Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The submucosal heterotopic gastric glands were found in 160 cases (10.7%) of 1500 resected stomachs; 15% in gastric ulcer, 9.9% in gastric carcinoma, 4% in duodenal ulcer and 11% in chronic gastritis. The heterotopic glands were usually found in the distal half of the stomach, diffusely or localized. Macroscopic submucosal tumor was found in 9 (5%) of 160 cases. Although the heterotopic glands were found with an intimate relation to the repeated mucosal damage and subsequent intestinal metaplasia, they had no specific relation to gastric carcinogenesis.
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PMID:Heterotopic gastric glands in the submucosa of the stomach. 45 98

The cases of the gastric carcinoma combined with distant benign gastric ulcer were 90 of 1257, 7.1%, and the carcinomas were frequently found in the lesser curvature of the antrum and the combined gastric ulcers frequently in the lesser curvature and posterior wall of the corpus. Average age in the combined cases was 58.8 which was older about 7 years than that in the cases of the gastric ulcer. The cases, in which the ulceration in the gastric ulcer was same or deeper than that in the gastric carcinoma, occupied about 70% of these combined cases. It should be considered that the malignant transformation does not always occur in the preceding ulcerative lesion. However, the intestinal metaplasia was usually severe, and so the well-differentiated carcinomas were twice frequent to the low-differentiated ones. The repeated regeneration of the epithelial cells associated with the erosive or ulcerative change may be of some relation to the carcinogenesis, because the intestinal metaplasia appears usually associated with the repeated defect and repair of the propria mucosae.
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PMID:Gastric carcinoma combined with distant gastric ulcer. 101 94

Over 3000 patients, treated surgically for peptic ulcers, were assigned to a Social Class and Occupation Group using information obtained either from their death certificates or from their hospital notes. An analysis of the relationship of socioeconomic status and occupation with the site of original ulcer and the risk of cancer is reported. The major observations were: (a) an association of gastric ulcer with manual and of duodenal ulcer with non-manual Social Class; (b) an association of gastric cancer with dusty occupation and colorectal cancer with professional and managerial workers; and (c) no association between post-surgery gastric cancer risk and social class. This implies that the early stages of gastric carcinogenesis are related to poor socioeconomic conditions but the progression from the precursor lesion (in this case gastric ulcer) to gastric cancer is not, and is consistent with the multistage hypothesis of gastric carcinogenesis proposed by Correa [Diet and Human Carcinogenesis (Edited by Joosens, J. V., Hill, M. J. and Geboers, J.), pp. 109-115. Excerpta Medica, Amsterdam (1985)].
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PMID:Occupational and socioeconomic factors associated with peptic ulcer and with cancers following consequent gastric surgery. 232 87

We reviewed 29 patients who developed carcinomas of the gastric remnant more than 10 years after the initial gastrectomy. The median age was 59 years (29-75), with a male-to-female ratio of 3.8:1. The reason for previous operation was stomach ulcer in 16 patients, chronic gastritis in 2, stomach polyp in 2, duodenal ulcer in 5 and stomach cancer in 4 patients. Regarding the type of the original operations, Billroth's operation I (B-I) was performed for 10 patients, Billroth's II (B-II) for 18 and Roux-en Y operation for one. The site of tumor was classified into three groups, stoma (gastroenterostomy), stump (gastric cut-end except stoma) and others (the site except stoma and stump). The patients reconstructed with B-II developed significantly more carcinomas in the stoma than those reconstructed with B-I, with the incidence of 10/18 and 0/10, respectively (p less than 0.05). The interval between the initial operation and the second one was significantly longer in patients with stomal cancer than in those with stump cancer (p less than 0.05). There were no significant difference in the frequency and degree of histologic change, such as intestinal metaplasia or glandular cystification in noncancerous areas, between the B-I and B-II patients. This study suggested that cancers of the gastric remnant, especially those developed in the stoma after B-II were different from the other remnant cancers in terms of carcinogenesis or cancer promotion, and that they were probably induced by duodenogastric reflux to the gastrojejunostomized area.
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PMID:[A study on 29 patients with cancers of the gastric remnant--a speculation on a remnant cancer-promoting factor from the aspect of tumor location]. 235 90

Gastric acid secretions and serum gastrin levels have been examined in 128 patients with early gastric cancer and in 98 gastric ulcer patients. Gastric cancer patients were found to have lower acid secretions than did gastric ulcer patients, and those with elevated types of a differentiated adenocarcinoma had lower acid secretions than did those with depressed types of an undifferentiated adenocarcinoma. Gastric acid secretions in patients with both a gastric ulcer and cancer were found to decrease with aging. However, the serum gastrin levels were found to be decreased in patients with a gastric ulcer and to be increased in patients with a gastric cancer. Incidences of a differentiated adenocarcinoma increased with aging. From these observations, it has been speculated that the carcinogenesis of a differentiated adenocarcinoma may be related to increasing endogenous gastrin levels and decreasing gastric acid secretions. These results suggest that a continuous check of the serum gastrin levels might be a good marker for cancer detection and that gastrin antibodies might be useful for treatment.
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PMID:[Gastric acid secretions and serum gastrin levels in patients with mucosal and submucosal gastric cancers]. 254 82

