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1. Hu X, Pandolfi PP, Li Y, Koutcher JA, Rosenblum M, Holland EC: mTOR promotes survival and astrocytic characteristics induced by Pten/AKT signaling in glioblastoma. Neoplasia; 2005 Apr;7(4):356-68
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  • [Title] mTOR promotes survival and astrocytic characteristics induced by Pten/AKT signaling in glioblastoma.
  • Combined activation of Ras and AKT leads to the formation of astrocytic glioblastoma multiforme (GBM) in mice.
  • Blockade of mTOR results in regional apoptosis in these tumors and conversion in the character of surviving tumor cells from astrocytoma to oligodendroglioma.
  • These data suggest that mTOR activity is required for the survival of some cells within these GBMs, and mTOR appears required for the maintenance of astrocytic character in the surviving cells.
  • Furthermore, our study provides the first example of conversion between two distinct tumor types usually thought of as belonging to specific lineages, and provides evidence for signal transduction-mediated transdifferentiation between glioma subtypes.

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  • (PMID = 15967113.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01CA894134-1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Proteins; 147336-22-9 / Green Fluorescent Proteins; 624KN6GM2T / temsirolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.67 / PTEN Phosphohydrolase; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC1501155
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2. Batistatou A, Kyzas PA, Goussia A, Arkoumani E, Voulgaris S, Polyzoidis K, Agnantis NJ, Stefanou D: Estrogen receptor beta (ERbeta) protein expression correlates with BAG-1 and prognosis in brain glial tumours. J Neurooncol; 2006 Mar;77(1):17-23
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  • [Title] Estrogen receptor beta (ERbeta) protein expression correlates with BAG-1 and prognosis in brain glial tumours.
  • Its expression declines in breast, ovarian, prostatic and colon carcinomas as well as in astrocytic tumours.
  • In astrocytic tumours low ERbeta expression correlated significantly with high grade (P < 0.001), higher expression of cytoplasmic BAG-1 (P < 0.001) and worse survival (log rank P = 0.02).
  • Moreover, ERbeta expression in astrocytic tumors might be an important prognostic factor for survival.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. DNA-Binding Proteins / metabolism. Estrogen Receptor beta / metabolism. Oligodendroglioma / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Female. Gene Expression Regulation, Neoplastic. HSP70 Heat-Shock Proteins / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Survival Analysis

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  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL2-associated athanogene 1 protein; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Estrogen Receptor beta; 0 / HSP70 Heat-Shock Proteins; 0 / Transcription Factors
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3. Yamamoto S, Tetsuka K, Sato Y, Endo S: Unsuspected tracheal web inhibits endotracheal intubation: report of a case. J Anesth; 2010 Feb;24(1):132-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A 66-year-old woman was scheduled for resection of a recurrent brain astrocytoma.
  • [MeSH-major] Intraoperative Complications. Intubation, Intratracheal. Trachea / pathology. Tracheal Stenosis / diagnosis
  • [MeSH-minor] Aged. Astrocytoma / complications. Astrocytoma / surgery. Brain Neoplasms / complications. Brain Neoplasms / surgery. Bronchoscopy. Female. Humans. Lasers, Gas / therapeutic use. Neoplasm Recurrence, Local / complications. Neoplasm Recurrence, Local / surgery. Reoperation. Video-Assisted Surgery / instrumentation

