PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Colonic Polyps”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,135 records · Page 63Linked to original sources
PubMed1989

Histopathological assessment of bleeding from polyps of the colon and rectum.

One hundred and twenty seven colorectal polyps were examined to assess histopathological evidence of recent and old haemorrhage to test the usefulness of faecal occult blood tests in detecting colorectal neoplasia, in particular premalignant adenomas. Evidence of haemorrhage was consistently found in adenomas but was rare in non-neoplastic polyps. Haemorrhage within adenomas was predominantly stromal and associated with dilated, congested vessels. Factors associated with more severe haemorrhage were size, pedunculation, and villous growth; the degree of epithelial dysplasia and the age and sex of the patient were not associated factors. Proximal polyps showed more old haemorrhage than rectal polyps, but there was no such difference for recent haemorrhage.

Aged↗
PubMed1986

The significance of synchronous carcinoma and polyps in the colon and rectum.

The relationship of colorectal carcinoma with polyps was studied retrospectively in 1202 patients. The incidence of synchronous carcinoma (SC) and metachronous carcinoma (MC), prognosis, and recurrence patterns were studied. Synchronous polyps (SP) were found in 36% of the patients. SC was found in 4.4% of the patients, and MC developed in 3.5% of patients. The incidence of SC and of MC increased with SP, and varied according to number, size, and histologic features of the polyps. The adjusted 5-year survival rate was improved in patients with SP compared with those without SP, both overall (79% versus 64%, respectively) and by Dukes' Stage B (87% versus 73%, respectively) and Dukes' Stage C (56% versus 39%, respectively). The pattern of relapse was the same for the SP and non-SP groups. Subtotal colectomy is recommended for colorectal carcinoma and SP in good-risk patients.

Adult↗
PubMed2002

Microadenomatous lesions involving loss of Apc heterozygosity in the colon of adult Apc(Min/+) mice.

Mutations in the human adenomatous polyposis coli (APC) gene are causative for familial adenomatous polyposis (FAP), a rare condition in which numerous colonic polyps arise during puberty and, if left untreated, lead to colon cancer. Mouse model for human FAP, Apc(Min/+) mouse, contains a truncating mutation in the Apc gene and spontaneously develops intestinal adenomas. However, the distribution of tumors along the intestine found in Apc(Min/+) mice is different from that in human FAP. A majority of intestinal polyps in the Apc(Min/+) mice is known to be located in the small intestine but rarely detected in the colon. We report here that adult Apc(Min/+) mice develop dozens of microadenomatous lesions in the colon (>20 lesions/colon). Surprisingly, the vast majority of such adenomatous lesions consisting of colonic crypts were <300 microm in their greatest dimension, whereas lesions in the small intestine showed various sizes. The allelic loss analysis revealed that these adenomatous crypts in the colon have already lost the remaining allele of Apc. Such findings suggest that, in contrast to tumorigenesis in the small intestine, loss of heterozygosity of the Apc gene is not sufficient for tumor development in the colon of Apc(Min/+) mice. Our results may give an account for the low incidence of colonic tumors in Apc(Min/+) mice.

Adenomatous Polyposis Coli↗
PubMed2004

Colorectal polyposis and immune-based therapies.

The progression from precancerous (adenomatous) colon polyps to malignant colorectal cancer involves the complex actions of various cytokines on T cell proliferation, cell-cell adhesion, apoptosis and host immunity. A broad spectrum of new treatments, including innovative molecular therapies such as gene therapy and treatment with cytokines, is under experimental and preclinical investigation. Nonsteroidal anti-inflammatory drugs and selective cyclooxygenase-2 inhibitors have traditionally been used as inflammation-reducing agents in cases of colon adenoma. Currently, adjuvant immunotherapies such as recombinant gene therapy and antibody-cytokine fusion proteins are assuming a more significant role in the management of colorectal neoplasia. Furthermore, advances in antitumour necrosis factor antibodies for the treatment of ulcerative colitis and Crohn's disease may have potential as chemoprotective agents for the treatment of colon polyposis. The present review aims to discuss the immunological mechanisms underlying colon tumour progression and the molecular and immune-based therapies that are leading to new methods of prognosis and treatment.

