Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The false positive and false negative computed tomography diagnoses of glioma made using an EMI 1010 machine on a consecutive series of patients seen over a period of two years are recorded. About 1.5% of gliomas were not detected on initial CAT scan, 6.5% were misdiagnosed as benign lesions, and in 6.5% of the cases identified as glioma a non-malignant condition was subsequently diagnosed.
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PMID:Difficulties in diagnosis of supratentorial gliomas by CAT scan. 46 55

Three cases of cystic meningioma encountered in one year are presented. It appears from a review of the literature, and an analysis of these three cases, that large xanthochromic cerebral cysts may be associated with meningiomas in any of three configurations: (1) centrally within the tumour; (2) peripherally within the tumour; (3) in the adjacent brain. Regardless of which configuration applies, the CAT scan appearance of such cystic meningiomas may mimic that of a glial tumour with cystic or necrotic change, and lead to an incorrect presumptive diagnosis. This false impression may be perpetuated by the gross appearance at operation, which can also mimic malignant glioma. Although several radiological features should suggest the possible presence of a cystic meningioma, we know of no definite radiological means of differentiating this lesion from the more common malignant glioma. This finding should underline the need to biopsy all suspected cerebral neoplasms, regardless of how much their appearance on CAT scan may suggest malignant glioma.
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PMID:Xanthochromic cysts associated with meningioma. 46 60

Two patients, one with multiple sclerosis (MS) and the other with a glioma of the splenium of the corpus callosum, were biopsied with the aid of CAT. Light microscopy, histochemistry, electronmicroscopy and morphometric analysis of counts of mitochondria, dense bodies, and pinocytotic vesicles within the capillary endothelial cells was done. Examination of the MS plaque showed endothelial cell tight junctions to be closed, basal lamina to be thinned, but endothelial cell mitochondria to be the same as in a patient without MS. Pinocytotic vesicles were markedly increased in endothelial cells in MS. Despite intense inflammation in the surround, endothelial lysosomes were as few as in a control.
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PMID:The capillaries in acute and subacute multiple sclerosis plaques: a morphometric analysis. 56 53

To investigate the regulatory processes involved in the expression of the D2 dopamine receptor gene, a rat genomic clone was isolated using a 21-mer oligonucleotide probe made of exon 1 sequences. A 1.3-kb region including all of exon 1, its 5'-flanking region, and part of intron 1 was sequenced. S1 nuclease analysis indicated three consecutive nucleotides as the main transcription start sites; several weaker sites were also noted between 321 and 363 nucleotides upstream from the 3' end of exon 1. The promoter region lacks TATA and CAAT boxes and is rich in G+C content with several putative Sp1 binding sites. Transient expression assays using chimeric constructs of D2 promoter deletion mutants-chloramphenicol acetyl-transferase gene in the neuroblastoma cell line NB41A3 which expresses D2 binding sites indicated strong transcription enhancing activity between nucleotides -75 and -30 and silencing activity between nucleotides -217 and -76. DNase I footprinting studies using nuclear extract from NB41A3 suggested Sp1 binding to its consensus sequence at nucleotide -48 but inhibition of Sp1 binding at nucleotide -86 by the extract. The D2 promoter could not induce transcription of the heterologous CAT gene in C6 glioma, embryonal NIH 3T3, or hepatic Hep G2 cells. It is concluded that the rat D2 gene shares with the human D1A dopamine receptor gene several features typical of "housekeeping" genes but they are both tissue-specific, regulated genes. Unlike the D1A gene, however, the D2 gene has a strong preference for transcription initiation to three consecutive nucleotides.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analysis of the promoter region of the rat D2 dopamine receptor gene. 139 Jun 23