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  • (PMID = 20052498.001).
  • [ISSN] 1438-8359
  • [Journal-full-title] Journal of anesthesia
  • [ISO-abbreviation] J Anesth
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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4. Allerstorfer S, Sonvilla G, Fischer H, Spiegl-Kreinecker S, Gauglhofer C, Setinek U, Czech T, Marosi C, Buchroithner J, Pichler J, Silye R, Mohr T, Holzmann K, Grasl-Kraupp B, Marian B, Grusch M, Fischer J, Micksche M, Berger W: FGF5 as an oncogenic factor in human glioblastoma multiforme: autocrine and paracrine activities. Oncogene; 2008 Jul 10;27(30):4180-90
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  • Here we report simultaneous overexpression of FGF5 and its predominant high-affinity receptor (FGFR1 IIIc) in astrocytic brain tumour specimens (N=49) and cell cultures (N=49).
  • Moreover, tumour cell migration was distinctly stimulated by rFGF5 but attenuated by FGF5 siRNA.
  • In summary, we demonstrate for the first time that FGF5 contributes to the malignant progression of human astrocytic brain tumours by both autocrine and paracrine effects.
  • [MeSH-major] Autocrine Communication / physiology. Brain Neoplasms / genetics. Fibroblast Growth Factor 5 / physiology. Glioblastoma / genetics. Oncogenes. Paracrine Communication / physiology
  • [MeSH-minor] Cell Death / drug effects. Cell Movement / drug effects. Cell Proliferation / drug effects. Culture Media, Conditioned / pharmacology. Disease Progression. Genes, Dominant / physiology. Humans. Mutant Proteins / genetics. Mutant Proteins / physiology. Neovascularization, Pathologic / chemically induced. Neovascularization, Pathologic / genetics. Recombinant Proteins / pharmacology. Transfection. Tumor Cells, Cultured

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  • (PMID = 18362893.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / P 19920
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / FGF5 protein, human; 0 / Mutant Proteins; 0 / Recombinant Proteins; 129653-64-1 / Fibroblast Growth Factor 5
  • [Other-IDs] NLM/ PMC2879862; NLM/ UKMS30927
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5. Louis DN: Molecular pathology of malignant gliomas. Annu Rev Pathol; 2006;1:97-117
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular pathology of malignant gliomas.
  • Malignant gliomas, the most common type of primary brain tumor, are a spectrum of tumors of varying differentiation and malignancy grades.
  • These tumors may arise from neural stem cells and appear to contain tumor stem cells.
  • Early genetic events differ between astrocytic and oligodendroglial tumors, but all tumors have an initially invasive phenotype, which complicates therapy.
  • Progression-associated genetic alterations are common to different tumor types, targeting growth-promoting and cell cycle control pathways and resulting in focal hypoxia, necrosis, and angiogenesis.
  • Knowledge of malignant glioma genetics has already impacted clinical management of these tumors, and researchers hope that further knowledge of the molecular pathology of malignant gliomas will result in novel therapies.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / pathology. Molecular Biology / methods. Oligodendroglioma / pathology
  • [MeSH-minor] Animals. Biomarkers, Tumor. Gene Expression Regulation, Neoplastic. Humans. Neoplasm Invasiveness. Neoplasm Staging

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  • (PMID = 18039109.001).
  • [ISSN] 1553-4006
  • [Journal-full-title] Annual review of pathology
  • [ISO-abbreviation] Annu Rev Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 76
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6. Sarkar C, Karak AK, Nath N, Sharma MC, Mahapatra AK, Chattopadhyay P, Sinha S: Apoptosis and proliferation: correlation with p53 in astrocytic tumours. J Neurooncol; 2005 Jun;73(2):93-100
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  • [Title] Apoptosis and proliferation: correlation with p53 in astrocytic tumours.
  • Apoptosis and cell proliferation occur simultaneously in tumour tissue with tumour suppressor gene, p53 being one of the key players in the complex relationship between these two key phenomena.
  • We, as well as several other groups, have earlier demonstrated the association of p53 immunopositivity with increased degree of cell proliferation in astrocytic tumours.
  • Here we have studied the extent of apoptosis in 62 primary human astrocytic tumours [25 Diffuse Astrocytoma (DA), 9 Anaplastic Astrocytoma (AA) and 28 Glioblastoma multiforme (GBM)] in relation to tumour grade, proliferative status and p53 protein expression.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Glioblastoma / metabolism. Glioblastoma / pathology. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 15981097.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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7. Arjona D, Rey JA, Taylor SM: Early genetic changes involved in low-grade astrocytic tumor development. Curr Mol Med; 2006 Sep;6(6):645-50
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  • [Title] Early genetic changes involved in low-grade astrocytic tumor development.
  • The most malignant grade of these tumors, glioblastoma multiforme, may arise as a malignant progression from low-grade astrocytoma through anaplastic astrocytoma to secondary GBM, or else it may arise "de novo" as primary GBM.
  • Since malignant transformation is a multistep process, we summarize in this review the earliest genetic changes that seem to be involved in the appearance and development of low-grade astrocytic tumors, where early detection and treatment could be possible.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Glioblastoma / genetics. Models, Genetic. Tumor Suppressor Proteins / genetics

