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)

Gastrin and somatostatin-like immunoreactivity (SLI) levels were studied by means of radioimmunoassay in peripheral venous blood of healthy volunteers and patients suffering from gastric adenocarcinoma or duodenal and gastric ulcers. Gastrin and SLI levels were also evaluated in patients in blood drawn from gastric veins during surgery. The elevations of gastrin and SLI levels were found in patients with gastric cancer as compared with healthy people and patients suffering from ulcers. The impairment of the negative feedback between gastrin and somatostatin secretions in patients with gastric cancer was suggested.
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PMID:Gastrin and somatostatin levels in patients with gastric cancer. 256 71

New, powerful gastric secretory inhibitors, such as omeprazole, produce gastric cancer in rats. The mechanism by which the drugs elicit gastric carcinogenesis is considered to depend on the production of therapeutic achlorhydria, with subsequent release in to the circulation of peptides (such as gastrin) which are trophic to the gastric mucosa. It has been argued that the drugs do not pose a carcinogenic risk to man because the neoplastic response to gastric inhibitors in rats is a reaction to a 'toxic' insult; or because rats and humans react differently to the drugs; or because the mechanisms of gastric carcinogenesis are different in the two species. In any case, since most of the powerful gastric secretory inhibitors produce carcinoid tumours in rats, and carcinoid tumours of the human stomach are rare and largely benign, there would be no risk even if the drugs did produce proliferative abnormalities of the human stomach. Not one of the above hypotheses has been confirmed or, indeed, even satisfactorily tested. The mechanisms of the drug-induced gastric carcinogenesis in rats has not been defined and consequently it is not even possible to attempt to guess the risk to man. Until information is available about the effects of the powerful gastric secretory inhibitors on the proliferative indices and patterns of the human gastric mucosa, the drugs must be categorized as too dangerous to use therapeutically, especially since the proposed therapeutic benefits are minimal.
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PMID:Therapeutic achlorhydria and risk of gastric cancer. 268 Jul 46

Antral G and D cells were microscopically counted by the immunoperoxidase method in the resected stomachs of 18 patients with duodenal ulcer (DU group), 4 with recurrent duodenal ulcer after selective proximal vagotomy (SPV-REC group) and 6 with early gastric cancer in the corpus (control group). In DU and SPV-REC groups, preoperative acid secretion stimulated by the tetragastrin (Tg-MAO, Tg-PAO) was examined. In 9 patients of DU and SPV-REC groups, adrenalin stimulated acid secretion (Adr-PAO) and integrated gastrin response (Adr-PGO) were also examined. The G cell count in DU group (Tg-MAO greater than or equal to 20) and SPV-REC group were significantly more than in DU group (Tg-MAO less than 20) and control group. In DU and SPV-REC groups, a significant correlation was observed between Tg-PAO and total G cell count. In 9 DU patients, a significant correlation was observed between the total G cell count and Adr-PGO or Adr-PAO, between Adr-PGO and Adr-PAO or Tg-PAO and between Tg-PAO and Adr-PAO. The above results suggested that increase of antral G cell counts is one of the great cause of duodenal ulcer and recurrent ulcer after SPV, greatly affecting on increase of acid secretion intermediating serum gastrin. Both Tg-PAO and Adr-PAO were regarded as good index of functional G cell mass of the antrum.
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PMID:[Effects of endocrinological function of antrum on acid secretion of parietal cell in patients with duodenal ulcer]. 279 54

This study evaluated the dose-related trophic effects of glutamine, gastrin, and somatostatin on the in vitro growth of human gastric cancer cells and normal human gastric mucosal cells. Quadruplicate cell cultures were seeded into growth medium with or without glutamine, gastrin, or somatostatin. After 72 hours' incubation, cells were counted and their numbers compared with those of controls. Glutamine and gastrin stimulated the growth of both normal and malignant gastric mucosal cells. Compared with normal cells, the malignant cells responded to these growth factors at lower concentrations. Somatostatin enhanced growth of gastric cancer cells at all concentrations and inhibited growth of normal cells at high concentrations. Further studies on the responsiveness of gastric adenocarcinoma to gastrointestinal tract hormones may elucidate mechanisms of oncogenesis and suggest new therapeutic avenues for patients with gastric cancer.
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PMID:Effects of gastrin, glutamine, and somatostatin on the in vitro growth of normal and malignant human gastric mucosal cells. 286 4

Eight patients with stomach cancer are described who had also a striking glandular hyperplasia of the fundic mucosa adjacent and remote from the tumor. Five of the eight patients were young women (30 to 37 years of age). The tumors were poorly differentiated carcinomas and six of the eight patients have died of their disease. None of the patients had clinical evidence of endocrine dysfunction including the Zollinger-Ellison syndrome. Immunohistochemistry revealed cells with endocrine differentiation in five of eight tumors, and in two tumors gastrin producing cells were found. Five of seven patients showed increased numbers of antral G-cells. In two patients numerous endocrine (chromogranin-positive) cells were present in the fundic mucosa, specific products of which could not be identified with the antigens tested. No satisfactory explanation exists for this coincidence and its apparent predominance in young female patients. It may be that endocrine substances are responsible for this fundic hyperplasia and that they may also act as promotors of tumor growth.
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PMID:Coincidence of fundic glandular hyperplasia and carcinoma of the stomach. 291 Apr 42

