Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

In view of the trophic action of gastrointestinal hormones on the exocrine pancreas, the effects of secretin, octapeptide of cholecystokinin (CCK-8), and desglugastrin on the growth of hamster pancreatic well differentiated adenocarcinoma were investigated in vitro. Desglugastrin exhibited the greatest effect on thymidine incorporation into these cells after a lag period of 96 h. Doses of desglugastrin in the range from 30 to 270 ng/mL caused a significant and dose-dependent increase in thymidine incorporation. Higher doses of this peptide led to a decreased response. Secretin also increased thymidine incorporation, but the response was less than that induced by gastrin. Prolonged incubation with secretin for 96 h increased tritiated thymidine incorporation in a log-dose fashion in the range of 30 to 270 ng/mL. Doses of CCK-8 in the range of 90 to 810 ng/mL significantly increased thymidine incorporation after 48 h of incubation. Following 72 h of incubation, only the dose of 270 ng/mL continued to exhibit a significant stimulation. Our study suggests that the gastrointestinal hormones could directly increase the growth of pancreatic carcinoma cells, act synergistically with endogenous growth factors, or stimulate the local production of these factors. In any event, our results that gastrin, secretin, and CCK can stimulate the growth of pancreatic ductal tumor cells in tissue cultures, support earlier findings on normal and malignant pancreatic parenchyma.
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PMID:The effect of gastrointestinal hormones on the incorporation of tritiated thymidine in the pancreatic adenocarcinoma cell line (WD PaCa). 260 Apr 53

A 7-year-old spayed female Cocker Spaniel was hospitalized with a history of chronic vomiting, anorexia, and weight loss. Laboratory abnormalities included leukocytosis, metabolic alkalosis, hypoglycemia, hypoproteinemia, and hyperinsulinemia. Gastroscopy and ultrasonography revealed multiple gastric masses and a possible pancreatic mass, respectively. Examination of tissues obtained at necropsy showed a pancreatic adenocarcinoma with hepatic metastasis, gastric hypertrophy, and multiple duodenal ulcers. Immunocytochemical staining of the neoplasia was positive for pancreatic polypeptide (PP) and insulin and negative for gastrin, calcitonin, adrenocorticotropic hormone (ACTH), serotonin, L-enkephalin, chromagranin, glucagon, and somatostatin. Subsequent serum gastrin and PP assays showed a fasting hypergastrinemia with a normal response of gastrin to provocative testing and extremely increased PP values. The high PP values may have resulted in the vomiting and gastrointestinal ulceration. A PP-secreting tumor has not previously been reported in the dog.
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PMID:Pancreatic polypeptide and insulin-secreting tumor in a dog with duodenal ulcers and hypertrophic gastritis. 267 25

A case of multiple gastric carcinoids and nonantral atrophic gastritis in which the larger tumor was a composite carcinoid-adenocarcinoma is presented. The two components of the composite tumor immunohistochemically showed clear-cut diverging functional differentiations although the available evidence supported a common histogenesis from the metaplastic intestinal epithelium of the gastric mucosa. The carcinoid tissue of the composite tumor, which showed "atypical" features, also differed from the other, pure carcinoids, in which the histologic appearance was "typical." Total gastrectomy performed 1 month after the original gastric resection with antrectomy disclosed regressive changes in the endocrine cell proliferations of the gastric stump consistent with the withdrawal of a stimulating effect of the antral gastrin.
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PMID:Composite carcinoid-adenocarcinoma of the stomach associated with multiple gastric carcinoids and nonantral gastric atrophy. 277 13

