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Results for “Intestinal Polyposis”

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At least 1,063 records · Page 59Linked to original sources
PubMed1988

Duodenal polyposis and malignancy in a case of familial polyposis coli.

Familial polyposis coli is characterized by progressive adenomatosis with ultimate progression to colon cancer. It is becoming clear that these patients also have a high incidence of upper gastrointestinal adenomatous polyps, with some developing periampullary malignancies similar to those seen in Gardner's syndrome. This has led to recommendations for periodic endoscopic screening of asymptomatic polyposis patients. We report a patient with familial polyposis coli who developed an adenocarcinoma in the distal duodenum. This case points out the importance of screening the upper gastrointestinal tract in patients at risk.

Adenocarcinoma↗
PubMed1995

Role of laparoscopic techniques in colorectal cancer surgery.

Laparoscopic intestinal resection is a relatively new application of endoscopic technology that has evolved as a direct result of the successes and benefits seen with laparoscopic gallbladder surgery. Currently acceptable and feasible laparoscopic intestinal resections include those for diagnostic procedures, fecal diversion, Crohn's disease, diverticulitis, familial polyposis, rectal prolapse, and palliative colorectal cancer surgery. However, the efficacy of laparoscopic resection for curative cancer surgery remains a topic of much debate. Issues surrounding curative laparoscopic oncologic resection include the ability to perform an acceptable oncologic resection, the question of morbidity and mortality compared to conventional surgery, and the problem of port site recurrences. Thus, at present, curative laparoscopic oncologic surgery must be conducted within the framework of a prospective, randomized clinical trial, which includes full informed patient consent.

Colonic Neoplasms↗
PubMed1998

Size-dependent increase in prostanoid levels in adenomas of patients with familial adenomatous polyposis.

Recent studies indicate that nonsteroidal anti-inflammatory drugs have a chemopreventive effect against colorectal neoplasia. Nonsteroidal anti-inflammatory drugs inhibit cyclooxygenases, principal enzymes that mediate the formation of prostanoids. To determine whether prostanoids are involved in the pathogenesis of colorectal adenomas, we compared the levels of five major stable metabolic products of the cyclooxygenase pathway in the normal-appearing mucosa and in adenomas of patients with familial adenomatosis polyposis. Of 12 patients tested, 6 had elevated levels of at least one prostanoid in the adenomas. More importantly, the relative levels of three prostanoids [prostaglandin (PG)D2, PGE2, and 6-keto-PGF1alpha] were elevated in adenomas compared to normal-appearing mucosa from the same patients, and the resulting ratios were correlated with the size of the adenoma. These results suggest a role for prostanoids in progression of colorectal polyposis in familial adenomatosis polyposis patients.

6-Ketoprostaglandin F1 alpha↗
PubMed2006

Smad4 haploinsufficiency in mouse models for intestinal cancer.

The Smad4(+/E6sad) mouse carries a null mutation in the endogenous Smad4 gene resulting in serrated adenomas and mixed polyposis of the upper gastrointestinal (GI) tract with 100% penetrance. Here, we show by loss of heterozygosity (LOH) analysis and immunohistochemistry (IHC) that, although the majority of the tumors appear at 9 months of age, somatic loss of the wild-type Smad4 allele occurs only at later stages of tumor progression. Hence, haploinsufficiency underlies Smad4-driven tumor initiation in the GI tract. As both the Apc and Smad4 tumor suppressor genes map to mouse chromosome 18, we have bred Smad4(+/E6sad) with the Apc(+/1638N) model to generate two distinct compound heterozygous lines carrying both mutations either in cis (CAS) or in trans (TAS). Strikingly, both models show increased tumor multiplicities when compared with the single mutant littermates, although CAS mice are more severely affected and became moribund at only 5-6 weeks of age. Phenotypic and molecular analyses indicate that Smad4 haploinsufficiency is sufficient to significantly affect tumor initiation and progression both prior to and upon loss of Apc function. Moreover, complete loss of Smad4 strongly enhances Apc-driven tumor formation.

Age of Onset↗
PubMed1994

Increased expression of mineralocorticoid receptor in human ileum after total colectomy: immunohistochemical and immunoblotting studies.

