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)

The binding of labeled insulin to dissociated R3230AC mammary adenocarcinoma cells from diabetic and intact rats was investigated in vitro. At 20 degrees, specific binding (total binding minus binding in the presence of 1000-fold excess or 10(-6) M unlabeled insulin) reached a plateau at 45 to 60 min and was directly related to the number of cells used. Degradation of labeled insulin, as measured by trichloroacetic acid precipitation, was related to the number of cells used, was not prevented by trasylol or phenylmethylsulfonyl fluoride (general proteolytic enzyme inhibitors), but was prevented by addition of 1 to 2% bovine serum albumin to the incubation medium. Specificity of insulisulin, and desoctapeptide insulin were capable of competing for insulin binding in an order of potency related to their relative biological activity; prolactin and glucagon were unable to compete for insulin binding. Scatchard analysis of the binding data demonstrated a curvilinear-plot; specific binding (over the concentration range of 10(-11) to 10(-10) M insulin) showed a high affinity (Kd approximately 1 to 3 X 10(-10) M), and the estimated number of sites was greater in tumors from diabetic animals than in tumors from intact animals or intact animals given insulin prior to sacrifice. Reversibility of insulin binding was studied by dissociation experiments; dissociation was enhanced in the presence of added unlabeled insulin compared to dissociation examined under conditions of "infinite" dilutions only. Maximum dissociation of bound insulin was observed in the presence of 10(-7) M unlabeled insulin, with less of an effect at lower or higher concentrations of added insulin (no effect seen at 10(-10) M insulin). Two techniques were investigated for separating cells from unbound labeled insulin; the procedure using centrifugation was found to be more efficient. Thus, in the R3230AC mammary adenocarcinoma, data obtained on saturability, reversibility, and specificity of insulin binding indicate the existence of an insulin receptor with properties similar to those found in normal cells.
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PMID:Identification and characterization of the insulin receptor in the R3230AC mammary adenocarcinoma of the rat. 13 40

A 39-year-old bus driver had been suffering for 2 years from a malignant polypoid mucosal proliferation of the upper nasal concha-ethmoid region, resembling a highly differentiated, villous-glandular adenocarcinoma of enteric type. There were numerous mono- and amphicrine cells and a massive quantity of oxyphilic, frequently Paneth-like goblet cells in the tumor. Immune-histochemically, a number of gastrin- and fewer glucagon-positive cells were identified. The somatostatin level in the serum was clearly increased. Electron-microscopically, 7 different endocrine cell types were identifiable, in order of decreasing frequency: A-like- and G-cells, both types of 5-HT-cells, A-cells, EG- and K-cell-like elements. Particularly impressive were the muco-argyrophilic amphicrine cells, containing A-granules. The unusual enteric character of the carcinoma seems to result from boundary movements and tissue displacements in an ecto-entodermal embryonic border region. There was no history of occupational wood dust inhalation.
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PMID:Endocrine-amphicrine enteric carcinoma of the nasal mucosa. 15 75

BK virus (BKV), a human papovavirus, was inoculated iv into 3-week-old Syrian golden hamsters. Between 2 1/2 and 9 months after inoculation, 82% of the animals developed tumors. The induced neoplasms were ependymoma, carcinoma of the pancreatic islets, osteosarcoma, adenocarcinoma, angiosarcoma, angioma, lymphoma, and seminoma. Hypersecretion of insulin, glucagon, C-peptide, and calcitonin was detected in tumors of pancreatic islets. BKV etiology of tumors was supported by the following evidence: 1) No tumors with BKV-specific markers appeared in animals given injections of buffer, animals inoculated with BKV neutralized by anti-BKV-specific serum, or uninoculated controls; 2) BKV tumor (T) antigen was detected by immunofluorescence and complement fixation tests in tumors of animals inoculated with infectious BKV and in transplanted tumors; 3) antibodies to BKV T-antigen were detected in sera of animals bearing primary or transplanted tumors; 4) BKV could be activated by Sendai virus-mediated fusion of neoplastic cells with susceptible Vero cells; and 5) no endogenous hamster oncornaviruses were found in tumors.
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PMID:Ependymomas, malignant tumors of pancreatic islets, and osteosarcomas induced in hamsters by BK virus, a human papovavirus. 21 Dec 43

Two cases of pancreatic exocrine tumors with endocrine component are reported. The first case concerned a microcystic cystadenoma including an endocrine tumor identified by Grimelius staining and positive immunostaining for neurone specific enolase and the second a tubular adenocarcinoma including cells with positive immunostaining for glucagon and neurone specific enolase. The malignant nature of the endocrine component of both tumors which was certain for the first one and probable for the second whose endocrine component was distinct from the hyperplastic endocrine reaction observed at the periphery of the tumor, seems to support the hypothesis of exocrine and endocrine differentiation from a common precursor cell. The precise value of such a sub-group of pancreatic tumors with double component need to be clarified.
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PMID:[Endocrine component of exocrine pancreatic tumors. Apropos of 2 cases]. 131 17

