Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Proliferation of endocrine cells was found to occur during early, i.e., first 12 weeks, exocrine pancreatic carcinogenesis after 6 weekly treatments of Syrian hamsters with the pancreatic carcinogen N-nitrosobis(2-oxopropyl)amine (BOP). Cells containing insulin (Ins), glucagon (Glu), and somatostatin (Som) were noted in all stages of tumor development and were present in adenocarcinomas and in metastases to the liver. Some of the cancer cells were of amphicrine (hybrid) type, i.e., produced both mucin and endocrine substances. Measurement of these hormones revealed a significant decrease in plasma Ins during early stages of carcinogenesis with concomitant increase of Ins level in pancreatic juice at 12 weeks after 6 weekly BOP treatments. Plasma Glu and Som were not changed. The changes noted, particularly in relation to Ins, suggest that proliferation of endocrine cells in pancreatic carcinogenesis may be associated with alterations in hormone secretion.
Cancer Res 1989 Nov 15
PMID:Alteration of pancreatic endocrine cell patterns and their secretion during pancreatic carcinogenesis in the hamster model. 257 21

The blood glucose level and serum levels of insulin, glucagon, and free fatty acids were examined in 7- to 8-mo-old female SHN mice with or without spontaneous mammary tumors (MT). Blood glucose levels in the females with MT were significantly higher than in those without MT, rising in proportion to the increase in size of MT up to 30 mm in diameter. In 4-mo-old male SHN and 11-mo-old female C57BL mice bearing mammary tumor grafts (MTg), the blood glucose level was significantly higher than in mice without MTg. Serum insulin and free fatty acids in female SHN mice with MT rose to higher levels than in mice without MT, whereas serum glucagon levels were unaltered. In 50% of mice with MT, pancreatic islets contained a large number of pyknotic cells. Livers of mice with MT or MTg were significantly heavier than those of mice without MT or MTg. In both female SHN mice with spontaneous MT and male SHN and female C57BL mice with MTg, the total number of hepatocytes and the total amount of liver DNA increased significantly compared with values from corresponding controls without MT or MTg. These findings suggest that MT or MTg induce a hyperglycemic state and an enhanced production of free fatty acids and insulin, which may in turn stimulate the growth of mammary tumors and the liver.
Cancer Res 1989 Feb 15
PMID:Correlation between mammary tumor and blood glucose, serum insulin, and free fatty acids in mice. 264 64

A facet of carcinoid tumors often not recognized is their close association with other, noncarcinoid malignancies. The clinical course of two patients with multiple ileal-jejunal carcinoids and multiple other noncarcinoid malignancies is described. These patients were found to have elevated circulating levels of gastrin, bombesin, glucagon, enteroglucagon, pancreatic polypeptide, and peptide tyrosine tyrosine. These regulatory peptides have been demonstrated to promote trophic effects on the gastrointestinal tract as well as malignant tumors. We propose that the release of these bioactive hormones into the portal and systemic circulation by carcinoid tumors may play some role in their association with these multiple second tumors.
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PMID:Malignant diathesis from jejunal-ileal carcinoids. 264 19

