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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↗
PubMed1977

Experimental carcinogenesis in the resected colon of the rat.

Until now, carcinoma of the large intestine resected previously for benign disease has not been published. However an increasing number of patients resected for Crohn's disease, diverticulitis or trauma may reach nowadays a high lifespan. On the other hand, it is known that the gastroenteral anastomosis is predisposed to cancer development. In this study, the question of whether the large intestine following colotomy or ileotransversostomy is sensitive to carcinogenesis is examined. Male Wistar rats, subjected to colotomy or resection and ileotransversostomy, were treated weekly by subcutaneous injection of 1,2-dimethylhydrazine (12 mg/kg body weight) for seven weeks. The animals were killed 54 weeks after the first injection. At autopsy, 21 out of 29 operated rats had developed adenocarcinomas of the remaining colon. Intact control animals had the same incidence of malignant degeneration of the large bowel. When the anastomosis is chronically irritated by inflammation or by formation of a diverticulum, development, of carcinoma near the stoma was observed. This was the case in three rats of 28 animals. The results demonstrate that the resected colon of the rat is not more sensitive to experimental carcinogenesis than the intact one.

Adenocarcinoma↗
PubMed2003

Exclusion of Madh2, Madh4, and Madh7 as candidates for the modifier of Min 2 (Mom2) locus.

We recently identified the Modifier of Min 2 (Mom2) locus. Mom2 is a new modifier of intestinal tumorigenesis that resulted from a spontaneous mutation in a B6 Apc(Min)/+ mouse. The presence of one resistant Mom2(R) allele results in a significant reduction in small intestinal polyp number and colon polyp incidence in Apc(Min)/+ mice. Through linkage analysis, we previously localized Mom2 to a 14-cM region on mouse Chromosome (Chr) 18, distal to the Apc gene. This region is syntenic with human Chr 18q, which frequently undergoes loss of heterozygosity (LOH) in several human cancers, including colorectal cancer. Residing in this region are the Madh2 and Madh4 genes, which have both been implicated in human colorectal cancer. Based on meiotic recombinations within the Mom2 region in the derivation of our congenic animals, we have narrowed the location of the Mom2 locus and excluded Madh2, Madh4, and Madh7, as well as Mbd1, Mbd2, Dcc, and Tcf4, as candidates for the Mom2 gene.

Alleles↗
PubMed1998

Ruby laser therapy for labial lentigines in Peutz-Jeghers syndrome.

UNLABELLED: Some patients with Peutz-Jeghers syndrome may be disturbed by the appearance of lentigines. Such patients require management of their lentigines as well as their gastro-intestinal polyps. We describe ruby laser therapy of labial lentigines in two children with Peutz-Jeghers syndrome. The response to treatment was excellent and no sequelae or recurrence of the lesions was noted. CONCLUSION: Our experience suggests that ruby laser therapy is safe and a suitable approach for the treatment of labial lentigines in children with Peutz-Jeghers syndrome.

Child↗
PubMed1986

The use of epidemiology, scientific data, and regulatory authority to determine risk factors in cancer of some organs of the digestive system. 4. Colon cancer.

Colon cancer accounts for over 10% of all cancers diagnosed from 1973 to 1976 in the United States. Many factors have been identified as having a role in its etiology, including the intestinal microflora, colonic mutagens, bile acids, cholesterol, estrogens, and diet. The evidence supporting or refuting the importance of each of these factors and others is discussed. Dietary factors appear to be the most important risk determinants for colon cancer. In particular, a high-fat, low-fiber diet has been most consistently incriminated as a promoting agent of this cancer. The incidence of colon cancer and consumption of total fat and animal protein are highly correlated internationally. However, further epidemiologic studies have given equivocal results. A high-fiber diet has been proposed as being protective against colon cancer although the mechanism of protection remains unclear. A major correlational study has shown that dietary fiber consumption was higher in areas with low incidence of colon cancer than in those areas with high incidence. A few case-control studies have been supportive of the fiber hypothesis but many more have shown no difference among cases and controls in their fiber consumption. More epidemiological studies are needed to clarify the role of diet in the etiology of colon cancer. Before a dietary change is recommended, the competing risks of other cancers and other diseases should be extensively researched.

Age Factors↗
PubMed1994

Gastric and small intestinal lesions after partial stomach resection with Billroth II or Roux-en-Y reconstruction in the rat.

The evolution and phenotypic expression of mucosal lesions of the gastric stump were investigated in male rats submitted to gastric resection with reconstruction by the Billroth II technique (BII with biliopancreatic reflux, BPR) or by the Roux-en-Y procedure (without BPR). Animals were studied at 24, 36, 54 and 64 weeks after surgery and the phenotypic expression of lesions analysed using routine hematoxylin and eosin staining, immunohistochemical staining for pepsinogen isoenzyme 1 and histochemical procedures for mucins (paradoxical concanavalin A, galactose oxidase Schiff (GOS) and sialidase GOS reactions). BPR was found to be responsible for the formation of adenomatous hyperplasia (AH), increasing in incidence and size with time, since the Roux-en-Y procedure failed to induce the gastric stump lesions observed after BII reconstruction. AHs always occurred in the transition of the gastrojejunal junction, a site offering special conditions for BPR influence, and were classified as gastric (G), intestinal (I) and G+I types according to their phenotypic expression. No pure I type AH was diagnosed at any time point. The G and G+I types developed at approximately equal incidences (i.e., G type 7/17, G+I type 10/17 at the 64th week). It was suggested that both gastric and intestinal mucosal elements were stimulated to proliferate by BPR, with the gastric mucosa tending to demonstrate AH. Intestinal type components of AH were found adjacent to the jejunum and not at the stomach margin, indicating an origin from intestinal mucosa. No metaplasia of the gastric mucosa was observed in any animal after partial gastric resection. In 101 rats submitted to the BII procedure, 5 mucinous adenocarcinomas were eventually diagnosed, mostly located in the subserosa of the gastrojejunal junction. All carcinomas expressed the phenotype of cells of the small intestine. Evidence of malignant transformation within the gastric components of AH was not observed even at the 64th week. In conclusion, all lesions induced by BPR in the rat remnant stomach are benign, and the few true cancers that arise in association are derived from the small intestine.

