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Query: UNIPROT:P01275 (
glucagon
)
26,492
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
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
.
...
PMID:[Gastrin]. 123 74
Vasoactive intestinal polypeptide (VIP) is a gut neuroendocrine polypeptide that increases cyclic adenosine monophosphate (cAMP) production in cells with VIP receptors. Some gastrointestinal cancer cells possess functional receptors for VIP; however, the role of VIP in regulation of growth of
gastric cancer
cells has not been determined. The purpose of this study was to determine whether VIP and other agents that increase cAMP regulate growth of a human
gastric cancer
cell line (AGS) and whether these agents regulate expression of c-myc proto-oncogene, which is required for cell proliferation. We measured levels of cAMP by radioimmunoassay, and we used Northern blot analysis to examine c-myc messenger RNA expression. Cell-growth studies were carried out in media supplemented with 3% serum, and cells were counted with a Coulter counter. We found that VIP significantly increased cAMP production of AGS cells in a dose-dependent manner, whereas secretin,
glucagon
, and peptide histidine methionine (PHM) did not stimulate cAMP production. Exogenous cAMP (8-bromo-cAMP) inhibited AGS cell growth in a dose-dependent manner. VIP acted synergistically with either isobutylmethyl-xanthine or forskolin to inhibit AGS cell proliferation. The increased c-myc expression, which was induced by serum, was inhibited by simultaneous treatment with VIP and isobutylmethyl-xanthine. We have found that AGS cells have specific, functional VIP receptors (activation of which are negatively correlated with cell growth) and that the mechanism by which VIP acts to inhibit cell growth appears to be due, in part, to cAMP-dependent regulation of c-myc proto-oncogene expression.
...
PMID:Vasoactive intestinal polypeptide inhibits c-myc expression and growth of human gastric carcinoma cells. 171 57
A distinct morphological variant of a diffuse type adenocarcinoma of the stomach with Paneth cell differentiation is reported. The tumor was a Borrmann's Type III carcinoma measuring 6.0 x 5.5 cm at the body along the greater curvature. It was composed of Paneth cell- and endocrine cell differentiated cancer cells in addition to tubular and poorly differentiated adenocarcinoma cells. The Paneth cell differentiation was characterized histologically by cytoplasmic distinct coarse eosinophilic granules stained red with periodic acid-Schiff and Masson trichrome reagents and reddish brown with phosphotungstic acid hematoxylin, and electron microscopically by lysozyme in cytoplasmic electron dense granules. In addition, electron microscopy revealed acid mucin globules and various intermediate forms between Paneth granules and the mucin globules which might be regarded as abortive forms of Paneth granules presumably resulting from defective incorporation of lysozyme-positive mucosubstances into acid mucin. Endocrine differentiated cancer cells consisted of serotonin-, peptide YY-, and
glucagon
/glicentin-positive cells. The various cell phenotypes found in the present tumor could be explained on the basis of intestinal differentiation of
gastric cancer
.
...
PMID:Predominant Paneth cell differentiation in an intestinal type gastric cancer. 206 3
We tested the truncated 7-37
glucagon-like peptide 1
(TGLP-1), a naturally occurring porcine intestinal peptide, and other members of the
glucagon
family, including pancreatic
glucagon
(G-29), GLP-1 and
GLP-2
for their ability to activate the cAMP generating system in rat gastric glands and HGT-1 human
gastric cancer
cells. In rat fundic glands, TGLP-1 was about 100 times more potent (EC50 = 2.8 X 10(-9) M) than GLP-1 of G-29, and 10 times more potent than G-29 in the HGT-1 cell line. Our results support the notion that TGLP-1 plays a direct role in the regulation of acid secretion in rat and human gastric mucosa.
...