When compared with a matched population group, 4466 ulcer patients who had had gastric surgery between 1940 and 1960 showed no difference in the risk of death from gastric cancer in the first 20 years of follow-up but a 4.5-fold increase thereafter. In duodenal ulcer patients there was an initial decrease in risk followed by a 3.7-fold increase after 20 or more years. Since the initial decrease was seen only in the gastrectomy patients and not in those who had truncal vagotomy and drainage, it may have been due to the reduction in mucosal surface. The increased risk 20 years after duodenal ulcer surgery was greater in vagotomy patients than in gastrectomy patients. In gastric ulcer patients a 3.0-fold increase in risk for the first 20 years rose to a 5.5-fold increase thereafter. After 20 years, patients treated with the Bilroth II operation were at higher risk than those treated with Bilroth I, consistent with a role for bile reflux in gastric carcinogenesis. The finding that the risk differs according to original pathology and type of operation may explain the discrepancies between previous studies.
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PMID:Mortality from gastric cancer following gastric surgery for peptic ulcer. 287 Dec 38

The current therapeutic approach to peptic ulcer disease includes agents that reduce gastric acidity and hence peptic activity, inactivate or adsorb pepsin, create a physical barrier against the effects of acid and pepsin, or enhance mucosal defence. Profound gastric acid reduction may predispose to infection, and it has been suggested that carcinogenesis is possible, although a cause-effect relationship has never been established. The side-effects of therapy are well-described, and may limit the therapeutic approach. Healing rates correlate closely with acid suppression in duodenal ulcer, but not entirely in gastric ulcer. Maintenance therapy lowers the relapse rate, but does not alter the ulcer diathesis. The optimal strategy for long-term management remains unclear, but in the future one should consider outcome measures which include a decrease in pain, improvement in the quality of life, reduction work loss, and a reduction of complications, in addition to ulcer healing. The ideal therapy should be efficacious, safe, and convenient--with no side-effects--and cost-effective. New agents should suppress acid and peptic activity, while enhancing the gastric mucosal defence mechanisms (such as mucosal blood flow, mucus, and bicarbonate secretion) and stimulating gastric cellular regeneration and restitution.
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PMID:The limitations of current therapy in peptic ulcer disease. 330 47

Patients with pernicious anaemia have a high risk of gastric cancer and we are investigating the role of N-nitroso compounds in their gastric carcinogenesis. We have carried out bacteriological studies and analyses of nitrite and N-nitroso compounds. Patients with duodenal or gastric ulcer are often treated with H2-receptor inhibitors such as cimetidine. This treatment induces hypochlorhydria similar to that in pernicious anaemia patients and it has been suggested that this might put these patients at risk of developing gastric cancer later. Analyses similar to those for p.a. patients have therefore been carried out in patients treated with cimetidine. We have set up an animal model of achlorhydria, using piglets, that will allow us to test in vivo the efficacy of compounds known to inhibit N-nitrosation in vitro. This is clearly necessary, in view of the growing size of the population now thought to be at risk.
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PMID:Gastric bacteria, nitrate, nitrite and nitrosamines in patients with pernicious anaemia and in patients treated with cimetidine. 722 82

N-Methyl-N-nitro-N'-nitrosoguanidine (MNNG) is a gastric carcinogen in several animal species and has been used in a number of systems to dissect the co-carcinogenic potential of various compounds in the induction of gastric adenocarcinoma. Recent epidemiological evidence suggests that Helicobacter pylori may play a role as a co-carcinogen in the etiology of this tumor in humans and we have been interested in developing an animal model to study this possibility. A related organism, H. mustelae, naturally colonizes the ferret stomach and causes persistent chronic gastritis. The pathology elicited by H. mustelae in ferrets has many similarities with the human disease including different stages of multifocal atrophic gastritis which underlie the gastric ulcer and gastric carcinoma syndrome. There is little evidence, however, demonstrating the susceptibility of ferrets toward chemical carcinogenesis. We have consequently undertaken a study to ascertain whether 10 6-month-old female ferrets given a single oral dose of MNNG (50-100 mg/kg) would develop adenocarcinoma of the stomach. Five age-matched unmanipulated control animals were included for comparative purposes. All 15 ferrets were infected with H. mustelae. Nine of 10 ferrets dosed with MNNG developed gastric adenocarcinoma (29-55 months after dosing), while none of the five historical control ferrets examined an average of 63 months after the initiation of the study developed gastric tumors. By comparison, we have not observed gastric adenocarcinoma, nor has it been reported, in > 10 years of observation of untreated ferrets naturally infected with H. mustelae. The H. mustelae-infected ferret, with demonstrated susceptibility to a gastric carcinogen, plus the recent availability of specific pathogen-free ferrets, should now allow longitudinal studies in vivo to probe the role of Helicobacter in the development of gastric cancer.
Carcinogenesis 1993 Sep
PMID:MNNG-induced gastric carcinoma in ferrets infected with Helicobacter mustelae. 840 24

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


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