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At least 19 recordsLinked to original sources
PubMed1993

The high frequency of upper gastrointestinal pathology in patients with fecal occult blood and colon polyps.

Colon polyps are commonly detected in the workup of fecal occult blood (FOB). It is, however, unclear whether colon polyps can adequately explain FOB. Our aim was to determine the frequency of upper gastrointestinal (UGI) pathology in patients with and without UGI symptoms and with and without risk factors for UGI pathology (such as smoking, drinking alcohol, taking nonsteroidal anti-inflammatory medications, or the presence of associated chronic diseases) who have colon polyps and FOB. Among our 67 study patients with colon polyps and FOB, 79% had associated UGI lesions. Presence or absence of UGI symptoms, risk factors associated with UGI lesions, and polyp characteristics such as size, location, number, and histology, did not appreciably affect this high frequency. Ulcers were the most common lesions in both symptomatic and asymptomatic patients. We conclude that patients with colon polyps found in the evaluation of FOB are likely to have concomitant UGI pathology, and UGI workup should be considered in both symptomatic and asymptomatic patients.

Colonic Polyps↗
PubMed1992

Colon polyps.

Colonic polyps commonly occur in all age groups and are of varied significance depending on the type of polyp and the symptoms manifested. There is some debate in the medical literature regarding the appropriate clinical management of polyps and the follow-up of patients after polypectomy. This discussion addresses the significance of colon polyps, including their etiology, histology, complications, detection, and management.

Adenoma↗
PubMed1997

Colon polyps.

Colon polyps may be single or multiple, noninherited or inherited, histologically may vary from inflammatory, hamartomatous, neurogenic, or adenomatous, and may be benign or malignant. The various recognized syndromes are discussed including their clinical presentation, malignant potential, and associated tumors. Recognition of these clinical syndromes will allow the clinician to categorize the patient and the relative risk. The discussion goes into the genetic studies identifying the adenomatous polyposis coli gene on chromosome 5 q21 and the identification of mutations arising in the DNA repair genes (MSA2, MLH1, PMSI, and M52) in the HNPCC syndrome. This identified two divergent pathologies, both involving "multiple hits" with mucosal cells going from normal to adenoma-dysplasia-carcinoma. The understanding of the multiple hit concept with the adenoma-dysplasia-carcinoma progression will aid in the further understanding of the broad neoplastic process.

Adenoma↗
PubMed1991

A mathematical computer stimulation model for the development of colonic polyps and colon cancer.

Currently known information about the development and progression of colon polyps and cancer is summarized and organized into a mathematical computer simulation model that successfully predicts the natural history of colon polyp and cancer development for an average patient with (1) familial polyposis coli (2) genetic susceptibility as measured by a positive family history, and (3) negative family history with a high fat diet. The mathematical model uses four distinct types of cells (normal, transformed, polypoid, and cancerous) and two kinetic processes (mutation and promotion). Arachidonic acid metabolites play a role in the model in the promotion of cancer from polyps, and account for that promotion through: (1) their effect on encouraging more polypoid cells in mitosis to move toward cancer; and (2) their immunosuppressive effect over time. The model also shows that one defect in allowing more cells to mutate to the transformed state is sufficient to account for the chain of events leading to the clinical sequelae of familial polyposis coli. A second genetic effect at another point in the process is unnecessary. The mechanism of action of Sulindac on colon polyps is explained by the model through inhibition of production of arachidonic acid metabolites, most notably prostaglandin E.

Adenomatous Polyposis Coli↗
PubMed2005

Aberrantly methylated CDKN2A, MGMT, and MLH1 in colon polyps and in fecal DNA from patients with colorectal polyps.

Colon cancer is the third leading cause of cancer-related death in the United States, affecting approximately 147,000 people each year. Most colon cancers arise from benign neoplasms and evolve into adenocarcinomas through a stepwise histologic progression sequence that starts from adenomas or hyperplastic polyps/serrated adenomas. Genetic alterations and, more recently, epigenetic alterations have been associated with specific steps in this polyp-adenocarcinoma sequence and likely drive the histologic progression of colon cancer. Consequently, we have assessed in colon adenomas and hyperplastic polyps the methylation status of MGMT, CDKN2A, and MLH1 to determine the timing and frequency of these events in the polyp-carcinoma progression sequence and subsequently to analyze the potential for these methylated genes to be molecular markers for adenomas and hyperplastic polyps. We have found that methylated MGMT, CDKN2A, and MLH1 occur in 49%, 34%, and 7% of adenomas and in 5%, 10%, and 7% of hyperplastic polyps, respectively, and that they are more common in histologically advanced adenomas. Furthermore, analysis of fecal DNA from persons who have undergone colonoscopic exams revealed methylated CDKN2A, MGMT, and MLH1 in fecal DNA from 31%, 48%, and 0% of individuals with adenomas and from 16%, 27%, and 10% of individuals with no detectable polyps, respectively. These results show that aberrant methylated genes can be detected frequently in sporadic colon polyps and that they can be detected in fecal DNA. Notably, improvements in the specificity and sensitivity of the fecal DNA-based assays will be needed to make them clinically useful diagnostic tests for polyps.