Biphasic contrast studies are generally advocated as the best current barium examination for the upper GI tract. Two recent prospective blinded trials compared the diagnostic results of a biphasic contrast examination--employing a medium-density barium suspension and glucagon--and endoscopy. Both methods appear to have nearly equal merit for the detection of peptic ulcer and gastric carcinoma. One of the trials demonstrated a relative inability of the barium examination to depict reflux esophagitis other than the severe variety, an inability that had been previously recognized. Earlier Japanese studies showed excellent results from biphasic studies in the detection of early and advanced gastric carcinoma. Because gastric carcinoma may present as a wide variety of lesions, ranging from minute alterations in mucosal relief through ulcers to masses, the values from these Japanese studies also test the sensitivity and specificity of the radiographic examination in demonstrating non-neoplastic lesions of the stomach. Ample data have shown that a radiographic examination compares favorably with endoscopy in the detection of esophageal carcinoma. The usefulness of a radiographic examination as a primary examination if disturbances of esophageal motor function are suspected is generally recognized. A state-of-the-art radiographic examination (ie, a biphasic examination, preferably with drug-induced hypotony) therefore appears to represent an appropriate initial examination in evaluation of most disorders of the upper GI tract. If this examination prompts the slightest suspicion of a malignant tumor, endoscopy should follow for the purpose of obtaining biopsy specimens. Endoscopy is not necessary if duodenal ulcers have been diagnosed by means of radiography; in typically benign gastric ulcers, radiographic follow-up without endoscopy may safely be considered. If in elderly patients multiple small gastric polyps have been detected, endoscopy is not needed. If complaints persist after negative results at radiographic examination, however, endoscopic intervention must be considered. If the complaints suggest reflux esophagitis, the clinician can choose between treatment and endoscopy. In a patient with acute upper GI bleeding, primary endoscopy may be preferred. This diagnostic approach in which endoscopy is employed as complementary to the barium examination is in most parts of the world a cost-effective one. It is also the safest possible option; although endoscopic complications are rare, their absolute number cannot be ignored if every patient had to undergo endoscopy. A biphasic approach with a medium-density barium suspension can be attempted in nearly every patient; if the patient proves unable to cooperate for an optimal double-contrast examination, a single-contrast examination can be performed with the same barium swallowed.
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PMID:Use of barium in evaluation of disorders of the upper gastrointestinal tract: current status. 268 69

Adult sarcoma-bearing mice were used to demonstrate whether hypoglycemia was the immediate cause of death in experimental animals with rapidly growing tumors without metastases. This kind of tumor model is representative of the majority of animal models used in experimental cancer research. Tumor-bearing animals died with severe hypoglycemia under all experimental conditions, while pair-killed controls were normoglycemic. Anorexia prevented tumor-bearing animals from attenuating the hypoglycemia by drinking glucose-containing water while completely starved control animals survived more than 14 days with glucose-containing water as the only energy source. Adrenalectomy shortened survival in tumor-bearing animals, but survival of adrenalectomized tumor-bearing animals could be normalized by daily injections of pharmacologic doses of hydrocortisone (25 mg/25 g body wt/day) but not by physiologic replacement (20 micrograms/25 g body wt/day). Injections of pharmacologic doses of hydrocortisone did not influence on survival or body composition in tumor-bearing animals with intact adrenals. Glucagon was without effect on either survival, tumor growth or body composition. Based on the results in this study and in our previous reports we conclude that hypoglycemia is the cause of death in the majority of murine tumor models. This hypoglycemic theory is important, since any treatment modality in animal experiments that influences glucose metabolism in the host may indirectly change tumor growth and may thus be misinterpreted as a direct tumor effect.
Eur J Cancer Clin Oncol 1989 Sep
PMID:The cause of death in non-metastasizing sarcoma-bearing mice. A study with relevance for tumor treatment experiments in mice. 280 52

Tumor necrosis factor (TNF) has been implicated in the toxic manifestations of overwhelming bacterial infection and in the tissue wasting that often accompanies prolonged infections and malignancy. We have examined a possible role of TNF in the early metabolic alterations following acute tissue injury or sepsis. Recombinant human TNF stimulated rat liver amino acid uptake up to 5-fold in vivo and there was a concomitant increase in plasma glucagon. In vitro TNF had no direct effect on hepatocyte amino acid uptake, but it markedly enhanced the stimulation of amino acid transport by glucagon, without an alteration in binding of glucagon to hepatocytes. This permissive effect of TNF on glucagon action represents an interrelationship between the immune and endocrine systems, and it may help to explain the mechanism of hormonal regulation of both the anabolic and catabolic responses to acute injury.
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PMID:Modulation of endogenous hormone action by recombinant human tumor necrosis factor. 282 98

