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Results for “Intestinal Polyposis”

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At least 757 records · Page 42Linked to original sources
PubMed2000

A case of cancerous familial adenomatous polyposis in urinary bladder due to migration of colonic mucosa through rectovesical fistula.

The patient was a 50-yr-old man who had undergone low anterior resection for rectal cancer at the age of 24 yr in 1966. At that time, gastric and colonic polyposis were indicated. Postoperative anastomotic dehiscence occurred and, by 1985, a rectovesical fistula had formed. In 1986, when the patient was 44 yr old, he was examined at our hospital for constriction of the rectum due to the rectovesical fistula. Abdominoperineal excision of rectum and surgical closure of the fistula were performed, and the patient was kept under observation because of a diagnosis of familial adenomatous polyposis. In 1988, when the patient was 46 yr old, early ascending colon cancer was discovered and total colectomy was performed. Then, in December, 1991, gross hematuria was found. Further examination revealed a tumor on the posterior wall of the urinary bladder lumen, and biopsy showed adenocarcinoma. Pelvic recurrence of the rectal cancer was diagnosed, and total pelvic exenteration was performed. There were no distant metastases; histologically, the tumor of the bladder was thought to be due to colonic mucosa of familial adenomatous polyposis that had migrated to the bladder lumen via the rectovesical fistula and had become cancerous.

Adenomatous Polyposis Coli↗
PubMedDate not supplied

[The dehiscence of colorectal anastomoses: the risk factors].

OBJECTIVE: To evaluate the results of emergency and elective colorectal resective surgery; to identify general and local factors that influence the anastomotic leak rate. MATERIAL AND METHOD: 200 selected consecutive patients (115 males and 85 females, medium age 50.6 years, range 16-87) underwent resective colorectal surgery between 1990 to 1997. 154 (77.0%) were operated in elective surgery and 46 (23.0%) in urgency, for carcinoma, diverticular disease, mesenteric infarction, chronic intestinal disease, dolicosigma, anastomotic leakage, familiar polyposis or lesions by firearm. The operations consisted in 58 right colectomy, 28 left colectomy, 6 resection of the transverse and 29 of the sigmoid colon, 40 anterior resection, 12 total colectomy, 19 closing of colostomy, 6 by-passes. Anastomoses were performed in 88 cases by manual and in 110 by mechanical sutures. RESULTS: We observed 12 (6%) anastomotic leakages. Mortality rate was 1.0%. 13%.0 of these patients were underwent before to emergency and 3.9% to elective surgery; 5.7% by manual and 6.4% by mechanical suture. Diagnosis of leakage was made by clinical features, blood vessel examinations and abdominal TC scan. DISCUSSION: The risk factors of anastomotic leakage are general or local. Chronic obstructive pulmonary disease, perioperative transfusion, level of serum albumin, use of corticosteroid in the first group and sepsis, bowel obstruction, anastomotic level and tension and poor blood supply in the second, appear the most important causative factors in the development of anastomotic leaks. CONCLUSION: The incidence of dehiscence in colo-rectal surgery was seen significatively lower when anastomoses were performed in ideal circumstances than in the presence of one or more unfavorable factors. Healing remains a process depending more on the patient than on any aspect of the surgical technique.

Adolescent↗
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↗
PubMed1995

Depressed adenomas of the colon in familial adenomatous polyposis. Histology, immunohistochemical detection of proliferating cell nuclear antigen (PCNA), and analysis of the background mucosa.

Depressed adenomas of the colon have been reported more often during the past several years, but there are few reports on the details of their characteristics or behavior. In this study, depressed and ordinary polypoid adenomas, especially those in an early stage, in the large intestine of 28 patients with familial adenomatous polyposis (FAP) were examined macroscopically, by dissecting microscope, and histologically. Proliferating cell nuclear antigen (PCNA) and the density of crypts in the background mucosa around depressed and polypoid adenomas were also compared. Depressed adenomas of < 1.0 mm in diameter showed horizontal growth between the normal adjacent crypts, which often left the normal crypts as islands, whereas polypoid adenomas grow expansively without including remnants of normal crypts. In depressed adenomas, PCNA shifted to the upper part of the crypts, and the background mucosa in their vicinity showed a low density of crypts. These findings indicate that a unique characteristic of growth of depressed adenomas at an early stage is superficial proliferation.

Adenoma↗
PubMed1992

The APC gene, responsible for familial adenomatous polyposis, is mutated in human gastric cancer.

Although gastric cancer is the most common cancer in the world, genetic changes during its carcinogenesis are not well understood. Since some gastric cancers are considered to originate from the intestinal metaplasia, it is likely that the adenomatous polyposis coli (APC) gene, the mutation of which causes adenomatous polyps in the colon, is associated with carcinogenesis of gastric cancer. Based on this idea, DNAs isolated from gastric cancers were examined by means of a RNase protection analysis coupled with polymerase chain reaction followed by sequencing of the polymerase chain reaction products. By screening nearly one-half of the coding region of the APC gene in 44 tumors, somatic mutations were detected in three tumors: a missense mutation, a nonsense mutation, and a 5-base pair deletion resulting in a frame shift which causes truncation of the gene product. These results suggest that the mutation of the APC gene also plays an important role during the carcinogenesis of at least some gastric cancers.

