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)

Basal and stimulated (after a standard meal) serum gastrin was determined by means of the radioimmunoassay method in 27 patients with epigastric pain that could not be diagnosed in the outpatient departement. An individual study of the patients with high (up to 300 pg/ml) basal and stimulated serum gastrin levels showed that most gastroduodenal diseases are situated within this range while levels of 500 pg/ml suggest Zollinger-Ellison syndrome. The test of serum gastrin stimulated with a standard protein-rich meal was proved more valuable than the basal one. Further investigations would be necessary to demonstrate the value of this test in the diagnosis of gastroduodenal ulcer, gastrites or gastric cancer.
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PMID:Radioimmunoassay of serum gastrin in chronic digestive diseases with epigastric pain. 59 18

In patients with gastric cancer who were to undergo gastrectomy, the fasting serum gastrin concentration in the peripheral vein was estimated by radioimmunoassay. The blood samples were also collected from the gastric veins and artery during the time of operations. These gastrin values were compared with morphological findings in the resected stomach. No significant differences in serum gastrin concentration was found between the patients of gastric cancer and normal subjects. In the patients with mucosal atrophy in the oxyntic gland area but with no atrophy in the pyloric gland area, however, significant increase in serum gastrin concentration was observed. In cases where fundal atrophy was accompanied by atrophy in the pyloric gland area, the increase was not observed. The amount of gastrin content in cancer tissue was negligible. These results indicate that the increase in serum gastrin concentration in some patients with gastric cancer might be due to the accompanied atrophy of oxyntic glands in the stomach.
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PMID:Studies on serum gastrin of the patients with gastric cancer. 91 Jul 86

Gastrin is released by food rich in proteins and by vagal mechanisms. HCI and possibly secretin and glucagon inhibit gastrin release. In the wide range of actions of gastrin, stimulation of gastric acid secretion is the most important. With the advent of radioimmunochemical methods for the determination of gastrinaemia, it has been shown that gastrin exists in a number of forms of different molecular weight. To estimate the validity of gastrin radioimmunoassay it is necessary to demonstrate that decrease in antibody-bound labelled antigen is unrelated to non-specific interference by unknown substances present in serum samples, and that the antiserum reacts with endogenous hormone in an identical manner. Heterogeneity of gastrin in serum may affect the validity of the radioimmunoassay. Hypergastrinaemia associated with hyper-normochlorhydria occures in gastrinoma, hyperplasia of antral gastrin cells, diseases with delayed gastric emptying, retained antrum, short bowel syndrome,renal failure. Hypergastrinaemia associated with hypo-achlorhydria occurs in atrophic gastritis without extensive antral lesion and after vagotomy. Gastrin radioimmunoassay can be used for the mass screening of subjects with atrophic gastritis, a high risk group for gastric cancer.
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PMID:[Gastrin]. 123 74

Patients with late-onset hypogammaglobulinaemia have a very high risk of developing gastric cancer. In such patients there is a high frequency of atrophy of the gastric mucosa. This is reflected in low gastrin content of the antral mucosa, low serum pepsinogen A level and pepsinogen A/C ratio, and reduced serum gastrin secretion in response to bombesin stimulation. There is no evidence to support a role of Helicobacter pylori infection in the aetiopathology of these gastric abnormalities, although prior infection cannot be excluded with certainty. Since patients with early-onset hypogammaglobulinaemia and X-linked agammaglobulinaemia do not show this increased frequency of gastric abnormalities, it is unlikely that the immunoglobulin deficiency per se is responsible for the development of the gastric abnormalities found in patients with late-onset hypogammaglobulinaemia. Because of the very high risk of gastric cancer, regular endoscopic screening is warranted in patients with late-onset hypogammaglobulinaemia.
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PMID:Gastric abnormalities in humoral immune deficiency syndromes. 129 45

Hypergastrinemia is a very important clinical condition for the reason that a growing body of evidence obtained from animal and human experiments has revealed gastric carcinoids induced by hypergastrinemia. We investigated 35 patients with Basedow's disease (BD) to elucidate the mechanism of hypergastrinemia associated with BD as well as the relationship between type A gastritis and BD. Fasting serum gastrin levels in BD (296.1 +/- 251.4 pg/ml; mean +/- S.D.) were significantly (p less than 0.001) higher than those in age-matched 27 healthy subjects (106.1 +/- 69.2), and in the BD group, significant positive correlation was detected between fasting serum gastrin levels and thyroid hormones (i.e. T3 and free T4). In the hyperchlorhydria group in BD with hypergastrinemia, the levels of fasting serum gastrin were normalized after euthyroidism was attained due to antithyroidal drugs. On the other hand, in the achlorhydria group in BD significant hypergastrinemia was persisted in spite of normalization of thyroid function. Twenty % of the BD patients had histologically proved type A gastritis with achlorhydria, and all patients with type A gastritis were older than 60 years old. Endoscopic examination revealed that one patient with type A gastritis had an early gastric cancer. However, no gastric carcinoids were demonstrated in this study. In conclusion, the results described as above suggested, 1) hypergastrinemia observed in patients with BD may be induced by gastrin hypersecretion due to hyperthyroidism as well as type A gastritis, 2) BD patients with type A gastritis were recommended to undertake regular endoscopic examination for detecting gastric cancers as well as gastric carcinoids.
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PMID:[Hypergastrinemia and type A gastritis in Basedow's disease]. 140 86

