UMLS:C0031511 - FACTA Search

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Query: UMLS:C0031511 (pheochromocytoma)
14,622 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ultrastructural features of neoplastic cells can provide clues for correct diagnosis when light microscopy fails. Secretory granules are characteristic in the following tumors: mucin granules in poorly differentiated adenocarcinomas, zymogen granules in acinic cell carcinomas, lysosomal granules in prostatic carcinomas, melanin granules in malignant melanoma, carcinoid, islet cell tumors, pheochromocytoma, and neuroblastoma granules in the corresponding neoplasms. Among cytoplasmic organelles, rough surfaced endoplasmic reticulum characterizes adrenocortical, ovarian, and hepatocellular carcinomas and plasmacytomas. Tonofibrils are characteristic of squamous cell carcinomas. Glycogen deposits distinguish Ewing's sarcoma from lymphoreticular neoplasms. Intercellular relationships and membrane specialization are important features in the differential diagnosis of various undifferentiated tumors. The frequent resolution of difficult diagnostic problems by electron microscopy outweighs the disadvantages of this technique, such as the expense and time required.
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PMID:The usefulness of electron microscopy in the diagnosis of human tumors. 115 Feb 21

Infection of a clonal rat pheochromocytoma cell line, PC12, with Japanese encephalitis (JE) virus produced successively higher titers of virus in the culture fluid during the 72-h experimental period. In electron microscopical observation, JE virus entered PC12 cells by direct penetration through the plasma membrane at 2 min postinoculation (p.i.) and caused marked cellular hypertrophy and extensive proliferation of the cellular secretory system including rough endoplasmic reticulum (RER) and Golgi complexes starting 24 h p.i. The proliferating RER of the virally infected cells contained progeny virions and characteristic endoplasmic reticulum vesicles in its cisternae, and the proliferating Golgi complexes contained virions in their saccules. These findings indicated that the proliferation of the cellular secretory system occurred in association with viral replication and maturation in the system. Seventy-two hours p.i., the cellular secretory system of infected PC12 cells showed degenerative changes with vesiculation, disorganization, and dispersion of the Golgi complexes and fragmentation, focal cystic dilation, and dissolution of the RER in the same manner as those seen in the secretory system of JE-virus-infected neurons in the mouse brain. Thus, JE-virus-infected PC12 cells seem to be a suitable neurogenic cell line for the study of the pathogenic mechanism of JE virus. At the same time, the virally infected cells seem to offer an interesting cell model for the study of the morphogenesis of the cellular secretory system.
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PMID:Cytopathology of PC12 cells infected with Japanese encephalitis virus. 136 19

Three spindle cell neoplasms were encountered in a series of 46 FNA of the adrenal performed between 1984 and 1991. These neoplasms included a recurrent undifferentiated adrenal cortical carcinoma (ACC) with a predominant spindle cell pattern, a pheochromocytoma (PC), and a metastatic desmoplastic malignant melanoma (DMM). Cytologically, the ACC was characterized by the presence of numerous microtissue fragments composed of spindle-shaped malignant cells with oval to spindle-shaped nuclei, one or more nucleoli, and bipolar cytoplasmic processes. In some areas the tumor cells were dissected by vascular channels. The background contained abundant metachromatic stroma as well as individually scattered tumor cells. The PC was composed predominantly of loosely cohesive spindle-shaped cells along with more polygonal shaped cells with delicate faintly staining granular cytoplasm. The tumor cells exhibited mild anisonucleosis. The tumor fragments were well vascularized by arborizing delicate capillary channels. The DMM was composed of microtissue fragments, interlacing fascicles and loose aggregates of spindle-shaped malignant cells with hyperchromatic nuclei, small nucleoli, and an absence of cytoplasmic pigment. In each case ancillary studies including immunocytochemistry and electron microscopy (EM) were helpful in the differential diagnosis. The ACC was negative for cytokeratins, neuron-specific enolase (NSE), and muscle-specific actin (HHF), but displayed strong positivity for vimentin as well as characteristic whorls of smooth endoplasmic reticulum by EM. The PC was positive for NSE and chromogranin with no EM performed. The DMM stained for S-100 and vimentin but was negative for HMB-45, cytokeratin, and HHF. EM examination revealed rare atypical premelanosomes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fine-needle aspiration cytology of spindle cell neoplasms of the adrenal gland. 160 81