Regulation of insulin release and transmembrane Ca2+ fluxes was examined using pieces of 3 benign medullary-type insulinomas removed from the pancreas of female patients at surgery. Immunocytochemical staining confirmed the presence of insulin-containing cells with no demonstrable glucagon, somatostatin or pancreatic polypeptide. After 3 days of culture in RPMI-1640, tumour pieces released 11-158 mg insulin kg-1 dry wt during acute 60 min incubations with the concomitant uptake of 2-47 mmol 45Ca kg-1 into the intracellular lanthanum-nondisplaceable pool. At 2.56 mM Ca2+, glucose alone or in combination with glyceraldehyde, mannoheptulose or diazoxide did not modify insulin release or 45Ca uptake. Theophylline significantly increased insulin release from 2 tumours with a small stimulatory effect on the third. A depolarising concentration of K+ enhanced insulin release from one tumour but this was not associated with an increase of 45Ca uptake. Calcium antagonists, (verapamil, D-600 and trifluoroperazine) and calcium ionophores (A23187 and Br-X537A) failed to modify insulin release or 45Ca uptake by each of the two tumours tested. Evaluation of 45Ca efflux from one tumour confirmed the unresponsiveness to glucose, K+, verapamil and A23187. Prolonged culture of 2 tumours for up to 16 days was associated with the gradual decline of insulin release to a steady output of 2-15 ng 24 h-1. Addition of verapamil to the cultures inhibited insulin output from one tumour, but mannoheptulose or diazoxide were without effect. The results indicate that inappropriate insulin release from these 3 benign medullary-type insulinomas is associated with disturbances in the regulation of transmembrane Ca2+ fluxes.
Br J Cancer 1987 Oct
PMID:Defective regulation of insulin release and transmembrane Ca2+ fluxes by human islet cell tumours. 282 49

Two cases of large cystic tumor of the pancreas in two young women are reported. Gross features and conventional light microscopic appearances of these tumors were consistent with those described as being the so-called papillary and cystic tumor (PCT) or solid and cystic tumor. Immunohistochemical staining for neuron-specific enolase was positive diffusely in both cases. Special stainings with Grimelius' silver impregnation, and stainings for insulin, glucagon, and somatostatin also were positive, although the population of positive cells was different in each case. Ultrastructural examinations confirmed the presence of numerous granules, probably neurosecretory, within the cytoplasm of many tumor cells in each case. Therefore, current cases were indistinguishable pathologically from the cystic nonfunctioning islet cell tumor. This study suggests that some PCT of the pancreas consist of endocrine cells predominantly.
Cancer 1988 Mar 15
PMID:Papillary and cystic tumor of the pancreas. Two cases indistinguishable from islet cell tumor. 283 9

We investigated the production, binding to cell membranes, and influence on cell proliferation of peptides and growth factors in 4 classic, 5 transitional, and 5 variant SCLC cell lines. Glucagon, neurotensin, and TGF-alpha were present in all cell lines. Bombesin was predominantly found in classic cell lines and insulin in variant cell lines. Neurokinin A, calcitonin, CGRP, GHRF, somatostatin, and CNTF were detectable in some cell lines without prevalence for a particular cell type. We could not detect AVP, growth hormone, neuropeptide Y, substance P, VIP, and NGF. Insulin binding sites were present on 11/14 cell lines, and some cell lines specifically bound bombesin, calcitonin, and EGF. Growth effects were detectable for insulin, GRP-related peptides, tachykinins, and VIP. Using serum-free conditions, insulin and VIP had a growth stimulating effect in liquid culture at nanomolar concentrations. Bombesin and neuromedin B stimulated the clonal growth at a concentration of 3-30 nM. The tachykinins neurokinin A, neurokinin B, physalaemin, and eledoisin inhibited the clonal and mass culture growth with a peak effect in the range of 0.1 to 10 pM. Peptide-induced stimulating and inhibiting effects were within a magnitude of 2-fold. All other peptides and growth factors tested, including ACTH, AVP, calcitonin, glucagon, neurotensin, somatostatin, EGF, CNTF, and NGF did not affect the growth of SCLC. We conclude that the growth of SCLC is partly controlled by such peptides in an autocrine/paracrine fashion.
J Cancer Res Clin Oncol 1988
PMID:Peptides and growth factors in small cell lung cancer: production, binding sites, and growth effects. 283 87

A 62-year-old man had necrolytic migratory erythema in association with hyperglucagonemia and multiple hepatic tumors. A diagnosis of metastatic glucagonoma was made. He was treated with human lymphoblastoid interferon given subcutaneously in the dose of 2.8 to 7.1 X 10(6) IU/day. This produced a considerable fall in plasma glucagon and resolution of the associated rash. The treatment was continued for 10 weeks over a 4-month period. Computed tomography demonstrated a reduction in hepatic tumor mass.
Cancer 1988 Sep 01
PMID:Hepatic tumors with hyperglucagonemia. Response to treatment with human lymphoblastoid interferon. 284 25


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