Adenomatous Polyps↗
PubMed1997

Telomerase and telomere length in the development and progression of premalignant lesions to colorectal cancer.

Telomerase and telomere length are increasingly studied as prognostic markers in malignancy. Telomerase is also known to be expressed in certain nonmalignant cells, although generally at low levels. We investigated telomerase activity and telomere length in premalignant, malignant, inflammatory, and normal colon specimens to determine whether significant differences exist and whether telomerase may serve as a marker for early- or late-stage colorectal cancer. Telomerase activity was evaluated in 130 frozen specimens from human colon cancer (n = 50), adjacent normal colon tissue (n = 50), colon polyps (n = 20), and colitis (n = 10) using a modified telomeric repeat amplification protocol assay, and telomere length was assessed by terminal restriction fragment analysis. High to moderate levels of telomerase activity were detected in 90% of colorectal tumors. Weakly positive activity was detected in 10%. None of the normal tissues exhibited telomerase activity. In polyps and colitis, telomerase activity was found in 60% (12 of 20) and 40% (4 of 10), respectively. Telomerase activity in both nonmalignant lesions was 25- to 54-fold lower than that detected in colon cancer (P < 0.001). We found a positive correlation between tumor cell infiltration determined in cryostat sections and telomerase activity (r = 0.886; P > 0.0001). Late-stage tumors (Dukes C + D) demonstrated increased telomerase activity compared to early-stage tumors (Dukes A + B). Telomere restriction fragments in colon tumors had peak values of 4.8 +/- 1 kbp that were significantly and consistently shorter than those of the adjacent normal tissues (7.54 +/- 1.3 kbp), polyps (7.5 +/- 0.7 kbp), and colitis specimens (7.7 +/- 0.5kbp; P < 0.0001). Telomeres were 0.6 kbp longer in tumors with high telomerase activity and in late-stage cancers (Dukes C + D) compared to those in tumors with low telomerase activity and in early-stage cancers (Dukes A + B). Our data demonstrate that telomerase in colon cancer was commonly acquired, and activity was higher than that in polyps and colitis. However, weak telomerase activity was detected in premalignant and inflammatory lesions. Telomeres in colon cancer were considerably shorter, an indication of extensive cell proliferation and population divisions, whereas adjacent normal colon specimens, polyps, and colitis had comparable telomere lengths. Our results indicate that increased telomerase activity occurs in colon cancer cells that have undergone extensive telomere shortening relative to surrounding normal tissues and in which telomerase-induced stabilization of telomeres may be critical for the continued proliferation of the malignant clone. The link between telomerase activity and stage suggests that telomerase is up-regulated as a function of increased tumor cell invasion, tumor progression, and metastatic potential in colon cancer.

Adult↗
PubMed1983

Colonoscopic polypectomy in a regional teaching hospital.

Five hundred and thirty-five polyps were found in 200 patients over 6 years at a regional teaching hospital. Eighty-five per cent of the patients were from the hospital area yet the presentation of the patients, the complications of polypectomy, the size, distribution and histological features of the polyps were similar to large series reported from metropolitan specialist centres of referral both in this country and the USA. However, a smaller proportion of our polyps were over 1 cm diameter. Between 25 and 53 per cent of patients had recurrent or residual polyps on the second and third colonoscopy. Patients with two or more polyps at the first endoscopy were significantly more likely (P less than 0.01) to have further polyps at follow-up. We therefore recommend that patients with colonic polyps are colonoscoped annually until free from polyps for 2 years, before being placed on colonoscopic review at 5-year intervals.

Colon↗
PubMed1999

Display modes for CT colonography. Part II. Blinded comparison of axial CT and virtual endoscopic and panoramic endoscopic volume-rendered studies.