Monoclonal antibody (MAb) 2H1, raised in mice immunized with membrane fractions from cultured rat pheochromocytoma cells (clonal line PC-12), detects a polypeptide from rat brain and PC-12 cell membranes of 60-65 KD apparent molecular mass. The polypeptide has been localized by immunoelectron microscopy in the rough endoplasmic reticulum (RER) of neurons. By light microscopic immunocytochemistry, several rat tissues and two rat-derived cultured cell types show selective patterns of staining with 2H1. In the central nervous system, the antibody stains neuronal cytoplasm; in the spleen, staining is seen only in certain cells of the marginal zone of the white pulp, and in lymph nodes, in plasma cells, and in areas populated by monocytes and macrophages. Whereas astrocytes and adrenal medullary cells in situ are virtually unstained with 2H1, primary cultures of astrocytes and PC-12 cells, which are derived from adrenal medullary cells, stain intensely with 2H1. The strong staining of cultured astrocytes and PC-12 cells with 2H1 suggests that the levels of the 60-65 KD polypeptide are up-regulated during cell proliferation and growth. Only a few hepatocytes stain with 2H1; intestinal epithelial and pancreatic cells are not stained with 2H1. The organelle-specific antibody 2H1 may prove a useful probe in structural and functional studies of membranes of the rough endoplasmic reticulum in neurons, and in certain cells of the immune system.
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PMID:Monoclonal antibody 2H1 detects a 60-65 KD membrane polypeptide of the rough endoplasmic reticulum of neurons and selectively stains cells of several rat tissues. 201 13

Pheochromocytoma cells (clone PC-12) were treated with 6-aminonicotinamide. Tetrahydrobiopterin content and DOPA production of the cells were determined by reverse-phase HPLC and subsequent electrochemical detection. The same chromatographic system was used to determine total biopterin (tetrahydrobiopterin, dihydrobiopterin and quinoide dihydrobiopterin) by fluorescence detection. Tetrahydrobiopterin plays a decisive role as cofactor of tyrosine hydroxylase for the biosynthesis of DOPA and dopamine. Addition of 6-aminonicotinamide to the culture medium resulted in the accumulation of 6-phosphogluconate, suggesting that PC-12 cells synthesize 6-aminonicotinamide-adenine-dinucleotide-phosphate (6-ANADP) by a glycohydrolase localized in the endoplasmic reticulum. This substance is known to be a strong inhibitor of 6-phosphogluconate dehydrogenase and leads to a blockade of the pentose phosphate pathway. In our experiments, the synthesis of biopterins was depressed after application of 6-aminonicotinamide. The decrease of intracellular tetrahydrobiopterin and total biopterin by 6-aminonicotinamide at different concentrations was strongly correlated with a reduced cellular DOPA production. The decreased content of biopterin cofactor was compensated by addition of the precursor sepiapterin, indicating that the NADPH2-dependent reductases in biopterin synthesis are not inhibited by the antimetabolite. However, DOPA production remained suppressed at the same time. After application of NADH2, we observed an increased DOPA production though the decreased biopterin levels remained almost unchanged. The results imply that the first step in the synthesis of biopterin from GTP as well as the recycling pathways of the oxidized cofactor might be the site of action of the antimetabolite.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of biopterin synthesis and DOPA production in PC-12 pheochromocytoma cells induced by 6-aminonicotinamide. 252 71