Adaptor Proteins, Signal Transducing↗
PubMed2003

Changes in the expression of the peroxisome proliferator-activated receptor gamma gene in the colonic polyps and colonic mucosa of acromegalic patients.

Acromegalic patients have an increased prevalence of colonic neoplasms and lower peroxisome proliferator-activated receptor gamma (PPARgamma) levels, the latter acting as a tumor suppressor gene. In this study we evaluated the expression of PPARgamma in the biopsy samples of the polyps and outside polyps colonic mucosa from seven patients with active, untreated acromegaly, 11 with cured disease, and 15 controls. Serum GH and IGF-I levels were higher in patients with untreated acromegaly than in those with acromegaly in remission or controls (P = 0.003 and P = 0.002, respectively) The expression of PPARgamma mRNA (mean +/- SE) was 1) mucosa outside polyps, 24,188 +/- 3,254 transcripts in the controls, 22,432 +/- 2,006 transcripts in acromegaly in remission, and 1,952 +/- 342 transcripts in untreated acromegaly (P < 0.0001 vs. controls and acromegaly in remission); and 2) polyps mucosa, 1,554 +/- 236 transcripts in the controls, 1,112 +/- 143 in acromegaly in remission, and 1,570 +/- 251 in untreated acromegaly (P = NS among polyps groups and mucosa outside polyps of untreated acromegaly; P < 0.0001 vs. mucosa outside polyps of controls and acromegaly in remission). Eighty-five percent of the cells in the mucosa outside polyps from controls or acromegaly in remission were positive at immunohistochemistry, at variance with 45% of the cells from polyps mucosa from each group and from those of mucosa outside polyps of untreated acromegaly (P = 0.0002). In conclusion, patients with untreated acromegaly have reduced expression of PPARgamma in the mucosa outside polyps, which might be reversed by curing the disease; conversely, patients with acromegaly in remission have the same low levels of expression of PPARgamma in the polyps mucosa as untreated acromegaly or controls, supporting the concept that reduced expression of PPARgamma might be an early event in colonic tumorigenesis.

Acromegaly↗
PubMed1989

Hyperplastic colonic polyps as a marker for adenomatous colonic polyps.

Hyperplastic colonic polyps are generally regarded as being of little or no clinical consequence. Recently, however, hyperplastic polyps have been found to share numerous functional similarities with colorectal carcinoma. To determine whether the presence of an isolated left-sided colonic hyperplastic (metaplastic) polyp could serve as a marker for more proximal synchronous adenomatous colonic polyps, we retrospectively analyzed all consecutive colonoscopic polypectomies performed over an 18-month period at two medical centers. It is the policy at both institutions to remove or biopsy all polyps, regardless of size. Indications for colonoscopy included known or previous colonic polyps or carcinoma, hemoccult positive stool, lower gastrointestinal bleeding, iron deficiency anemia, abnormal barium enema, inflammatory bowel disease, abdominal pain, and family history of colon cancer. The location of adenomatous polyps and hyperplastic polyps was recorded and compared. One hundred sixty-three of 845 consecutive patients (19.3%) had at least one colonic polyp. The prevalence of adenomatous polyps alone was 10.3%, hyperplastic polyps 9%, and both types 1.9%. The prevalence rate for an adenomatous polyp in patients without a hyperplastic polyp was 15%. In contrast, among patients with a hyperplastic polyp, 49% had a synchronous adenomatous polyp. Only 3.4% of patients had an adenomatous polyp proximal to the splenic flexure when no polyps were present in the left colon. Conversely, among the 29 patients in whom an isolated hyperplastic polyp was found in the left colon, there was a 32.5% prevalence of adenomatous polyps in the proximal colon (p less than 0.01). The results of this study suggest that left-sided hyperplastic colonic polyps (generally within the reach of a screening sigmoidoscopy) serve as a marker for neoplastic polyps.

Adolescent↗
PubMed1991

Pre-elastofibroma-like colonic polyp: another cause of colonic polyp.