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  • (PMID = 17022734.001).
  • [ISSN] 1566-5240
  • [Journal-full-title] Current molecular medicine
  • [ISO-abbreviation] Curr. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Tumor Suppressor Proteins
  • [Number-of-references] 80
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8. Nakamura JL, Haas-Kogan DA, Pieper RO: Glioma invasiveness responds variably to irradiation in a co-culture model. Int J Radiat Oncol Biol Phys; 2007 Nov 1;69(3):880-6
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  • PURPOSE: We developed a co-culture system to quantitate the growth and invasion of human malignant gliomas into a background of confluent normal human astrocytes, then used this assay to assess independently the effects of irradiating both cell types on glioma invasion.
  • METHODS AND MATERIALS: Enhanced green fluorescent protein (EGFP)-labeled immortalized human astrocytes, human malignant glioma cells, or transformed human astrocytes were focally plated onto a confluent layer of normal human astrocytes, and the invasiveness of EGFP-labeled cells was scored after 96 h.
  • To address the consequences of irradiation on glioma invasion, the invasiveness of irradiated glioma cell lines and irradiated astrocytic backgrounds was assessed.
  • In contrast, all malignant human glioma cell lines and transformed human astrocytes demonstrated various degrees of infiltration into the astrocytic bed.
  • Independently irradiating the human astrocytic bed did not alter the invasiveness of nonirradiated U251, whereas the matrix metalloproteinase (MMP) inhibitor GM6001 reduced U251 invasiveness in the co-culture assay.
  • [MeSH-major] Astrocytes / cytology. Brain Neoplasms / radiotherapy. Glioma / radiotherapy
  • [MeSH-minor] Cell Line, Transformed. Cell Line, Tumor. Coculture Techniques / methods. Dipeptides / pharmacology. Flow Cytometry. Green Fluorescent Proteins. Humans. Matrix Metalloproteinase 2 / secretion. Matrix Metalloproteinase Inhibitors. Neoplasm Invasiveness. Protease Inhibitors / pharmacology

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  • (PMID = 17889268.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dipeptides; 0 / Matrix Metalloproteinase Inhibitors; 0 / N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide; 0 / Protease Inhibitors; 0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins; EC 3.4.24.24 / Matrix Metalloproteinase 2
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9. Stegh AH, Kim H, Bachoo RM, Forloney KL, Zhang J, Schulze H, Park K, Hannon GJ, Yuan J, Louis DN, DePinho RA, Chin L: Bcl2L12 inhibits post-mitochondrial apoptosis signaling in glioblastoma. Genes Dev; 2007 Jan 1;21(1):98-111
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  • Glioblastoma (GBM) is an astrocytic brain tumor characterized by an aggressive clinical course and intense resistance to all therapeutic modalities.
  • Enforced Bcl2L12 expression confers marked apoptosis resistance in primary cortical astrocytes, and, conversely, its RNA interference (RNAi)-mediated knockdown sensitizes human glioma cell lines toward apoptosis in vitro and impairs tumor growth with increased intratumoral apoptosis in vivo.
  • Thus, Bcl2L12 contributes to the classical tumor biological features of GBM such as intense apoptosis resistance and florid necrosis, and may provide a target for enhanced therapeutic responsiveness of this lethal cancer.