Aldosterone is known to regulate transmembrane ion transport and water absorption through its binding to mineralocorticoid receptor (MR) in the mammalian colon. A possible roles of aldosterone has been suggested in increased water absorption from remnant ileum in the patients with total colectomy. We, therefore, studied immunolocalization of MR in remnant ileal mucosa in the patients with total colectomy in order to study the role of aldosterone in water and sodium absorption in these patients. Immunohistochemical localization of MR was performed in ileal mucosa of 7 patients with total colectomy and 5 cases of normal ileum obtained from the resection of ascending colon due to carcinoma by using a polyclonal antibody raised against a mineralocorticoid receptor fusion protein as a primary antibody and a biotinstreptavidin system for immunostaining. Immunoblotting was also performed. Positive MR immunoreactivity was observed in both cytoplasm and nucleus of absorptive cells of ileum of total colectomy patients but not in control normal ileum. Immunoblotting revealed the presence of an approximately 100 kDa immunoreactive product corresponding to mineralocorticoid receptor. Aldosterone is considered to act on ileal mucosa following total colectomy and the aldosterone dependent sodium transport and water absorption may be accelerated in ileal mucosa after total colectomy, which is consistent with the postoperative decrease in the stool volume observed in these patients. In conclusion, increased expression of the mineralocorticoid receptor in remnant ileum may play an important role in intestinal adaptation in total colectomized patients.

Adenomatous Polyposis Coli↗
PubMed2006

Dietary anthocyanin-rich tart cherry extract inhibits intestinal tumorigenesis in APC(Min) mice fed suboptimal levels of sulindac.

A promising approach for cancer chemoprevention might be a combination therapy utilizing dietary phytochemicals and anticarcinogenic pharmaceuticals at a suboptimal dosage to minimize any potential adverse side effects. To test this hypothesis, various dosages of anthocyanin-rich tart cherry extract were fed in combination with suboptimal levels of the nonsteroidal anti-inflammatory drug sulindac to APCMin mice for 19 weeks. By the end of the feeding period, fewer mice that were fed the anthocyanin-rich extract in combination with sulindac lost more than 10% of body weight than mice fed sulindac alone. Mice that were fed anthocyanin-rich extract (at any dose) in combination with sulindac had fewer tumors and a smaller total tumor burden (total tumor area per mouse) in the small intestine when compared to mice fed sulindac alone. These results suggest that a dietary combination of tart cherry anthocyanins and sulindac is more protective against colon cancer than sulindac alone.

Adenomatous Polyposis Coli↗
PubMed2001

Suppression of intestinal polyps in Msh2-deficient and non-Msh2-deficient multiple intestinal neoplasia mice by a specific cyclooxygenase-2 inhibitor and by a dual cyclooxygenase-1/2 inhibitor.

Epidemiological studies suggest that nonsteroidal anti-inflammatory agents decrease the risk of colorectal cancer. This is believed to be mediated, at least in part, by inhibition of cyclooxygenase (COX) activity. There are two COX isoenzymes, namely the constitutively expressed COX-1 and the inducible COX-2. COX-2 is overexpressed in adenomas and colorectal cancers, and COX-2-specific inhibitors have been shown to inhibit intestinal polyps in Apc(Delta716) mice more effectively than dual COX-1/COX-2 inhibitors such as sulindac. Various Apc knockout mice, including the multiple intestinal neoplasia (Min) mouse and the Apc(Delta716) mouse, are limited by their lack of large numbers of colonic adenomas and aberrant crypt foci, the putative precursors of large-bowel polyps and cancers. Our DNA mismatch-repair-deficient Min mouse model (Apc+/-Msh2-/-) has genetic features of both familial adenomatous polyposis and hereditary nonpolyposis colorectal cancer, and most importantly, rapidly develops numerous small- and large-bowel adenomas, as well as colonic aberrant crypt foci. The purpose of this study was to determine the effects of COX inhibitors on intestinal adenomas and colonic aberrant crypt foci in this accelerated polyposis, mismatch-repair-deficient Min mouse model, in addition to a standard Min mouse model. Weanling Apc+/-Msh2-/- and Min mice were fed diets containing no drug, sulindac, or a specific COX-2 inhibitor (MF-tricyclic). Apc+/-Msh2-/- and Min mice were sacrificed after 4 weeks and 5 months on diet, respectively. Apc+/-Msh2-/- mice treated with MF-tricyclic had significantly fewer small-bowel polyps (mean +/- SD, 178 +/- 29) compared with mice on sulindac (278 +/- 80), or control diet (341 +/- 43; P < 0.001). There was no difference in numbers of large-bowel polyps or aberrant crypt foci in mice in the three groups. MF-tricyclic was also effective in reducing both small- and large-bowel polyps in Min mice. Western analysis demonstrated COX-2 expression in both large- and small-bowel polyps from mice of both genotypes. This study demonstrates that a specific COX-2 inhibitor is effective in preventing small-bowel polyps in mismatch-repair-deficient Min mice and both small- and large-bowel polyps in standard Min mice. Therefore, specific COX-2 inhibitors may be useful as chemopreventive and therapeutic agents in humans at risk for colorectal neoplasia.

Adenoma↗
PubMedDate not supplied

[Massive rectorrhagia and acute intestinal occlusion revealing Peutz-Jeghers syndrome: apropos of 3 cases].

