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 activity of transglutaminase (TGase) was measured in cultured C6 glioma cells after their stimulation by either isoproterenol and isobutyl-methylxanthine or by a serum-containing medium. The activity fluctuated in a biphasic manner, with the peaks at 2-3 hr and 7-8 hr poststimulation. The first peak of TGase activity was affected neither by cycloheximide nor by actinomycin D, which inhibited protein synthesis. The second peak, on the other hand, was completely eliminated by cycloheximide and was reduced by actinomycin D. Immunological procedures were employed to find out whether or not the activity of TGase corresponded with the presence of the TGase antigen in the cultured cells. Indirect immunofluorescent staining and radioimmunoblot techniques suggested that unstimulated cells contained an inactive enzyme. This inactive, or cryptic, enzyme had the same molecular weight as its active counterpart. Activation of the enzyme was mediated by cell stimulation, probably by its release from the membrane. This step did not require protein synthesis, unlike the second step, which was dependent on de novo protein synthesis.
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PMID:Activation and de novo synthesis of transglutaminase in cultured glioma cells. 241 53

Over 35 intraaxial lesions in 15 patients suspected of having intracranial tumors were studied with MR before and after injection of Gadolinium-DTPA (Gd-DTPA). Diseases included primary and metastatic brain tumors, plaques of multiple sclerosis, occult arteriovenous malformations, lymphoma, toxoplasmosis, and pituitary adenoma. The precontrast T2-weighted sequence (SE 2000/30, 60) was found to be most sensitive in detecting intraaxial lesions, showing 17 lesions that were not seen on the post-Gd-DTPA T1-weighted sequence (SE 500/30). In one case of multiple sclerosis, several lesions seen on the pre-Gd-DTPA study on T2-weighted images faded after injection of Gd-DTPA (due to T2 shortening). In two patients with large metastatic foci, other small metastatic lesions were seen better after Gd-DTPA on both T1- and T2-weighted sequences. Four other patients with only one focal-enhancing lesion and one patient with multifocal lesions on T1-weighted images actually had a much larger single glioma depicted on pre-Gd-DTPA T2-weighted images. In a patient with AIDS, a ring-enhancing lesion thought to be an abscess proved to be lymphoma. The cryptic arteriovenous malformations enhanced but showed more characteristic findings, such as hemorrhage, on pre-Gd-DTPA studies. Our experience suggests that Gd-DTPA may not improve sensitivity of MR in the detection of intraaxial lesions. However, functional aspects of brain disease, such as the presence of perfusion of a lesion and active breach of the blood-brain barrier, are depicted well with Gd-DTPA and are vital for proper diagnosis in many instances.
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PMID:Gd-DTPA in clinical MR of the brain: 1. Intraaxial lesions. 349 Jul 58

Five cases of brain-stem hematoma are described. The cause of these hematomas was identified as "cryptic angioma" (1 cavernous angioma, 1 telangiectasia, 3 arteriovenous malformations). So, they are so-called "secondary hematoma", as opposed to brain-stem hematoma in relation with hypertension. Such secondary hematomas are reported in the literature: 37 operated on cases and 22 untreated cases were found. The clinical picture does not seem to be typical. The presentation appears to be either with the acute onset of a stroke, or with a subacute onset including relapsing symptoms. A progressive deterioration suggesting a pontine glioma or mimicking demyelination is not rare. The CT scanner appearance is often characteristic showing a high density area in the brain-stem which enhanced after injection of contrast medium with an aspect of "halo". Angiography is usually negative. The natural history of brain-stem hematoma due to rupture of a cryptic angioma is not well documented, but it seems that prognosis is very poor. So, the authors insist on surgical evacuation which is effective and safe allowing the diagnosis of brain-stem hematoma and in some cases the identification of the malformation.
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PMID:[Secondary hematoma of the brain stem. Apropos of 5 cases]. 376 36

Six patients with angiographically cryptic vascular malformations involving the brainstem were examined with computed tomography (CT). The clinical and CT findings of cryptic vascular malformations of the brainstem are described and distinguished from those of brainstem glioma and multiple sclerosis. Calcification within a brainstem lesion that displays relatively little mass effect and shows little contrast enhancement, particularly when associated with a long history of waxing and waning brainstem symptoms, should suggest a vascular malformation.
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PMID:Cryptic vascular malformations involving the brainstem. 684 69