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  • (PMID = 17210792.001).
  • [ISSN] 0890-9369
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA099041; United States / NCI NIH HHS / CA / P01 CA095616; United States / NINDS NIH HHS / NS / K08 NS042737; United States / NCI NIH HHS / CA / R01 CA57683; United States / NCI NIH HHS / CA / R01 CA057683; United States / NCI NIH HHS / CA / P01 CA95616; United States / NINDS NIH HHS / NS / K08NS42737
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosomes; 0 / BCL2L12 protein, human; 0 / Bcl2l2 protein, mouse; 0 / Immunoglobulin G; 0 / Muscle Proteins; 0 / Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Small Interfering; 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspase 7; EC 3.4.22.- / Caspase 9
  • [Other-IDs] NLM/ PMC1759904
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10. Franco-Hernández C, Martínez-Glez V, de Campos JM, Isla A, Vaquero J, Gutiérrez M, Casartelli C, Rey JA: Allelic status of 1p and 19q in oligodendrogliomas and glioblastomas: multiplex ligation-dependent probe amplification versus loss of heterozygosity. Cancer Genet Cytogenet; 2009 Apr 15;190(2):93-6
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  • Identification of the 1p/19q allelic status in gliomas, primarily those with a major oligodendroglial component, has become an excellent molecular complement to tumor histology in order to identify those cases sensitive to chemotherapy.
  • We used MLPA to explore the 1p and 19q allelic constitution in a series of 76 gliomas: 41 tumors with a major oligodendroglial component, 34 glioblastomas, and one low-grade astrocytoma.
  • Thirty-eight of 41 oligodendrogliomas displayed identical findings by both LOH and MLPA, and losses at either 1p and/or 19q were identified in 12 of 35 (34%) astrocytic tumors.
  • These findings agree with data previously reported comparing MLPA versus FISH or CGH in gliomas and suggest that MLPA can be used in the identification of the 1p/19q allelic deletions on these brain neoplasms.
  • [MeSH-major] Alleles. Brain Neoplasms / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Glioblastoma / genetics. Loss of Heterozygosity / genetics. Oligodendroglioma / genetics

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  • (PMID = 19380026.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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11. Horger M, Fenchel M, Nägele T, Moehle R, Claussen CD, Beschorner R, Ernemann U: Water diffusivity: comparison of primary CNS lymphoma and astrocytic tumor infiltrating the corpus callosum. AJR Am J Roentgenol; 2009 Nov;193(5):1384-7
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  • [Title] Water diffusivity: comparison of primary CNS lymphoma and astrocytic tumor infiltrating the corpus callosum.
  • OBJECTIVE: The purpose of this study was to determine whether lymphoma and astrocytic tumor infiltrating the corpus callosum can be reliably differentiated with measurement of water diffusivity.
  • MATERIALS AND METHODS: Echo-planar diffusion-weighted MR images of 27 patients with glioblastoma multiforme, five patients with low-grade astrocytoma, five patients with gliomatosis cerebri, and nine patients with primary lymphoma infiltrating the corpus callosum were reviewed retrospectively.
  • Regions of interest were drawn on apparent diffusion coefficient (ADC) maps inside the callosal tumor.
  • ADCs were normalized by calculation of the ratio between the ADC of the tumor and the ADC of an uninvolved region of corpus callosum.
  • RESULTS: The mean ADC of glioblastoma multiforme was 1.13 +/- 0.31 (SD) x 10(-3) mm(2)/s, and the mean tumor to corpus callosum ADC ratio was 1.51 +/- 0.46; of low-grade astrocytoma, 1.14 +/- 0.23 x 10(-3) mm(2)/s and 1.54 +/- 0.28; gliomatosis cerebri, 1.01 +/- 0.20 x 10(-3) mm(2)/s and 1.31 +/- 0.36; and lymphoma, 0.71 +/- 0.13 x 10(-3) mm(2)/s and 0.93 +/- 0.19.
  • The difference between the mean tumor to corpus callosum ADC ratio of lymphoma and that of all grades of astrocytoma (1.48 +/- 0.43) was statistically significant (p < 0.001).
  • The optimal ADC threshold for discriminating astrocytic tumor and lymphoma was 0.90 x 10(-3) mm(2)/s (sensitivity, 84%; specificity, 89%).
  • The optimal threshold for tumor to corpus callosum ADC ratio was 1.22 (sensitivity, 73%; specificity, 100%).
  • CONCLUSION: The water diffusivity and the ADC ratio of the tumor to normal-appearing corpus callosum of astrocytic tumor differ significantly from those of lymphoma infiltrating the corpus callosum, allowing reliable differentiation of the two types of tumor.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Corpus Callosum / pathology. Diffusion Magnetic Resonance Imaging / methods. Glioblastoma / pathology. Lymphoma / pathology. Water / metabolism

