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 gross, histomorphologic, cytochemical, and immunocytochemical findings in 16 dogs with medullary thyroid carcinoma were evaluated. Grossly, the neoplasms were encapsulated, firm, lobulated, and grey-white to tan. The typical histologic pattern was groups or sheets of round to polygonal cells with fibrovascular stroma, which was thickened and hyalinized in places. Variants of clear cell (two dogs), giant cell (one dog), and oxyphil cell (one dog) types were also seen. In all 16 dogs, Grimelius-stained sections of the neoplasms revealed intracytoplasmic silver granules; ten tumors contained amyloid and four contained mucin. Immunohistochemically, the neoplasms reacted to AE1/AE3 (n = 13), S-100 protein (n = 5), neuron specific enolase (n = 14), synaptophysin (n = 11), calcitonin (n = 16), somatostatin (n = 4), gastrin (n = 7), and serotonin (n = 6). Only one neoplasm was positive for vimentin. None of the neoplasms reacted to antibodies for neurofilaments, thyroglobulin, insulin, glucagon, or adrenocorticotrophic hormone. Eleven neoplasms contained multiple (two to four) peptides, in various combinations. It was concluded that in dogs, gross and histologic features can be used to distinguish medullary thyroid carcinoma from other thyroid malignancies. Cytochemical and immunocytochemical studies with neuron specific enolase, synaptophysin, and calcitonin can be used to establish the diagnosis of medullary thyroid carcinoma in dogs.
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PMID:Gross, histologic, cytochemical, and immunocytochemical study of medullary thyroid carcinoma in sixteen dogs. 190 46

Neuroendocrine (NE) neoplasms of the human bronchopulmonary tract were examined by electron microscopy, immunocytochemistry, and gel electrophoresis of cytoskeletal proteins from microdissected tissue samples. All samples (carcinoids, well-differentiated NE carcinoma, NE carcinomas of intermediate type, NE carcinomas of the small cell type) contained significant numbers of cells that immunostained for one or more of the following neuroendocrine markers tested: bombesin, calcitonin, ACTH, leu-enkephalin, gastrin, serotonin, somatostatin, alpha-melanocyte-stimulating hormone, vasoactive intestinal peptide, glucagon, insulin, substance P, and neuron-specific enolase. Electron microscopy revealed typical NE cell features, including variable abundant and frequently heterogeneous neurosecretory granules. Tumor cells contained filaments specifically stained with different conventional and monoclonal antibodies to cytokeratins and displayed punctate plasma membrane staining with antibodies to desmoplakins, in agreement with the electron microscopic demonstration of tonofilament bundles and desmosomes. Immunocytochemistry for NE markers and cytoskeletal proteins on consecutive sections revealed both cytokeratins and neuroendocrine substances in single cells. Using gel electrophoresis of cytoskeletal proteins of tissue regions extracted with high salt buffer and detergent, we could detect, in the tumors tested, appreciable amounts of cytokeratin polypeptides 8, 18, and 19, i.e., major cytokeratins also found in certain other lung carcinomas such as adenocarcinomas. Tumor cells were not significantly stained with antibodies to other intermediate filament proteins such as vimentin, desmin, glial filament protein, and neurofilament protein. The results show that NE substances can be synthesized in cells containing a typical epithelial cytoskeleton, i.e., cytokeratin filaments and desmosomes. These findings support the notion of an epithelial character of these tumors and appear in contrast with recent reports that neurofilaments are the only type of intermediate filaments present in carcinoids and other pulmonary NE tumors. These observations may have important implications for the histogenesis of NE carcinomas and for diagnostic pathology.
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PMID:Coexpression of neuroendocrine markers and epithelial cytoskeletal proteins in bronchopulmonary neuroendocrine neoplasms. 298 72

