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)

To evaluate beta-cell function in patients with pancreatic cancer, the glucagon stimulation test was performed in seven patients with pancreatic adenocarcinoma, seven patients with type I diabetes mellitus, seven patients with type II diabetes mellitus, and in seven healthy controls. C-peptide serum levels were determined before and after a 1-mg i.v. glucagon injection. Basal C-peptide values were normal or slightly increased in pancreatic cancer and type II diabetic patients and low in type I diabetic patients. Following glucagon stimulation, no significant increase was observed in C-peptide values of type I diabetics and pancreatic cancer patients, whereas significant increases occurred in controls and type II diabetics. It is concluded that the altered beta-cell function found in pancreatic cancer patients may lead to hyperglycemia, which is frequently associated with this tumor type.
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PMID:Beta-cell function in pancreatic adenocarcinoma. 802 55

The occurrence of endocrine cells in 350 cases of colorectal adenocarcinoma was studied by immunohistochemistry for chromogranin A (CGA). The hormone profile of endocrine tumor cells, the correlation between endocrine differentiation and presence of other colorectal epithelial-cell lineages and the prognostic relevance of endocrine differentiation in colorectal cancer were investigated. CGA-positive tumor cells were found in 30% of cases, 21% showing moderate positivity and 9.0% extensive positivity. Of CGA-positive tumors, 70% additionally produced neurohormones, mainly indigenous to normal colorectal epithelium: 55% showed immunoreactivity for glucagon-like substances, 20% for serotonin and 10% for somatostatin, PYY and HCG. No immunoreactivity was found for various neurohormones not normally produced by colorectal endocrine cells. CGA-positive tumors tended to be more aggressive than CGA-negative tumors. Especially, tumors with extensive CGA positivity showed shorter survival, which was most apparent within Dukes' stage C. In multivariate analysis, extensive CGA positivity was an independent indicator of poor prognosis. CGA immunoreactivity significantly correlated with mucin production, but not with expression of secretory component (SC), a columnar-cell marker. Mucin production significantly correlated with SC expression. Tumors positive for CGA but not for mucin and/or SC showed the worst prognosis. SC expression was a relatively favorable feature, and mucin-producing tumors showed intermediate behavior.
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PMID:Endocrine cells in colorectal adenocarcinomas: incidence, hormone profile and prognostic relevance. 810 Aug 8

Diabetes occurs frequently in patients with pancreatic cancer. To investigate the impact to tumour removal, seven patients were studied before and after 85 per cent subtotal pancreatectomy for adenocarcinoma of the pancreas. The frequency of diabetes was determined by the oral glucose tolerance test. Fasting levels of C peptide and insulin were measured in plasma, and insulin secretion was investigated by hyperglycaemic glucose clamp and glucagon stimulation. Six of the seven patients were diabetic before surgery and four required insulin treatment. Improvements in diabetic status and glucose metabolism were found in all seven patients after operation, as demonstrated by increased glucose metabolic capacity during hyperglycaemia. This occurred despite a postoperative reduction in insulin secretion and is explained by the observed augmentation of whole-body insulin sensitivity after surgery. A diabetogenic factor may be produced by pancreatic adenocarcinoma that may be responsible, directly or indirectly, for the high frequency of diabetes in patients with pancreatic cancer.
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PMID:Improved glucose metabolism after subtotal pancreatectomy for pancreatic cancer. 840 64

Two cases are described of an unusual form of primary adenocarcinoma of the pancreas characterized histologically by their striking resemblance with a neuroendocrine neoplasm. The tumors were composed of a population of relatively small, uniform cells arranged in sheets admixed with small microglandular structures resulting in a cribriform pattern of growth. The tumor cells displayed scant cytoplasm with indistinct cell borders and round to oval nuclei with irregular clumping of chromatin and small, inconspicuous nucleoli. Immunohistochemical studies in both cases showed positivity of the neoplastic cells with CAM 5.2 antibodies and negative staining with a battery of neuroendocrine-related markers including chromogranin, NSE and synaptophysin, as well as with a variety of peptide hormones including insulin, glucagon, vasoactive intestinal polypeptide, gastrin and serotonin. Ultrastructural examination revealed a cohesive population of cells forming abortive glandular lumens lined by imperfectly formed microvilli and showing well-developed junctional complexes. No dense core neurosecretory granules or zymogen granules could be identified in any of the cells, supporting a ductal type of differentiation for these tumors. The main importance of recognizing this rare variant of pancreatic adenocarcinoma lies in avoiding misdiagnosis with other primary and metastatic neuroendocrine neoplasms of this organ. Immunohistochemical and ultrastructural examination will be of value in such cases for differential diagnosis.
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PMID:Microglandular carcinoma of the pancreas: immunohistochemical and ultrastructural study of an unusual variant of pancreatic carcinoma that may closely resemble a neuroendocrine neoplasm. 916 70