Bombesin, a 14-amino acid peptide, exhibits direct and indirect effects on the gastrointestinal tract, including release of hormones, stimulation of pancreatic, gastric, and intestinal secretion and intestinal motility. Cholecystokinin (CCK) and gastrin, two of the hormones released by bombesin, have been shown to play a role in maintaining the growth of normal gastrointestinal mucosa as well as in eliciting trophic responses in normal and neoplastic tissue. We studied the effects of chronic bombesin treatment on the growth of a human ductal pancreatic adenocarcinoma (SKI) xenografted into nude mice, and on the growth of the normal nude mouse pancreas. Thirteen nude mice were implanted with SKI tumor and divided into two groups. Mice received 0.1 ml intraperitoneal injections of either bombesin (20 micrograms/kg) or the vehicle alone three times per day. Tumor areas were measured twice weekly until death (week 8), at which time the tumors and the host pancreas were excised, weighed, and assayed for protein, RNA, and DNA content. Significant inhibition of tumor growth was found in the bombesin-treated group at weeks 4, 5, 6, 7, and 8. Tumor area and weight at death (day 57) were significantly less in the bombesin-treated group (48 and 46%) as compared with control. We observed similar inhibition of tumor DNA (39%), RNA (38%), and protein (43%) content compared with controls. In contrast, bombesin significantly increased the weight (64%), protein (81%), and DNA (73%) content of the mouse pancreas compared with controls. We conclude that bombesin acts concurrently as both a trophic agent for normal host pancreas and a growth inhibitory agent in xenografted pancreatic cancer tissue.
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PMID:Bombesin inhibits growth of human pancreatic adenocarcinoma in nude mice. 283 42

The importance of distinguishing between malignant islet cell tumour and pancreatic carcinoma is emphasized in this report of a 57-year-old woman who presented with an epigastric mass. Clinically and radiologically it was diagnosed as a pancreatic adenocarcinoma. A fine-needle aspiration biopsy specimen obtained under ultrasonic guidance showed tumour cells suggestive of an islet cell tumour. Immunostaining and electron microscopy were performed on the aspirate. The tumour cells stained positive with antibodies to keratin, glucagon and gastrin; ultrastructural examination revealed neurosecretory granules, confirming the diagnosis of an islet cell tumour. Angiography was performed to assess the possibility of debulking the mass. This case demonstrates the value of immunohistochemistry and electron microscopy on fine-needle aspiration biopsy specimens of the pancreas to differentiate islet cell tumours, which are potentially curable, from pancreatic adenocarcinomas, which carry a 5-year survival rate of less than 2%.
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PMID:Fine-needle aspiration biopsy of an islet cell tumour simulating pancreatic carcinoma. 284 41

A case of primary adenocarcinoma of the urinary bladder occurring in a patient with type 1 multiple endocrine adenomatosis (MEA) is presented. The patient was a 36-year-old female who had a past history of type 1 multiple endocrine adenomatosis, namely, adenomatosis of the parathyroid gland, insulin and gastrin-producing adenomatosis of the pancreas, and prolactin-producing pituitary adenoma. She was admitted in January 1981 with the complaints of gross hematuria, pollakisuria and micturition pain lasting for about one year and a half. Cystoscopic examination revealed four solid tumors in the posterior and left lateral walls of the bladder with diffuse mucosal hyperemia. Biopsy of the tumors disclosed that they were adenocarcinoma. Clinical examinations revealed that there was no extravesical primary malignant neoplasm in this case. Radical cystectomy with urinary diversion by ileal conduit was performed on January 22, 1981. Histological examination revealed that the tumor was adenocarcinoma originating from the vesical mucosa. Follow-up for over three years since the time of surgery has not shown any sign of tumor recurrence or occurrence of extravesical malignant neoplasm. In addition, 28 cases of primary adenocarcinoma of urinary bladder in Japan reported during the last 25 years are reviewed and analyzed.
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PMID:[A case of primary adenocarcinoma of the urinary bladder occurring in a patient with type 1 multiple endocrine adenomatosis (MEA)]. 286 84

The effect of hydrochlorhydria caused by vagotomy on carcinogenesis in the glandular stomach of male rats was studied. Group A (35 rats): After N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) 80 mg/l solution was orally administered during the first 15 weeks of life, vagotomy was performed. Group B (35 rats): After the oral administration of MNNG 80 mg/l solution during the first 15 weeks of life, laparotomy was done. Group C (10 rats): As the control, vagotomy was undertaken at the 15th week of life. Group D (10 rats): As the control, laparotomy was done at the same time. At the 52nd week, all surviving rats were autopsied, and gastrin cell counts and body weight were ascertained. The incidence of adenocarcinoma was 62% in Group A, 32% in Group B (p less than 0.05) and nil in Group C and D. These results strongly support the view that the hypochlorhydria plays the role of a promoting factor in producing gastric carcinoma.
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PMID:[The effect of vagotomy on carcinogenesis in the glandular stomach of rats, induced by N-methyl-N'-nitro-N-nitrosoguanidine]. 286 62

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


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