PURPOSE: To determine the sensitivity of radiologist observers for detecting colonic polyps by using three different data review (display) modes for computed tomographic (CT) colonography, or "virtual colonoscopy." MATERIALS AND METHODS: CT colonographic data in a patient with a normal colon were used as base data for insertion of digitally synthesized polyps. Forty such polyps (3.5, 5, 7, and 10 mm in diameter) were randomly inserted in four copies of the base data. Axial CT studies, volume-rendered virtual endoscopic movies, and studies from a three-dimensional mode termed "panoramic endoscopy" were reviewed blindly and independently by two radiologists. RESULTS: Detection improved with increasing polyp size. Trends in sensitivity were dependent on whether all inserted lesions or only visible lesions were considered, because modes differed in how completely the colonic surface was depicted. For both reviewers and all polyps 7 mm or larger, panoramic endoscopy resulted in significantly greater sensitivity (90%) than did virtual endoscopy (68%, P = .014). For visible lesions only, the sensitivities were 85%, 81%, and 60% for one reader and 65%, 62%, and 28% for the other for virtual endoscopy, panoramic endoscopy, and axial CT, respectively. Three-dimensional displays were more sensitive than two-dimensional displays (P < .05). CONCLUSION: The sensitivity of panoramic endoscopy is higher than that of virtual endoscopy, because the former displays more of the colonic surface. Higher sensitivities for three-dimensional displays may justify the additional computation and review time.

Colonic Polyps↗
PubMed1982

Atherosclerosis and polyps of the colon. Quantification of precursors of coronary heart disease and colon cancer.

The prevalence of adenomatous and hyperplastic polyps of the colon and the degree of involvement of the aorta by atherosclerotic lesions were evaluated in 842 autopsies from New Orleans. A positive statistical association between the two variables was found in white males under 75 years of age. In black males a positive correlation between atherosclerotic lesions and adenomatous (but not hyperplastic) polyps was found. The most extensive involvement of the aorta by atherosclerosis was found in patients in whom adenomatous and hyperplastic polyps coincided. The possibilities that dietary factors may account for these findings and its relevance in relation to colon cancer and coronary heart disease are discussed.

Adult↗
PubMed1997

High prevalence of Helicobacter pylori infection in patients with colonic adenomas and carcinomas.

In some uncontrolled studies, a high prevalence of Helicobacter pylori infection unexpectedly has been found in patients with colorectal cancer. The purpose of the study was to investigate the prevalence of H. pylori infection in patients with colonic polyps or cancer. We reviewed 50 consecutive patients with either colonic adenomas or cancer who entered a preliminary case-control study. For each patient, 2 age- and gender-matched control subjects were selected (72 males; mean age, 63.1 years). A further 44 consecutive patients (30 with polyps and 14 with cancer) subsequently were enrolled. The H. pylori prevalence in patients with either polyps or cancer was compared with that in control subjects. Anti-H. pylori immunoglobulin G antibodies were assayed by an immunoenzymatic method. The prevalence of H. pylori antibodies was 49 (49%) of 100 in control subjects, 40 (71.4%) of 56 in patients with polyps (p < 0.006 vs. control subjects), and 21 (55%) of 38 in patients with cancer (not significant). Among patients with colorectal cancer, H. pylori prevalence was 9 (69.2%) of 13 for patients evaluated at the time of diagnosis and 12 (48%) of 25 for patients evaluated 1 to 9 years after surgery. We conclude that colonic neoplastic lesions, especially adenomas, are associated with an increased prevalence of H. pylori infection. The mechanisms underlying this association need to be elucidated.

Adenoma↗
PubMed1987

Characterization and tissue specificity of a monoclonal antibody against human uridine 5'-diphosphate-glucuronosyltransferase.

A monoclonal antibody against human liver uridine 5'-diphosphate-glucuronosyltransferase (UDPGTase) was developed. Enzyme inhibition studies with this monoclonal antibody showed inhibition of human liver UDPGTase activity with bilirubin, 4-methylumbelliferone, and 4-nitrophenol as substrates. Testosterone, estrone, and phenolphthalein UDPGTase activity was not inhibited. The monoclonal antibody probably recognizes the uridine 5'-diphosphate-glucuronic acid binding site at 4-nitrophenol UDPGTase. Proteins with a molecular mass of 54,000 daltons were immunopurified from solubilized human liver using the monoclonal antibody as ligand coupled to Sepharose 4B beads. The distribution of UDPGTase isoforms in various human tissues was studied by immunofluorescence. The enzyme could be detected in liver, kidney, stomach, small intestine, colon, and skin. In liver, only hepatocytes contain UDPGTase. In kidney, the enzyme was localized exclusively in proximal tubuli and in stomach in epithelial mucous cells. In small intestinal epithelium, maximal fluorescence was seen at the villous tip. In colon, all lining epithelial cells were stained. In colon polyps, staining for UDPGTase was clearly decreased, and in colon carcinoma it was undetectable. In skin, the stratum corneum was intensely stained, whereas the stratum basale showed no fluorescence.

