colorectal carcinomas. Only one case showed a mutation of the APC gene, involving an insertional mutation of an adenine at codons 1554-1556 with formation of a stop codon immediately downstream. Since the occurrence of an APC mutation is considered an early event in colorectal carcinogenesis, our findings indicating an extremely low frequency of such changes in and around the MCR suggest that carcinomas of the small intestine arise via a genetic pathway distinct from that involved in the development of carcinomas of the colorectum.

Adult↗
PubMed2000

Pathology of intestinal lymphomas.

The advent of immunohistological and molecular techniques has enabled the comprehensive characterization of many lymphoma entities. Furthermore, it has increased the consensus in lymphoma classification among pathologists. In this review we describe the pathological features of primary intestinal lymphomas classified according to the revised European-American classification of lymphoid neoplasms. The majority of primary intestinal lymphomas are of B-cell lineage and most of these are high-grade tumors. By morphology they may be classified as diffuse large B-cell lymphomas of centroblastic, immunoblastic or plasmablastic type and Burkitt lymphomas. The latter occur predominantly in the terminal ileum and affect children or young adults. Low-grade extra-nodal marginal-zone lymphoma of the mucosa-associated lymphoid tissue (MALT) type and, less frequently, follicular center-cell lymphomas are the low-grade B-cell lymphomas most commonly observed in this region. The first mentioned tumor and its specific intestinal variant, alpha-chain disease or immunoproliferative small intestinal disease are well known for their indolent clinical course. Primary intestinal mantle-cell lymphoma often presents as multiple lymphomatous polyposis and similarly to its node-based equivalent is associated with an unfavorable prognosis. Most primary intestinal T-cell lymphomas display a characteristic immunophenotype, particular histological features with prominent epitheliotropism and are often associated with celiac disease indicating that these tumors form a specific lymphoma type. It has been termed intestinal T-cell lymphoma or enteropathy-type T-cell lymphoma. Clinically, these are aggressive diseases with a high mortality rate. In summary, primary intestinal lymphomas consist of several entities which display distinct clinicopathological features thus confirming the relevance of lymphoma typing.

Humans↗
PubMed1990

Turcot's syndrome with intestinal lymphoma in a child: an unusual case of triple tumor.

Turcot's syndrome, the association of brain tumor (usually glioblastoma, medullo-blastoma, or astrocytoma) and colonic polyps, is a very rare condition of which about 20 cases have been reported. It has been described only once previously with cancer in a third organ system. In this paper, we report a child affected with colonic polyposis and astrocytoma (i.e., Turcot's syndrome) associated with intestinal non-Hodgkin's lymphoma.

Adenomatous Polyposis Coli↗
PubMed1975

The Paneth cell in the adenoma of familial polyposis coli.

It is said that the Paneth cells are found in the large intestine in a pathological state such as ulcerative colitis or adenoma. We examined the Paneth cells in the adenomas of familial polyposis coli. Nine cases including one case of Gardner's syndrome comprised the material for the examination of the Paneth cells because the caecum was available for the examination. The remaining one case had no Paneth cells. In two cases, the Paneth cells were found among the adenomas in the areas beyond the caecum and the proximal part of the colon ascendens. In one remarkable case, the Paneth cells were found in 43% of the adenomas in the caecum. Seven cases were carcinomas but no Paneth cells were found in or near the carcinoma. In the control cases, which were taken from the resected colon with a disease other than familial polyposis coli, the Paneth cells were found confined to the caecum. We concluded that the distribution of the Paneth cell-bearing adenomas reflects the distribution of the Paneth cells in the normal mucosa of the large intestine and that the Paneth cells in the adenoma may have differentiated in the adenoma.

Adenoma↗
PubMed2003

Reduction in alkaline sphingomyelinase in colorectal tumorigenesis is not related to the APC gene mutation.