PMID:Effect of truncated glucagon-like peptide 1 on cAMP in rat gastric glands and HGT-1 human gastric cancer cells. 284 Nov 60
Endocrine-like cells containing
glucagon
, glicentin or pancreatic polypeptide immunoreactivity in human foetal and adult stomach, with or without disease, were studied with the indirect immunoperoxidase method and mirror sectioning technique. In foetal and neonatal oxyntic mucosae, there were endocrine-like cells with
glucagon
and glicentin immunoreactivities and argyrophilia. Cells containing glicentin immunoreactivity alone were detected earlier than
glucagon
cells during foetal development, and were also distributed throughout foetal to neonatal life. Bovine pancreatic polypeptide immunoreactivity coexisted in a subpopulation of the
glucagon
-glicentin cells. These cells were absent from normal oxyntic mucosa in the postneonatal period and from normal antral mucosa throughout life. Hamartomatous polyp in adult oxyntic mucosa, hyperplastic oxyntic mucosa in Menetrier's disease and atrophic oxyntic mucosa in a remnant stomach with cancer showed scattered
glucagon
-glicentin cells, but few or no cells containing bovine pancreatic polypeptide. Intestinalized mucosa showed plentiful glicentin cells with occasional
glucagon
and/or bovine pancreatic polypeptide immunoreactivity. Some
gastric cancer
cells of both diffuse and adenoplastic types contained immunoreactive glicentin and, less frequently,
glucagon
. Bovine pancreatic polypeptide immunoreactivity was detected in a few adenoplastic cancer cells, but not in diffuse type cells. Three different anti-pancreatic polypeptide sera against bovine, porcine or human pancreatic polypeptide detected basically the same cells mentioned above, but pancreatic polypeptide cells lacking human pancreatic polypeptide immunoreactivity were also present in foetal oxyntic mucosa. Immunoabsorption tests revealed that the bovine pancreatic polypeptide immunoreactivity was remote from peptide YY and neuropeptide Y.
...
PMID:Immunohistochemical studies on glucagon, glicentin and pancreatic polypeptide in human stomach: normal and pathological conditions. 620 42
Various hormones and peptides were added to rat
stomach cancer
cells growing in vitro in a serum-free medium and the cell number was determined by a spectro-photometric method. Five gastro-entero-pancreatic hormones or related peptides (tetragastrin,
glucagon
, secretin, cholecystokinin-pancreozymin and cerulein) significantly increased the number of
stomach cancer
cells from 15% to 310% of the number of control cells cultivated in a serum-free, hormone-free medium. On the other hand, insulin and vasoactive intestinal peptide, and other hormones (thyroxin, epinephrine, hydrocortisone, beta-estradiol, progesterone, testosterone), peptone broth and bovine serum albumin had no significant growth effect. All the active substances belong to the two major families of gastro-entero-pancreatic polypeptide hormones, suggesting the existence of hormone receptors at the surface of
stomach cancer
cells.
...
PMID:Growth responses of rat stomach cancer cells to gastro-entero-pancreatic hormones. 711 98
The purpose of this study was to investigate the peculiarities of hormonal regulation of adenylate cyclase (AC) of blood lymphocytes in colorectal cancer patients and to compare these peculiarities with hormone sensitivity of AC of colorectal tumors and normal colonic mucosa. Basal and stimulated lymphocyte AC activity was studied in 51 healthy persons and 52 cancer patients (14 with colon cancer, 21 with rectal cancer and 17 with
stomach cancer
) aged 20-75 years. In 31 of 35 patients with colorectal cancer the AC activity was studied simultaneously in lymphocytes, tumor tissue and normal colonic mucosa. To evaluate basal and stimulated AC activity the measurement of c-AMP (Amersham kits) formed in the presence of ATP regenerating system was used. Basal and by VIP, pentagastrin and sodium fluoride stimulated AC activity in lymphocytes of gastrointestinal cancer patients was lower than in lymphocytes of healthy subjects of similar age. Stage dependence of the parameters under study was not found. There was a tendency for higher basal and stimulated lymphocyte AC activity in colon cancer patients as compared to stomach and rectal cancer patients. In colorectal cancer patients the peculiarities of lymphocyte AC reactions to stimulation were closer to those in tumor tissue but not to those in normal colonic mucosa. The reaction of lymphocyte AC to VIP and
glucagon
coincided more frequently with tumor AC reactions to the same hormones in case of hormone nonsensitive tumors. Thus, basal and stimulated lymphocyte AC activity in colorectal cancer patients was modified to some degree by tumor factors. Lymphocyte AC reactions to VIP and
glucagon
may be considered as indirect markers of hormone sensitivity of colonic tumors. Moreover, the probability of discovery of hormone nonsensitive tumors by this way is more reliable than hormone sensitive ones.