Three cases of clinically benign pancreatic papillary cystic tumors in young female patients were studied by immunohistochemistry and electron microscopy in order to define the cellular nature of this type of neoplasm. Two of the tumors showed focal cytokeratin- and desmoplakin-positivity as evidence of focal epithelial differentiation, while the tumor cells were in all cases positive for vimentin--the intermediate filament protein typical of (but not specific for) mesenchymal cells. Electron microscopy showed some cell-cell junctions, but there was no evidence of acinar or islet cell differentiation. The tumors were at least focally positive for neuron-specific enolase, and small clusters of polypeptide hormone immunoreactive cells were present in all cases (glucagon 3/3, somatostatin 2/3, insulin 2/3). However, the tumors were negative for synaptophysin and neurofilament proteins, unlike most islet cell tumors. Trypsin and chymotrypsin immunoreactivity was found in all tumors, but because many nonpancreatic carcinomas were also positive, we doubt whether these two enzyme proteins can act as specific markers for pancreatic acinar cell differentiation. Two of the tumors that were studied immunohistochemically for the presence of nuclear estrogen receptors, were negative. Therefore no proof of the suggested hormone dependence of this tumor could be obtained. We conclude that papillary cystic tumor is a neoplasm of primitive pancreatic epithelial cells, that may exhibit focal endocrine cell differentiation.
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PMID:Papillary cystic tumor of the pancreas. An analysis of cellular differentiation by electron microscopy and immunohistochemistry. 367 83

The patterns of distribution of insulin (INS), glucagon (GLU), atrial natriuretic peptide (ANP), neuropeptide-Y (NPY), cholecystokinin-octapeptide (CCK-8), neurofilament-200 protein (NF), S-100 protein (S-100), and vimentin (VIM) in the pancreas of the one-humped camel (Camelus dromedarius) were investigated using immunohistochemical techniques. INS-immunoreactive cells were observed in the central and peripheral parts of the islets of Langerhans, but some solitary INS-positive cells were found outside the islets. INS-positive cells constituted 44.26-90.91% [mean +/- standard deviation (std): 67.34 +/- 14.20] of the total number of islet cells. GLU-immunopositive cells were located mainly in the peripheral region of the islets, and they constituted 11.43-44.44% [mean +/- std: 23.54 +/- 8.27] of the total number of islet cells. ANP and CCK-8 immunoreactivity was observed in neurons and perivascular nerves fibers. NPY was identified in pancreatic neurons and in some peripheral and central cells of the islets of Langerhans. VIM immunoreactivity was observed in the endothelial cells of blood vessels and the nerves located in the perivascular, interlobular and periacinar regions. VIM was also detected immunohistochemically in the periductal nerves of the pancreas. NF occurred only in nerves. S-100 was discerned mainly in the nerves of the interlobular connective tissue and in nerves lying close to blood vessels and acinar tissue. It is concluded that INS, GLU, ANP, NPY, CCK-8, NF, S-100, and VIM are well distributed in the pancreas of the camel.
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PMID:Immunohistochemical identification of pancreatic hormones, neuropeptides and cytoskeletal proteins in pancreas of the camel (Camelus dromedarius). 898 75

Some cytologic specimens may be limited in quantity, and this may hamper or preclude the performance of immunocytochemistry (ICC) in cases where more than one antibody (ab) is required by ICC to arrive at a definitive diagnosis. There is very little information in the cytology literature regarding the use of ICC for specimens that are limited in quantity. In this study, we describe a method, derived from the principles of double immunolabelling, whereby more than one ab test can be repeatedly used on the same Papanicolaou stained slide. Multiple cytologic scrape preparations fixed in 95% ethanol were obtained from fresh surgical specimens including carcinomas of the breast, endometrium, stomach, ovary and colon. Nonneoplastic tissues included tonsil (2), lymph node (2) and myometrium. Papanicolaou stained slides or unstained slides were subjected to two sequential ICC procedures, the first in which the ab was known to be nonreactive with the cells (insulin, glucagon, or somatostatin) and the second in which the ab was known to be positive in the cells. Positive controls for the known positive abs included a single-step ICC procedure as well as the tissue section. The test abs included CAM 5.2, AE1/3, K903, LCA, L26, UCHL-1, s-100, mCEA, GCDFP-15, vimentin, muscle specific actin and desmin. Identical two-step ab procedures were carried out on the tissues from the same surgical specimens. For Papanicolaou stained cytologic specimens, abs were reactive and gave excellent results for the repeat second-step ICC method. There was no false positive or false negative staining. This "repeat ICC" method also gave excellent results on the tissue sections. Immunocytochemistry can be performed more than once on the very same cytologic specimen if the initial ICC antibody attempt is negative. This method may be especially useful in situations where more than one antibody is needed on a very limited cytologic sample size.
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PMID:Immunocytochemistry on cytologic specimens of limited quantity. 948 46

