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Gastric Adenoma (gastric + adenoma)
Selected AbstractsCOMPARISON OF ENDOSCOPIC DETECTION RATE OF EARLY GASTRIC CANCER AND GASTRIC ADENOMA USING TRANSNASAL EGD WITH THAT OF TRANSORAL EGDDIGESTIVE ENDOSCOPY, Issue 4 2008Yukiya Yoshida Background:, To investigate the influence of the reduced image quality of transnasal esophagogastroduodenoscopy (EGD) with the ultrathin endoscope (transnasal EGD) on endoscopic diagnoses, we compared the detection rate (DR) of early gastric cancer and gastric adenoma by transnasal EGD with that of transoral EGD using a standard endoscope. Methods:, Transnasal EGD was carried out in 2791 examinations for the purposes of screening or other reasons. Controls were examined by transoral EGD and numbered 3591 examinations. The transnasal endoscope used was an EG530N. Lesions graded C-3 or higher by Kimura-Takemoto's classification were regarded as endoscopic atrophy. Results:, (i) DR in all subjects and those with atrophy were not different between transnasal and transoral EGD. (ii) Multivariate analysis of DR in subjects with atrophy was carried out using five variables: gender, age, purposes of endoscopy, endoscopic insertion route and the four endoscopists. DR was significantly higher in males or subjects ,60 years. No difference was noted between the endoscopic insertion routes (transnasal vs transoral). (iii) The subjects analyzed in (ii) were divided into the transnasal and transoral groups, and multivariate analysis of DR was carried out using four variables. DR was not different among the endoscopists in the transoral group. However, in the transnasal group, DR increased as the years of endoscopic experience was prolonged. Conclusions:, Multivariate analysis detected no significant difference in DR between transnasal and transoral EGD. However, a significant difference in DR by transnasal EGD among the endoscopists is detected. Transnasal EGD should be carefully carried out by experienced endoscopists. [source] LARGE HYPERPLASTIC POLYP DEVELOPING AFTER ENDOSCOPIC MUCOSAL RESECTION OF GASTRIC ADENOMA IN A PATIENT RECEIVING IMMUNOSUPPRESSIVE THERAPYDIGESTIVE ENDOSCOPY, Issue 2 2006Geum-Youn Gwak A 59-year-old man underwent endoscopic mucosal resection (EMR) for gastric adenoma. He had suffered from end-stage renal disease for several years and had received renal transplantation some 5 months before EMR. Subsequently, he took immunosuppressive agents. Follow-up gastrofiberscopy 6 months after EMR showed a sessile polyp at the resection site twice as large as the original adenoma; biopsy specimens revealed a hyperplastic nature. At the time of writing, this hyperplastic polyp has neither increased in size nor developed adenomatous or carcinomatous changes by histological examinations over the past 5 years. Therefore, this is a case of hyperplastic polyp occurring at the gastric adenoma resection site, and suggests the possible effect of immunosuppressive therapy on the post-EMR healing process and hyperplastic polyp development. [source] COMPARISON OF ENDOSCOPIC DETECTION RATE OF EARLY GASTRIC CANCER AND GASTRIC ADENOMA USING TRANSNASAL EGD WITH THAT OF TRANSORAL EGDDIGESTIVE ENDOSCOPY, Issue 4 2008Yukiya Yoshida Background:, To investigate the influence of the reduced image quality of transnasal esophagogastroduodenoscopy (EGD) with the ultrathin endoscope (transnasal EGD) on endoscopic diagnoses, we compared the detection rate (DR) of early gastric cancer and gastric adenoma by transnasal EGD with that of transoral EGD using a standard endoscope. Methods:, Transnasal EGD was carried out in 2791 examinations for the purposes of screening or other reasons. Controls were examined by transoral EGD and numbered 3591 examinations. The transnasal endoscope used was an EG530N. Lesions graded C-3 or higher by Kimura-Takemoto's classification were regarded as endoscopic atrophy. Results:, (i) DR in all subjects and those with atrophy were not different between transnasal and transoral EGD. (ii) Multivariate analysis of DR in subjects with atrophy was carried out using five variables: gender, age, purposes of endoscopy, endoscopic insertion route and the four endoscopists. DR was significantly higher in males or subjects ,60 years. No difference was noted between the endoscopic insertion routes (transnasal vs transoral). (iii) The subjects analyzed in (ii) were divided into the transnasal and transoral groups, and multivariate analysis of DR was carried out using four variables. DR was not different among the endoscopists in the transoral group. However, in the transnasal group, DR increased as the years of endoscopic experience was prolonged. Conclusions:, Multivariate analysis detected no significant difference in DR between transnasal and transoral EGD. However, a significant difference in DR by transnasal EGD among the endoscopists is detected. Transnasal EGD should be carefully carried out by experienced endoscopists. [source] LARGE HYPERPLASTIC POLYP DEVELOPING AFTER ENDOSCOPIC MUCOSAL RESECTION OF GASTRIC ADENOMA IN A PATIENT RECEIVING IMMUNOSUPPRESSIVE THERAPYDIGESTIVE ENDOSCOPY, Issue 2 2006Geum-Youn Gwak A 59-year-old man underwent endoscopic mucosal resection (EMR) for gastric adenoma. He had suffered from end-stage renal disease for several years and had received renal transplantation some 5 months before EMR. Subsequently, he took immunosuppressive agents. Follow-up gastrofiberscopy 6 months after EMR showed a sessile polyp at the resection site twice as large as the original adenoma; biopsy specimens revealed a hyperplastic nature. At the time of writing, this hyperplastic polyp has neither increased in size nor developed adenomatous or carcinomatous changes by histological examinations over the past 5 years. Therefore, this is a case of hyperplastic polyp occurring at the gastric adenoma resection site, and suggests the possible effect of immunosuppressive therapy on the post-EMR healing process and hyperplastic polyp development. [source] Review article: should we kill or should we save Helicobacter pylori?ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2001R.H. Hunt 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. [source] Genomic profiling of gastric carcinoma in situ and adenomas by array-based comparative genomic hybridization,THE JOURNAL OF PATHOLOGY, Issue 1 2010Masahiro Uchida Abstract Although genomic copy number aberrations (CNAs) of gastric carcinoma at the advanced stage have already been extensively characterized by array comparative genomic hybridization (array CGH) analysis, those of gastric carcinoma in situ (CIS) are still poorly understood. Furthermore, no reports have demonstrated correlations between CNAs and histopathological features of gastric adenoma. In this study, we investigated CNAs of 20 gastric CISs (Vienna category 4.2) and 20 adenomas including seven low-grade adenomas (LGA; Vienna category 3) and 13 high-grade adenomas (HGA; Vienna category 4.1), using oligonucleotide-based array CGH. The most frequent aberrations in CIS were gains at 8q (85%) and 20q (50%), and losses at 5q (50%) and 17p (50%), suggesting that these CNAs are involved in the development of CIS. We found that the pattern of CNAs in HGA was quite different from that in LGA. The most frequent CNAs in HGA were gains at 8q (62%) and 7pq (54%), whereas those in LGA were gain at 7q21.3-q22.1 (57%) and loss at 5q (43%). Interestingly, gains at 8q and 7pq, both of which occurred most frequently in HGA, were not detected in any cases of LGA. Of note, 8q gain was detected most frequently in both HGA and CIS but was undetected in LGA. Since HGA is believed to have a higher risk of progression to invasive carcinoma than LGA, these data suggest that 8q gain is important for the malignant transformation of gastric adenoma. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] Genetic and epigenetic analysis of the KLF4 gene in gastric cancer,APMIS, Issue 7 2007YONG GU CHO KLF4, which is also known as the gut-enriched Kruppel-like factor, plays important roles during the proliferation and differentiation of gastrointestinal epithelial cells. A loss of KLF4 expression has been observed in human tumors, particularly in the gastrointestinal tract. In this study, the molecular basis of the KLF4 inactivation in gastric cancer was investigated by analyzing the somatic mutation, the allelic loss with two microsatellite markers, D9S53 and D9S105, and hypermethylation of the KLF4 gene in 47 gastric adenomas and 81 gastric adenocarcinomas. Mutational analysis revealed one mutation of the KLF4 gene in a diffuse-type advanced gastric adenocarcinoma, but not in the gastric adenoma. This mutation was a somatic missense mutation, GGG,AGG (Gly,Arg) at codon 107 in exon 3, which encodes a transcriptional activation domain of the protein. An allelic loss was found in 7 (22.6%) of the 31 informative gastric adenoma cases and 15 (31.3%) of the 48 informative cancer cases at one or both markers. In addition, promoter hypermethylation of the KLF4 gene was observed in only two gastric cancers. These results suggest that genetic and epigenetic alterations of the KLF4 gene might play a minor role in gastric carcinogenesis. [source] Cyclooxygenase-2 and gastric carcinogenesisAPMIS, Issue 10 2003KIRSI SAUKKONEN Epidemiological studies have shown that the use of nonsteroid anti-inflammatory drugs (NSAIDs) is associated with reduced risk of gastric cancer. The best-known target of NSAIDs is the cyclooxygenase (Cox) enzyme. Two Cox genes have been cloned, of which Cox-2 has been connected with gastric carcinogenesis. Expression of Cox-2 is elevated in gastric adenocarcinomas, which correlates with several clinicopathological parameters, including depth of invasion and lymph node metastasis. This suggests that Cox-2,derived prostanoids promote aggressive behavior of adenocarcinomas of the stomach. Cox-2 expression is especially prominent in intestinal-type gastric carcinoma and it is already present in dysplastic precursor lesions of this disease, which suggests that Cox-2 contributes to gastric carcinogenesis already at the preinvasive stage. Our most recent data show that Cox-2 is expressed in gastric adenomas of trefoil factor 1 deficient mice. Treatment of these mice with a Cox-2 selective inhibitor, celecoxib, reduced the size of the adenomas. Taken together these data support efforts to initiate clinical studies to investigate the effect of Cox-2 inhibitors as chemotherapeutic agents and as adjuvant treatment modalities against gastric neoplasias. [source] | ||||||||||