Five primary ovarian carcinomas composed of a high-grade neuroendocrine tumor of non-small-cell type and a surface-epithelial-stromal tumor are reported. The five tumors presented in women aged 36 to 77 (mean, 57) years with abdominal distension or a palpable mass in three cases, right lower quadrant pain with tenderness and fever in one case, and a cervicovaginal smear showing a high estrogen effect in one postmenopausal patient. The tumors were unilateral, 9 to 30 (mean, 16) cm in greatest dimension, and had solid and cystic components. Three tumors were stage I; one, stage II; and one, stage III. Two patients who received chemotherapy died of tumor 8 and 36 months postoperatively, another who refused chemotherapy but later received radiation died of tumor after 19 months, a fourth was lost to follow-up, and a fifth was treated recently. Microscopically, the neuroendocrine components of all the tumors were composed predominantly of sheets, closely packed islands, cords, and trabeculae of epithelial cells with little intervening stroma. The tumor cells in the neuroendocrine areas were medium-sized to large compared with the cells of small cell carcinoma, and they contained scanty to moderate amounts of cytoplasm and hyperchromatic nuclei with coarse chromatin clumping in three cases and abundant cytoplasm and vesicular nuclei with single, large eosinophilic nucleoli in the other two. In all the cases, areas of necrosis and single-cell necrosis were extensive, and mitotic figures were abundant. Positive argyrophil and argentaffin reactions were observed in occasional to many cells in all cases. The glandular components of the tumors were grade 1/3 endometrioid adenocarcinoma (one case), grade 2/3 mucinous adenocarcinoma (2 cases), and mucinous borderline tumor with small foci of mucinous adenocarcinoma (two cases). Numerous enterochromaffin cells were identified in hematoxylin and eosin sections of the borderline mucinous components of two tumors; occasional nonargentaffin argyrophilic cells were present in the endometrioid and mucinous carcinoma components. Luteinized stromal cells were present focally in two cases, including the case in which there was evidence of a high estrogen level. Immunohistochemical studies in five cases showed staining of most cells in the solid components for cytokeratin and chromogranin A and some to most cells for serotonin and neuron-specific enolase. Neuropeptides that were detected in the solid component of one or more of the cases included vasoactive intestinal peptide, somatostatin, gastrin, and glucagon; negative results were obtained for pancreatic polypeptide and insulin. Flow cytometry in four tumors revealed that the neuroendocrine component was aneuploid in two, suspicious for aneuploidy in one, and diploid in one. Tumors of the type described are distinct pathologically from primary ovarian carcinoid tumors and small cell carcinoma of pulmonary type. Although experience with this type of tumor is limited, the prognosis appears to be poor.
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PMID:Ovarian neuroendocrine carcinomas of non-small-cell type associated with surface epithelial adenocarcinomas. A study of five cases and review of the literature. 888 77

Twelve cervical tumors showing morphologic evidence of neuroendocrine differentiation and lesional cells larger than those of typical small cell carcinoma are reported in women 21 to 62 (mean 34) years of age. The patients presented with an abnormal Papanicolaou smear or vaginal bleeding. Two tumors were stage Ia2, nine were stage Ib, and one was stage IIa. All patients were treated by radical hysterectomy, and most received adjuvant chemotherapy. Seven of 10 patients with > 1 year of follow-up died of tumor 6 to 24 months after hysterectomy. The tumors had insular, trabecular, glandular, and solid growth patterns and contained medium to large cells with moderate to abundant cytoplasm; eosinophilic cytoplasmic granules were present in nine cases. The tumors were mitotically active, and necrosis was present in 10 of them. Nine of 10 tumors were argyrophilic, and all 12 were immunoreactive for chromogranin. Individual cells containing somatostatin, serotonin, or glucagon were identified in four of eight cases. Adenocarcinoma in situ was present adjacent to the tumor in eight cases; invasive adenocarcinoma of non-neuroendocrine type was present in three of these tumors. Using diagnostic criteria established for pulmonary neuroendocrine tumors, the 12 tumors were classified as large cell neuroendocrine carcinomas. Cervical large cell neuroendocrine carcinomas are distinctive cervical carcinomas that are frequently misdiagnosed and have an unfavorable outcome, similar to that of small cell carcinoma.
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PMID:Large cell neuroendocrine [corrected] carcinoma of the uterine cervix: a clinicopathologic study of 12 cases. 925 53

