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At least 217 records · Page 12Linked to original sources
PubMed1997

Morphological and molecular processes of polyp formation in Apc(delta716) knockout mice.

Mutations in the human adenomatous polyposis coli (APC) gene are responsible for not only familial adenomatous polyposis but also many sporadic cancers of the digestive tract. Using homologous recombination in embryonic stem cells, we recently constructed Apc gene knockout mice that contained a truncation mutation at codon 716 (Apc(delta716)). The heterozygous mice developed numerous intestinal polyps. All microadenomas dissected from nascent polyps had already lost the wild-type allele, indicating the loss of heterozygosity (M. Oshima et al., Proc. Natl. Acad. Sci. USA, 92: 4482-4486, 1995). We also demonstrated that cyclooxygenase 2 is induced in the polyps at an early stage and plays a key role in polyp development (M. Oshima et al., Cell 87: 803-809, 1996). We have analyzed the process of polyp development in these mice both at morphological and molecular levels. A small intestinal microadenoma is initiated as an outpocketing pouch in a single crypt and develops into the inner (lacteal) side of a neighboring villus forming a double-layer nascent polyp. The microadenoma then enlarges and gets folded inside the villus. When it fills the intravillous space, it expands downward and extends into adjoining villi, rather than rupturing into the intestinal lumen. During this course of development, the basement membrane remains intact, and the labeling index of the microadenoma cells is similar to that of the normal crypt epithelium. As in the crypt cells, neither transforming growth factor beta1 nor its receptor type II is expressed in the microadenoma cells. No hot spot mutations in the K-ras gene are found in the microadenoma tissue during these early stages of polyp development. Essentially, the same results have been obtained for the colonic polyps as well. These results suggest that early adenomas in the Apc(delta716) polyps are very similar to the normal proliferating cells of the crypt except for the lack of directed migration along the crypt-villus axis.

Activin Receptors, Type I↗
PubMed1986

Orbital osteoma in Gardner's syndrome.

A 30-year-old woman developed proptosis secondary to a left ethmoidal compact osteoma. At age 29 years, a mandibular eburnated (ivory) osteoma was excised. At age 25 years, multiple adenomatous polyps of the colon were resected. Her father, age 61 years, had multiple intestinal polyps and bilateral mandibular osteoma. A 24-year-old sister had an osteoma of the forehead. Gardner's syndrome is an autosomal dominantly inherited disorder characterized by intestinal polyposis, various skin and soft tissue tumors, and osteomas of the bony skeleton. Orbital osteomas occur rarely.

Adult↗
PubMed1992

Lack of association among typical congenital hypertrophy of the retinal pigment epithelium, adenomatous polyposis, and Gardner syndrome.

BACKGROUND: It has been recently documented that multiple bilateral pigmented lesions at the level of the retinal pigment epithelium may be an indicator of patients with familial adenomatous polyposis who are prone to develop intestinal cancer, particularly if there is a positive family history of these intestinal disorders. Although atypical, such lesions have been called congenital hypertrophy of the retinal pigment epithelium (CHRPE). This study was undertaken to determine whether the typical lesions of CHRPE, seen frequently by ophthalmologists, also were indicators of familial adenomatous polyposis. METHODS: Review of charts and follow-up studies were performed on all patients diagnosed and coded as having solitary CHRPE or its multifocal variant (congenital grouped pigmentation; bear tracks). Patients and their physicians were contacted by telephone to complete a detailed questionnaire designed to detect signs or symptoms of familial adenomatous polyposis or Gardner syndrome among these patients with CHRPE and their relatives. RESULTS: Of the 132 patients with previously diagnosed CHRPE, there were none with familial adenomatous polyposis, Gardner syndrome, or intestinal cancer, and only one patient had a history of intestinal polyps. Among more than 2000 of their blood relatives, only 20 had intestinal polyposis or colonic cancer (1%). This is much lower than would be expected from a survey of patients with the typical fundus lesions seen with familial adenomatous polyposis. CONCLUSIONS: It appears that solitary CHRPE and congenital grouped pigmentation differ clinically from the multiple pigmented lesions seen with familial adenomatous polyposis and that patients with these conditions, as well as their relatives, are not at a greater risk of developing intestinal cancer.

Adenomatous Polyposis Coli↗
PubMed1999

Tumor burden and clonality in multiple intestinal neoplasia mouse/normal mouse aggregation chimeras.

