Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Being pepsinogen A (PGA) levels generally reduced and pepsinogen C (PGC) increased in gastric cancer patients, PGA/PGC ratio has been proposed as a useful marker of the tumour. We tested PGA, PGC and Gastrin (G) levels in patients with gastric cancer (39) and, as a control, in patients with epithelial dysplasia (21), chronic atrophic gastritis (57), gastric ulcer (11) or subjects lacking major or minor endoscopic and microscopic changes at gastroscopy (48). PGA and PGA/PGC levels were significantly reduced in gastric cancer patients (p less than 0.005 and p less than 0.0001 respectively with analysis of variance). Gastrin levels were also reduced in the same patients (p less than 0.005). We therefore adopted an index number (PGA x Gastrin) which was also dramatically reduced in gastric cancer (p less than 0.005); using an arbitrarily chosen cut-off, the "marker" showed very high sensitivity (76%), specificity (96%) and overall accuracy (74%, by Youden J test). We therefore suggest the use of the index number PGA x G in the diagnosis of gastric cancer, as the most useful gastrin presently available, to our knowledge.
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PMID:Pepsinogen A/pepsinogen C or pepsinogen A multiplied by gastrin in the diagnosis of gastric cancer? 175 13

A study on DNA ploidy by flow cytometry was carried out on human gastric tissues with normal mucosa, chronic atrophic gastritis, varying grades of gastric dysplasia or early carcinoma. The results showed that no DNA aneuploidy was found in all 8 cases with normal mucosa, 13 cases with chronic atrophic gastritis, and 18 cases with grade I gastric dysplasia. DNA aneuploidy was found in 2 among 19 cases with grade II gastric dysplasia, in 8 among 14 cases with grade III gastric dysplasia, and in all 12 cases with early gastric cancer. There was significant differences in DNA index and S% phase cells from cases with gastric dysplasia of varying grades. The findings indicate that DNA aneuploidy might be a marker of malignant change of gastric precancerous lesions.
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PMID:[DNA ploidy in gastric precancerous lesions]. 178 53

To assess the evolution of gastric epithelial dysplasia (GED), a prospective multicenter study was based on a protocol of repeated endoscopies and biopsies. To date, 134 cases (0.4% of all patients endoscopically examined in the same period) have been diagnosed as having GED and 80 of those have had an "adequate" follow-up (at least three endoscopies). Mean follow-up time was 18 months. Gastric epithelial dysplasia was mild in 59% of cases, moderate in 25%, and severe in 10%. Six percent of the patients had lesions that were "indefinite for dysplasia." Chronic atrophic gastritis (40%), gastric ulcer (32%), gastrectomy (10%), and polyps (9%) were the most frequently associated lesions. The term "regression" was adopted for GED no longer detectable during follow-up and the term "progression" was used when more severe changes or cancer was detected. Mild GED regressed in 66% of cases, persisted in 15%, and progressed in 19% (three cases to moderate, one to severe, and five to cancer). Moderate GED regressed in 30% of patients, persisted in 30%, and progressed in 40% (one to severe GED and seven to cancer). Severe GED regressed in 12.5% of patients, persisted in 12.5%, and progressed to cancer in 75%. Of the five patients with lesions indefinite for dysplasia, two had no dysplastic changes at follow-up and three had cancer diagnosed. Ten of 21 cases of cancer (48%) were at the early stage. The diagnosis was reached within the first year of follow-up in 14 cases and after 1 year in seven (13 to 39 months). Fifteen of 21 cases of cancer were diagnosed in gastric ulcer patients. In conclusion, GED is an infrequent finding and its biologically neoplastic significance is confirmed by the results of the follow-up study: (1) in its mild form, it tends to regress but adequate subsequent check-ups are mandatory as it may associate with or evolve as cancer; (2) patients with moderate GED require strict follow-up since the lesion shows a higher cancer risk; (3) surgery is indicated for severe GED because gastric cancer develops in 75% of cases; and (4) patients with lesions indefinite for dysplasia should immediately undergo repeat endoscopy and biopsy. Such an approach allows gastric cancer to be detected at an early stage in a much higher percentage of cases than may be expected.
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PMID:Gastric epithelial dysplasia: a prospective multicenter follow-up study from the Interdisciplinary Group on Gastric Epithelial Dysplasia. 184 72

Although gastric cancer is the most common cause of mortality from cancer, its etiology is not yet clear. To elucidate the role of N-nitroso compounds, we investigated 30 cases of gastric cancer by determination of the contents of nitrate and ascorbic acid and by detection of mutagens in urine. Cases were paired 1:1 with patients with dysplasia and normal controls of the same sex and age group. In comparison with normal controls, the gastric cancer group had higher nitrate and lower ascorbic acid levels in urine. Mutagenicity was observed in the urines of 83.3% of the gastric cancer cases and in 16.6% of the dysplasia group, but in none of those from normal controls. When the N-nitroso compound content of gastric juice was determined, the levels in control subjects were significantly lower than those in persons with gastric cancer. These results support the hypothesis that the cause of gastric cancer may be N-nitroso compounds.
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PMID:An approach to establishing N-nitroso compounds as the cause of gastric cancer. 185 38

