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PubMed1996

Familial polyposis syndromes. Advances in molecular genetic characterization.

Many gastrointestinal polyposis syndromes have well-defined clinical and histopathologic features. Recent advances in our ability to analyze these syndromes at the genetic level have allowed for further characterization of these entities and their pathophysiology. Elucidation of the underlying molecular genetic alterations that result in the various forms of adenomatous polyposis syndromes has been reported recently and is discussed in this article. Defining these syndromes at the genetic level has important biologic and practical implications.

Adenomatous Polyposis Coli↗
PubMed1997

Short-chain fructo-oligosaccharides reduce the occurrence of colon tumors and develop gut-associated lymphoid tissue in Min mice.

C57BL/6J-Min/+ mice, which are heterozygous for a non-sense mutation in the Apc gene, provide a model for both familial adenomatous polyposis and sporadic colon cancers. In our study, gut tumors and small intestine lymphoid nodules were counted in Min mice fed fiber-enriched diets for 6 weeks. Neither starch-free wheat bran nor resistant starch modified the number of tumors. However, short-chain fructo-oligosaccharides dramatically reduced the incidence of colon tumors and concomitantly developed gut-associated lymphoid tissue. Our experiment shows that short-chain fructo-oligosaccharides counteract advanced stages of colon carcinogenesis, possibly via stimulation of antitumoral immunity by modulation of the colonic ecosystem.

Animals↗
PubMed1998

[Hemostatic therapy of gastroduodenal hemorrhage of non-ulcer genesis by the use of reserve mechanisms of hemostasis].

The article presents summarized results of treatment and examinations of 216 patients with gastro-intestinal bleedings due to acute errosive hemorrhagic gastritis and gastroduodenitis, cancer and polyposis of the stomach, liver cirrhosis and portal hypertension, hemorrhage against the background of atherosclerosis and arterial hypertension by administration of hemostatic medicine into the lymphatic system for activation and reinforcement of the reserve monocyte-macrophage mechanism of hemocoagulation. The results obtained confirm the expedience of this method of influencing the monocyte-macrophage hemostasis, having no complications and giving better medical effects.

Acute Disease↗
PubMed1991

[Results and late sequelae of colectomy].

Results after 55 colectomies are reported in the period from 1962-1986. The surgical intervention was indicated by ulcerative colitis in 19, Crohn's disease in 18 and familial polyposis of the colon in 18 cases. 37 total colectomies, 12 subtotal colectomies with ileorectal anastomosis and 6 colectomies with a remaining terminal closed stump of the rectum were performed. During the period of observation postoperative lethality decreased from 37% to 6%. Death was most frequently caused by thromboemboli and peritonitis. In 44% of the patients ill with familial polyposis malignant degeneration could be observed. 3 died by generalized metastases. Metabolism of protein, lipid and electrolyte showed no essential disturbances after colectomy. Intestinal assimilation was nearly standard. More difficult is social reintegration.

Adenomatous Polyposis Coli↗
PubMed1997

[Genetic and environmental factors in colorectal cancer. Mutations in the familial adenomatous polyposis gene].

The incidence of colon cancer has increased during the last 30 years in Norway and is now the second most common newly diagnosed type of cancer in women and the third in men. Familial adenomatous polyposis, hereditary colorectal cancer, is caused primarily by inactivation of the tumour suppressor gene adenomatous polyposis coli (APC). The protein coded for by this gene has a possible role in cell-cell signalling or adhesion by binding to catenins which bind to the cell adhesion molecule E-cadherin, or in anchoring the cytoskeleton. Both germ-line and somatic APC gene mutations result in a truncated protein, due to introduction of a stop codon. The positions of the germ-line mutations seem to correlate with the seriousness of polyposis. The food mutagen PhIP causes specific mutations in the Apc gene in rats, and is a possible environmental mutagen also in humans. The Min mouse with mutated Apc-gene is a good model for studies of both induction and prevention of inherited and sporadic intestinal cancer.