This study deals with the effect of four types of COOH-terminal cholecystokinin (CCK) fragments on the growth of xenotransplantable human gastric cancer (SC-6-JCK, a poorly differentiated adenocarcinoma) whose growth has been promoted by pentagastrin. The growth of the tumor was inhibited using daily s.c. injections of CCK-octapeptide (CCK-8) and glutaryl-CCK-8 at a dose of 500 micrograms/kg body weight. After 30 days of treatment with CCK-8 or glutaryl-CCK-8, a significant decrease was observed in the tumor weight (P less than 0.05) and the tumor size P less than 0.01) in comparison with those of the control. But treatment with CCK-12 and pyroglutamyl-CCK-8 did not produce inhibition of tumor growth. Furthermore the correlation between the effect of CCK-8 on the normal rise in tumor cyclic adenosine 3':5'-monophosphate (cAMP) levels caused by pentagastrin injection and tumor growth was studied. The increase of cAMP by a single i.p. injection of pentagastrin at a dose of 20 micrograms/mouse was significantly inhibited by pretreatment with CCK-8 at concentrations equimolar to pentagastrin (P less than 0.05), while cAMP in the tumor was slightly elevated by a single i.p. injection of CCK-8 alone. Also in the in vitro study, CCK-8 inhibited the increase of cAMP and the activation of cAMP-dependent protein kinase which was stimulated by pentagastrin. These results suggest that proliferation of gastrin-dependent human gastric cancers may be suppressed by CCK in competition with gastrin.
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PMID:Cholecystokinin inhibition of tumor growth and gastrin-stimulated cyclic adenosine 3':5'-monophosphate metabolism in human gastric carcinoma in nude mice. 300 May 84

The authors tried to clarify relations between autoimmune gastritis and isolated atrophic corpus gastritis by bioptic corporal and antral examinations from 150 probands as well as examinations of gastrin in serum and parietal cell antibody tests. Only 30% of all patients examined with isolated atrophic gastritis of the corpus part revealed criteria of an autoimmune gastritis. Therefore investigations of antibodies against parietal cells are necessary to mark off both clinical pictures. This differentiation seems to be necessary regarding the high risk of gastric cancer following an autoimmune gastritis.
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PMID:[Atrophic corpus gastritis and autoimmune gastritis]. 331 4

The effect of cysteamine (2-aminoethanethiol hydrochloride) on the incidence and histology of gastric adenocarcinomas induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) was investigated in inbred Wistar rats. Prolonged administration of 25 or 50 mg per kg body weight of cysteamine after treatment with MNNG for 25 weeks significantly reduced the incidence and number of adenocarcinomas of the glandular stomach. Histological examination showed that the adenocarcinomas that did develop in rats treated with these 2 doses of cysteamine had high mucin-producing activity. Furthermore, treatment with cysteamine caused significant increases in serum gastrin level and gastric acid secretion, together with significant decreases in the antral mucosal pH and the labelling indices of pyloric and oxyntic gland mucosae and gastric cancer. These findings indicate that cysteamine inhibits the development of gastric adenocarcinomas and that its effect may be related to decreasing proliferation of cells in the gastric mucosae.
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PMID:Inhibitory effect of prolonged administration of cysteamine on experimental carcinogenesis in rat stomach induced by N-methyl-N'-nitro-N-nitrosoguanidine. 334 7

Mucosal atrophy of the gastric antrum (type B atrophic gastritis) is generally accepted as predisposing to the development of the intestinal type of gastric cancer. Since bombesin stimulates gastrin release selectively from the antral mucosa, the response can be used as a marker for antral mucosal atrophy. In this study we have investigated bombesin-stimulated plasma gastrin responses in 21 patients with the intestinal type of gastric cancer and we have compared the results with 12 patients with the diffuse type of gastric cancer, 17 patients with benign gastric ulcer, and 30 dyspeptic patients without endoscopical or histological abnormalities. Gastrin concentrations were also measured in extracts of antral biopsies. Basal plasma gastrin concentrations were not significantly different. In contrast, patients with the intestinal type of gastric cancer had a significantly lower plasma gastrin response to bombesin than did the normal subjects (P less than 0.01) and patients with the diffuse type of gastric cancer (P less than 0.05), but the result was not significantly different from that of the gastric ulcer patients. The antral gastrin content of the patients with the intestinal type of gastric cancer was significantly lower than in controls (P less than 0.005), the patients with the diffuse type of gastric cancer (P less than 0.05), and those with gastric ulcer (P less than 0.05). It is concluded that patients with the intestinal type of gastric cancer have, in contrast to those with the diffuse type of gastric cancer, an abnormally low plasma gastrin response to bombesin. This low response is due to a reduced gastrin content of the antral mucosa.
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PMID:Plasma gastrin responses to bombesin and antral gastrin concentrations in patients with the intestinal type of gastric cancer. 334 93

The effect of ad libitum feeding of a defined diet in liquid form on the incidence of gastric adenocarcinomas induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) was investigated in Wistar rats. Fresh defined diet was supplied once every 24 h from 2 weeks before oral administration of MNNG to the end of the experiment in week 52. Oral administration of the defined diet resulted in significant decrease in the incidence of gastric cancers in experimental week 52. It also caused a significant increase in the incidence of atypical glandular hyperplasia, which is a precursor of gastric cancer. Furthermore, administration of the defined diet for 30 and 52 weeks also resulted in significant decrease in the serum gastrin level and the marked gastric mucosal hypoplasia. These findings indicate that the defined diet in liquid form inhibited the development of gastric cancers and that this effect may have been related to its effect in decreasing proliferation of cells in the antral mucosa.
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PMID:Effect of a defined diet in liquid form on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats. 336 20


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