Animals↗
PubMed2002

Inhibition of beta-catenin/Tcf activity by white tea, green tea, and epigallocatechin-3-gallate (EGCG): minor contribution of H(2)O(2) at physiologically relevant EGCG concentrations.

Epigallocatechin-3-gallate (EGCG) is the major polyphenol present in white tea and green tea. Recently, it was reported that the addition of EGCG and other tea polyphenols to cell culture media, minus cells, generated significant levels of H(2)O(2), with the corollary that this might represent an "artifact" in cell culture studies which seek to examine the chemopreventive mechanisms of tea. We show here that in cell growth media with and without serum, and in growth media containing human embryonic kidney 293 (HEK293) cells plus serum, physiologically relevant concentrations of EGCG (< or =25 microM) generated H(2)O(2) with a peak concentration of the order of 10-12 microM. However, addition of 20 microM H(2)O(2) directly to HEK293 cells transiently transfected with wild-type or mutant beta-catenin constructs and TCF-4 had no significant effect on beta-catenin/TCF-4 reporter activity or beta-catenin expression levels. In contrast, 2-25 microM EGCG inhibited beta-catenin/TCF-4 reporter activity in a concentration-dependent fashion and there was a concomitant reduction in beta-catenin protein levels in the cell lysates without changes in TCF-4 expression. The inhibition of reporter activity was recapitulated by white tea and green tea, each tested at a 25 microM EGCG equivalent concentration in the assay, and this was unaffected by the addition of exogenous catalase. The results indicate that physiologically relevant concentrations of tea and EGCG inhibit beta-catenin/TCF-4 reporter activity in HEK293 cells due to reduced expression of beta-catenin and that this is unlikely to be an artifact of H(2)O(2) generation under the assay conditions used here. These data are consistent with the findings from in vivo studies, showing the suppression of intestinal polyps by tea, via an apparent down-regulation of beta-catenin and Wnt target genes.

Anticarcinogenic Agents↗
PubMed2003

Requirement for tumor suppressor Apc in the morphogenesis of anterior and ventral mouse embryo.

Tumor suppressor Apc (adenomatous polyposis coli) is implicated in the Wnt signaling pathway that is involved in the early embryonic development and tumorigenesis in vertebrates. While the heterozygous null mutant mice develop intestinal polyps, the homozygous embryos die before gastrulation. To investigate the role of Apc in later embryonic development, we constructed a novel hypomorphic Apc allele whose expression was attenuated by approximately 80%. In the hypomorphic Apc homozygous ES cells, reduction in Apc expression caused beta-catenin accumulation and Wnt signaling activation. The homozygous mutant mouse embryos survived 3 days longer than the null mutant embryos. Interestingly, they showed anterior truncation, partial axis duplication, and defective ventral morphogenesis. To determine the tissues where Apc functions for anterior and ventral morphogenesis, we constructed chimeric embryos whose epiblast was derived predominantly from the Apc hypomorphic homozygous cells but the visceral endoderm was from the wild type. Although these chimeric embryos still showed some anterior defects, their ventral morphogenesis was rescued. In addition, marker studies indicated that the axial mesendoderm was also defective in the homozygous embryos. Our results provide genetic evidence that expression of Apc at the normal level is essential for both anterior and ventral development, in the epiblast derivatives and visceral endoderm.

Alleles↗
PubMed1998

Apoptosis induced by sulindac sulfide in epithelial and mesenchymal cells from human abdominal neoplasms.

We investigated whether the therapeutic action of sulindac, used for the treatment of familial adenomatous polyposis, desmoid tumors, and against colon cancer, could be mediated by its active metabolite, sulindac sulfide, in cell growth and apoptosis on cell lines derived from abdominal neoplasms. Sulindac sulfide actions on cell growth and apoptosis were evaluated in epithelial human colon tumor 8 (HCT8) cell line and mesenchymal cell lines (bovine bone endothelial (BBE) cell line, desmoid tumor-derived cells, human colorectal cancer-derived fibroblasts). Sulindac sulfide (0.1-60 microg/ml) induced a dose-dependent inhibition of cell proliferation of all cell lines tested. Apoptosis was induced at doses of 20 and 40 microg/ml, respectively, in BBE and HCT8 cells with no effect on desmoid tumor cells and colorectal cancer-derived fibroblasts. Since mesenchymal cells respond to clinically effective concentrations of the compound, its preferential action on the stromal compartment of intestinal polyps, desmoid tumors and colon cancer can be proposed, with consequent regression of the tumor.

Abdominal Neoplasms↗