Adenomatous Polyposis Coli↗
PubMed2000

More frequent beta-catenin gene mutations in adenomas than in aberrant crypt foci or adenocarcinomas in the large intestines of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-treated rats.

Alteration of adenomatous polyposis coli (APC) is known to be an early event in neoplasia, causing activation of the beta-catenin / Tcf pathway. Although it is thought that alterations in APC and beta- catenin may complement one another, the contribution of beta-catenin mutations to colorectal carcinogenesis remains unclear. We therefore performed PCR-single strand conformation polymorphism analysis and direct sequencing of exon 3 of beta-catenin gene in adenomas, adenocarcinomas, and aberrant crypt foci (ACF), considered to be putative precursor lesions of colorectal neoplasias, in 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) treated F344 rats. beta-Catenin mutations were identified in all of 7 adenomas (100%) and 6 of 12 (50%) adenocarcinomas. All of the mutations were found in codons 32 through 34, the serine encoded by codon 33 being an important phosphorylation site by glycogen synthase kinase-3beta. Regarding ACF, 14 of 46 (30.4%) were found to be mutated, eleven (78%) in codon 34, and the others in codon 45 (frequently altered in human colon cancer), and codons 47 and 56 (which have not been previously reported). The frequency of beta-catenin mutations in adenomas was significantly higher than in ACF (P < 0.001) and adenocarcinomas (P < 0.05). Thus, beta-catenin mutations may have more importance in the genesis of adenomas than ACF or adenocarcinomas in rat colon carcinogens by PhIP.

Adenocarcinoma↗
PubMed2007

Aneuploidy arises at early stages of Apc-driven intestinal tumorigenesis and pinpoints conserved chromosomal loci of allelic imbalance between mouse and human.

Although chromosomal instability characterizes the majority of human colorectal cancers, the contribution of genes such as adenomatous polyposis coli (APC), KRAS, and p53 to this form of genetic instability is still under debate. Here, we have assessed chromosomal imbalances in tumors from mouse models of intestinal cancer, namely Apc(+/1638N), Apc(+/1638N)/KRAS(V12G), and Apc(+/1638N)/Tp53-/-, by array comparative genomic hybridization. All intestinal adenomas from Apc(+/1638N) mice displayed chromosomal alterations, thus confirming the presence of a chromosomal instability defect at early stages of the adenoma-carcinoma sequence. Moreover, loss of the Tp53 tumor suppressor gene, but not KRAS oncogenic activation, results in an increase of gains and losses of whole chromosomes in the Apc-mutant genetic background. Comparative analysis of the overall genomic alterations found in mouse intestinal tumors allowed us to identify a subset of loci syntenic with human chromosomal regions (eg, 1p34-p36, 12q24, 9q34, and 22q) frequently gained or lost in familial adenomas and sporadic colorectal cancers. The latter indicate that, during intestinal tumor development, the genetic mechanisms and the underlying functional defects are conserved across species. Hence, our array comparative genomic hybridization analysis of Apc-mutant intestinal tumors allows the definition of minimal aneuploidy regions conserved between mouse and human and likely to encompass rate-limiting genes for intestinal tumor initiation and progression.

Aneuploidy↗
PubMed2000

[Clinical features and current progress of familial adenomatous polyposis].

Familial adenomatous polyposis(FAP) is inherited disease as an autosomal dominant trait in which the large intestine is diffusely carpeted by numerous adenomas with a high incidence of colorectal cancer. Current clinical aspects and biological progress were discussed with emphasis on diagnostic imaging, natural histories of gastrointestinal polyps and intra-mandibular osteomas. Genotype-phenotype correlation including attenuated type and function of APC gene, identified in 1991 as a responsible tumour suppressor one for FAP and Gardner syndrome, were also reviewed.

