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Results for “Intestinal Polyps”

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At least 145 records · Page 8Linked to original sources
PubMed1999

Inhibitory effect of intestinal bacteria on spontaneous multiple polyps in the small intestine of gnotobiotic BALB/c mice.

The incidence of multiple polyps and number of polyps per mouse were significantly lower in conventionalized (CVz), and chloroform-resistant bacteria (CRB)- or fusiform bacteria (FB)-associated mice than in germfree (GF) BALB/c mice. The concentration of fecal fatty acids was also higher in mice associated with either CRB or FB than in GF mice. The incidence of multiple polyps and number of polyps per mouse were significantly correlated with the concentration of fatty acids in the feces of CVz and CRB-GB mice. This study demonstrated that inhibition of multiple polyps in the small intestine of BALB/c mice was affected by the production of intestinal fatty acids.

Animals↗
PubMed2002

COX selectivity and animal models for colon cancer.

Early experiments performed during 1980s and 1990s using carcinogen-induced rat intestinal tumor models demonstrated the inhibitory effects of non-steroidal anti-inflammatory drugs (NSAIDs) on intestinal tumorigenesis. Furthermore, epidemiological studies and clinical trials for familial adenomatous polyposis (FAP) patients supported the possibility that NSAIDs can be used as chemopreventive agents. The major target molecules of NSAIDs are cyclooxygenases (COX), which catalyze the rate-limiting step of prostaglandin biosynthesis. Two isoenzymes of COX have been identified; COX-1 and COX-2. Whereas COX-1 is expressed constitutively in most tissues and responsible for tissue homeostasis, COX-2 is inducible and plays an important role in inflammation and intestinal tumorigenesis. A genetic study using compound mutant mice of COX-2(-)/(-), and Apc(Delta716) which is a model for human familial adenomatous polyposis (FAP), directly demonstrated that induction of COX-2 is critical for intestinal polyp formation. Numerous studies have also demonstrated that COX-2 selective inhibitors suppress intestinal polyp formation in Apc gene-mutant mice, and xenografted cancer cell growths. In addition, stimulation of angiogenesis is one of the major effects by COX-2 expression that is induced in the polyp stromal cells. On the other hand, another study indicated that COX-1 also plays an important role in the early stage of intestinal tumorigenesis. These data from animal model studies should be helpful in understanding the in vivo mechanism(s) of tumor suppression by NSAIDs or COX-2 inhibitors. Here, we review the animal studies that have been published as of August 2001, and reported to suppress intestinal tumor growths by NSAIDs or COX-2 inhibitors.

Animals↗
PubMed1976

[Juvenile colonic mucosal polyps in adults].

The histology of all intestinal polyps removed endoscopically during the last 30 months has been reviewed. Among the 90 patients with a total of 154 polyps, 3 cases of juvenile polyps were found. All three were male adults who were aged 29, 34, and 50 years. In two patients the lesion was solitary, while one had polyposis with about 100 polyps. Macroscopically the juvenile polyps cannot be distinguished from adenomatous polyps, but their histologic appearance is typical. They are considered to be hamartomas and have no tendency to become malignant. Thus, juvenile polyposis does not represent a precancerous lesion as adenomatous polyposis does, and must therefore be treated differently. Therapy consists of endoscopic removal of all polyps. In order to differentiate juvenile from adenomatous polyps with certainty, histological examination of at least one polyp is necessary. This differential diagnosis is the indispensable precondition for appropriate therapy.

Adenoma↗
PubMed2003

Peutz-Jeghers syndrome in children: high recurrence rate in short-term follow-up.

We have managed four cases of Peutz-Jeghers syndrome (PJS) in children. Fathers of three of these patients had PJS. There was also a family history of cancer in three cases, with pancreatic cancer in a father, colonic and laryngeal cancers in a grandfather, and hepatic and gastric cancers in a grandmother. It is presumed that in each of the cases, the largest polyp was responsible for initial symptoms. Preoperative examination revealed additional small polyps in the whole alimentary tract except for the oesophagus. Patients underwent laparotomy to remove the largest polyps and subsequent intraoperative endoscopic polypectomy for other small polyps, to minimize intestinal resection. Follow-up gastrointestinal examinations, including upper gastrointestinal series, small intestinal contrast study, and barium enema, were repeated about once a year. Three of four cases showed recurrent small intestinal polyps, and one required a second laparotomy because of recurrent abdominal pain. In conclusion, patients with PJS occurring in childhood have a strong hereditary family history of cancer and a high incidence of recurrence. Careful follow-up examination is mandatory for the gastrointestinal tract, as well as other solid organs that are susceptible to malignant change, throughout a patient's life.