BACKGROUND AND AIMS: The sphingomyelin pathway is an important intracellular mechanism in regulating cell growth. The first step in this pathway is catalysed by sphingomyelinases. Alkaline sphingomyelinase is specifically located in the intestinal tract. Markedly reduced alkaline sphingomyelinase activities have been found in sporadic colorectal tumours and in familial adenomatous polyposis adenomas. Since the adenomatous polyposis coli (APC) gene is mutated in about 80% of sporadic colorectal tumors, and familial adenomatous polyposis is the consequence of a germline mutation of the same gene, we examined whether low alkaline sphingomyelinase activity is linked to APC gene mutations. PATIENTS AND METHODS: Both germline and sporadic adenomatous polyposis coli gene mutations were studied. Alkaline, neutral, and acid sphingomyelinase activities were measured in the intestinal mucosa and content of multiple intestinal neoplasia mice, a murine model of familial adenomatous polyposis and compared to control mice. Alkaline sphingomyelinase activity was also measured in 11 human rectal tumors with APC gene mutation and compared with 9 control tumors without mutation. RESULTS: Alkaline, neutral, and acid sphingomyelinase activities were present in the small intestine and colon in both mice types with no differences in hydrolytic capacity or distribution pattern. In sporadic rectal tumors similar alkaline sphingomyelinase activities were identified in tumors with somatic APC gene mutations as in samples without mutations. In the tumors without detectable APC mutations beta-catenin was analyzed, but no mutation was detected. CONCLUSION: Alkaline sphingomyelinase is not directly linked to adenomatous polyposis coli gene mutations.

Adenomatous Polyposis Coli↗
PubMed1996

Polyclonal origin of colonic adenomas in an XO/XY patient with FAP.

It is widely accepted that tumors are monoclonal in origin, arising from a mutation or series of mutations in a single cell and its descendants. The clonal origin of colonic adenomas and uninvolved intestinal mucosa from an XO/XY mosaic individual with familial adenomatous polyposis (FAP) was examined directly by in situ hybridization with Y chromosome probes. In this patient, the crypts of the small and large intestine were clonal, but at least 76 percent of the microadenomas were polyclonal in origin.

Adenomatous Polyposis Coli↗
PubMed2006

Bmp signaling is required for intestinal growth and morphogenesis.

Intestinal growth, morphogenesis, differentiation, and homeostasis are regulated by reciprocal interactions between the epithelium and the underlying mesenchymal stroma. The identification of BMPR1A mutations in patients with Juvenile Polyposis implicates Bmp signaling as an important mediator of these interactions. To test this hypothesis, we inhibited Bmp signaling in the mouse proximal intestine by transgenic misexpression of the BMP antagonist, noggin, using regulatory elements of the fatty acid binding protein (Fabp1) gene. This leads to abnormal villus morphogenesis, stromal and epithelial hyperplasia, and ectopic crypt formation. The resulting intestinal histopathology resembles that seen in human Juvenile Polyposis. Misexpression of noggin in the large intestine gives a similar abnormal phenotype in this region of the gut. Analysis of gene expression in the transgenic small intestine raises the possibility that Hedgehog and Pdgf signaling play a role in the development of the Juvenile Polyposis-like phenotype.

Animals↗
PubMed2005

Evidence for active Wnt signaling during postresection intestinal adaptation.

BACKGROUND: In the intestine, Wnt proteins are powerful regulators of cell proliferation, differentiation, and adhesion. Mutations of the adenomatous polyposis coli (APC) gene elevate nuclear beta-catenin and provoke intestinal tumor formation. We sought to determine whether Wnt signaling is involved in adaptive response to massive small bowel resection (SBR). METHODS: Male Min mice with a mutation of the APC gene and wild-type controls underwent a 50% proximal SBR or sham operation. After 3 days, villus height, crypt depth, and rates of proliferation and apoptosis were recorded in the remnant ileum. RESULTS: After SBR, villus height and enterocyte proliferation were significantly greater in the Min mice. Western blotting demonstrated resection-induced increases in beta-catenin, c-Myc, and E-cadherin after SBR, which was more pronounced in Min mice. CONCLUSIONS: Mutation of the APC gene and augmented Wnt signaling in the intestine results in an enhanced adaptive response to massive SBR. These data, for the first time, implicate an important role for Wnt signaling during the pathogenesis of resection-induced intestinal adaptation.