...
PMID:Hormonal regulation of adenylate cyclase activity in circulating lymphocytes and its interrelationship with hormone sensitivity of tumor tissue in colorectal cancer patients. 761 78
The HGT-1
gastric cancer
cell line was used to determine the actions of protein kinase C on the stimulation of adenylate cyclase by the human histamine H2 receptor, and the receptors for gastric inhibitory polypeptide and truncated
glucagon
like peptide 1 (TGLP-1). Suspensions of HGT-1 cells were preincubated with the activator of protein kinase C, 12-O-tetradecanoylphorbol 13-acetate (TPA, 100 nmol/l), for 10 minutes. The subsequent cyclic adenosine monophosphate (AMP) response to 0.5 mmol/l histamine or 100 nmol/l TGLP-1 was reduced by comparison with control cells preincubated in the absence of TPA. The cyclic AMP response to 100 nmol/l gastric inhibitory polypeptide was enhanced by preincubation with TPA, while the responses to cholera toxin and forskolin were unaffected. Preincubation with pertussis toxin prevented the enhancement of the gastric inhibitory polypeptide response by TPA, suggesting an involvement of an inhibitory guanine nucleotide regulatory subunit of the Gi class, but did not change the inhibition of histamine stimulation. In conclusion, activation of protein kinase C produces a specific inhibition of the effects of histamine and TGLP-1 on adenylate cyclase activity in a human
gastric cancer
cell line by acting at a site close to their receptors.
...
PMID:Protein kinase C inhibits cyclic adenosine monophosphate generation by histamine and truncated glucagon like peptide 1 in the human gastric cancer cell line HGT-1. 839 30
Thirty-five patients with
gastric cancer
were preoperatively examined with CT performed in the prone position. Patient preparation consisted in filling the stomach with tap water and i.v.
glucagon
administration. The CT images were independently reviewed by two radiologists, who staged each tumor according to the TNM classification. The results were compared with surgical and histological findings. The overall accuracy for T staging ranged 74-77%, overstaging 17-23%; understaging was 3%. Diagnostic sensitivity, specificity and accuracy for serosal invasion were 100%, 80%, 85% and 100%, 84% e 88%, respectively, for the two radiologists. The overall accuracy for N staging was 48% and 51% for the two observers, respectively. Considering N1 and N2 as a single group, accuracy ranged 68-77%. The interobserver agreement analyzed by the "K tests" was 80%, with a K index of 60%. CT performed with the patient in the prone position, after preparation with gastric wall hypotony and distension with water, is a valid technique permitting excellent depiction of the gastric wall and providing useful preoperative information to the surgeon.
...
PMID:[The diagnostic accuracy and reproducibility of computed tomography with water distention and induced hypotonia in the preoperative staging of gastric tumors]. 946 14
In order to observe the regulative effects of pentagastrin (PG) and somatostatin (SS) on the growth of two human
gastric cancer
cell lines (HGC803 and HGC823) in vitro, we observed the effects of PG and SS on proliferation of human
gastric cancer
cells by means of MTT. The contents such as gastrin, insulin, and
glucagon
were determined by radioimmunoassay (RIA), and the hexosamine content was determined by Neuhaus' method. The results showed that the growth of the two human
gastric cancer
cell lines were obviously promoted by PG. On the contrary, the growth and secretion of gastrin and
glucagon
were inhibited by SS. In addition, the hexosamine content of human
gastric cancer
cells was significantly increased by PG (7.58 +/- 0.66 versus 4.20 +/- 0.39 pg/cell, (P < 0.05). But the hexosamine content was decreased by SS (2.62 +/- 0.29 versus 4.20 +/- 0.39 pg/cell, P < 0.05). These findings indicate that the growth of
gastric cancer
cells is regulated by PG and SS, nevertheless a host of problems need to be elucidated.
...
PMID:[Regulative effects pentagastrin and somatostatin on growth of human gastric cancer cells in vitro]. 1068 96
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