Gastric cancer is the leading cause of death from cancer in China. Samples of fish sauce, a traditional seasoning, were collected in the high-risk area for gastric cancer in the Fuzhou area, Fujian Province. When fish sauce samples were nitrosated at pH 2.0, direct mutagenicity and high contents of N-nitrosamide were detected (30.9-78.0 microM); the N-nitrosamide content of three samples of fish sauce made in Guangdong and purchased from a market outside Fujian were low (2.1-6.0 microns). When the nitrosated fish sauce extract was given to newborn rats by gavage, dysplasia and adenocarcinoma were induced in the glandular stomach in the 4th and 16th experimental week, respectively. N-Nitrosamides were also found in fasting gastric juice from patients with chronic gastritis in the high-risk area of Putian. The mean concentration of total N-nitrosamides in the extracts correlated with the severity of gastritis in the stomach. These findings indicate that N-nitrosamides may play an important role in causing gastric cancer in China.
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PMID:Role of nitrosamides in the high risk for gastric cancer in China. 185 40

Research over the past several years in an area of Shandong, China, with one of the world's highest rates of gastric cancer, has yielded clues to the environmental determinants of this tumour. Interviews with 564 gastric cancer patients and 1131 population-based controls revealed increased risks associated with consumption of sour pancakes, a fermented staple unique to the area, in samples of which volatile N-nitrosamines have been detected. Lower risks were found among people who had a higher intake of fresh vegetables, including garlic and other Allium vegetables which contain constituents that can inhibit carcinogenesis by N-nitrosamines and other substances in experimental animals. A pilot study involving assays of urine and gastric juice from 60 individuals in a screening programme showed higher levels of N-nitrosoproline and of cis- and trans-N-nitroso-2-methylthiazolidine 4-carboxylic acid among persons with gastric dysplasia than in either normal controls or those with chronic atrophic gastritis. We are trying to characterize the transition and progression of precursor lesions to gastric cancer and to evaluate the role of dietary variables, nutrients, N-nitroso compounds and other factors in particular stages of the carcinogenic process.
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PMID:Etiological research on gastric cancer and its precursor lesions in Shandong, China. 185 74

Evidence is presented suggesting that infection by Helicobacter pylori triggers and continuously contributes to the pathophysiology of progressive gastric changes that can ultimately lead to gastric cancer. In Peru, especially in population groups of low socioeconomic status, infection by H. pylori begins earlier in life and is more prevalent and persistent than in developed countries. The infection produces a destructive lesion of the mucinous surface epithelium which probably enables other aggressive luminal factors to cause further mucosal damage. As a consequence, active chronic gastritis appears. The gastritis is of the superficial type at the beginning but may progressively change to atrophic. Chronic atrophic gastritis is found more frequently and at a younger age in dyspeptic patients with low socioeconomic status--that is, in patients having higher prevalence of persistent infection by H. pylori since earlier in life. When chronic atrophic gastritis becomes severe and extensive, hypochlorhydria ensues. Hypochlorhydria favors the appearance of bacterial overgrowth, nitrites, and N-nitroso compounds in the gastric lumen. N-nitroso compounds, because of their mutagenic-carcinogenic properties, probably induce gastric premalignant lesions like intestinal metaplasia and dysplasia of the gastric mucosa. Oral bismuth therapy apparently reverses H. pylori-associated gastric dysplasia. It is proposed that future programs designed for the control of gastric cancer would be incomplete if they do not include further evaluation of the many effects of infection by H. pylori on the gastric mucosa and of cost-effective methods to eradicate the infection.
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PMID:Helicobacter pylori and progressive gastric pathology that predisposes to gastric cancer. 186 95

Endoscopic and pathologic examinations were conducted in a randomly chosen population in a high risk area of gastric cancer, Linqu County, Shandong Province. A high prevalence of chronic atrophic gastritis, intestinal metaplasia and dysplasia was found. Gastric mucosal lesions changed from mild to severe with a decline in transition rate. The prevalence rate of severe dysplasia was close to that of gastric cancer. The study indicates that gastric precancerous lesions are related to malignant changes implying that gastric cancer develops on the damaged gastric mucosa. It is also shown that the progression from chronic atrophic gastritis to dysplasia may take an average of 20 years.
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PMID:[Gastric mucosal lesions and their transition rates in high risk population of gastric cancer]. 187 85

We analyzed 850 gastric biopsy specimens: 643 were obtained from patients with gastric symptoms, and 207 from apparently normal individuals. We evaluated the incidence of precancerous lesions (PL) of the stomach (chronic atrophic gastritis, intestinal metaplasia and gastric dysplasia) in both groups of patients (symptomatic and assymptomatic). We also studied the relationship between these lesions and diverse clinical and morphological parameters (age, sex, location and endoscopic findings). Our results indicate a higher incidence than expected of PL in an area of low risk of the gastric cancer, both in symptomatic patients (CAG: 65%, IM: 50% and GD: 23%) and in the normal population (CAG: 24%, IM: 17.4% and GD: 2%). These lesions were preferentially located in the antral region and the antro-corporal transitional zone. The incidence of the PL was highest in patients 50 and 60 years of age. These parameters should be considered as risk factors in the development of a gastric carcinoma of the intestinal type.
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PMID:[Precancerous lesions of gastric cancer (I): incidence in 2 population groups: symptomatic and asymptomatic]. 191 Sep 17

We studied a group of gastric precancerous lesions in order to analyze their mutual relationship as well as and their association with the development of gastric carcinoma of the intestinal type. This study was performed on 850 gastric biopsy specimens. Our results demonstrate the strong association of atrophic gastritis, intestinal metaplasia and gastric dysplasia (p less than 0.001) which should be considered as precursor lesions of gastric cancer. Moreover, the relations between these lesions and the intestinal type of gastric carcinoma suggest their active participation in the genesis of this type of malignancy. Our results also suggest that chronic atrophic gastritis and intestinal metaplasia evolve to the dysplasia stage before developing gastric cancer.
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PMID:[Precancerous conditions in gastric cancer (II): relationship between atrophic gastritis-intestinal metaplasia-gastric dysplasia-gastric carcinoma]. 193 Dec 40


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