Peutz-Jeghers syndrome is a rare hereditary disorder involving digestive polyposis with hamartomatous gastrointestinal polyps and mucocutaneous lentiginosis. We report three cases in which this syndrome was detected by complications: a massive rectal hemorrhage requiring a blood transfusion in one case and acute impaction of the bowel requiring emergency surgery in the other two. This work demonstrates the importance of the complications that may indicate that the patient has this syndrome. We also discuss the cancers of the digestive system and other organs that may be associated with PJS and recent progress in genetic research into this disease.

Adolescent↗
PubMed2007

Impact of Phospholipase A2 group IIa gene polymorphism on phenotypic features of patients with familial adenomatous polyposis.

PURPOSE: Phospholipase A2 Group IIa has been suggested to be a possible disease modifier gene in familial adenomatous polyposis. This investigation was designed to elucidate possible association between phospholipase A2 Group IIa polymorphism and phenotypes of patients with familial adenomatous polyposis. METHODS: Phospholipase A2 Group IIa was examined by polymerase chain reaction-based single strand conformation polymorphism and direct sequencing in 55 patients from 45 families with familial adenomatous polyposis. The patients were examined by gastroduodenoscopy plus biopsy with respect to fundic gland polyposis and gastroduodenal adenomas. Helicobacter pylori status was determined by rapid urease test. Contributions of genetic alteration and Helicobacter pylori infection to intestinal and extraintestinal lesions were investigated. RESULTS: Four types of single nucleotide polymorphism were found in exon 3 of phospholipase A2 Group IIa, among which single nucleotide polymorphism in codon 32 was the most frequent. The prevalence of fundic gland polyposis was higher in patients positive for single nucleotide polymorphism of phospholipase A2 Group IIa than those negative for single nucleotide polymorphism (61 vs. 33 percent; P < 0.05). In contrast, positive rate of Helicobacter pylori infection was lower in the former than in the latter (22 vs. 52 percent; P < 0.05). The prevalence of the other phenotypes was not different significantly. Logistic regression analysis revealed a possibility toward single nucleotide polymorphism of phospholipase A2 Group IIa as an independent risk factor for fundic gland polyposis (95 percent confidence interval, 00.9-14.3; P = 0.06). CONCLUSIONS: Phospholipase A2 Group IIa may be a modifier gene for fundic gland polyposis in patients with familial adenomatous polyposis.

Adenomatous Polyposis Coli↗
PubMed1981

Polyposis coli presenting with Streptococcus bovis endocarditis.

Streptococcus bovis bacteremia is an important early clue to the presence of serious and clinically unexpected gastrointestinal disease, particularly carcinoma of the colon. S. bovis bacteremia has also been associated with carcinoma of the esophagus and stomach, gastric lymphoma, pancreatic adenocarcinoma, intestinal diverticulosis and single adenomatous polyps and villous polyps of the colon. We report a patient with S. bovis endocarditis as the initial clinical manifestation of extensive polyposis of the colon and rectum. All patients with S. bovis bacteremia need thorough investigation of their gastrointestinal tract even in the absence of symptoms, signs, or positive laboratory tests suggestive of gastrointestinal pathology.

Adenoma↗
PubMed2002

Peroxisome proliferator-activated receptors modulate K-Ras-mediated transformation of intestinal epithelial cells.

Activation of peroxisome proliferator-activated receptors (PPARs) exerts diverse effects on neoplastic cells. Recent work has shown that PPARdelta is up-regulated after loss of adenomatous polyposis coli tumor suppressor gene function and that transcriptional activation of the PPARgamma nuclear receptor can lead to inhibition of carcinoma growth. In this study, we elucidate the regulation and functional importance of PPARgamma and delta after K-Ras-transformation of intestinal epithelial cells. In conditionally K-Ras-transformed rat intestinal epithelial cells (IEC-iK-Ras), the level and activity of PPARdelta were markedly increased. PPARdelta up-regulation occurred due to increased mitogen-activated protein kinase activity and receptor activation required the endogenous production of prostacyclin via the cyclooxygenase-2 pathway. We also demonstrate that activation of the PPARgamma nuclear receptor has antineoplastic effects in Ras-transformed cells. Activation of PPARgamma resulted in a delay in transit through the G(1) phase of the cell cycle that was associated with inhibition of phosphatidylinositol 3'-kinase/Akt activity and a reduction of cyclin D1 expression. Therefore, these two PPAR nuclear receptors, which are structurally related, have distinct roles during neoplastic transformation. PPARgamma appears to modulate differentiation and signal growth inhibition, whereas PPARdelta is up-regulated by oncogenic Ras and activated by cyclooxygenase-2-derived prostaglandins.

Animals↗