To identify potential cell surface receptors for chicken cytotactin (CT), we have characterized the ability of recombinant fusion proteins spanning the proximal fibronectin (FN) type III repeats of the molecule to support attachment of glioma and carcinoma cell lines. The third FN type III repeat, which contains the RGD tripeptide, supported cell attachment and cell spreading; however, mutation of RGD to RAD did not result in significant loss of either activity. In addition, the same repeat of mouse CT, which contains a natural mutant, RVD, also supported cell attachment and spreading, although at a lower level; both activities were increased by mutation of the RVD sequence to RGD. Studies utilizing RGD-containing peptides and well-characterized antibodies to integrins indicated that cell attachment to the third FN type III repeat was mediated by at least two different integrin receptors of the alpha v subtype. Additional cellular receptors may also be involved in cell attachment to CT. For example, an antibody to the beta 1 subfamily of integrins partially inhibited binding of cells to intact CT but did not inhibit cell binding to the third FN type III repeat. These findings suggest that the RGD site in CT is able to mediate cell attachment to integrins and thus is not a cryptic adhesion site. They also open the possibility that the functions of CT in processes such as counteradhesion, cell migration, cell proliferation, and cell differentiation may be mediated in part by interaction with multiple integrins.
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PMID:Multiple integrins mediate cell attachment to cytotactin/tenascin. 769 84

A novel endogenous retrovirus (ERV) designated XA34 was isolated from a human glioma cDNA library using low stringency hybridization with an ERV-9 env probe. Southern blot hybridizations with human genomic DNA revealed the presence of approximately 16 genomic copies closely related to XA34. Sequencing of a 2303 bp cDNA clone of XA34 showed that it belongs to a new ERV family. The XA34 ERV has recombined with an ERV-9-like retrovirus resulting in a truncated ERV-9-like env region that ends with an Alul-like 3' LTR. By using PCR, we isolated approximately 940 bp pol fragments from three additional members of this family, XA35, XA36 and XA37. A fifth member, XA38, was isolated and sequenced as a 4729 bp genomic clone. The genomic XA38 clone spans from pol towards the 3' flanking region. The XA38 virus contains a more cryptic env region. The XA38 env is truncated in the transmembrane region and the virus then ends with three Alu repeats. Southern blot studies with human, chimpanzee, orangutan and squirrel monkey DNA show the presence of the XA34 family in all these species. That both the New and Old World monkeys have this ERV family means that the integration and/or amplification in the primate germ-line of XA34 probably took place about 40-45 million years ago. The phylogeny and the closet relatives to ERV XA34 are discussed.
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PMID:The structure and phylogeny of a new family of human endogenous retroviruses. 876 Apr 9

Human glioma cell line KG-1C contains GM3 ganglioside as its sole glycolipid. The degree of M2590 antibody binding to GM3 was found to be regulated by the cell density; the percentage of positive cells in FACS analysis decreased from approximately 20% to close to none as the cells increased their density from sparse to confluent. The contents of GM3 with different cell densities were consistent, being more than 0.4 micromol/g of the cellular weight, which was high enough to be recognized by the antibody. Trypsin treatment of the cells did not increase antibody reactivity. The extracted GM3 retained its antigenicity, being intensely stained with M2590 on a TLC plate; there was no change in chromatographic mobility either, indicating no modification of its chemical structure. The fluorescent microscope disclosed scattered dot-like staining of GM3, particularly at the periphery of the cells. We were able to expose cryptic GM3 fully within 12 h by dispersion of the cells to a sparse density. Surface labeling of GM3 with the use of limited sodium periodate oxidation of sialylated residue equally labeled GM3 either from the confluent cells or the sparse cells. Disassembly of actin filaments with cytochalasin B (10 microM) partially exposed cryptic GM3 of confluent cells, indicating reversibility of the crypticity. All together, the results indicate that cryptic GM3 actually exists on the cell surface, hidden from the surface not by other molecules but by other mechanisms associated with the cellular architecture. We are beginning to explore the possibility of selective localization of GM3 in small caves or folds of the cell membrane produced upon cell-to-cell contact.
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PMID:Cell density regulates crypticity of GM3 ganglioside on human glioma cells. 918 84

