Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An assessment of treatment methods for the Zollinger-Ellison syndrome over 25 years suggests that the dual surgical approach of excision of resectable tumor and total gastrectomy provides the greatest possibility of attaining tumor and serum gastrin control. Normal serum gastrin levels and reduction of tumor status, not observed with nonoperative management, were attained by surgical treatment, particularly when the tumor (or hyperplasia) was limited to the pancreas, stomach, duodenum and regional lymph nodes. Eleven of 16 such operations resulted in tumor control, and 10 of these patients developed normal serum gastrin concentrations. In elective clinical situations combined medical and surgical therapy is a rational approach allowing confirmation of diagnosis and safe, definitive surgical control of the syndrome before metastases occur.
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PMID:Treatment of the Zollinger-Ellison syndrome. A 25 year assessment. 646 Dec 68

A method for measurement of gastrin in human antral mucosa or in extragastric tissue has been developed and validated. Tissue gastrin was extracted by boiling followed by homogenization at neutral pH. Extractable gastrin immunoreactivity was measured by radioimmunoassay using an antiserum with equal affinity towards G-17 I, G-17 II, G-34 I and G-34 II molecular forms. Almost all extractable gastrin immunoreactivity was recovered after a single extraction and no significant interference by other peptides and/or substances present in tissue was found. The mean gastrin concentration in antral mucosa of healthy subjects was similar to that observed in duodenal ulcer patients, while patients with type A chronic atrophic gastritis or with antral gastrin cell hyperplasia had mean values significantly higher. Gastrin concentration in all specimens from gastrinoma or its metastases was above the upper limit of the range of control tissue. Measurement of tissue gastrin seems to be a valuable tool in the diagnosis of antral gastrin cell hyperplasia and Zollinger-Ellison syndrome.
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PMID:Measurement of immunoreactive gastrin in tissue. 650 40

Gastric endoscopy of a 40 year old woman suffering from ill-defined epigastralgy revealed a carcinoid tumor apparently located at the mucous membrane. The tumor was neither argyrophil nor argentaffin. Immunohistochemical tests for VIP, gastrin and serotonin were negative. Biological examinations indicated hypochrome anemia and hypergastrinemia (greater than 800 pg/ml). The excision was completed by a gastrectomy of 2/3 with a Pean anastomosis. No residual tumor was detected but the fundic mucous membrane showed considerable atrophic gastritis together with a marked hyperplasia of endocrine cells giving an aspect of microcarcinoidosis. Immunohistochemical studies showed that most of the cells produced serotonin while a few cells produced gastrin or VIP. Control biopsies of the stump showed similar hyperplasia of the endocrine cells and ultrastructural studies confirmed the polymorphism of the islets. The present observation is compared to analogous cases cited in the literature. The pathogenic mechanism possibly linked to the capacity of gastrin in stimulating endocrine cells is discussed. The prognosis in these carcinoid tumors appears to be the same as in other gastric carcinoid tumors. In particular, a recent observation (Goldman et al., 1981) illustrated their aptitude to lead to metastases.
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PMID:[Chronic atrophic gastritis with carcinoid tumor and microcarcinoidosis. Report of a case with immunohistochemistry and ultrastructure study]. 662 98

A series of 156 patients with gastrointestinal carcinoid tumors is presented. The tumors were grouped as foregut, midgut and hindgut carcinoids. The appendiceal tumors were grouped separately. Lack of specific symptoms resulted in only 26% correct presumptive diagnoses. This also reflected the patient's delay greater than 2 years in 10% and doctor's delay greater than 2 years in 29%. In the larger group (midgut), 41% were multiple primary tumors. Liver metastases were found in 46% and tumors bigger than 1 cm metastasized to the liver in 58%. The five-year survival of patients with liver metastases was 43% while the figure for those without metastases was 80%. In 47 patients with appendiceal carcinoids, 68% had tumors less than 1 cm. No metastases to the regional lymph nodes, viscera or skeleton were found. Thirty-three patients were traced and none had died of the tumor. Two foregut and 4 hindgut tumors were re-examined using immunocytochemistry. In one of the foregut tumors, cells containing serotonin were found while the other one contained gastrin cells. In 3 hindgut tumors PP-cells were seen and one of them also harbored glucagon/glicentin cells. In one hindgut tumor no peptides were found.
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PMID:Carcinoid tumors in the gastrointestinal tract--an analysis of 156 cases. 665 73