Adenomatous Polyposis Coli↗
PubMed2003

Purified intestinal alkaline sphingomyelinase inhibits proliferation without inducing apoptosis in HT-29 colon carcinoma cells.

PURPOSE: Sphingomyelin (SM) hydrolysis by sphingomyelinase (SMase) has become an important signalling pathway, with the product ceramide implicated in regulation of cell growth, differentiation and apoptosis. Alkaline SMase is specifically located in the intestinal tract. Marked reductions of the enzyme activity have been found in sporadic colorectal carcinomas and in both adenomas and flat mucosa of patients with familial adenomatous polyposis, indicating an anti-proliferative role in colonic cell growth. METHODS: We examined the effects of a purified alkaline SMase from rat intestine and a bacterial neutral SMase on cell growth parameters in HT-29 colonic carcinoma cells. RESULTS: Alkaline SMase was found to inhibit proliferation of HT-29 cells in both dose-dependent and time-dependent manners. The threshold concentration of the enzyme was approximately 2.5 microU/ml, and the maximum effect was obtained at approximately 20 microU/ml, which inhibited the cell growth by 50%. The inhibition occurred rapidly, and maximum effect was reached after 12 h of incubation. Dose-dependent inhibition of DNA synthesis was also demonstrated. The effect of alkaline SMase was preceded and accompanied by increased hydrolysis of SM and production of ceramide. Neutral SMase with equivalent hydrolytic capacity did not inhibit cell growth. Alkaline SMase did not induce apoptosis in HT-29 cells. Alkaline SMase did not inhibit growth of IEC-6 cells. CONCLUSION: Alkaline SMase, at doses that induce SM hydrolysis, inhibits growth of colon cancer cells. The inhibition is attributed to an anti-proliferative effect rather than an apoptotic effect.

Animals↗
PubMed1987

Hyperplastic polyposis of the colorectum and adenocarcinoma in a 24-year-old man.

Hyperplastic polyps in the large intestine are considered common after the age of 40, devoid of neoplastic transformation capability, and have a well-defined histological picture. Nevertheless, there exists evidence that hyperplastic polyps can present with adenomatous areas, eventually leading to carcinoma. There has been a suggestion in certain cases that a transformational sequence might exist in the genesis of colorectal cancer: hyperplastic polyp-adenoma-adenocarcinoma. Adenocarcinoma resulting from a pure hyperplastic polyp has also been described. These data have generated reconsideration of the significance of hyperplastic polyps in relation to cancer. In this paper we present a 24-year-old man with adenocarcinoma of the colon who underwent a right hemicolectomy. Twenty-eight hyperplastic polyps were found in the surgical specimen. Two of these polyps had adenomatous areas. The patient died 18 months after the surgical resection.

Adenocarcinoma↗
PubMed1994

Duodenal adenomas in familial adenomatous polyposis: relation of cell differentiation and mucin histochemical features to growth pattern.

We performed a clinicopathologic analysis of 74 periampullary and duodenal adenomas from 30 patients with familial adenomatous polyposis to evaluate the growth pattern, mucin histochemical profile, and degree and significance of Paneth cell and endocrine cell differentiation in these lesions. A trend toward more numerous adenomas was seen in patients with the longest intervals since their previous colectomies. Adenomas were most often clustered in the periampullary region and were numerous (> 20) in 40% of patients. Periampullary and duodenal adenomas were morphologically similar; both exhibited the same size-villous shape-dysplasia relationship as sporadic and familial adenomatous polyposis-associated colonic adenomas. Adenomas showed a heterogenous pattern of mucin production (mixed small intestinal-large intestinal types), with a shift toward the colonic type (sulfomucin) in lesions that were larger, villous, or severely dysplastic. Ninety-two percent of adenomas showed Paneth cell differentiation (average n Paneth cells/high power field = 24.5), and 99% showed endocrine cell differentiation (average n endocrine cells/high power field = 64.4). In general, the proportion of these specialized cell types was inversely related to size, villous shape, and degree of epithelial dysplasia. These results suggest that periampullary and duodenal adenomas in familial adenomatous polyposis arise from the neoplastic transformation of an undifferentiated stem cell that retains its ability for multidirectional differentiation.

