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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A morphological study of biopsy samples of gastric polyps from 224 patients was carried out. Four stages in gastric polyp morphogenesis were distinguished: foveolar hyperplasia, hyperplastic polyp, "two-floor" adenoma and adenoma. The correlation was established between the degree of Helicobacter pylori infection in the polyp mucous membrane on the one hand, and epithelial and stromal reactions (immuno-inflammatory reaction of stroma, chronic inflammation, formation of Russel bodies, cystes and chronic erosions) on the other. Greater content of stromal collagens, type IV collagen in case of gastric hyperplastic lesions was observed. Appearance and progression of gastric adenomatous growth in hyperplastic polyp correlates with an increase of type III collagen content, decrease of types I, IV, V collagens and fibronectin.
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PMID:[Morphological characteristics of hyperplastic and adenomatous stomach polyps]. 961 4

Although epidemiological studies strongly suggest an association between Helicobacter pylori infection and gastric carcinogenesis via a multistage process, a causal link between them has not been demonstrated. We evaluated the endoscopic and histological changes of gastric adenoma, which is considered a premalignant condition, after eradication of H. pylori. Thirty-five H. pylori-infected patients with gastric adenoma were treated with triple therapy (lansoprazole 30mg/day, clarithromycin 400mg/day, and amoxicillin 1500 mg/day) for 1 week. Of these 35 patients, 30 (86%) exhibited no H. pylori by culture or histology after the therapy. Of the 30 gastric adenomas, 7 decreased in size endoscopically; three gastric adenomas especially showed apparent remission, although histological cure in these three patients was not apparent. Our results suggest that removal of H. pylori infection may only mask a gastric adenoma endoscopically owing to the change around the gastric mucosa.
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PMID:Endoscopic and histological reversibility of gastric adenoma after eradication of Helicobacter pylori. 1061 74

To assess a role of microsatellite instability (MSI) in the development of gastric adenocarcinoma or adenoma from chronic gastritis, we analysed mutations of five microsatellite loci in gastritis, adenoma and adenocarcinoma retrospectively. Gastric mucosa was biopsied from the same area in each patient at different periods and examined for MSI. Only one of 55 patients with chronic gastritis revealed MSI-H phenotype and the other 54 patients showed microsatellite stable (MSS) phenotypes. In six of 17 patients with gastric adenoma or well-differentiated adenocarcinoma, MSI-positive phenotypes were demonstrated. Interestingly, all of six patients showing MSI, including three high-level MSI (MSI-H) cases and three low-level (MSH-L) cases, had already revealed MSI at the stage of chronic gastritis. In two of three MSI-H cases, the identical MSI patterns had been observed at the stage of gastritis 1.5-7 years before the final diagnosis of adenocarcinoma. The adjacent gastritis mucosa within 10 mm from the carcinoma demonstrated MSI as well. MSI was not found in any of 35 patients with Helicobacter pylori infection, but found in one of 30 patients without infection. Moreover, two of three cases of gastric adenoma or well-differentiated adenocarcinoma with MSI-H at the stage of chronic gastritis showed no evidence of Helicobacter pylori infection throughout the observation periods. These results indicate that MSI in biopsy specimens at the stage of chronic gastritis may predict the risk of the progression to adenoma and well-differentiated adenocarcinoma, and that Helicobacter pylori infection itself may not induce MSI directly in the gastric mucosa.
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PMID:Clinical usefulness of microsatellite instability for the prediction of gastric adenoma or adenocarcinoma in patients with chronic gastritis. 1083 96

Results from epidemiological studies and therapeutic clinical trials have shown that Helicobacter pylori infection causes acute and chronic active gastritis and is the initiating factor for the majority of peptic ulcer disease. Eradication of the infection with antibiotics resolves gastritis and restores normal gastric physiology, accelerates healing of peptic ulcer disease, and virtually eliminates recurrence of duodenal ulcer disease. The infection also plays an important role in the initiation and/or progression of gastric atrophy and intestinal metaplasia, which may eventually lead to the development of distal gastric cancer. Furthermore, almost all patients with gastric MALT lymphoma are infected with H. pylori and cure of the infection leads to histological regression of the tumor and maintains the regression in over 80% of patients during long-term follow-up. Preliminary uncontrolled data from Japan show that eradication of the infection significantly reduced metachronous intestinal-type gastric cancer following initial endoscopic resection of early gastric cancer and might also prevent the progression of gastric adenoma to gastric dysplasia or gastric cancer. Although this overwhelming evidence has demonstrated that H. pylori infection is bad for humans, some have questioned the wisdom of eradicating the infection in all those infected. Their arguments are largely based on hypothesis and circumstantial evidence: 1) Less than 20% of all H. pylori infected persons will develop significant clinical consequences in their lifetime. 2) H. pylori strains are highly diverse at a genetic level and are of different virulence. 3) The antiquity of H. pylori infection in humans and their co-evolution suggests that H. pylori may be a commensal to humans. Eradication of H. pylori may remove some beneficial bacterial strains and may provoke esophageal disease or gastric cancer at the cardia. However, careful review of the literature confirms that H. pylori infection is a serious pathogen albeit in a minority of those infected. It remains for carefully designed prospective studies, rather than hypothesis to make changes in the current consensus position.
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PMID:Review article: should we kill or should we save Helicobacter pylori? 1148 62