Genomic and cDNA clones encoding the rat D1 receptor were isolated and sequenced. Comparison of the D1 receptor cDNA and genomic sequences revealed that the rat D1 receptor gene is organized into two exons separated by a small intron in the 5' untranslated region of its mRNA. The transcription start site is located 864 bp upstream from the translational initiation site. The 5'-flanking sequences of the D1 receptor gene do not contain TATA and CAAT canonical sequences, but have a high G+C content, potential cyclic AMP and glucocorticoid response element sequences, and binding sites for transcription factors such as Sp1, Ap1, and Ap2. Transfection studies using the D1 5'-flanking sequence and CAT gene fusion constructs have demonstrated that (1) the D1 promoter is active in D1-expressing neuroblastoma NS20Y cells, but inactive in D1-deficient glioma C6 and kidney 293 cells, (2) the information contained within 735 bp of 5'-flanking sequence of the D1 gene appears to be sufficient to confer its cell-specific expression, and (3) the D1 gene promoter responds to cyclic AMP induction, suggesting the existence of an auto-regulation mechanism by which the stimulation of D1 receptor exerts a positive feedback on its own gene expression.
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PMID:Characterization of gene organization and promoter region of the rat dopamine D1 receptor gene. 140 30

DNA methylation at HpaII (CmCGG) sites inhibits expression of a human proenkephalin-CAT fusion gene when it is transiently expressed in CV-1 cells or stably expressed in C6-glioma cells. The inhibitory effects of HpaII methylation have been mapped to a site within the human proenkephalin promoter located at position -72 relative to the start site of transcription. This region spans a cAMP and phorbol ester inducible enhancer and methylation at this position inhibits both basal transcription and transcription induced by either cAMP or TPA. The HpaII site is located within an element which binds the transcription factor AP-2. In vitro methylation at this HpaII site inhibits the binding of AP-2. These results suggest that CpG methylation inhibits proenkephalin gene expression by directly interfering with the binding of a positively acting transcription factor previously shown to be essential for maximal basal, cAMP, and TPA inducible transcription.
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PMID:CpG methylation inhibits proenkephalin gene expression and binding of the transcription factor AP-2. 169 33

A genomic clone spanning a large portion of the 5' untranscribed region of the CD20 gene was isolated. Deletion analysis of subcloned fragments identified several regulatory elements. A major positive cis-acting element was localized between base pairs -290/-186. A second positive regulatory element was localized between -454/-280 and negative regulatory elements were present in the region between bp -828/-454. The sequence -280/-186 conferred B cell-specific expression on a heterologous, TATA box containing c-fos promoter. Electrophoretic mobility shift assays with overlapping oligonucleotide probes spanning -280/-186 revealed that a 25-bp probe (-225/-201) bound a nuclear protein present in B cell lines expressing the CD20/B1 antigen but not in Jurkat (T cell), U937 (promonocytic), U251 (glioma), or HeLa cells. To confirm the functional significance of this sequence, a trimer of this region was subcloned into the c-fos promoter containing CAT plasmid. Expression was observed only in BJA-B and HS-Sultan cells but not in CD20/B1- cell lines. This sequence element is also important in phorbol ester-induced CD20 expression in the pre-B cell line BP-697. These results partially characterize several regulatory elements present in the CD20 promoter that are likely important in the B cell-specific expression of the CD20 gene.
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PMID:Analysis of cis-acting elements present in the CD20/B1 antigen promoter. 171 97

Mouse lactoferrin is expressed in a variety of tissues under different types of control. To understand how molecular mechanisms govern the mode of lactoferrin expression, we isolated and characterized the 5'-flanking region of the lactoferrin gene. Several clones containing lactoferrin gene fragments were isolated from a mouse (129/J) genomic library including clone lambda J14, which contains a 7.5-kilobase pair 5'-flanking sequence. Sequence analysis of the region flanking the transcription initiation site revealed the following: a TATA-like sequence, two CAAT boxes, three GC boxes including one within the first intron, an AP2 site, seven PU boxes, an AC-rich region, a B1 sequence, and an estrogen-responsive element consensus sequence over-lapping with a chicken ovalbumin upstream promoter-binding element. Footprinting analysis demonstrated that several regions, including the putative estrogen-responsive element region, in the 5'-flanking sequence were protected from DNase I digestion. Promoter fragments were cloned into a chloramphenicol acetyltransferase receptor plasmid to study functional activity. The mouse lactoferrin gene promoter was active in human endometrium carcinoma RL 95-2 cells and in rat glioma C6 cells. Multiple upstream elements modulated the basal transcriptional promoter activity. The transcription level directed by this minimal promoter was controlled by both positive (between -1739 and -922) and negative (between -2644 and -1739, and between -589 and -291) regulatory sequences. A tissue-specific regulatory sequence was critical for the establishment of lactoferrin expression in human endometrium carcinoma cells, but not in rat glioma cells located between -1739 and -922. Reporter plasmid 0.6 mL14-CAT, containing the estrogen-responsive element sequence, was estrogen-responsive in the presence of estrogen receptor in human endometrium carcinoma RL 95-2 cells.
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PMID:Characterization of estrogen-responsive mouse lactoferrin promoter. 193 12

