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Results for “Intestinal Polyps”

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At least 415 records · Page 23Linked to original sources
PubMed1997

A Drosophila homolog of the tumor suppressor gene adenomatous polyposis coli down-regulates beta-catenin but its zygotic expression is not essential for the regulation of Armadillo.

Mutations in the adenomatous polyposis coli gene (which encodes a protein called APC) are associated with the formation of intestinal polyps and colon cancers. To facilitate the functional study of APC we have isolated its Drosophila homolog (D-APC) by screening an expression library with an antibody against human APC. The isolated cDNA encodes a predicted 2416-amino acid protein containing significant homology to multiple domains of mammalian APCs. D-APC has seven complete armadillo repeats with 60% identity to its human homolog, one beta-catenin binding site, and up to 7 copies of a 20-amino acid repeat with the average of 50% identity to human APC at amino acid level. D-APC, like its human counterpart, also contains a basic domain. Expression of the domain of D-APC homologous to the region required for beta-catenin down-regulation resulted in down-regulation of intracellular beta-catenin in a mammalian cell line. This same region bound to the Armadillo (Arm) protein, in vitro, the Drosophila homolog of beta-catenin. D-APC RNA and protein expression is very low, if detectable at all, during stages when Arm protein accumulates in a striped pattern in the epidermis of the Drosophila embryos. Removing zygotic D-APC expression did not alter Arm protein distribution, and the final cuticle pattern was not affected significantly. As observed in the rodent, high levels of D-APC expression have been detected in the central nervous system, suggesting a role for D-APC in central nervous system formation.

Adenomatous Polyposis Coli Protein↗
PubMed2003

Silencing of CDX2 expression in colon cancer via a dominant repression pathway.

CDX2 is a caudal-related homeobox transcription factor whose expression in the adult is normally restricted to intestinal epithelium. Mice heterozygous for germ line Cdx2 inactivation develop intestinal polyps, and the lesions lack Cdx2 expression. Prior studies indicate some human colon carcinomas also lack CDX2 expression. To address the role of CDX2 defects in colon cancer development, we analyzed CDX2 expression in 45 primary colorectal carcinomas. Four carcinomas lacked CDX2 expression, and three others showed aberrant cytoplasmic localization of CDX2, although no significant CDX2 gene defects were seen in the seven tumors. Marked reductions in CDX2 transcript and protein levels were seen in five of 13 colorectal cell lines, and nuclear run-off data indicated reduced transcription was a major factor in CDX2 silencing. Treatment with the DNA demethylating agent 5-aza-2'-deoxycytidine and/or the histone deacetylase inhibitor trichostatin A did not restore CDX2 expression in CDX2-negative lines. However, consistent with a role for dominant repression mechanisms in CDX2 silencing, all somatic cell hybrids resulting from pairwise fusions between colon cancer lines with intact CDX2 expression and lines lacking CDX2 had reduced CDX2 transcripts and protein. A roughly 9.5-kb 5'-flanking region from the human CDX2 gene contained key cis elements for regulating transcription in colon cancer cells. Restoration of CDX2 expression suppressed proliferation and soft agar growth in the CDX2-negative HT-29 colon cancer cell line. Our findings suggest CDX2 inactivation in colon cancer results from defects in trans-acting pathways regulating CDX2 transcription, and CDX2 silencing contributes to the altered phenotype of some colorectal cancers.

Adenoma↗
PubMed1976

The production of urinary phenols by gut bacteria and their possible role in the causation of large bowel cancer.

Epidemiological evidence is presented to relate the amount of dietary meat to the risk of large bowel cancer; it has been suggested that this may be due to the production of cocarcinogenic volatile phenols by intestinal bacteria from tyrosine. This paper describes preliminary experiments to test this suggestion. In vitro, aerobic bacteria tended to produce phenol from tyrosine while anaerobic bacteria produced p-cresol. Urine from 10 normal healthy persons contained a mean of 9.8 mg phenol/day and 51.8 mg p-cresol/day. Results from studies on patients with ileostomy, colostomy, and diverticular disease indicated that p-cresol is largely produced by the anaerobic flora of the left colon while phenol was produced in the ileum (when colonized) and cecum. In patients with familial polyposis the activity of the aerobic flora was apparently normal but there was greatly reduced amounts of p-cresol produced. The amounts of urinary volatile phenols in six patients with newly diagnosed large bowel cancer were not different from the normal values, indicating that cocarcinogenic phenols were unlikely to be a major cause of the disease.

