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At least 1,207 records · Page 67Linked to original sources
PubMed2007

Intestinal microbiota: a potential diet-responsive prevention target in ApcMin mice.

We previously reported that two dietary regimens, calorie restriction (CR) and a high olive oil-containing diet supplemented with a freeze-dried fruit and vegetable extract (OFV), reduced the development of intestinal adenomas in Apc(Min) mice by 57% and 33%, respectively, compared to control mice fed a defined diet ad libitum. The OFV diet was designed to have a strong effect on the composition of the intestinal microbiota through its high content of fiber, which represents a major source of fermentable substrate for the gut bacteria. We hypothesized that some of the observed effects of diet on intestinal carcinogenesis might be mediated by diet-related changes in the bacterial species that thrive in the gut. Therefore, we determined by fluorescent in situ hybridization (FISH) and denaturing gradient gel electrophoresis (DGGE) how the dietary interventions affected the composition of the intestinal microbiota, and we characterized specific microbiota changes that were associated with diet and reduced intestinal carcinogenesis. The OFV diet changed the overall composition of the intestinal microbiota, smaller changes were observed for the CR diet. Furthermore, we detected a 16S rDNA fragment associated with mice that did not develop polyps. Sequence analysis suggested that hitherto unidentified bacteria belonging to the family Lachnospiraceae (order Clostridiales) were its source. Thus, these bacteria may be an indicator of intestinal conditions associated with reduced intestinal carcinogenesis in Apc(Min) mice.

Adenoma↗
PubMed2001

Actin-dependent membrane association of the APC tumour suppressor in polarized mammalian epithelial cells.

Adenomatous polyposis coli (APC) is mutated in most colorectal cancers. APC downregulates nuclear beta-catenin, which is thought to be critical for its tumour suppressor function. However, APC may have additional and separate functions at the cell periphery. Here, we examine polarized MDCK and WIF-B hepatoma cells and find that APC is associated with their lateral plasma membranes. This depends on the actin cytoskeleton but not on microtubules, and drug wash-out experiments suggest that APC is delivered continuously to the plasma membrane by a dynamic actin-dependent process. In polarized MDCK cells, APC also clusters at microtubule tips in their basal-most regions. Microtubule depolymerization causes APC to relocalize from these tips to the plasma membrane, indicating two distinct peripheral APC pools that are in equilibrium with each other in these cells. Truncations of APC such as those found in APC mutant cancer cells can neither associate with the plasma membrane nor with microtubule tips. The ability of APC to reach the cell periphery may thus contribute to its tumour suppressor function in the intestinal epithelium.

Actins↗
PubMed1976

Familial 'minor' adenomatous polyposis coli associated with gastric carcinoma - a hiterto undescribed phenotype of polyposis coli?

A clinical study of a family (Sch.) with a high incidence of death from gastric cancer in the second generation is presented. Endoscopic and/or surgical evaluation of the stomach, upper small intestine, and colon in 14 mainly asymptomatic members of the third and fourth generations revealed single or multiple (solitary) papillary adenomas in the colon or jejunum in 2 members each of the two generations. In addition, single or multiple hyperplastic polyps in the stomach or colon were found in 5 members, in 4 of them in association with papillary adenomas. The findings in family Sch. are consistent with 'minor' adenomatous polyposis coli associated with gastric carcinoma. Gastric carcinoma probably represents another phenotype among the vast variety of extra-colonic and extra-alimentary neoplastic changes known to occur in association with familial polyposis coli (FPC). The relationship of hyperplastic polyps to papillary adenoma in the colon and to gastric carcinoma respectively is discussed. Finally, evidence for a genetic relationship between family Sch. and a case with probable FPC is presented.

Adenocarcinoma, Papillary↗
PubMed2002

[Tumors of the small intestine].