We have detected a tyrosine phosphorylated 200 kDa glycoprotein (gp200) on the surface of two tumour cells of neural origin, namely A1235 glioma and A172 glioblastoma. gp200 (polypeptide mass of 165-170 kDa) has all the structural features of a growth factor receptor and it appears to display high basal tyrosine kinase activity, a characteristic associated with transforming proteins. Another interesting feature of gp200 is that it is immunologically highly related to the EGF receptor (polypeptide mass of 135 kDa), a member of the erb-B family of proteins; however, it lacks EGF binding activity. gp200 also differs from all other EGF-receptor-related oncogenic proteins, namely erb-B-2, erb-B-3 and erb-B-4 gene products, and hence appears to be yet another member of the erb-B family of proteins. This is further strengthened by the fact that both gp200 and the EGF receptor are also recognized by a conformation-specific anti-peptide antibody to the cytoplasmic domain of the beta-type PDGF receptor. In the EGF- and the PDGF receptors, this peptide epitope is cryptic and receptor phosphorylation unmasks this site [Panneerselvam K, Reitz H, Khan S A, and Bishayee S (1995) J Biol Chem 270, 7975-7979] indicating that this epitope might be important in biological message transmission. In this context, the expression of a novel EGF-receptor-related 200 kDa protein with high basal kinase activity in certain tumour cells of neural origin and the fact that it contains an important peptide epitope suggest its possible role in normal and abnormal cell growth.
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PMID:A novel 200 kDa plasma membrane glycoprotein with high basal tyrosine kinase activity in tumour cells. 934 24

Human malignant gliomas are highly vascularized and aggressive tumors. Angiogenesis inhibitors have been shown to induce regression of a variety of primary and metastatic tumors in vivo. However, their usefulness in treating brain tumors is not well understood. Angiostatin, a multiple kringle (1-4 of 5)-containing fragment of plasminogen, is one of the highly effective natural cryptic angiogenesis inhibitors. In our study, the therapeutic efficacy of non-glycosylated and small molecular size recombinant kringles 1-3 (rPK1-3) was examined in the treatment of brain tumors generated by stereotactic intracerebral implantation of U-87 human glioma cells in nude mice. Mice bearing tumors 7 days post-implant were treated daily with rPK1-3 (100 mg/kg) s.c. for 21 days. Treated animals showed suppressed brain tumor growth by greater than 71.2% along with a 3-fold increase of apoptotic index and suppressed vascularization by 78.9%, without any observable signs of toxicity. Analysis of bFGF and VEGF expression in the tumors of treated animals using immuno-histochemical methods showed near complete absence of growth factors. Our results indicate that the non-glycosylated, small molecular size rPK1-3 is an efficient tumoristatic agent for the treatment of intracranial human glioma xenografts in mice and might provide new strategies for the treatment of brain tumors.
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PMID:Inhibition of human malignant glioma growth in vivo by human recombinant plasminogen kringles 1-3. 1041 67

Identification of genetic losses and gains is valuable in analysis of brain tumors. Locus-by-locus analyses have revealed correlations between prognosis and response to chemotherapy and loss or gain of specific genes and loci. These approaches are labor intensive and do not provide a global view of the genetic changes within the tumor cells. Bacterial artificial chromosome (BAC) arrays, which cover the genome with an average resolution of less than 1 MbP, allow defining the sum total of these genetic changes in a single comparative genomic hybridization (CGH) experiment. These changes are directly overlaid on the human genome sequence, thus providing the extent of the amplification or deletion, reflected by a megabase position, and gene content of the abnormal region. Although this array-based CGH approach (CGHa) seems to detect the extent of the genetic changes in tumors reliably, it has not been robustly tested. We compared genetic changes in four newly derived, early-passage glioma cell lines, using spectral karyotyping (SKY) and CGHa. Chromosome changes seen in cell lines under SKY analysis were also detected with CGHa. In addition, CGHa detected cryptic genetic gains and losses and resolved the nature of subtle marker chromosomes that could not be resolved with SKY, thus providing distinct advantages over previous technologies. There was remarkable general concordance between the CGHa results comparing the cell lines to the original tumor, except that the magnitude of the changes seen in the tumor sample was generally suppressed compared with the cell lines, a consequence of normal cells contaminating the tumor sample. CGHa revealed changes in cell lines that were not present in the original tumors and vice versa, even when analyzed at the earliest passage possible, which highlights the adaptation of the cells to in vitro culture. CGHa proved to be highly accurate and efficient for identifying genetic changes in tumor cells. This approach can accurately identify subtle, novel genetic abnormalities in tumors directly linked to the human genome sequence. CGHa far surpasses the resolution and information provided by conventional metaphase CGH, without relying on in vitro culture of tumors for metaphase spreads.
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PMID:Application of bacterial artificial chromosome array-based comparative genomic hybridization and spectral karyotyping to the analysis of glioblastoma multiforme. 1512 Sep 9


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