Today the upper gastrointestinal endoscopy is the diagnostic tool of choice to detect peptic gastroduodenal lesions. In case of substantial gastric outlet obstruction or strong suspicion of perforated ulcer, an upper gi-transit with barium or water soluble contrast medium in suspected perforated ulcers may be useful. Gastric ulcers are endoscopically controlled up to their complete healing and biopsies taken at each endoscopy in order to rule out gastric cancer. In contrast, duodenal ulcers are rarely malignant and uncomplicated duodenal ulcers, correctly treated with omeprazole over 8 weeks do not necessarily need a final endoscopic control. Since about 5% of duodenal ulcers treated with H2 blockers or mucosal protective agents do not heal within 8 weeks however, an endoscopic control of the healing is recommended. In peptic ulcer patients tests for detection of helicobacter pylori are only needed in presence of a hard indication for immediate eradication: Frequent ulcer recurrencies, complicated ulcer disease or very painful ulcer relapses, because the eradication therapy is often not well tolerated and the patient compliance therefore compromised. 30% of helicobacter infected patients have antibiotic resistant strains and there is no sufficient longterm experience with the eradication therapy available (4) to 8 weeks after treatment of the helicobacter pylori infection the effect on ulcer healing and infection should be verified. Determinations of plasma gastrin levels in peptic ulcer patients are mandatory in patients with suspected Zollinger-Ellison syndrome or patients with treatment resistant ulcers or recurrent ulcers after vagotomy or partial gastric resection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diagnosis of peptic ulcer disease]. 147 69

Gastrin is known as a trophic factor for some stomach and colorectal cancer cells; however, the roles of gastrin receptors and the intracellular signal transduction pathways by which gastrin regulates cell growth are still unknown. The authors examined the effect of synthetic human gastrin-17 on growth of human stomach cancer cells (the parent line, AGS-P, and two different clones, AGS-10 and AGS-12), which were established (and have been maintained) in our laboratory. Gastrin stimulated growth of AGS-P and AGS-10 cells, which have gastrin receptors, in a dose-dependent fashion. A highly selective gastrin receptor antagonist, JMV 320, inhibited the growth-stimulatory effect of gastrin on AGS-P cells in a dose-dependent fashion. Concentrations of gastrin (10(-8) to 10(-6) M), which stimulated growth of AGS-P cells, did not affect either cyclic adenosine monophosphate production or phosphatidylinositol hydrolysis. Gastrin (10(-11) to 10(-5) M) mobilized calcium from the intracellular organelles to increases intracellular calcium level in AGS-P cells. The AGS-12 clone has no gastrin receptors, and gastrin did not affect growth or mobilization of intracellular calcium in these cells. Our findings indicate that gastrin stimulates growth of AGS cells through a mechanism that involves binding to specific gastrin receptors that are linked to the system for mobilization of intracellular calcium.
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PMID:The effect of gastrin on growth of human stomach cancer cells. 161 89

After proton pump inhibitors (omeprazole) became available, discussions about safety aspects of (particularly long-term) inhibition of gastric acid secretion have been renewed. In contrast to animals, hypergastrinaemia does not seem to be a relevant problem in man: marginal increases of serum gastrin during proton pump inhibition may induce proliferation of gastric endocrine ("enterochromaffin-like"; ECL-) cells in some cases which are without clinical importance, the risk for development of gastric carcinoids seems negligible if existent at all. Other aspects of acid inhibition (e.g. protein malabsorption, diminished iron and cobalamin absorption, bacterial overgrowth of the stomach, risk of gastric cancer) do also not appear to be of clinical relevance. However, data from larger numbers of patients on long-term therapy with proton pump inhibitors should be available until such treatment can be generally recommended.
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PMID:[Reduction of gastric acid secretion: pathophysiologic and clinically relevant sequelae]. 168 86

Gastrin may play a role in gastric carcinogenesis, as indicated by an increased frequency of gastric carcinomas in patients with pernicious anaemia and the fact some human gastric cancer cell lines carry the gastrin receptor. Recently, it has been shown that the acid-stimulatory effect of gastrin may be solely mediated by histamine release from the enterochromaffin-like (ECL) cell, on which gastrin has a specific trophic effect. We therefore found it of interest to examine human gastric carcinomas for the presence of ECL tumour cells by using silver staining and chromogranin immunohistochemistry. We found evidence of ECL cell-derived tumour cells in 40% of the diffuse gastric carcinomas but no such tumour cells in the intestinal type of gastric carcinoma. This may suggest that diffuse gastric carcinomas, like malignant gastric tumours of the mastomys, are in fact malignant ECLomas.
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PMID:Enterochromaffin-like tumour cells in the diffuse but not the intestinal type of gastric carcinomas. 171 Mar 71

Although cell proliferation studies on gastric mucosa are relatively few compared to the results obtained in the large bowel, they brought important contributions to our knowledge of the mechanisms involved in the development and progression of neoplasia. In normal gastric mucosa, the proliferative zone is limited to the neck region of the glands. In diseases at risk for gastric cancer, such as chronic atrophic gastritis, two main features have been observed: an increased cell proliferation rate and expansion or upward displacement of the proliferative compartment. However, while a high cell turnover rate can be due to many stimuli such as inflammation or the effect of hormones (i. e. gastrin), the expansion of the proliferative compartment is more evident with the development and progression of neoplasia. It could be due to an error in the control of cell proliferation and maturation. This kinetic pattern is probably a marker of gastric cancer risk. Application of these observations in clinical investigations are the search for proliferative abnormalities and other phenotypical markers in order to define an individual profile of cancer risk, and to evaluate the effects of xenobiotics or dietary intervention in controlled trials.
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PMID:Cell proliferation kinetics as a marker of gastric cancer risk. 174 97


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