Tumors of the small bowel are uncommon. Most of them are malignant neoplasmas with bad outcome. To ameliorate the doubtful prognosis tumors should be clarified carefully by means of histological, immunohistochemical and molecular methods. Patients suffering from familial adenomatous polyposis are at high risk to develop adenomas and adenocarcinomas of the duodenum. Therefore, the upper gastrointestinal tract should be monitored endoscopically in regular intervals. Surgically unresectable or metastatic malignant gastrointestinal stromal tumors should be included in an EORTC trial assessing the clinical activity of STI-571. This agent inhibits KIT-tyrosine kinase activity thus leading to a reduction of the tumor mass. Moreover, the WHO classification of lymphomas enables a more precise prognosis and individually tailored therapeutic strategies in primary lymphomas of the small bowel.

Adenocarcinoma↗
PubMed2003

Frequent loss of hMLH1 by promoter hypermethylation leads to microsatellite instability in adenomatous polyps of patients with a single first-degree member affected by colon cancer.

The first-degree relatives of patients affected by colorectal cancer, who do not belong to familial adenomatous polyposis and hereditary nonpolyposis colorectal cancer families, have a doubled risk of developing tumors of the large intestine. We have previously demonstrated that subjects with a single first-degree relative (SFDR) with colon cancer have a doubled risk for developing colorectal adenomas, and in these cases, polyps recur more frequently. The mechanism underlying this predisposition has not been clarified. In this study, we evaluated the frequency of microsatellite instability (MSI) using the five markers suggested by the National Cancer Institute workshop, target gene mutations, hMLH1 and hMSH2 expression, and hMLH1 promoter hypermethylation in the adenomas of patients with and without a SFDR affected by colon cancer. Seventy polyps were obtained from 70 patients: 27 with a single FDR with colon cancer and 43 without such a history. Of the 70 polyps, 12 were MSI-H (17.1%), 20 were MSI-L (28.6%), and 30 were microsatellite stable (42.9%). Of the 27 patients with positive family history, 8 polyps (29.6%) were MSI-H compared with those with negative history in which 4 polyps (9.3%) were MSI-H (P < 0.02). Of the 12 MSI-H polyps, all of the polyps obtained from patients with positive family history had loss of hMLH1 immunostaining versus one with negative family history (P < 0.02). Of the MSI-H polyps, 2 had a somatic frameshift mutation of the MBD4 gene, 1 of MSH6, 1 of BAX, and 2 of transforming growth factor betaRII. Furthermore, 6 of 8 polyps from patients with positive family history with MSI-H and loss of MLH1 had hypermethylation of the MLH1promoter versus none of the MSI-H with negative family history (P < 0.02). All 6 polyps of the 27 from SFDR positive subjects, with hMLH1 promoter hypermethylation loss of hMLH1 and MSI, were located in the right colon (P < 0.02). Hypermethylation of the promoter of hMLH1, consequent loss of hMLH1 expression, and MSI are at the basis of approximately 25% of adenomatous polyps developed in subjects with a SFDR affected by colorectal cancer.

Adaptor Proteins, Signal Transducing↗
PubMed2004

ApcMin/+ mouse model of colon cancer: gene expression profiling in tumors.

The Apc(Min/+) mouse is a popular animal model for studies of human colon cancer, but the molecular changes associated with neoplasia in this system have only been partially characterized. Our aim was to identify novel genes involved in tumorigenesis in this model. RNA from intestinal adenomas and from pre-neoplastic small intestine were prepared from six Apc(Min/+) mice. The tumor transcriptomes were analyzed with high-density oligonucleotide microarrays representing approximately 12,000 probe sets; we compared their profiles with those of matched pre-neoplastic intestine. Stringent analysis revealed reproducible changes for 98 probe sets representing 90 genes, including novel observations regarding 50 genes whose involvement in this mouse model has never been reported. In addition to the expected changes in growth regulatory genes, the altered gene products could be assigned to four functional groupings that should enhance tumorigenesis: metabolic changes that would result in a high rate of glycolysis, alterations in enzymes involved in reactive oxygen species or carcinogen metabolism, cytoskeletal elements, and proteins involved in tumor invasion or angiogenesis. A fifth group consisted of expression changes that might restrict tumor progression, suggesting that the adenomatous state reflects a balance of pro- and anti-tumorigenic factors. Since many of the altered genes had not previously been reported to be involved in any tumorigenic processes, our observations provide a host of new candidates for potential modulation to prevent or treat intestinal neoplasia.

