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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↗
PubMedDate not supplied

Molecular biology of gastric cancer.

Gastric cancer involves changes in multiple oncogenes and multiple suppressor genes, and it causes genetic instability. Aberrant expression and amplification of the c-met gene, inactivation of the p53 gene, and CD44 abnormal transcripts are common events of both well differentiated and poorly differentiated gastric cancers. Amplification of the cyclin E gene is also observed in gastric cancer regardless of histologic type. Decreased expression of the pic1 (p21) gene occurs independent of the p53 mutations. In addition, K-ras mutations, c-erbB-2 gene amplification, loss of heterozygosity (LOH) and mutations of the APC gene, LOH of the bcl-2 gene, and LOH at the DCC locus are preferentially associated with well differentiated gastric cancer. Moreover, LOH on chromosome 1q is involved in the progression of well differentiated cancer. Precancerous lesions, including hyperplastic polyp, intestinal metaplasia, and adenoma, share genetic changes found in well differentiated cancers. Conversely, genetic instability may be involved in the first step of stomach carcinogenesis of the poorly differentiated type. Reduction or loss of cadherin and catenins, K-sam gene amplification, and c-met gene amplification are necessary for the development and progression of poorly differentiated or scirrhous carcinoma. Interaction between cell-adhesion molecules in the c-met expressed tumor cells and hepatocyte growth factor from stromal cells is implicated in the morphogenesis of two types of gastric cancer.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1976

[The surgical treatment of villous tumours of the large bowel (author's transl)].

The treatment of 12 patients with villous tumours of the rectum is described. In benign lesions a sphincter conserving operation should be employed. With the technique of submucosal local excision per anum which was described by A.G. Parks it is possible to remove large villous tumours of the rectum. If there is malignant change with invasion of the muscularis muscosae which is found in about 20% of the cases resection therapy is necessary.

Aged↗
PubMed1977

[Reversal of small bowel segments to delay intestinal passage after total colectomy (author's transl)].

Five female mini-pigs underwent total colectomy including resection of the ileocecal valve. Sparing the terminal rectum, we reformed an end-to-end anastomosis between terminal ileum and remaining rectal cuff. In a second series 8 female mini-pigs have been colectomized using the same model. To delay intestinal passage, in addition a 10-12 cm long reversed segment of terminal ileum has been inserted between small bowel and rectal stump. Both groups were compared with a group of normal unoperated mini-pigs in a study up to 1 year, observing intestinal transit time, blood chemistry and general development of the animals. It could be proved that the reversal of a small bowel segment in colectomized animals leads to a prolongation of the intestinal transit time, to normalization of electrolytes and general appearance. Colectomy was only survived by animals with a reversed segment. The clinical application of a reversed small bowel segment following total colectomy in 1 patient was successful.

Adult↗
PubMed1989

Angiodysplasia. Natural history and efficacy of therapeutic interventions.

Angiodysplasia, a disease for which the optimal treatment is uncertain, is a frequent cause of lower intestinal bleeding among older patients. To study the natural history of angiodysplasia and compare the efficacy of medical therapy, endoscopic electrocoagulation, and surgery, the course of 101 patients evaluated from 1974 through 1983 at the Massachusetts General Hospital was reviewed. Angiodysplasia caused bleeding that ranged from occult blood in stools to massive hemorrhage and was also observed incidentally in nonbleeding patients. Patients were followed for up to 10 years (mean of 22 months). Rebleeding was defined as evidence of hemorrhage requiring hospital admission, transfusion, or surgery. Thirty-one patients were treated surgically, 19 patients were treated endoscopically, and 36 patients were treated medically. Using life table analysis we observed similar rebleeding rates among medically and endoscopically treated groups. The surgically treated group had a frequency of rebleeding less than half that of the other groups (P = 0.15). A multivariate regression analysis failed to identify any factors other than coagulopathy to explain the different incidence of rebleeding in the patients treated by endoscopic electrocoagulation and surgery.

Diverticulum↗
PubMed1985

The role of bile acids in colonic carcinogenesis.

Several line of evidence suggest that bile acids may be implicated in the pathogenesis of colonic cancer. A high consumption of fat and animal protein and a low dietary intake of fiber have been shown to be related to the incidence of colonic cancer. From these epidemiologic observations the hypothesis was proposed that the correlation between diet and colon cancer might be explained by the involvement of bile acids. Populations at a high risk of developing cancer were shown to have an increased excretion both of total and bacterially modified bile acids in their feces. Animal studies demonstrated a cocarcinogenic effect of bile acids and experimental diets containing large amounts of fat did not only induce an increased bile acid excretion but also an enhanced tumor formation in the colon. Furthermore, microbial in vitro tests showed a comutagenic activity of secondary bile acids. However, case control studies comparing the fecal bile acid excretion pattern in colonic cancer patients and control subjects failed to show such a clear relationship, which might be explained by rather similar dietary habits within one population and individual differences in sensitivity to environmental factors contributing to the tumor development. Cholecystectomy, leading to an increased exposure of bile acids to the intestinal microflora, has been suggested as a predisposing factor for the development of colonic cancer, but the results of experimental and epidemiologic studies so far are rather inconsistent.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Clinical and roentgen features of the intestinal polyposis syndromes.

The intestinal polyposis syndromes represent a challenging diagnostic problem for the radiologist. These syndromes include: familial multiple polyposis, Gardner's, Peutz-Jeghers, Turcot's, Cronkhite-Canada and juvenile polyposis. The polyposis syndromes can usually be differentiated from one another on the basis of the clinical history, examination of the mucocutaneous tissues and roentgen findings. Numerous other conditions, however, may mimmic a polyposis syndrome, and must be considered in the differential diagnosis.

Adolescent↗
PubMedDate not supplied

Concurrent colonic carcinoma and small-bowel carcinoid tumor. Case reports and review of the literature.

Recent reviews stressing the existence of synchronous and metachronous noncarcinoid neoplastic lesions in the same segment of an organ stimulated a review of experience with simultaneous small-bowel carcinoids and colonic carcinoma. Four cases of colonic malignancy associated with small-bowel carcinoid are presented. Included are cases with multiple carcinoids and concurrent multiple carcinomas; two metachronous carcinomas with subsequent ileal carcinoids, and three cases explored for colonic carcinoma with the discovery of incidental ileal carcinoids. There are few reports describing this variety of situations. The occurrence of concurrent malignant lesions, particularly more than one metachronous lesion in primary carcinoid cases, is uncommon.

Adenocarcinoma↗
PubMed1983

Background mucosal changes of primary advanced large intestinal cancer in patients without familial polyposis coli.

In 337 cases of primary advanced large intestinal cancer in patients without familial polyposis coli, the risk factor for cancer was discussed chiefly from the background mucosa surrounding and apart from the cancers. The following findings were obtained: (1) in the mucosa surrounding cancers, adenoma was seen in 23 cases (6.8 per cent), adenomatous changes of the basal cells in 211 cases (62.6 per cent), and hyperplastic glands in 167 cases (49.6 per cent), (2) in the mucosa at least 10 mm from the cancers, adenoma, adenomatous changes of the basal cells, and hyperplastic glands were seen in 42 cases (12.5 per cent), 129 cases (38.3 per cent), and 40 cases (11.9 per cent), respectively. Therefore, it is suggested that microscopic adenoma and adenomatous changes of the basal cells might be a sign of premalignancy in patients without familial polyposis coli.

Adenocarcinoma↗