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  • (PMID = 19843757.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 059QF0KO0R / Water
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12. Kunitz A, Wolter M, van den Boom J, Felsberg J, Tews B, Hahn M, Benner A, Sabel M, Lichter P, Reifenberger G, von Deimling A, Hartmann C: DNA hypermethylation and aberrant expression of the EMP3 gene at 19q13.3 in Human Gliomas. Brain Pathol; 2007 Oct;17(4):363-70
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  • However, the tumor suppressor genes (TSG) on 19q are still elusive.
  • Our data corroborate that oligodendroglial and astrocytic gliomas often show EMP3 hypermethylation and aberrant expression.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 19 / genetics. DNA Methylation. Gene Expression Regulation, Neoplastic / genetics. Glioma / genetics. Membrane Glycoproteins / genetics
  • [MeSH-minor] Adult. Astrocytoma / genetics. Astrocytoma / metabolism. Astrocytoma / physiopathology. Gene Expression Profiling. Gene Silencing / physiology. Genetic Predisposition to Disease / genetics. Humans. Oligodendroglioma / genetics. Oligodendroglioma / metabolism. Oligodendroglioma / physiopathology. Oligonucleotide Array Sequence Analysis

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  • (PMID = 17610521.001).
  • [ISSN] 1015-6305
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / EMP3 protein, human; 0 / Membrane Glycoproteins
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13. Jiang L, Bao Y, Luo C, Hu G, Huang C, Ding X, Sun K, Lu Y: Knockdown of ubiquitin-conjugating enzyme E2C/UbcH10 expression by RNA interference inhibits glioma cell proliferation and enhances cell apoptosis in vitro. J Cancer Res Clin Oncol; 2010 Feb;136(2):211-7
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  • PURPOSE: To address the role of ubiquitin-conjugating enzyme, E2C/UbcH10, in astrocytic carcinogenesis.
  • RESULTS: Levels of UbcH10 protein were significantly upregulated in U251 cells compared with normal brain tissues.
  • [MeSH-minor] Blotting, Western. Cell Cycle. Cell Line, Tumor. Central Nervous System Neoplasms / enzymology. Central Nervous System Neoplasms / genetics. Down-Regulation. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry

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  • (PMID = 19657671.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 2.3.2.23 / UBE2C protein, human; EC 2.3.2.23 / Ubiquitin-Conjugating Enzymes
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14. Takarada T, Yoneda Y: Transactivation by Runt related factor-2 of matrix metalloproteinase-13 in astrocytes. Neurosci Lett; 2009 Feb 20;451(2):99-104
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  • We have previously shown functional expression by osteoblasts of signaling machineries required for neurotransmission in the brain.
  • In this study, we have evaluated possible functional expression of different osseous genes in the brain.
  • In pluripotent P19 progenitor cells, Runx2 mRNA expression was drastically increased along with mRNA expression of an astrocytic marker, but not with neuronal marker mRNA expression.
  • Both mRNA and corresponding protein were detected for Runx2 in cultured rat neocortical astrocytes and astrocytic C6 glioma cells.
  • [MeSH-major] Astrocytes / metabolism. Brain / metabolism. Core Binding Factor Alpha 1 Subunit / genetics. Core Binding Factor Alpha 1 Subunit / metabolism. Matrix Metalloproteinase 13 / genetics. Transcriptional Activation / genetics
  • [MeSH-minor] Animals. Brain Neoplasms / genetics. Brain Neoplasms / metabolism. Cell Line, Tumor. Core Binding Factor beta Subunit / genetics. Core Binding Factor beta Subunit / metabolism. Gene Expression Regulation, Enzymologic / genetics. Glial Fibrillary Acidic Protein / analysis. Glial Fibrillary Acidic Protein / metabolism. Glioma / genetics. Glioma / metabolism. Luciferases / genetics. Mice. Microtubule-Associated Proteins / analysis. Microtubule-Associated Proteins / metabolism. Osteopontin / genetics. Osteopontin / metabolism. Pluripotent Stem Cells / metabolism. Promoter Regions, Genetic / genetics. Rats. Signal Transduction / genetics. Transfection