In a series of 130 cases of adenocarcinoma of the large intestine, enterochromaffin (EC) cells were detected in 54 cases (41.5%) by immunocytochemistry with anti-chromogranin monoclonal antibody. Among the 54 cases, 30 were found positive for serotonin, 14 for somatostatin, 11 for glucagon, 5 for pancreatic polypeptide, and only one for gastrin. The cases with EC cells (++) or polypeptide positive cells exhibited higher grade of differentiation, earlier stage of tumour extension and higher survival rate than those without EC cells. A significant difference of the EC cell population pattern among different histological grades of the tumours and nonneoplastic mucosa was found. The proportion of hormone, especially polypeptide positive cells was the highest in the mucosa and lowest in the moderately poorly differentiated carcinomas. The incidence, methodology and clinicopathological significance of EC cells found in the tumours are discussed.
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PMID:[Immunocytochemical study of enterochromaffin cells in carcinoma of the large intestine]. 197 23

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.
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PMID:Predominant Paneth cell differentiation in an intestinal type gastric cancer. 206 3

Scattered argyrophil cells were present in normal, large, medium-sized and small pancreatic ducts (ductules). There was marked increase in argyrophil cells in ducts with hyperplastic epithelium. Argyrophil cells were also found in 67.7% of all exocrine pancreatic carcinomas. In a well differentiated group including cystadenocarcinoma, mucinous carcinoma and well differentiated ductal adenocarcinoma argyrophil cells were found in all cases examined. Using four antisera (against insulin, glucagon, somatostatin and gastrin), insulin, glucagon and somatostatin cells were identified in 2.65%, 0.001% and 1.2% of normal ducts, and 7.5%, 2.4% and 4.6% of ducts with hyperplastic epithelium respectively and were also greatly increased in numbers in the latter group. Immunoreactive cells were present in 66.7% of exocrine carcinomas. Cells reactive for insulin were found in 7/15 cases; glucagon in 6/15 cases; somatostatin in 5/15 cases and gastrin in 2/15 cases. Eight cases contained two or more than two types of immunoreactive cells. The presence of argyrophil and hormone immunoreactive cells in pancreatic ducts and carcinomas is indicative of the close developmental relationship between endocrine and exocrine parts of the pancreas. The inter-relationship of response in the different cell types following stimulus suggests that injury to a common precursor may be involved.
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PMID:Argyrophilic and hormone immunoreactive cells in normal and hyperplastic pancreatic ducts and exocrine pancreatic carcinoma. 245 41

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

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

The non-ionic detergent n-octyl-beta-D-glucopyranoside was used to solubilize the VIP (vasoactive intestinal peptide) receptor from human colonic adenocarcinoma cell line HT29-D4. The binding of monoiodinated 125I-VIP to the solubilized receptor was specific, time-dependent, and reversible. Scatchard analysis of data obtained from competitive displacement of monoiodinated 125I-VIP by native VIP suggested the presence of two classes of VIP binding sites with Kd values of 0.32 and 46.7 nM. The binding capacities of these two classes were 1.7 x 10(10) and 30.2 x 10(10) sites/mg of proteins, respectively. The solubilized receptor retained the specificity of the human VIP receptor towards the peptides of the VIP/secretin/glucagon family. The order of potency in inhibiting monoiodinated 125I-VIP binding was VIP (IC50 = 1.0 x 10(-9) M) much greater than peptide histidine methionine amide (IC50 = 10(-7) M) greater than growth hormone-releasing factor (IC50 = 3 x 10(-7) M) greater than secretin (IC50 greater than 10(-6) M); glucagon had no effect on VIP binding. The reducing agent dithiothreitol inhibited in a dose-dependent manner the binding of 125I-VIP. Covalent cross-linking experiments between the solubilized receptor and 125I-VIP showed that after sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography two major and one minor polypeptides of Mr 67,000, 72,000, and 83,000 were specifically labeled. When analyzed by gel filtration, the n-octyl-beta-D-glucopyranoside-solubilized 125I-VIP-receptor complex was resolved into two major peaks with molecular mass in the range of 60-70 and 270-300 kDa. Thus, the soluble form of the VIP receptor was probably a multimeric complex in which disulfide bonds may play an important role to hold the receptor in an active configuration.
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PMID:Solubilization of the active vasoactive intestinal peptide receptor from human colonic adenocarcinoma cells. 284 75


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