Adenomatous Polyposis Coli Protein↗
PubMed2001

Role of cyclooxygenase inhibitors for the prevention of colorectal cancer.

Eicosanoids play an important role in numerous physiologic and pathophysiologic processes in the gastrointestinal tract, including maintenance of mucosal integrity, stimulation of mucus and electrolyte secretion, and inflammation. A rapidly growing body of evidence implicates COX-2 in colorectal carcinogenesis. COX-2 has been shown to alter cellular adhesion, apoptosis, and angiogenesis, contributing to its neoplastic potential. NSAIDs appear to attenuate this potential by mechanisms that are COX-2 dependent and independent. Several advances have been made in understanding the details of COX-2 regulation. The downstream effect of COX-2-dependent metabolites varies with the enzymatic machinery present in a particular cell, the level of COX activity, differences in location and types of prostaglandin receptors, and differences in signal transduction pathways. Further studies are needed to understand better these complex interactions, which may provide insight into the role of COX-2 in pathologic conditions, such as intestinal inflammation and colorectal cancer.

Adenomatous Polyposis Coli↗
PubMed1976

[Multiple adenomatous papillary colonic polyps in a family with frequent cases of stomach carcinoma--a new phenotype of familial colonic polyposis].

A kindred of "minor adenomatous polyposis" associated with a high incidence of gastric cancer is described. Five out of 14 mainly asymptomatic individuals in 2 generations of kindred examined clinically, by panendoscopy and coloscopy exhibited multiple polyps of colon or/and stomach and jejunum. Single or multiple papillary adenomas were detected mainly in the right or middle colon (3 times or in the jejunum (once). Hyperplastic polyps were found in the stomach (3 times) and in the colon (twice of these 5 individuals. Our findings suggest that "minor adenomatous polyposis" associated with gastric cancer may represent another, hitherto unrecognized, phenotype of familial multiple polyposis.

Colonic Diseases↗
PubMed1996

Polyps and polypoid lesions of the jejunum and ileum. Clinical aspects.

Polyps and polypoid lesion of the small intestine present a major challenge to the surgeon. In contrast to similar lesions in the large intestine, small bowel polyps present late in their course and are difficult to diagnose. Small bowel tumors produce vague symptoms and screening tests are poor. Most of these polyps are found at autopsy or during exploration for another cause. In this article, the authors outline the problem as well as discuss the diagnosis and treatment options.

Adenomatous Polyposis Coli↗
PubMed2004

Nonfamilial juvenile polyposis coli in a child: report of a case.

Juvenile polyposis coli (JPC) is an uncommon condition, manifesting as hamartomatous gastrointestinal polyposis with potential malignancy. This report describes a 15-month-old girl who was diagnosed to have nonfamilial JPC accompanied by macrocephaly, clubbed fingers, and mental retardation. Radiography of the colon by a barium enema and total colonoscopy demonstrated numerous colonic polyps. A barium meal study did not show any abnormality in the stomach, duodenum, or small intestine. She died at 6 years of age from hemorrhagic shock due to massive lower gastrointestinal bleeding associated with a rectal prolapse. The related literature is reviewed, and the treatments and complications of JPC in children are also discussed. We emphasize that family members of patients diagnosed with juvenile polyposis should be questioned and undergo appropriate examinations of the entire intestine from the stomach to the rectum.

Adenomatous Polyps↗
PubMed1986

Epithelial polyps of the large intestine. A classification based on biologic behavior.