Animals↗
PubMed1994

[Endoscopy of the small intestine].

Small bowel pathology has been a difficult problem for all the scientists related with the study of these diseases. Small bowel position; far from the oral cavity and rectum, makes it quite inaccessible to exploration. Although double-contras technique in radiology has improved the study of this part of the digestive tract, many of these lesions cannot be evaluated. During the last few years, endoscopy has developed a great deal and at present, equipments capable of exploring this segment are available, even though the technique needs to be improved making it less troublesome and uncomfortable to the patient. We present a study of 32 patients who underwent "push" jejunoscopy with a large sterilized colonoscope. The main indications were bleeding and diarrhea of unknown cause. Three patients had jejunitis; one had a lymphoma; the second had a bleeding polyp and the third patient had a multiple polyposis. Five patients with partial atrophy of intestinal villi were found to have a normal endoscopic appearance of the mucosa. This indicates the necessity of performing biopsy in all cases. The absence of complications accounts for the confidence and safety of the exploration.

Adolescent↗
PubMedDate not supplied

[The Peutz-Jeghers syndrome and intestinal invagination].

Peutz-Jeghers syndrome is a autosomal dominant disorder characterized by hamartomatous polyposis of the gastrointestinal tract and mucocutaneous melanin pigmentation. This condition can occur and cause symptoms at any age, but intestinal obstruction due to intussusception is a frequent complication. Two cases of this syndrome associated to intussusception are reported. Both patients were girls, 2 and 8 years old respectively and underwent surgical treatment.

Child↗
PubMed2005

Loss of imprinting of IGF2: a common epigenetic modifier of intestinal tumor risk.

Epigenetic alterations in cancer occur at least as commonly as genetic mutations, but epigenetic alterations could occur secondarily to the tumor process itself. To establish a causal role of epigenetic changes, investigators have turned to genetically engineered mouse models. Here, we review a recent study showing that a mouse model of loss of imprinting (LOI) of the insulin-like growth factor II gene (Igf2), which shows aberrant activation of the normally silent maternal allele, modifies the risk of intestinal neoplasia caused by mutations of the adenomatous polyposis coli (Apc) gene. This increased risk corresponds to the apparent increased risk of colorectal cancer in patients with LOI of IGF2. The model suggests that preexisting epigenetic alterations in normal cells increase tumor risk by expanding the target cell population and/or modulating the effect of subsequent genetic alterations on these cells, providing a novel idea for cancer risk management.

Adenomatous Polyposis Coli Protein↗
PubMed1987

[Hypothesis on the existence of an adenoma-carcinoma sequence in the small intestine].

An analysis of a literature survey of 104 adenomas of the ampulla of Vater, 94 of the duodenum and 20 of the jejunum and ileum, as well as 735 carcinomas of Vater's ampulla, 180 carcinomas of the duodenum and 72 carcinomas of the jejunum and ileum, demonstrated, in spite of small case collectives, that there is probably a similar close relationship between adenomas and carcinomas in the small intestine, as in the large intestine. In adenomas of the small intestine signs of malignancy sometimes can be seen, as well as in some case of carcinoma of the small intestine rests of adenomas have been described. The age and sex distribution of the epithelial neoplasms of the small intestine permits an adenoma-carcinoma-sequence. The relative distribution of the adenomas over the different parts of the small intestine corresponds with that of the carcinomas. The adenomas and carcinomas of the small intestine in patients with adenomatosis coli have the same relationship to the neoplasms of the small intestine in patients without adenomatosis coli, as it is valid in the large intestine. The hypothesis of an adenoma-carcinoma-sequence in the small bowel with a great significance, which explains the results best, is therefore proposed. As the distribution of adenomas and carcinomas of the small bowel in patients with and without familial polyposis is equal, the theory is suggested, that the principle of the adenomatosis intestine disease is a general increase of the overall liability to adenomas in the large and small intestine.