Urocanic acid (UCA) has been shown to mediate the UVB radiation-induced immunosuppression initiated in the skin by UV-induced isomerization from the trans to the cis isomer. However, the mechanism by which cis-UCA acts is still unclear. Therefore, the present study was undertaken to determine the effect of trans- and cis-UCA on cyclic adenosine 3',5'-monophosphate (cAMP) synthesis in human dermal fibroblasts, Golden Syrian hamster hepatocytes and in the human adenocarcinoma cell line, HT29. Neither trans- nor cis-UCA was able to stimulate cAMP synthesis directly in any of the models tested. In human dermal fibroblasts, cis-UCA, in contrast to trans-UCA, specifically inhibited cAMP synthesis induced by either prostaglandin (PG) E1 or PGE2 with a maximum inhibitory effect of 25-30% at cis-UCA concentrations greater than 1 microM and half-maximum inhibitory effect (EC50) observed at 35 nM. The effect of cis-UCA was not to stimulate phosphodiesterase and cAMP breakdown. The inhibitory effect of cis-UCA (an imidazole derivative) was not mediated through stimulation of the alpha 2-adrenergic receptor. The inhibitory effect of cis-UCA on stimulated cAMP synthesis was a function of the cell density and was only significant when the fibroblasts were confluent or postconfluent. In contrast to the studies with human dermal fibroblasts, an inhibitory effect of cis-UCA was not observed in either isolated hamster hepatocytes or HT29 cells, in which cAMP synthesis was stimulated by glucagon and vasoactive intestinal peptide, respectively. These results point to a possible regulation of cAMP synthesis in fibroblasts as one mechanism by which cis-UCA exerts its biological effect in the skin.
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PMID:Regulation of stimulated cyclic AMP synthesis by urocanic acid. 952 31

A 37-year-old male patient, without any particular symptoms apart from moderate right upper quadrant postprandial pain, was found to have a liver mass identified as a glucagon-producing tumor. Plasma glucagon levels were slightly increased, whereas those of other gut peptides were within the normal range. Despite an extensive pre- and intraoperative diagnostic work-up, a presumed primary glucagonoma remained undetected. This unusual presentation with the absence of any symptoms typical of glucagonoma, as well as the presence of histopathological features characteristic of both benign and malignant forms of glucagonoma, make this case very peculiar. A clinically silent, apparently unrelated adenocarcinoma of the left colon was also found. The concomitant presence of a glucagonoma and a carcinoma of the large intestine has not been previously reported, and its significance remains unclear.
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PMID:Asymptomatic glucagonoma presenting with an isolated hepatic nodule. 975 12

The diagnosis of adenocarcinoid (mucinous/goblet cell carcinoid) is usually unexpected by both clinicians and pathologists. We report here the case of a 74-year-old man with gastric lymphoma (B-cell MALToma) diagnosed by endoscopy, who was found on exploratory laparotomy also to have extensive intraabdominal involvement by adenocarcinoid, arising from the ileum and/or appendix. The patient died two years after diagnosis with bladder outlet and small bowel obstruction due to diffuse metastases. In addition to mucin positivity, immunohistochemical stains demonstrated the tumor to be positive for chromogranin, synaptophysin, serotonin, gastrin, and glucagon. Of histogenetic interest, some individual neoplastic cells appeared to be positive for both mucin and chromogranin, and this was confirmed by the electron microscopic finding of microvilli, intracytoplasmic mucin droplets, and neurosecretory granules involving the same neoplastic cells. This also appears to be the first reported case of adenocarcinoid associated with lymphoma and demonstration of histochemical/immunohistochemical and ultrastructural evidence of cellular components with dual mucinous adenocarcinoma and neuroendocrine features, and the second reported case to have prostatic metastases.
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PMID:Adenocarcinoid of ileum and appendix, incidentally discovered during exploratory laparotomy for gastric MALT lymphoma, with subsequent diffuse prostatic metastases: report of a case with light, immunohistochemical, and electron microscopic studies. 995 28

Somatostatin is a neuropeptide produced by neuroendocrine, inflammatory and immune cells in response to different stimuli. Somatostatin inhibits various cellular functions including secretions, motility and proliferation. Its action is mediated by five specific somatostatin receptors (sst1-sst5) which belong to the G protein-coupled receptor family. The five receptors bind the natural peptide with high affinity but only sst2, sst5 and sst3 bind the short synthetic analogues used to treat patients with neuroendocrine tumors. The five receptors are expressed in various normal and tumor cells, the expression of each receptor being receptor subtype and cell-type specific. In neuroendocrine tumors, sst2 is highly expressed whereas in advanced pancreatic adenocarcinoma as well as high-grade colorectal carcinomas, its expression is lost. Each receptor subtype is coupled to different signal transduction pathways through G protein-dependent and -independent mechanisms. The synthesis of selective agonists for each receptor and the recent development of genetic animal models with selective deletion of receptor subtype provide tools for establishing some of the biological roles of the receptors. sst1, 2 and 5 mediate inhibition of GH secretion whereas sst2 and sst5 mediate inhibition of glucagon secretion and insulin secretion, respectively.
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PMID:Somatostatin receptors. 1094 Jun 84


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