Adenoma↗
PubMed2002

Immunohistochemical study of myofibroblasts in normal colonic mucosa, hyperplastic polyps, and adenomatous colorectal polyps.

CONTEXT: Myofibroblasts are distinct cells with characteristics of both smooth muscle cells and fibroblasts. Through their ability to secrete cytokines, chemokines, prostaglandins, growth factors, and matrix components, they are thought to play critical roles in inflammation, growth, repair, and neoplasia. OBJECTIVE: The goal of this study was to identify the distinct cell populations of the lamina propria of normal colon and colorectal polyps. DESIGN: We studied the expression of alpha-smooth muscle actin (alphaSMA), smooth muscle myosin (SMM), desmin, vimentin, and c-kit by intestinal mesenchymal (stromal) cells in the normal colonic mucosa (n = 5), as well as in hyperplastic polyps (n = 5), sporadic colorectal adenomas (n = 47), and adenomas from patients with familial polyposis (n = 36). RESULTS: In the normal colonic mucosa, the pericryptal stromal cells were alphaSMA+, SMM+, desmin-, and vimentin+, defining them as myofibroblasts. In contrast, cells of the muscularis mucosae were alphaSMA+, SMM+, desmin+, and vimentin-, defining them as smooth muscle cells. alpha-Smooth muscle actin also highlighted direct connections between the muscularis mucosae and the pericryptal myofibroblasts, and vimentin immunostaining showed a network of connections between the alphaSMA+ pericryptal myofibroblasts and the alphaSMA- fibroblasts in the interstitium. In all hyperplastic polyps and adenomatous polyps, the interstitial stromal cells (fibroblasts) now also express alphaSMA and form a syncytium of alphaSMA+ networklike connections throughout the lamina propria. Stromal cells of sporadic adenomas demonstrated the same immunohistochemical staining characteristics displayed by adenomas from patients with familial polyposis and by hyperplastic polyps. Conclusions.-These findings indicate that in normal colon, alphaSMA- fibroblasts are the predominant cell type in the lamina propria. However, the pericryptal (subepithelial) stromal cells are a distinct cell type (alphaSMA+ myofibroblast) that is immunophenotypically different from muscularis mucosae smooth muscle cells and are connected to the interstitial, nonpericryptal fibroblasts with which they exist as a network throughout the lamina propria of the normal colon. Furthermore, in both hyperplastic and neoplastic polyps, there are changes in nonpericryptal fibroblasts from vimentin+, alphaSMA-, and SMM- to vimentin+, alphaSMA+, and SMM+; thus, the interstitial fibroblasts are replaced by myofibroblasts. The factors that cause these changes and the origin of the myofibroblasts need to be determined to clarify the biology of colorectal tumorigenesis.

Adenoma↗
PubMed1978

beta-Glucuronidase in schistosomal intestinal polypi of the colon.

The results of a clinical, histopathological and biochemical study on twenty patients with schistosomal polyposis of the large bowel and ten patients with normal colon as a control are reported. The biopsy showed clearly the absence of any malignant or premalignant changes in all the twenty bilharzial patients. Results of the biochemical study showed that there is a statistically significant increase in beta-glucuronidase activity in schistosomal polypi compared to normal mucosa. This enzymatic activity is absent in schistosoma ova. The causes of the increase in the enzyme activity have been attributed to leucocytic infiltration present in schistosomal granulomata and possible to some degree of liver disfunction. The protein content of the excess mucus present in the colon could also activate the enzyme. Our results also show that the increased enzyme activity does not necessarily have carcinogenic properties. We did not come across a single case of malignancy even in a patient with very high level of enzyme activity (11615 units) or in those patients with a prolonged history of the disease.

Colonic Neoplasms↗