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  • (PMID = 19121369.001).
  • [ISSN] 0304-3940
  • [Journal-full-title] Neuroscience letters
  • [ISO-abbreviation] Neurosci. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Cbfb protein, mouse; 0 / Core Binding Factor Alpha 1 Subunit; 0 / Core Binding Factor beta Subunit; 0 / Glial Fibrillary Acidic Protein; 0 / Microtubule-Associated Proteins; 0 / Mtap2 protein, rat; 0 / Runx2 protein, rat; 0 / Spp1 protein, rat; 106441-73-0 / Osteopontin; EC 1.13.12.- / Luciferases; EC 3.4.24.- / Matrix Metalloproteinase 13; EC 3.4.24.- / Mmp13 protein, rat
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15. Nakao K, Shirakawa H, Sugishita A, Matsutani I, Niidome T, Nakagawa T, Kaneko S: Ca2+ mobilization mediated by transient receptor potential canonical 3 is associated with thrombin-induced morphological changes in 1321N1 human astrocytoma cells. J Neurosci Res; 2008 Sep;86(12):2722-32
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  • [Title] Ca2+ mobilization mediated by transient receptor potential canonical 3 is associated with thrombin-induced morphological changes in 1321N1 human astrocytoma cells.
  • In the present study we revealed a novel function of astrocytic Ca(2+) dynamics through investigation of thrombin-induced unique Ca(2+) entry.
  • Using 1321N1 human astrocytoma cells, which have been shown to be a good model for detecting morphological dynamics, we observed rapid retraction of bipolar protrusions that were reversibly evoked by 0.03-3 U/mL thrombin.
  • These results suggest a novel function of astrocytic Ca(2+) dynamics, including Ca(2+) entry, in the pathophysiological effects of PAR-1-mediated astrocytic activation.
  • TRPC3 forms a functional Ca(2+) channel and might modulate astrocytic activation in response to brain hemorrhaging.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Calcium / metabolism. TRPC Cation Channels / physiology. Thrombin / physiology
  • [MeSH-minor] Calcium Signaling / physiology. Humans. Receptor, PAR-1 / genetics. Receptor, PAR-1 / metabolism. Tumor Cells, Cultured