Animals↗
PubMed1998

Effects of sulindac and its metabolites on growth and apoptosis in human mammary epithelial and breast carcinoma cell lines.

Nonsteriodal anti-inflammatory drugs (NSAIDs) are among the most commonly used medications in the United States and elsewhere, mainly for the treatment of arthritis. The NSAID sulindac causes regression and prevents the recurrence of premalignant colonic polyps in patients with familial adenomatous polyposis and inhibits colon carcinogenesis in rodents. Sulindac and sulindac sulfone, a metabolite of sulindac that lacks cyclooxygenase (cox) inhibitory activity, also inhibit mammary carcinogenesis in rats. To obtain insights into the relevance of these findings to human breast cancer, we examined the mechanism of action of sulindac and its sulfide and sulfone metabolites on the normal human mammary epithelial cell line MCF-10F and the human breast cancer cell line MCF-7. Of the three compounds, the sulfide was the most potent inhibitor of cell growth, although the sulfone and sulfoxide were also active at higher concentrations. Treatment of MCF-10F and MCF-7 cells with 100 microM sulindac sulfide resulted in accumulation of cells in the G1 phase of the cell cycle and induction of apoptosis. Apoptosis occurred within 24 h as determined by the TUNEL assay and DNA laddering was observed at 72 h. The accumulation of cells in G1 was associated with decreased levels of expression of cyclin D1 but no effect was seen on the expression of CDK4 or the immediate early response gene c-jun. Treatment with sulindac sulfide caused a striking induction of the CDK inhibitor p21WAF1 in MCF-10F cells. The MCF-7 cell line expressed a high basal level of p21WAF1 which did not change significantly after drug treatment. The pro-apoptotic gene BAX was not induced in either MCF-10F or MCF-7 cells by sulindac sulfide. Stable overexpression of cyclin D1, which frequently occurs in breast cancers, did not protect mammary epithelial cells from inhibition by the sulfide. These studies suggest that this class of compounds warrants further study with respect to breast cancer prevention and treatment.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1996

Location of tumour cells in colon tissue by Texas red labelled pentosan polysulphate, an inhibitor of a cell surface protease.

Pentosan polysulphate (PPS), a highly negatively charged polysaccharide, is a significant inhibitor of an isoenzymic form of a cell surface protease referred to as guanidinobenzoatase GB, associated with colonic carcinoma tissues in frozen sections and free GB in solution, in a concentration-dependent manner. However PPS failed to recognise and bind to the isoenzymic form of GB associated with normal colon epithelial cell surfaces. Texas red labelled PPS (TR-PPS) binds to the tumour cell surfaces of colonic carcinoma and colonic polyps and these cells fluoresce red, whilst the normal colon cell surfaces failed to bind the TR-PPS, and hence lacked red fluorescence. Polysulphonated suramin also selectively recognised and inhibited the colonic carcinoma GB isoenzyme. The kinetic data indicated that this inhibition was not caused by a mere polyanionic effect, since highly sulphated heparin failed to show a significant inhibition of colonic carcinoma GB, however trypan blue did show 50% inhibition. Kinetic studies have also shown that PPS is a non-competitive, reversible inhibitor of colonic carcinoma GB, with an apparent Km 6.8 x 10(-7) M. Gel analysis has shown that PPS binds to another site, distinct from the active centre, and after binding PPS changed the conformation of GB. These studies suggest that TR-PPS is a potent inhibitor of colonic carcinoma GB, and can be used as a novel fluorescent probe for the location of tumour cells in frozen sections of human colon tissues. PSS could also have potential as a vehicle for the transport of cytotoxic compounds to carcinoma cells of the colon.

Carboxylic Ester Hydrolases↗