Histopathologic and clinical data strongly suggest a causal relation between Helicobacter pylori infection and gastritis, peptic ulcer disease, or both. However, little has been written about the potential association between H. pylori infection and Brunner's gland adenoma. Therefore, we carried out a prospective study to determine the presence of H. pylori infection among patients with Brunner's gland adenoma. From November 1996 till October 1999, 19100 patients who had undergone upper gastrointestinal endoscopy at two clinical centers in Zagreb, Croatia, were candidates for participation in the study. Brunner's gland adenoma was diagnosed on the basis of histologic samples taken from the polyp (four patients) or after the entire polyp was made available upon endoscopic removal (three patients). When all endoscopic examinations had been performed, biopsy samples were taken from the antrum and body of the stomach, so that gastritis could be classified and H. pylori determined by histology. Biopsy samples were also taken from the duodenal bulb to verify duodenitis. Two other samples were taken from the antrum for rapid urease test. The patients were considered positive for H. pylori when both histology and rapid urease test were positive. Brunner's gland adenoma was diagnosed in seven patients (five women and two men; median age, 49 yrs). Five (71%) patients with diagnosed Brunner's gland adenoma had concurrent H. pylori infection. Duodenitis associated with gastric metaplasia was observed in six patients. Complete eradication of H. pylori was achieved in only two patients. Symptoms disappeared or markedly diminished in all patients with significant improvement during therapy or immediately upon endoscopic removal of the polyp. Although limited by a very small number of patients, our results suggest that concurrent H. pylori infection is very common in patients with Brunner's gland adenoma. However, the role of H. pylori infection in the pathogenesis and development of Brunner's gland hyperplasia remains unclear.
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PMID:Helicobacter pylori infection in patients with Brunner's gland adenoma. 1239 18

Although debates still exist whether Helicobacter pylori infection is really class I carcinogen or not, H. pylori has been known to provoke precancerous lesions like gastric adenoma and chronic atrophic gastritis with intestinal metaplasia as well as gastric cancer. Chronic persistent, uncontrolled gastric inflammations are possible basis for ensuing gastric carcinogenesis and H. pylori infection increased COX-2 expressions, which might be the one of the mechanisms leading to gastric cancer. To know the implication of long-term treatment of antiinflammatory drugs, rebamipide or nimesulide, on H. pylori-associated gastric carcinogenesis, we infected C57BL/6 mice with H. pylori, especially after MNU administration to promote carcinogenesis and the effects of the long-term administration of rebamipide or nimesulide were evaluated. C57BL/6 mice were sacrificed 50 weeks after H. pylori infection. Colonization rates of H. pylori, degree of gastric inflammation and other pathological changes including atrophic gastritis and metaplasia, serum levels and mRNA transcripts of various mouse cytokines and chemokines, and NF-kappaB binding activities, and finally the presence of gastric adenocarcinoma were compared between H. pylori infected group (HP), and H. pylori infected group administered with long-term rebamipide containing pellet diets (HPR) or nimesulide mixed pellets (HPN). Gastric mucosal expressions of ICAM-1, HCAM, MMP, and transcriptional regulations of NF-kappaB binding were all significantly decreased in HPR group than in HP group. Multi-probe RNase protection assay showed the significantly decreased mRNA levels of apoptosis related genes and various cytokines genes like IFN-gamma, RANTES, TNF-alpha, TNFR p75, IL-1beta in HPR group. In the experiment designed to provoke gastric cancer through MNU treatment with H. pylori infection, the incidence of gastric carcinoma was not changed between HP and HPR group, but significantly decreased in HPN group, suggesting the chemoprevention of H. pylori-associated gastric carcinogenesis by COX-2 inhibition. Long-term administration of antiinflammatory drugs should be considered in the treatment of H. pylori since they showed the molecular and biologic advantages with possible chemopreventive effect against H. pylori-associated gastric carcinogenesis. If the final concrete proof showing the causal relationship between H. pylori infection and gastric carcinogenesis could be obtained, that will shed new light on chemoprevention of gastric cancer, that is, that gastric cancer could be prevented through either the eradication of H. pylori or lessening the inflammation provoked by H. pylori infection in high risk group.
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PMID:Chemoprevention of Helicobacter pylori-associated gastric carcinogenesis in a mouse model: is it possible? 1254 79