The study of intermediate filament expression in the pancreatic epithelium has been previously focused almost exclusively on cytokeratins. Transient vimentin immunoreactivity has also been detected in duct cells of rat fetal pancreas. Here we report that, in rat pancreas, intense GFAP-like immunoreactivity is detectable in a subpopulation of endocrine cells located in the periphery of the islet of Langerhans. In addition, staining appeared to be preferentially localized to the apical pole of the cells. Two different polyclonal antibodies were employed in this study, with analogous results. Staining of consecutive sections with anti-GFAP, anti-glucagon, and anti-somatostatin antibodies demonstrates that GFAP-like immunoreactivity is present in glucagon-secreting cells. The relevance of this finding is discussed. (J Histochem Cytochem 48:259-265, 2000)
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PMID:Glial fibrillary acidic protein (GFAP)-like immunoreactivity in rat endocrine pancreas. 1063 92

Persistent hyperinsulinemic hypoglycemia of infancy (PHHI) is characterized by hyperinsulinism and profound hypoglycemia, with most children requiring pancreatic resection. The histological classification of PHHI is controversial. Most authors acknowledge the existence of focal areas of islet cell proliferation (adenomatosis) in 30%-50% of cases and a diffuse disorganisation of islet architecture, termed "nesidiodysplasia," in others. De Lonlay et al. reported that cases with adenomatosis are focal with normal remainder of pancreas and that focal and diffuse disease can be differentiated intraoperatively, on the basis of increased beta-cell nuclear size found only in the diffusely abnormal pancreas. We have examined pancreatic histology in a blinded controlled study of PHHI patients. Pancreatic tissue was obtained at autopsy from 60 normal subjects (age 17 weeks gestation to 76 years) and from surgical specimens of 31 PHHI patients. Sections from PHHI subjects (n = 294 blocks) and control sections were stained with hematoxylin and eosin, insulin, glucagon, somatostatin, NSE, cytokeratin 19, and vimentin. Three sections from each PHHI patient were randomly chosen for further analysis. Age-matched control (n = 34) and PHHI sections (n = 66) were examined, with the identity of subjects concealed. A diagnosis of normal histology, adenomatosis, or diffuse nesidiodysplasia was recorded for each section. The presence of large beta-cell nuclei (>19 microm), ductuloinsular complexes, and centroacinar cell proliferation was noted. Of a total of 65 subjects examined (34 control and 31 PHHI), 37 subjects were identified as normal on both sections examined. All the control cases were correctly identified as normal and none had large beta-cell nuclei or centroacinar cell proliferation. Of 31 PHHI patients, 28 were identified as abnormal, either on the basis of abnormal architecture and/or abnormally large beta-cell nuclei. Three patients were identified as normal in both sections. Fifteen of 31 patients had diffuse nesidiodysplasia only. Of 13 patients with areas of adenomatosis, 2 had resection of a nodule with adenomatosis present in most of the tissue removed at surgery. Nine patients had a diagnosis of adenomatosis in one section and a diagnosis of diffuse nesidiodysplasia in the other sections from nonadjacent pancreas. Only 2 of 31 PHHI cases had adenomatosis on one section examined and normal pancreas on the other section examined. Large beta-cell nuclei were variably found in PHHI sections. Only 5 of 15 patients with diffuse nesidiodysplasia had large nuclei in both sections examined. Centroacinar cell proliferation was identified in 12 PHHI subjects, 6 with adenomatosis and diffuse nesidiodysplasia and 6 with diffuse changes only. It was patchy in distribution within sections and present in only one section in 7 of the 12 subjects. In summary, we have shown that a blinded observer could differentiate control and PHHI pancreatic tissue. Only 2 of 31 patients (6%) had focal adenomatosis with normal nonadjacent pancreas, the majority (24 of 31) had diffuse nesidiodysplasia affecting the remainder of their pancreas, with 38% (9 of 24) also having areas of adenomatosis. Large beta-cell nuclei did not reliably identify those with diffuse disease in this study. There was evidence of significant ductal and centroacinar proliferation in 39% of PHHI cases, which was not observed in any of the controls. We have shown that PHHI subjects have a spectrum of pancreatic histological abnormalities, from no abnormality to diffuse subtle changes to florid adenomatosis. Patients could not be segregated into subtypes for different operative intervention despite the availability of full immunohistochemical staining.
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PMID:Histologic findings in persistent hyperinsulinemic hypoglycemia of infancy: Australian experience. 1100 Mar 31