Adenocarcinoma↗
PubMedDate not supplied

Piroxicam-induced regression of intestinal adenomatous polyps in APC(delta474) mice.

Mutation of adenomatous polyposis coli (APC) gene results in incidence or development of polyps and colorectal cancer. It has been reported that nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cell growth, cause cell cycle arrest, and induce apoptosis. The aims of this study are to investigate chemopreventive effects of piroxicam and elucidate its mechanism. All APC(delta474) mice have intestinal polyps. Thirty-five APC(delta474) mice were divided into three groups: 0.005% solution of piroxicam in tap water was given for P group (n = 15) and 0.001% solution for P' group (n = 5), and water without piroxicam for C group (n = 15) from 4 weeks of age to 12 weeks, respectively. All mice were sacrificed at the 12th week after birth. Hematoxylin-eosin staining for number and size of polyps, immunohistochemical staining for cyclooxygenase (COX)-1 and -2, proliferating cell nuclear antigen (PCNA), vascular endothelial growth factor (VEGF), TUNEL method, and Western blot analysis of COX-2 and VEGF were performed. Polyps were divided into two types of large polyps of >or=300 microm in diameter and small polyps of <300 microm. The number of large polyps in P group decreased significantly compared with C group (p <.0001), but without significant difference in small polyps. There were no significant differences in PCNA index in both of large and small polyps among the three groups. Apoptotic index of polyps in P group increased more than those in C group (p <.05). There was immunohistochemically no significant difference in COX-1 positivity of normal intestinal epithelia and adenomas among three groups. Both numbers of VEGF-positive cells and COX-2 positive cells in the stroma of the small intestine were significantly downregulated in P group (p <.05). COX-2 expression was inhibited in dose-dependent manner without significant difference. There were no significant differences in VEGF expression between P' and C groups. In conclusion, piroxicam suppressed the development of large polyps in APC(delta474) mice by inducing apoptosis and inhibiting VEGF expression in interstitial cells of polyps.

Adenomatous Polyposis Coli↗
PubMed2002

Intestinal adenomas can develop with a stable karyotype and stable microsatellites.

Loss of function of the adenomatous polyposis coli (APC)/Apc tumor suppressor gene occurs early in the etiology of intestinal cancer in mammals. In human colonic tumors, genomic instability is proposed to be associated with tumor initiation by inducing loss of APC function. We have used a mouse model of inherited intestinal cancer (Apc(Min)/+, Min/+) to analyze the earliest stages of tumorigenesis in this organ. We find that tumors from C57BL/6 Min/+ mice have a stable karyotype and stable microsatellites. In contrast to previous claims, we find that homozygosity for the Min allele of Apc in tumors can proceed by homologous somatic recombination. Further, our analysis of early, benign human colorectal adenomas failed to reveal any evidence for generalized chromosomal or microsatellite instability. These results cast doubt on the hypothesis that either of these forms of genomic instability is necessary for the initial development of colorectal adenomas. We contrast our analysis of autochthonous primary tumors to other studies involving xenografts or cultured cells.

Adenoma↗
PubMedDate not supplied

Cyclin D1 expression in the intestinal mucosa and tumors of Apc1638N mice.

Altered expression of cyclin D1 contributes to the development of several types of cancer, including colorectal cancer. This study examined cyclin D1 expression in 32 intestinal tumors in different stages of tumorigenesis in Apc1638N mice, a mouse model for human familial adenomatous polyposis (FAP). Three morphological patterns of expression of cyclin D1 in intestinal epithelial cells were found: nuclear, punctate-cytoplasmic and fine granular cytoplasmic. The nuclear pattern of cyclin D1 was detected in all of the tumors, including adenomas (n = 18) and adenocarcinomas (n = 14); this pattern was found predominantly in the tubular region of the tumors and in flat mucosa adjacent to a subset of the tumors (67% of adenomas and 57% of carcinomas). The punctate-cytoplasmic pattern of cyclin D1 expression was found in all adenocarcinomas and a majority of adenomas (80%), mainly in invasive and villous areas of the tumors; it was not found in normal flat adjacent mucosa suggesting that this pattern and altered cytoplasmic/nuclear expression were associated with tumor progression. Fine cytoplasmic granules were located in normal duodenum in the basal portion of the crypts and in colon in epithelial cells at the surface of the colonic crypts; in both duodenum and colon the number of cells with fine cytoplasmic granules significantly increased after feeding a Western-style diet. These altered patterns of expression of cyclin D1 may provide useful biomarkers of abnormal cell development for studies of tumorigenesis and the effects of chemopreventive agents.

Adenomatous Polyposis Coli↗