Helicobacter pylori infection is a known risk factor of gastric carcino-genesis. This article presents early molecular alterations associated with H. pylori chronic gastritis and advances in the molecular characterization of preneoplastic intestinal metaplasia (IM) and premalignant gastric mucosal lesions. H. pylori infection induces changes in gene expression, genomic instability and accumulation of gene mutations in the stomach epithelium. Mutations, including LOH and microsatellite instability, and gene hypermethylation are seen not only in gastric cancer, but are already detectable in IM and gastric dysplasia/adenoma. Recent reports using microarray expression analysis identified several gastric epithelial genes that are regulated by H. pylori. Among the many genes showing altered epithelial expression in response to H. pylori, some might be useful as markers to assess gastric cancer risk. Profiles of mutagenesis and gene expression in IM and dysplasia/adenoma have been characterized and represent potential markers of preneoplastic and premalignant lesions during gastric carcinogenesis.
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PMID:Molecular markers in Helicobacter pylori-associated gastric carcinogenesis. 1574 38

Stem cells share many properties with malignant cells, such as the ability to self-renew and proliferate. Cancer is believed to be a disease of stem cells. The gastrointestinal tract has high cancer prevalence partly because of rapid epithelial cell turnover and exposure to dietary toxins. The molecular pathways of carcinogenesis differ according to the tissue. Work on hereditary cancer syndromes including familial adenomatous polyposis (FAP) has led to advances in our understanding of the events that occur in tumour development from a gastrointestinal stem cell. The initial mutation involved in the adenoma-carcinoma sequence is in the 'gatekeeper' tumour-suppressor gene adenomatous polyposis coli (APC). Somatic hits in this gene are non-random in FAP, with the type of mutation selected for by the position of the germline mutation. In the stomach, a metaplasia-dysplasia sequence occurs and is often related to Helicobacter pylori infection. Clonal expansion of mutated cells occurs by niche succession. Further expansion of the aberrant clone then occurs by the longitudinal division of crypts into two daughter units--crypt fission. Two theories seek to explain the early development of adenomas--the 'top down' and 'bottom up' hypotheses. Initial studies suggested that colorectal tumours were monoclonal; however, later work on chimeric mice and a sex chromosome mixoploid patient with FAP suggested that up to 76% of early adenomas were polyclonal. Introduction of a homozygous resistance allele has reduced tumour multiplicity in the mouse and has been used to rule out random collision of polyps as the cause of these observations. It is likely that short-range interaction between adjacent initiated crypts is responsible for polyclonality.
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PMID:From gene mutations to tumours--stem cells in gastrointestinal carcinogenesis. 1630 Jun 52

Gastric adenomas are rare neoplastic growths characterized by localized polypoid proliferations of dysplastic epithelium that tend to progress to infiltrating adenocarcinoma. Therefore, the identification of molecular markers that could reliably recognize adenomas at risk of progression is advocated in the clinical management. In this study we investigated, in a series of gastric adenoma specimens from an area at high risk of gastric cancer, the relationship between clinicopathological characteristics of adenoma and Helicobacter pylori infection, APC mutational status, and COX-2 and the down-stream enzyme mPGES1 expression. Helicobacter pylori infection, detected in 24%, and 33% by histology and PCR analyses, respectively, did not show any relationship with growth pattern, localization, size, dysplasia grade and presence of synchronous cancer. Pathogenetic mutations of MCR region (codons 1269-1589) of the APC gene were detected only in one case corresponding to a single, small size, low grade, H. pylori-negative adenoma. The expression of COX-2 largely matched that of mPGES(1). Both were overexpressed in 79% of cases showing a relationship with high-grade dysplasia, size >10 mm and presence of a synchronous carcinoma. In conclusion, COX-2 may play a key role in the development and progression of gastric adenoma and could be an attractive target in the management of gastric adenoma at major risk of cancer development.
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PMID:Gastric adenomas: relationship between clinicopathological findings, Helicobacter pylori infection, APC mutations and COX-2 expression. 1676 Feb 71

Atrophic gastritis, intestinal metaplasia, autoimmune corpus atrophic gastritis, gastric remnant man 15 years after gastrectomy, hyperplastic or adenoma polyps and gastric ulcer are conditions associated with an increased risk of gastric carcinoma of intestinal or diffuse type. The role of Helicobacter pylori infection is major but the usefulness of H. pylorieradication to revert precancerous lesions is questionable. Except for patients with dysplasia, no consensus exists for endoscopic surveillance of these premalignant conditions in countries with low incidence of gastric cancer.
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PMID:[Premalignant gastric lesions (except lymphomas)]. 1892 29


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