Middle ear adenoma (MEA) is a rare tumor postulated to take origin from the lining epithelium of the middle ear cavity. The authors report on a case of MEA arising in a 53-year old woman suffering from a sensation of fullness in her left ear, otalgia, and light left-sided hearing loss. Histopathologically, the lesion was composed of cuboidal and polygonal cells displaying a trabecular, tubulo-glandular, and solid pattern of growth. Immunohistochemically, neoplastic cells diffusely stained with anti-vimentin antibodies and were focally positive for chromogranin A, neuron-specific enolase, lysozyme, and cytokeratins AE1/AE3. The majority of tumor cells showed weak and diffuse staining with both anti-PP and anti-ACTH antibodies and intense positivity with anti-glucagon and anti Leu-7 antibodies. Ultrastructural investigation revealed both mucinous-glandular and neuroendocrine differentiation. The authors suggest that the appropriate terminology would be adeno-carcinoid or amphicrine tumor of the middle ear rather than "adenoma," a term that does not reflect its dual nature.
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PMID:Middle ear adenoma is an amphicrine tumor: why call it adenoma? 1129 23

Malignant mesenchymal neoplasms of the pancreas are rare and malignant islet cell tumors with sarcomatous dedifferentiation are rarer still. We present a case of malignant islet cell tumor with sarcomatous differentiation, which to our knowledge is only the second reported case showing such a combination of morphologic features. Clinically, the neoplasm was not hormonally active and immunohistochemical staining was negative for gastrin, glucagon, insulin and somatostatin. The sarcomatous component strongly reacted with an antibody directed against vimentin, and a minority of cells stained strongly with antisera directed against desmin and smooth muscle actin. The spindle cell component was nonreactive with antibodies directed against Factor VIII. The myogenous direction of differentiation in the present tumor is similar to that seen in the prior case report of malignant islet cell tumor with rhabdomyosarcomatous differentiation.
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PMID:Malignant islet cell tumor with sarcomatous differentiation. 1170 83

Type I diabetes is characterized by destruction of insulin-producing beta-islet cells in the pancreas resulting in hyperglycemia and associated morbidity. The successful treatment of diabetes by transplanted islets has resulted in renewed efforts to identify methods to augment islet availability. One approach is to identify and expand islet precursor cells able to later differentiate into functional endocrine cells. A population of cytokeratin 19-negative, vimentin-positive, insulin-negative, glucagon-negative, and nestin-positive cells was cultured from human fetal pancreas and passaged for over 20 population doublings. These cells were stimulated to form cell aggregates when grown on poly-D-lysine (PDL)-coated surfaces and then evaluated for differentiation potential using in vivo function as a surrogate marker for the presence of differentiated precursor cells. Streptozotocin-induced diabetic SCID mice implanted with PDL-induced cell aggregates were able to maintain glucose concentrations below 200 mg/dL for over 70 days (n = 5). In addition, human C-peptide was detectable in implanted animals but not in control animals. These findings show that a population of human fetal pancreas-derived cells (1) can be cultured and expanded in vitro, (2) can maintain the ability to differentiate into beta-islet-like cells, and (3) can correct hyperglycemia in a mouse model of diabetes. Further improvements in isolation, culture, and differentiation of human pancreas-derived beta-cell precursors may one day help to provide a novel source of islets for use in transplantation therapy to treat type I diabetes.
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PMID:Long-term correction of hyperglycemia in diabetic mice after implantation of cultured human cells derived from fetal pancreas. 1521 Nov 20


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