Adenomatous Polyposis Coli↗
PubMed2006

Capsule endoscopy: where are we after 6 years of clinical use?

Capsule endoscopy has revolutionised the management of digestive tract diseases by providing a new non-invasive way to view the entire small bowel mucosa directly. Obscure gastrointestinal bleeding is the primary and best validated indication to capsule endoscopy, which when used as first-line exploration is the most efficient strategy as regards diagnosis. In these patients, the technique is also helpful for effective decision-making concerning subsequent treatments. There is significant uncertainty regarding the role of capsule endoscopy in patients with Crohn's disease. Although it is clearly more sensitive than conventional imaging modalities, the implications of the lesions identified with this technique are not fully understood. Further prospective studies are required to identify the clinical settings where capsule endoscopy is most effective in these patients. Capsule endoscopy may potentially lead to diagnosis of small bowel tumours earlier in their course; it should be used as first-line surveillance procedure in patients with Peutz-Jeghers syndrome, and it may be of clinical value in selected patients with familial adenomatous polyposis. Although preliminary results are promising, additional research is necessary to determine its role in the diagnosis and management of coeliac disease, as well as for the diagnosis of oesophageal and large bowel disorders. Well-designed studies are also needed to better define the impact of capsule endoscopy on health care use and clinical outcome of patients with intestinal diseases.

Adenomatous Polyposis Coli↗
PubMed1993

[The syndrome of juvenile polyposis].

Juvenile polyposis (JP) was first distinguished from other gastrointestinal polyposis syndromes in 1964. Since then, some 272 cases of this entity have been reported in the literature. The underlying polyps found in JP are of the hamartomatous type, but it is known that juvenile polyps may contain adenomatous tissue, or may be accompanied by adenomas. For the most part, juvenile polyps are found in the colon, but may also develop in the stomach, duodenum, jejunum or ileum. In 20 to 50% of the cases, juvenile polyposis occurs as a familial condition. Extra-intestinal anomalies are found in approximately 11% of JP patients. A particular clinical feature is anaemia caused by chronic gastrointestinal bleeding. In infants and young children, however, massive diarrhoea may become life-threatening. A reported malignant degeneration rate of 17.6% (among known cases) justifies the classification of JP as a precancerous condition, and has both therapeutic and, in particular, prophylactic consequences. These include the need to carry out regular follow-up examinations of the entire gastrointestinal tract, and also screening examinations in other members of the family.

Adenomatous Polyposis Coli↗
PubMed2004

Immunolocalization of protein 4.1B/DAL-1 during neoplastic transformation of mouse and human intestinal epithelium.

Recently, we have reported that the protein 4.1B immunolocalization occurred only in matured columnar epithelial cells of normal rat intestines. This finding suggested that protein 4.1B expression could be examined for a possible change during neoplastic transformation of the intestinal mucosa. In the present study, we first present the distribution of mouse protein 4.1B in normal intestinal epithelial cells and tumor cells using the adenomatous polyposis coli (Apc) mutant mouse model. A low level of protein 4.1B expression coincided with the phenotypic transition to carcinoma. To examine the protein 4.1B expression in human intestinal mucosa, we used another antibody against an isoform of the human protein 4.1B, DAL-1 (differentially expressed adenocarcinoma of the lung). Human DAL-1 was also expressed in matured epithelial cells in human colons, with a definite expression gradient along the crypt axis. In human colorectal cancer cells, however, DAL-1 expression was not detected. These results suggest that mouse protein 4.1B and human DAL-1 might have a striking analogy of functions, which may be integrally involved in epithelial proliferation. We propose that loss of protein 4.1B/DAL-1 expression might be a marker of intestinal tumors, indicative of a tumor suppressor function in the intestinal mucosa.

Animals↗