Histological and ultrastructural studies were performed to examine 6 paragangliomas of various sites: carotid glomus, aortic body, sympathetic chain, and stomach. Five of the tumors in question had a histological structure typical of a paraganglioma. The gastric tumor was distinguished by being similar to a pheochromocytoma. With regard to the degree of infiltrative growth, the paragangliomas of the sympathetic chain and stomach were regarded as malignant. The ultrastructures of the paragangliomas examined were found to be of the same type. In all the neoplasms, tumor cells had signs of neuroendocrine and neurogenous differentiations that were characteristic of the ultrastructural organization of postganglionic neurons in the autonomic nervous system. The neurogenous differentiation was evidenced by cytoplasmic portions that are structurally similar to rough-surface endoplasmic reticulum, which is pertaining to Nissl's bodies; neurofilaments that form concentric structures containing neuroendocrine granules such as fibrous or Pick's bodies; intracytoplasmic cilia; specialized cytoplasmic processes of two types: axons and dendrites; partially reduced intercellular contacts, such as axosomatic and axodendritic synapses; sustentacular cells (sustenocytes). In the neoplasms evaluated as malignant, the neurogenous differential signs were more pronounced by reducing the number of neurosecretory granules, which might, apparently, serve as an ultrastructural criterion for establishing the degree of paraganglioma malignancy.
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PMID:[Morphology and histogenesis of paraganglioma]. 254 76

The localization of tyrosine hydroxylase (TH) immunoreactivity in rat adrenal chromaffin and pheochromocytoma (PC12) cells was investigated by immunoelectron microscopy using monoclonal and polyclonal antisera against TH purified from rat adrenal medulla. Strong TH immunoreactivity was found uniformly in the granules of the adrenaline cells; the immunoreactivity was visible mainly within the periphery, but not in the clear space of the granules of the noradrenaline cells. In the PC12 cells, strong TH immunoreactivity was also observed uniformly in the granules. In addition, TH immunoreactivity was seen in the cytoplasm, the ribosomes attached to the endoplasmic reticulum and the free ribosomes of both the rat adrenal chromaffin and PC12 cells. These results suggest that TH may be localized in the granules, cytoplasm and ribosomes of rat adrenal chromaffin and PC12 cells.
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PMID:Intracellular localization of tyrosine hydroxylase immunoreactivity in the rat adrenal chromaffin and pheochromocytoma cells. 257 25

Cells of the PC-12 rat pheochromocytoma cell line respond to nerve growth factor (NGF) by sprouting neurites and biochemically differentiating into sympathetic ganglion-like cells. NGF-stimulated ('differentiated') and unstimulated ('undifferentiated') cells were studied by cytochemical techniques for the localization of the enzymes acid phosphatase (ACPase) and thiamine pyrophosphatase (TPPase), and by a morphometric analysis of the distribution of endocytosed wheat-germ agglutinin labelled with horseradish peroxidase (WGA-HRP). Both cytochemical stains showed the enzymes to be distributed in lysosomes and certain cisternae of the Golgi apparatus in both NGF stimulated and unstimulated cells. ACPase was not confined to GERL (Golgi-endoplasmic reticulum-lysosome) as in certain other cells. The morphometric studies demonstrated that the reaction product of the internalized WGA-HRP occupied 4.7% of the cytoplasmic area in unstimulated cells and 4.5% in NGF-stimulated ones. Despite this similarity, the distribution of the WGA-HRP among the studied intracellular compartments in these two cell groups varied. In the NGF-stimulated cells 3.3% of the WGA-HRP reaction product was found in the innermost Golgi cisterna(e) while in unstimulated cells only 0.3% was seen in this compartment. Similarly, 4.3% of the WGA-HRP stain was found in small vesicles at the 'trans' aspect of the Golgi apparatus in stimulated cells, when only 0.3% of the stain occupied this compartment in 'undifferentiated' cells. The morphometric analysis also revealed that when the PC-12 cells were stimulated with NGF, the Golgi apparatus increased in area by approximately 70%. These findings are consistent with the hypothesis that NGF induced differentiation of PC-12 cells is coupled with enhanced endocytosis of WGA and probably of its 'receptor' to the innermost Golgi cisterna(e) and the closely associated vesicles.
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PMID:Nerve growth factor induced changes in the Golgi apparatus of PC-12 rat pheochromocytoma cells as studied by ligand endocytosis, cytochemical and morphometric methods. 613 21