We present a case of pre-elastofibroma-like lesion, a kind of elastic-producing fibrous tumor. The small colonic polyp, which was found in a 49-year-old asymptomatic man in association with a large colonic adenoma, showed submucosal nodular deposits of fine granular or fibrillar eosinophilic materials with interspersed fibroblastic cells. Elastic stain revealed these deposits to consist mainly of dark gray granular or partially fibrillar dense elastinophilic materials, most of which were digested with elastase. This stromal lesion somewhat resembled a pre-elastofibroma. Therefore, pre-elastofibroma-like lesions should be kept in mind as a possible origin of colonic polyp.

Colonic Polyps↗
PubMedDate not supplied

Molecular biology of colon polyps and colon cancer.

From a histologic and endoscopic standpoint, colon and rectal cancer (CRC) begins as a small neoplastic polyp which progressively enlarges and transforms through a dysplasia stage into invasive cancer. Recently, molecular abnormalities underlying the adenomacarcinoma progression have been defined. The adenomatous polyposis coli (APC) gene and mismatch repair genes are found to be dysfunctional early in the neoplastic process; either as inherited or somatic mutations. Subsequently, polyps progress to cancer along one of two paths depending on which gene is abnormal. When the APC gene is the initial mutation tumor development follows the "loss of heterozygocity" (LOH) pathway. If mismatch repair genes are altered, the "replication error" (RER) pathway is followed. Somatic mutations of the K-ras oncogene and the MCC, DCC, and p53 tumor suppressor genes accumulate in the LOH pathway and mark the progression through polyp stages. Microsatellite instability is a characteristic of the RER pathway but the precise genes involved in this pathway currently are not known. Defining these pathways has led to a new classification scheme for CRC with resultant changes in our clinical approach to screening, surveillance, and treatment.

Adenomatous Polyposis Coli↗
PubMedDate not supplied

OVX1 and CEA in patients with colon carcinoma, colon polyps and benign colon disorders.

The OVX1 tumor marker promises to complement CA125 for detection of early stage ovarian carcinoma. OVX1 has also been shown to be elevated in colon cancer patients. This study is designed to assess serum OVX1 levels in patients with specific stages of colon cancer, colon polyps or other GI disorders. Serum OVX1 and CEA were measured by radioimmunoassay or enzyme immunoassay for 206 patients at the time of colonoscopy or staging for colon carcinoma. In patients with stage I, II, III, or IV colon carcinoma, serum OVX1 was positive in 37%, 48%, 74% and 63%, respectively. Fifty-three percent of patients with colon polyps had elevated OVX1 levels, while OVX1 levels were positive in only 7% of healthy controls. If both OVX1 and CEA were considered, at least one of these markers was elevated in 36%, 60%, 79% or 89% of patients with stage I, II, III or IV colon carcinoma, respectively. The majority of patients with inflammatory bowel disease or diverticulosis also had elevated OVX1 levels. Both markers were positive in 27% of patients with colon carcinoma, and not in any patients with a normal colonoscopy or with a diagnosis of diverticulosis or hemorrhoids. In conclusion, serum OVX1 improves the sensitivity of CEA for detecting colon polyps and colon cancer; however, the use of OVX1 in this setting is hindered by its elevation in non-malignant colonic processes.

Antigens, Tumor-Associated, Carbohydrate↗
PubMed1983

[Methods for the early detection of colonic polyps and colonic cancers].

The dramatically rising incidence of colorectal cancer and the fact that survival rates can only be improved by earlier diagnosis call for increased efforts aimed at early detection of colonic neoplasias. Present diagnostic methods--occult blood testing, digital exam, rigid and flexible sigmoidoscopy, double contrast barium enema and colonoscopy--are analyzed with regard to diagnostic yield, time requirement and patient acceptability. Flexible sigmoidoscopy has proved to be of high diagnostic value, to take relatively little time and to cause only minimal patient discomfort. It will therefore gradually replace rigid sigmoidoscopy. Various populations at risk for colorectal cancer are outlined and appropriate diagnostic screening methods are described. Finally, a plan for monitoring of the normal risk population is proposed.

Colonic Neoplasms↗
PubMed1993

Leiomyomatous colonic polyp.

Leiomyomatous colonic polyps are rare. We report a patient with an asymptomatic 15-mm submucosal polyp in the sigmoid colon. The tumor was successfully removed by endoscopy. Histopathological examination revealed a leiomyoma originating in the muscularis mucosa.

Colon, Sigmoid↗
PubMed1992

Pedunculated colonic polyp diagnosed by colonic sonography.

A solitary hamartomatous polyp of the colon in a four year old boy was diagnosed by colonic sonography while barium enema and colonoscopy were non-diagnostic. Colonic sonography provides an additional simple, relatively non-invasive modality for evaluation of the colon.

Barium Sulfate↗