In a patient with Zollinger-Ellison syndrome, control of the peptic ulcer diathesis was attempted by excision of a small duodenal gastrinoma and removal of three lymph nodes containing metastases. The patient has been asymptomatic for 2.5 years with basal achlorhydria, a normal serum gastrin level and a negative gastrin response to secretin. Our experience with this patient emphasizes the fact that the presence of metastatic disease does not preclude the possibility of long-term control of hypergastrinemia by resection of the tumor. Attempts to cure the Zollinger-Ellison syndrome by tumor resection alone, however, should only be made in patients whose hypersecretion is adequately controlled by antisecretory drugs.
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PMID:Control of the Zollinger-Ellison syndrome by excision of primary and metastatic tumor. 670 15

We determined the relative concentrations of gastrin molecular species in serum samples from 21 patients with Zollinger-Ellison syndrome with localized gastrinoma (n = 11) or gastrinoma with hepatic metastases (n = 10). Gastrin molecular species were separated by gel-filtration chromatography and quantitated by radioimmunoassay with a gastrin antiserum produced in our laboratory. The percentage gastrin-17 of the total gastrin in the two groups differed significantly (nonparametric Wilcoxon rank test; p less than 0.01). Patients with the Zollinger-Ellison syndrome with apparently localized gastrinoma had a lower percentage of G- 17 (7.6%, SEM 1.6%) than did patients with gastrinoma with hepatic metastases (31.1%, SEM 6.1%). This procedure may be useful in the early classification of tumors in patients with Zollinger-Ellison syndrome.
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PMID:Serum gastrins in Zollinger-Ellison syndrome: identification of localized disease. 737 8

Prior to total gastrectomy, serum levels of gastrin and human chorionic gonadotropin (HCG) and its alpha- and beta-subunits (alpha-HCG and beta-HCG) were determined by radioimmunoassays in 40 patients with the Zollinger-Ellison syndrome. Basal serum gastrin levels greater than 1,500 pg/mL were found only in patients with metastases to lymph nodes or liver, while levels greater than 8,000 indicated massive liver replacement by tumor. Gastrin levels less than 1,500 pg/mL had no correlation with malignant behavior. Neither the calcium-infusion nor secretin-injection test was useful in identifying tumors as benign or malignant. Basal serum levels of alpha-HCG were elevated (> 7 ng/mL) in four of 20 patients with metastatic gastrinoma and were normal in all 16 patients with benign disease. There was a significant correlation between basal gastrin and alpha-HCG levels in patients with malignant gastrinoma but not for those with benign tumors. The results suggest that serum gastrin and alpha-HCG levels can be useful in assessing the biologic behavior of gastrinomas and in planning appropriate surgical and nonsurgical treatment.
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PMID:Serum gastrin and human chorionic gonadotropin in the Zollinger-Ellison syndrome. 741 55

Among endocrine tumors arising in the intestinal tract, midgut argentaffin EC cell carcinoids, duodenal gastrin cell tumors and rectal trabecular L cell carcinoids, in order of decreasing frequency, are those better represented. Together they account for more than 80% of such tumors. Duodenal somatostatin cell tumors, gangliocytic paragangliomas and poorly differentiated neuroendocrine carcinomas, are also well defined tumor entities. The carcinoid syndrome with intermittent flushing, hypotension and diarrhea, and the Zollinger-Ellison syndrome with severe peptic ulcer disease, are the only hyperfunctional syndromes consistently found in association with these tumors. The carcinoid syndrome arises in about 10% of intestinal carcinoids, usually in their advanced metastatic stage. The Zollinger-Ellison syndrome occurs in association with about 40% of gastrin cell tumors, including small intramural growths. Tumor prognosis depends on mode and site of presentation, histology, cell type(s), size, level of invasion, metastases (especially distant metastases) and associated clinical syndrome or background disease.
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PMID:Endocrine tumors of the small and large intestine. 747 53