Aggregation chimeras were formed between C57BL/6 mice heterozygous for the Apc(min) (Min) mutation and wild-type SWR mice, that differ in their Pla2g2a status, a modifier of Apc(min), and also in their resistance to intestinal polyp formation. Variation in the dolichos biflorus agglutinin-staining patterns of the intestines of these mouse strains was used to determine the chimeric composition of the intestine in individual mice and to examine the clonal composition of adenomas. Macroscopic adenoma numbers in chimeric mice were compared with the expected adenoma numbers based on the percentage of C57BL/6J-Apc(min/+) epithelium in individual mice. These results unexpectedly show that there was no apparent inhibitory effect of the SWR-derived (Pla2g2a wild-type) tissue on adenoma formation in the C57BL/6J-Apc(min/+) epithelium. This suggests that the main genetic modifiers of the Min phenotype act at a cellular or crypt-restricted level with no discernable systemic effect. All adenomas were seen to contain C57BL/6J-Apc(min/+)-derived epithelium, confirming that the germ-line mutation of the mApc gene is necessary to initiate tumorigenesis in this model system, and that the mApc gene acts in a cell autonomous fashion.

Adenoma↗
PubMed2001

[Peutz-Jegher's syndrome].

Peutz-Jeghers syndrome is a rare hereditary disease, although in about 20 % of patients there is no known family history. Its clinical hallmarks are facial mucocutaneous pigmentation and diffuse gastrointestinal polyposis of hamartomatous origin. The major difficulty in the management of this disease lies in the complications of surgery for small bowel polyposis and the high incidence of tumors presented by these patients as adults. We present the case of a 10-year-old girl with treatment-resistant anemia and no other clinical symptoms. Further investigation revealed pigmentation in the oral mucosa and polyposis in the stomach and small intestine. Hamartomatous lesions were confirmed by histological study of intestinal biopsy. No familial antecedents of pigmentation or intestinal polyps were found. During evolution the patient required subtotal resection of the small intestine due to invagination.

Child↗
PubMed1994

Hamartomatous polyps in the intestine of two dogs.

Partly obstructing, proliferative mucosal masses in the small intestine of two dogs were shown histologically to be hamartomatous polyps. They were characterized by an extension of smooth muscle from the muscularis mucosae into the lamina propria of the lesion. This is the first report of such lesions in domestic animals. In one of the dogs the lesion had become malignant.

Adenocarcinoma↗
PubMed1976

Nature of juvenile polyps in the large intestine.

Forty-five juvenile polyps were found among approximately 390 mucosal polyps of the large intestine. Various degrees of epithelial pseudostratification were found among juvenile polyps and the larger-sized polyps of both juvenile type and adult one tended to have a more advanced degree of epithelial pseudostratification. The glands of both juvenile polyps and adult ones revealed a closely resembled or almost identical pattern of size-distribution-pattern of the glandular size in both normal mucosae and hyperplastic mucosae of long-standing ulcerative colitis. Transition of juvenile polyps into adult ones was suggested by the cases with increase in numbers of glands and their orifices to the surface of the polyp and there were some polyps showing an intermediate form between juvenile polyps and adult ones. On the basis of histologic characteristics and age incidence of the patients, it may be said that a juvenile polyp is an immature variant of an adult polyp.

Adolescent↗
PubMed1999

Inflammatory fibroid polyp presenting with intestinal invagination: sonographic and correlative imaging findings.

We report a case of a large inflammatory fibroid polyp of the small bowel presenting with intussusception in a 22-year-old man. Sonography demonstrated a solid, mobile, homogeneous, echogenic mass surrounded by the typical mural layers of an invaginated ileum. CT demonstrated a well-defined intraluminal solid mass with an attenuation of 17 HU. The pathologic diagnosis after segmental ileal resection was ileal inflammatory fibroid polyp.

Adult↗
PubMed1997

Homeosis and polyposis: a tale from the mouse.

Homeobox genes play essential roles in specifying the fates of different cell types during embryogenesis. In Drosophila, the homeotic gene caudal is important for the generation of posterior structures. In the mouse, the caudal homologue Cdx2 has been implicated in directing early processes in intestinal morphogenesis and in the maintenance of the differentiated phenotype. A recent study showed that Cdx2 null mutation was embryonically lethal, whereas Cdx2+/- mice developed multiple intestinal polyps in the proximal colon in addition to developmental defects. There are striking phenotypic similarities and differences between Cdx2+/- and other mice predisposed to intestinal neoplasia. The possible role of Cdx2 in human colorectal tumorigenesis is discussed.

Adenomatous Polyposis Coli↗
PubMed1995

Endorectal pull-through of transplanted colon as part of intestinal transplantation.

BACKGROUND: Two children with life-threatening disorders underwent intestinal transplantation; one multivisceral transplantation excluding the liver, and the second transplantation of the liver, small bowel, and colon. METHODS: Involvement of the native rectum necessitated resection and replacement with the transplanted allograft. To prevent a permanent colostomy, a pull-through of the allograft colon was performed. RESULTS: Both patients had a stormy early postoperative course, mainly because of the complexities of intestinal transplantation, but with eventual recovery, including improvement of rectal function. CONCLUSIONS: These are the first two known cases in which a transplanted large intestine was used for a pull-through procedure.

Colon↗