Classifications of colonic polypoid lesions are often based on their pathogenesis. Little attention is paid to the biologic behavior (or predicted behavior, based on experience) of these lesions. Classification based on biologic behavior separates these lesions, regardless of histogenesis, according to possible malignant potential. This helps the clinician to explain the implications of the histopathologic diagnosis to the patient and to understand when aggressive or prophylactic therapy should be pursued.

Adenoma↗
PubMed1999

Mucosa-associated lymphoid tissue (MALT) lymphoma manifesting as multiple lymphomatosis polyposis of the gastrointestinal tract.

There have been a number of previous case reports of lymphomas in the form of multiple mucosal polyps affecting variable lengths of colonic and intestinal mucosa. Invariably these have been classified histologically as mantle cell lymphomas. We report a case of this rare syndrome that illustrates many of its typical features but which demonstrates significant histological and immunophenotypic differences. A 67-yr-old man was referred with a 3-month history of altered bowel habit and a barium enema suggestive of extensive ulcerative colitis. At colonoscopy, diffuse umbilicated mucosal polyps were seen throughout the colon and a larger circumferential mass lesion at the ileocecal valve. Biopsies demonstrated a diffuse B-cell lymphoma consistent with "multiple lymphomatous polyposis" of the colon. Flow cytometry revealed CD25 positive/CD5 negative lymphoid cells confirming marginal B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) type. Upper gastrointestinal investigations confirmed similar involvement of the stomach, duodenum, and small bowel. Helicobacter pylori was absent. Flow cytometry abnormalities consistent with marrow involvement were present. These features led to a diagnosis of stage IV marginal zone B-cell lymphoma of MALT type, presenting as multiple lymphomatous polyposis of the gastrointestinal tract. Three months of combination chemotherapy resulted in an excellent symptomatic and endoscopic response.

Aged↗
PubMed1997

Plasma (carotenoids, retinol, alpha-tocopherol) and tissue (carotenoids) levels after supplementation with beta-carotene in subjects with precancerous and cancerous lesions of sigmoid colon.

OBJECTIVES: (1) To compare tissue and plasma carotenoids status of healthy subjects and subjects with pre-cancer and cancer lesions; (2) to evaluate the effect of beta-carotene supplementation on the concentrations of other carotenoids in tissue (luteine + zeaxanthin, cryptoxanthin, lycopene, alpha-carotene) and in plasma and also retinol and alpha-tocopherol levels. DESIGN: Eighteen subjects were divided into three groups on the basis of colonoscopy and histological analytical findings: four healthy subjects (control group A); seven subjects affected by adenomatous polyps (group B with pre-cancer lesions); seven subjects suffering from colonic cancer (group C). Blood and colonic biopsy samples were taken (of colon and rectal mucosa) before and after beta-carotene supplementation in all subjects. Groups A and B received a daily dose of beta-carotene (30 mg/die) for 43 d. Group C's supplementation was terminated at the time which was performed, usually within 15 d. The tissue and plasma concentration of carotenoids, retinol and alpha-tocopherol were determined by high-performance liquid chromatography. RESULTS: The tissue concentrations of each carotenoid were similar in all the intestinal sites examined as regards groups A and B, although there was a high degree of intra individual variability within each group. Only beta-carotene made significant increases (P < 0.001) after supplementation. The subjects with cancer show tissue levels for each carotenoid lower than those of healthy subjects or subjects with polypous. The plasma levels of alpha-tocopherol did not change after supplementation while significant increases were noted of retinol, alpha-carotene (P < 0.01) and of beta-carotene (P < 0.001). CONCLUSIONS: The patients with colonic cancer seemed to undergo a significant reduction in their antioxidant reserves with respect to the normal subjects and or polyps. We can confirm that oral B-carotene supplementation induces also an increase in plasma alpha-carotene in all groups.

Adenomatous Polyposis Coli↗