To determine the role of protein phosphorylation in transcription regulation, we have treated mouse neuroblastoma N18TG2 cells with the protein kinase inhibitor H-7 and tested its effect on transcription. After the preculture and transfection in the presence of H-7, the cell preparation was divided in half and cultured with and without H-7. The level of CAT expression of pSV2-CAT was found to be higher in the cells cultured in the absence of H-7 than in those cultured in the presence of H-7. This difference was observed only after pretreatment of the cells with H-7, suggesting that withdrawal of H-7 from the culture medium after preculture with H-7 gave an enhancing effect on CAT expression. This phenomenon was also observed with transformants that expressed the CAT gene of pSV2-CAT stably. The 72 base-pair (bp) repeat of SV40 DNA was responsible for this difference in CAT expression. A similar effect of H-7 on the SV40 enhancer activity was observed in mouse neuroblastoma x rat glioma hybrid NG108-15 cells, but not in rat glioma C6-BU-1 cells.
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PMID:A novel enhancement of SV40 enhancer activity by treatment of mouse neuroblastoma N18TG2 with protein kinase inhibitor H-7. 284 18

Acetylcholine metabolism has been studied in sister cultures of E13 rat spinal cord cells cultured for 1 to 3 weeks with or without conditioned medium (CM) from rat skeletal muscle cells. Spinal cord cells grown with CM synthesized and accumulated 3 to 4 times more [3H]ACh from [3H]choline than cultures grown without CM. This effect of CM was accompanied by a comparable increase in CAT activity and could not be mimicked by increasing the density of the spinal cord cultures. A 2- to 3-fold increase in AChE activity was also observed in 2- to 3-week-old CM cultures, whereas the activity of lactate dehydrogenase was identical in cultures grown with and without CM. We have compared the effects of CMs from various non-neuronal cell cultures on [3H]ACh synthesis and storage by spinal cord cultures and by sympathetic neuron cultures. CM by skeletal muscle greater than skin fibroblasts greater than rat heart muscle greater than C6 glioma cells were the most active on both types of neuron cultures, whereas CM from rat brain, L6 myoblasts, mouse 3T3, and PYT21 fibroblasts was inactive on spinal cord cultures and only weakly active on sympathetic neurons. Serum-free CM from skeletal muscle was inactive on both types of neuron cultures. The CM factor active on spinal cord cultures has been purified several thousand-fold by using a four-step fractionation scheme which has previously led to a partial purification of the CM factor involved in the regulation of CAT, AChE, and catecholamine-synthesizing enzymes in sympathetic neuron cultures ( Swerts , J. P., A. Le Van Thai, A. Vigny , and M. J. Weber (1983) Dev. Biol. 100: 1-11). Moreover, a comparison of dose-response curves established with this purified material showed that it exerted its effects on spinal cord and on sympathetic neuron cultures in the same range of concentration. Thus, these results suggest that the same macromolecule is involved in the regulation of neurotransmitter phenotype in both types of cultures despite their different embryological origins.
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PMID:Acetylcholine metabolism in rat spinal cord cultures: regulation by a factor involved in the determination of the neurotransmitter phenotype of sympathetic neurons. 614 37


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