Adult↗
PubMed1994

Recurrent benign intracranial hypertension due to iron deficiency anemia. Case report and review of the literature.

PURPOSE: Iron deficiency anemia (IDA) causes benign intracranial hypertension (BIH). PATIENTS AND METHODS: A case of an 11-year-old girl with severe IDA and benign intracranial hypertension is presented. RESULTS: Treatment of iron deficiency resulted in the resolution of BIH. Recurrence of BIH is observed with the recurrence of IDA. Chronic intermittent blood loss from the intestinal polyps was the etiology of recurrent IDA. CONCLUSIONS: A thorough search to determine the etiology of IDA is essential for proper treatment. Although BIH is a rare complication of IDA, its association with IDA should be recognized for prompt treatment before an extensive and costly workup for BIH is done.

Adolescent↗
PubMed2003

Rofecoxib (Vioxx), a specific cyclooxygenase-2 inhibitor, is chemopreventive in a mouse model of colon cancer.

The ApcDelta716 knockout mouse develops hundreds of intestinal polyps and smaller numbers in the colon because of the truncation of the suppressor protein Apc. We show inhibition of polyposis in the ApcDelta716 mouse by rofecoxib (Vioxx), a specific cyclooxygenase-2 (COX-2) inhibitor. Both the number and size of polyps in the ApcDelta716 mouse were markedly reduced by rofecoxib (Vioxx) treatment at plasma concentrations similar to those achieved in humans with antiinflammatory concentrations of Vioxx. Sulindac, a dual cyclooxygenase-1/2 inhibitor, also diminished size and number of polyps but to a lesser extent than rofecoxib. The protein expression of COX-1 or COX-2 was unchanged by treatment with rofecoxib or sulindac because these agents inhibit enzyme activity and prostaglandin product formation rather than transcription of the COX genes. The proangiogenic protein vascular derived endothelial growth factor was decreased in polyps treated with rofecoxib, whereas membrane-associated beta-catenin increased in rofecoxib-treated polyps. DNA proliferation was decreased in polyps by both rofecoxib and sulindac treatment. Rofecoxib (Vioxx) is used clinically for osteoarthritis and pain, and in addition the results described here suggest that Vioxx may be useful as a chemopreventive in humans at risk for colorectal neoplasia.

Animals↗
PubMed2005

Suppression of azoxymethane-induced colon cancer development in rats by a prostaglandin E receptor EP1-selective antagonist.

Prostaglandin E(2) is involved in colon carcinogenesis through its binding to the PGE(2) receptor subtypes EP(1), EP(2), EP(3) and EP(4). We have demonstrated that administration of ONO-8711, an EP(1)-selective antagonist, suppresses development of AOM-induced ACF in C57BL/6 mice and F344 rats. ONO-8711 also reduced the numbers of intestinal polyps in Min mice. In the present study, we investigated the long-term effects of ONO-8711 on colon cancer development in rats treated with AOM. Male F344 rats were injected subcutaneously with AOM (15 mg/kg body weight) once a week for the first 2 weeks to develop colon cancer. Administration of 400 or 800 p.p.m. ONO-8711 in their diets for 32 weeks reduced the incidence, multiplicity and volume of colon carcinomas. The incidence of colon adenocarcinomas in AOM-treated rats was 97, 83 and 76% (P < 0.05) in the 0, 400 and 800 p.p.m. of ONO-8711 groups, respectively. The multiplicity of adenocarcinomas was also decreased significantly, being 3.31 +/- 0.33, 2.34 +/- 0.27 (P < 0.05) and 2.06 +/- 0.34 (P < 0.01) with 0, 400 and 800 p.p.m. of ONO-8711, respectively. Moreover, treatment with 800 p.p.m. ONO-8711 reduced the mean volume of adenocarcinomas to 49% (P < 0.05) of the value for the AOM treatment alone. Furthermore, the BrdU labeling index was decreased significantly in colon cancer cells by 800 p.p.m. ONO-8711. These results confirm that EP(1) is involved in colon carcinogenesis and that EP(1)-selective antagonists might be promising candidates for colon cancer chemopreventive agents.

Animals↗