Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As for precancerous lesion of the stomach detail analysis of endoscopic follow-up cases and histopathological investigations brought some new informations on its carcinogenesis. In this paper recent several reports were introduced and discussed on new opinion of precancerous conditions such as adenoma, intestinal metaplasia, gastric ulcer, remnant stomach and H. pylori. Gastric adenoma was considered to be neoplastic because of high incidence of carcinoma in situ. The stomach coexisted with adenoma showed high percentage of new arising tumor in same stomach and therefore, we can say that these are thought to be high risk group for well differentiated adenocarcinoma. Concerning the relation between intestinal metaplasia and gastric cancer we have never obtained final conclusion. However, it is likely that incomplete type of intestinal metaplasia appeared to be coexistent with gastric cancer, especially intestinal type carcinoma, which was thought to be paracancerous lesions. Recent advance of molecular biology has indicated new knowledge on gastric carcinogenesis, suggestive of multistep pathways. According to their reports, genomic instanbility appeared frequently in gastric adenoma and intestinal metaplasia as well as gastric carcinoma. Gastric carcinogenesis for ulcer, remnant stomach and H. pylori was also discussed. In near future the mechanism of gastric carcinogenesis is expected to be solved from view point of genetic events.
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PMID:[New concepts on precancerous lesions of the stomach]. 860 11

Gastric adenoma is a precancerous lesion of the stomach and its malignant transformation is thought to result from accumulative series of gene alterations. The aim of this study was to determine the pattern of chromosomal changes during gastric carcinogenesis. Pairs of adenoma and carcinoma tissues from 15 gastrectomy cases containing both adenomas and carcinomas in the same (adjacent pairs, 6 cases) and different (non-adjacent pairs, 9 cases) lesions, were analyzed for chromosomal alterations of 39 non-acrocentric chromosomal arms by comparative genomic hybridization (CGH). CGH analysis identified frequent chromosomal alterations in most of the gastric adenomas (14/15, 93%) and all of the carcinomas. The mean number of chromosomal alterations was higher in carcinoma (5.5 for adenoma and 11.7 for carcinoma; P = 0.006, by nonparametric Wilcoxon's test). Losses on the short arm of chromosome 17 were most common in both adenomas (43%) and carcinomas (67%). The pattern of chromosomal alterations in paired gastric adenomas and carcinomas showed greater similarity compared to the non-case pairs and this similarity was increased in the adjacent pairs. Deletion mapping analysis on chromosome 17p also demonstrated that the conserved deletion area was more frequent in the adjacent pairs. Among these 6 adjacent pairs, all had common deletion areas. In contrast, among the 9 non-adjacent pairs, 2 (22%) had common area of deletion, 5 (56%) showed deletion only in the carcinoma, and the remaining 2 (22%) had no deletion on 17p, suggesting diverse genetic changes might be involved in the multiple tumor formation. Our results that common clonal genetic changes between adjacent pairs of gastric adenomas and carcinomas and accumulated genetic changes in the carcinomas provide evidences for the stepwise mode of gastric carcinogenesis through the accumulation of a series of genetic alterations.
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PMID:Chromosomal alterations in paired gastric adenomas and carcinomas. 1115 2