Adolescent↗
PubMed2002

[COX inhibitor, suppression of polyposis, and chemoprevention].

Early experiments using carcinogen-induced rat intestinal tumor models demonstrated the inhibitory effects of non-steroidal anti-inflammatory drugs (NSAIDs) on intestinal tumorigenesis. Furthermore, epidemiological studies and clinical trials for familial adenomatous polyposis (FAP) patients supported the possibility that NSAIDs can be used as chemopreventive agents. The major target molecules of NSAIDs are cyclooxygenases (COX), which catalyze the rate-limiting step of prostaglandin biosynthesis. Two isoenzymes of COX have been identified: COX-1 and COX-2. Whereas COX-1 is expressed constitutively in most tissues and responsible for tissue homeostasis, COX-2 is inducible and plays an important role in inflammation and tumorigenesis. A genetic study using compound mutant mice of COX-2-/- and Apc delta 716, a model for human familial adenomatous polyposis (FAP), directly demonstrated that induction of COX-2 is critical for intestinal polyp formation. Numerous studies have also demonstrated that COX-2-selective inhibitors suppress intestinal polyp formation in Apc gene-mutant mice and xenografted cancer cell growths. In addition, stimulation of angiogenesis is one of the major effects by COX-2 expression that is induced in the polyp stromal cells. These data from animal model studies should be helpful in understanding the in vivo mechanism(s) of tumor suppression by NSAIDs or COX-2 inhibitors. Here, we review the animal studies that reported the suppression of intestinal tumor growths by NSAIDs or COX-2 inhibitors.

Adenomatous Polyposis Coli↗
PubMed2004

Prevention of colorectal cancer through the use of COX-2 selective inhibitors.

Colorectal cancer is a major cause of morbidity and mortality accounting for an estimated 550,000 deaths annually worldwide. Colonic neoplasia develops in a stepwise fashion progressing from normal mucosa to adenomatous polyps to carcinoma, a process that takes years, thereby providing a prime opportunity for intervention. Although early detection by fecal occult blood testing and sigmoidoscopy can decrease the risk of cancer-related death by 20-30%, most persons never undergo appropriate screening. Population-based studies have previously determined that long-term ingestion of aspirin or other nonsteroidal antiinflammatory drugs (NSAIDs) leads to a 40-50% reduction in mortality. from colorectal cancer. These observational studies fueled subsequent mechanistic investigations that led to the identification of a molecular target, cyclooxygenase-2 (COX-2). COX-2 has tumor-promoting properties. Expression of COX-2 is virtually undetectable in normal intestinal mucosa, but is increased in approximately 50% of colonic adenomas and in 90% of colorectal carcinomas. Experimental studies in mice have revealed that genetic ablation or pharmacologic inhibition of COX-2 attenuates the number and size of intestinal polyps that develop in animals harboring a mutation in Apc, which confers an increased risk for intestinal neoplasia. Recent clinical studies using specific COX-2 inhibitors have shown that these compounds can: (1) reduce intestinal polyp burden in patients with familial adenomatous polyposis; (2) prevent the occurrence and/ or recurrence of colorectal adenomas and cancers; and (3) negatively regulate angiogenesis in colorectal cancer liver metastases. Compared to nonselective NSAIDs, COX-2 specific inhibitors cause substantially fewer gastrointestinal side effects. These findings indicate that a widely used and relatively safe class of drugs may represent a viable and effective anticancer strategy for a disease that causes over a half-million deaths per year.

Animals↗
PubMed2005

The threshold level of adenomatous polyposis coli protein for mouse intestinal tumorigenesis.