The organelle specificity of the uranaffin reaction was determined by subjecting two human neoplasms (a pheochromocytoma and islet cell carcinoma) to four different experimental conditions. In Uranaffin Procedure (UP) I, fixed tissue was immersed in 0.9% sodium chloride (NaCl) before reacting with 4% uranyl acetate (pH 3.9) for 24 hours. In UP II, the tissue was prepared as in UP I with the exception that the tissue was immersed in uranyl acetate for 48 hours. In UP III, fixed tissue was prepared as in UP I with the exception that tissue was immersed in 0.1M cacodylate buffer (pH 7.2) instead of 0.9% NaCl. In UP IV, fixed tissue was prepared as in UP III with the exception that the tissue was immersed in uranyl acetate for 48 hours instead of 24 hours. When UPs I and II were utilized, only three cell organelles showed electron-dense reactivity: the nucleus, ribosomes, and cytoplasmic neurosecretory-like granules. In the nucleus, the nuclear chromatin, nucleolus, interchromatinic granules and perichromatinic granules were intensely stained. The reaction product in all of the uranaffin-positive organelles had a finely granular appearance. When fixed tissue was immersed in cacodylate buffer instead of isotonic saline, a non-specific reactivity was observed. The reaction product in some areas had a distinct crystalline appearance and filled some areas of the cytosol, the cisternae of the endoplasmic reticulum, the Golgi apparatus, the perinuclear cisternae, the nucleus, nucleolus, mitochondria, neurosecretory-like granules and larger lysosome-like bodies. There was a statistically significant (p less than 0.05) increase in the number of uranaffin-positive granules/mu2 when both endocrine neoplasms were reacted with uranyl acetate for 48 hours instead of 24 hours. The increase in uranaffin-positive granules using UP II did not result in an increase in non-specificity of the staining reaction.
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PMID:An ultrastructural evaluation of the cell organelle specificity of the uranaffin reaction in two human endocrine neoplasms. 630 75

In previous experiments it has been demonstrated that nerve growth factor (NGF), subsequent to its binding to specific membrane receptors, is internalized. Ultrastructurally, this internalized NGF is localized in membrane-confined compartments which ultimately fuse with lysosomes. The present experiments were designed, first, to evaluate whether a very small but functionally important portion of the internalized NGF might reach the free cytoplasm (and subsequently the nuclear chromatin) and might be responsible for the induction of choline acetyltransferase (ChAT) in PC12 cells. Second, we investigated whether a lysosomal proteolytic degradation product of NGF might act as a second messenger in the NGF-mediated ChAT induction. In one series of experiments, guinea pig erythrocyte ghosts, loaded with NGF (or NGF antibodies), fluorescein isothiocyanate-coupled bovine serum albumin, and/or horseradish peroxidase (HRP) were fused with PC12 pheochromocytoma cells. Electron microscopy showed that [125I]NGF and HRP reaction product were located throughout the cytoplasm and the nucleus but did not penetrate membrane compartments such as the endoplasmic reticulum, the Golgi complex, the perinuclear space, or mitochondria. Biochemically, NGF injected into the cytoplasm did not produce an induction of ChAT, whereas NGF acting via cell surface receptors resulted in a 2-fold increase in ChAT. Conversely, injection of NGF antibodies did not prevent the receptor-mediated ChAT induction. In a second series of experiments, the half-life of internalized NGF was increased from 40 min to 24 hr by the administration of leupeptin, a protease inhibitor which is accumulated in lysosomes. However, the NGF-mediated ChAT induction was not affected by this treatment. It is concluded that NGF itself does not act directly on cytoplasmic or nuclear target sites, nor is a proteolytic degradation product of NGF responsible for the NGF-mediated ChAT induction. Thus, NGF must act via a second messenger mechanism, the nature of which remains to be established.
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PMID:Nerve growth factor-mediated induction of choline acetyltransferase in PC12 cells: evaluation of the site of action of nerve growth factor and the involvement of lysosomal degradation products of nerve growth factor. 650 22

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