Endocrine pancreatic tumors are neuroendocrine neoplasms with malignant potential and give rise to varied clinical syndromes due to excessive secretion of multiple hormones. In this study 22 endocrine pancreatic tumors and 11 carcinoid tumors were examined for the expression of CD44 using a monoclonal antibody. CD44 gene activity of 11 endocrine pancreatic tumor tissues and five carcinoid tumor tissues was also studied by amplifying messenger RNA with the polymerase chain reaction followed by electrophoresis and blot hybridization. Strong immunoreactivity was detected on all gastrinomas examined (P < 0.001), and in two non-functioning endocrine pancreatic tumors. Such immunoreactivity was not observed in other subtypes of endocrine pancreatic tumors. In the normal human pancreas, the acinar portion and ductal epithelial cells stained strongly positive but pancreatic islet cells did not show any significant immunostaining. Furthermore, in endocrine pancreatic tumors with metastatic disease, CD44-positive tumors had a tendency to metastasize to lymph nodes (P = 0.005), as compared with CD44-negative tumors which were locally invasive or metastasized to the liver. Although, in this limited material and short follow-up, we were not able to show any statistical significance, patients with CD44-negative endocrine pancreatic tumors had prolonged survival time compared with patients with CD44-positive tumors (73% versus 59% at 5 years; P = 0.7). Of 10 carcinoid tumors examined, all three foregut carcinoids and one midgut carcinoid stained strongly positive, whereas all other midgut carcinoids were negative. Analysis of CD44 splice variants showed that in all five gastrinomas there was overproduction of alternatively spliced larger molecular variants as compared with other types of endocrine pancreatic tumors and carcinoid tumors. The band pattern from one case of carcinoid tumor with a fulminant clinical course was similar to that of gastrinomas, whereas other carcinoid tumors expressed the epithelial form of CD44. The earlier identified splice variants which confer metastatic behavior on a pancreatic tumor cell line were not expressed in neuroendocrine tumors. Our data indicate that CD44 expression in endocrine pancreatic tumors correlates with the ability to give rise to lymph node metastases and may play a vital role in determining the fate of metastasizing cells. Moreover, because gastrin is not detectable in the normal human pancreas, the pancreatic ductal cell positivity for CD44 strengthened the ductal origin concept of gastrinomas. The band pattern of CD44 splice variants suggests that the previously described splice variants conferring metastatic behavior do not accompany metastatic activity of neuroendocrine tumors.
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PMID:Different splice variants of CD44 are expressed in gastrinomas but not in other subtypes of endocrine pancreatic tumors. 750 23

To investigate further the presence of an autocrine proliferative loop involving gastrin in colorectal carcinomas and to clarify the receptor responsible, 102 human colorectal carcinomas and 10 hepatic metastases were investigated for the expression of the genes encoding gastrin, the gastrin/CCK-B receptor and the gastrin/CCK-C receptor. Levels of RNA expression were assayed by RNase protection assay. In addition, gastrin/CCK receptors on crude membranes of tumour tissue were assayed by radioligand binding. High-affinity gastrin/CCK-B receptors were not detected in any of the carcinomas investigated, whereas in 36% low-affinity binding was observed, consistent with the expression of the gastrin/CCK-C receptor. RNase protection assay detected the RNA for the gastrin/CCK-B receptor in 11% of the carcinomas investigated, whereas the RNA for the gastrin/CCK-C receptor was demonstrated in 75% and the RNA for gastrin in 86% of the carcinomas investigated. These results confirm the recent demonstration of progastrin fragments in colorectal carcinomas. One possible explanation for progastrin expression is that such progastrin fragments may participate in an autocrine proliferative loop. The receptor involved in this loop is more likely to be the low-affinity gastrin/CCK-C receptor rather than the gastrin/CCK-B receptor, which is rarely expressed in colorectal carcinomas.
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PMID:Expression of gastrin, gastrin/CCK-B and gastrin/CCK-C receptors in human colorectal carcinomas. 759 30


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