The adenomatous polyposis coli (APC) gene, whose mutations are responsible for familial adenomatous polyposis, is a major negative controller of the Wnt/beta-catenin pathway. To investigate the dose-dependent effects of APC protein in suppressing intestinal tumorigenesis, we constructed mutant mice carrying hypomorphic Apc alleles Apc(neoR) and Apc(neoF) whose expression levels were reduced to 20% and 10% of the wild type, respectively. Although both hypomorphic heterozygotes developed intestinal polyps, tumor multiplicities were much lower than that in Apc(Delta716) mice, heterozygotes of an Apc null allele. Like in Apc(Delta716) mice, loss of the wild-type Apc allele was confirmed for all polyps examined in the Apc(neoR) and Apc(neoF) mice. In the embryonic stem cells homozygous for these hypomorphic Apc alleles, the level of the APC protein was inversely correlated with both the beta-catenin accumulation and beta-catenin/T-cell factor transcriptional activity. These results suggest that the reduced APC protein level increases intestinal polyp multiplicity through quantitative stimulation of the beta-catenin/T-cell factor transcription. We further estimated the threshold of APC protein level that forms one polyp per mouse as approximately 15% of the wild type. These results also suggest therapeutic implications concerning Wnt signaling inhibitors.

Adenomatous Polyposis Coli Protein↗
PubMed2003

Potential role for peroxisome proliferator activated receptor (PPAR) in preventing colon cancer.

BACKGROUND: Peroxisome proliferator activated receptors (PPARs) are nuclear hormone receptors involved in genetic control of many cellular processes. PPAR and PPAR have been implicated in colonic malignancy. Here we provide three lines of evidence suggesting an inhibitory role for PPAR in colorectal cancer development. METHODS: Levels of PPAR mRNA and protein in human colorectal cancers were compared with matched non-malignant mucosa using RNAse protection and western blotting. APC(Min)/+ mice were randomised to receive the PPAR activator methylclofenapate 25 mg/kg or vehicle for up to 16 weeks, and small and large intestinal polyps were quantified by image analysis. The effect of methylclofenapate on serum stimulated mitogenesis (thymidine incorporation), linear cell growth, and annexin V and propidium iodide staining were assessed in human colonic epithelial cells. RESULTS: PPAR (mRNA and protein) expression levels were significantly depressed in colorectal cancer compared with matched non-malignant tissue. Methylclofenapate reduced polyp area in the small intestine from 18.7 mm(2) (median (interquartile range 11.1, 26.8)) to 9.90 (4.88, 13.21) mm(2) (p=0.003) and in the colon from 9.15 (6.31, 10.5) mm(2) to 3.71 (2.71, 5.99) mm(2) (p=0.009). Methylclofenapate significantly reduced thymidine incorporation and linear cell growth with no effect on annexin V or propidium iodide staining. CONCLUSIONS: PPAR may inhibit colorectal tumour progression, possibly via inhibition of proliferation, and may be an important therapeutic target.

Animals↗
PubMed2005

A prospective trial comparing wireless capsule endoscopy and barium contrast series for small-bowel surveillance in hereditary GI polyposis syndromes.

BACKGROUND: Capsule endoscopy has demonstrated its clinical utility in the evaluation of the small bowel, and, accordingly, it has been suggested that it could be useful for the identification of small-intestinal polyps in patients with polyposis syndromes. The objective was to establish the effectiveness of wireless capsule endoscopy for detecting small-bowel polyps in patients with hereditary GI polyposis syndromes in comparison with barium contrast series. METHODS: Consecutive patients with GI polyposis syndromes were included. Small-bowel follow-through series and capsule endoscopy were performed within 1 week, in a blind fashion. The number and the location of polyps were analyzed. RESULTS: Twenty-four patients with familial adenomatous polyposis (n = 20) or Peutz-Jeghers syndrome (n = 4) were included. Capsule endoscopy detected small-bowel polyps in 7 of 24 patients (29%), whereas a barium contrast study identified small-intestinal polyps in only 3 of these 7 patients. In the 4 remaining patients, all of them with familial adenomatous polyposis, polyps detected by the capsule but missed in radiographic series were located at either ileum (2 patients), jejunum (1), or duodenum (1). No procedure-related complication was observed in any patient. CONCLUSIONS: Wireless capsule endoscopy is a highly accurate technique for the detection of small-bowel polyps in patients with hereditary GI polyposis syndromes, and it represents a valuable alternative to barium contrast series in the surveillance of patients with Peutz-Jeghers syndrome.

Administration, Rectal↗