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18478545.001).
  • [ISSN] 1097-4547
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptor, PAR-1; 0 / TRPC Cation Channels; 0 / TRPC3 cation channel; EC 3.4.21.5 / Thrombin; SY7Q814VUP / Calcium
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16. Mitsuhashi T, Shimizu Y, Ban S, Ogawa F, Matsutani M, Shimizu M, Hirose T: Anaplastic oligodendroglioma: a case report with characteristic cytologic features, including minigemistocytes. Acta Cytol; 2007 Jul-Aug;51(4):657-60
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  • BACKGROUND: Absolute criteria for grading oligodendrogliomas are somewhat poorly defined in contrast to those for grading astrocytic tumors, and cytologic features of anaplastic oligodendrogliomas have been poorly described.
  • Intraoperative smears of the tumor showed hypercellular, loosely cohesive cell clusters and single cells with nuclear pleomorphism, numerous apoptotic cells and no discernible fibrillary processes.
  • Cryostat sections showed cellular nests consisting of tumor cells with oval nuclei and clear cytoplasm.
  • These cells were proliferating in the finely reticulated vascular stroma, and the tumor had an infiltrative margin with areas of focal necrosis and numerous calcifications.
  • The diagnosis of anaplastic oligodendroglioma, World Health Organization grade 3, was made, and the results of fluorescence in situ hybridization (chromosome 1q deletion) supported the diagnosis.
  • CONCLUSION: Intraoperative diagnosis of anaplastic oligodendroglioma may not be easy but is possible with judicious consideration of several features: high cellularity, no fibrillary processes, nuclear atypia, pleomorphism, abundant apoptotic cells, occasional mitotic figures, coagulative necrosis, endothelial hyperplasia and characteristic conspicuous minigemistocytes.
  • [MeSH-major] Brain Neoplasms / pathology. Oligodendroglioma / pathology


17. Balkanov AS, Makarenko MF, Poliakov PIu, Kachkov IA: [Results of hyperfractionated radiation therapy used in combination with lomustin in malignant gliomas of the brain]. Zh Vopr Neirokhir Im N N Burdenko; 2005 Jul-Sep;(3):14-16; discussion 16-7
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  • [Title] [Results of hyperfractionated radiation therapy used in combination with lomustin in malignant gliomas of the brain].
  • The postoperative use of lomustin, a nitrosourea agent, was investigated for its impact on the efficiency of hyperfractionated radiation therapy performed in patients with glioblastoma and anaplastic astrocytoma of the brain.
  • A total of 35 patients (26 and 9 patients with glioblastoma and anaplastic astrocytoma, respectively) were followed up.
  • Lomustin in combination with hyperfractionated radiation therapy was found to have no effect on the survival of patients with glioblastoma and anaplastic astrocytoma.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Glioma / drug therapy. Glioma / radiotherapy. Lomustine / therapeutic use

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  • (PMID = 16485820.001).
  • [ISSN] 0042-8817
  • [Journal-full-title] Zhurnal voprosy neĭrokhirurgii imeni N. N. Burdenko
  • [ISO-abbreviation] Zh Vopr Neirokhir Im N N Burdenko
  • [Language] rus
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7BRF0Z81KG / Lomustine; 7S5I7G3JQL / Dexamethasone
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18. Nasonkin I, Mahairaki V, Xu L, Hatfield G, Cummings BJ, Eberhart C, Ryugo DK, Maric D, Bar E, Koliatsos VE: Long-term, stable differentiation of human embryonic stem cell-derived neural precursors grafted into the adult mammalian neostriatum. Stem Cells; 2009 Oct;27(10):2414-26
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  • NPs inoculated in white matter tracts showed a tendency toward glial (primarily astrocytic) differentiation, whereas NPs inoculated in the ventricular epithelium persisted as nestin(+) precursors.
  • Our findings demonstrate the long-term ability of noggin-derived human NPs to structurally integrate tumor-free into the mature mammalian forebrain, while maintaining some cell fate plasticity that is strongly influenced by particular central nervous system (CNS) niches.

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  • (PMID = 19609935.001).
  • [ISSN] 1549-4918
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] ENG
  • [Grant] United States / NIDCD NIH HHS / DC / DC000232; United States / NINDS NIH HHS / NS / R01 NS045140; United States / NINDS NIH HHS / NS / NS45140-03; United States / NEI NIH HHS / EY / P30 EY001765; United States / NIDCD NIH HHS / DC / DC000232-23; United States / NIDCD NIH HHS / DC / R01 DC000232-23; United States / NIDCD NIH HHS / DC / DC005211-089002; United States / NIDCD NIH HHS / DC / R01 DC000232; United States / NIDCD NIH HHS / DC / P30 DC005211; United States / NINDS NIH HHS / NS / R01 NS045140-03; United States / NEI NIH HHS / EY / EY01765; United States / NINDS NIH HHS / NS / NS045140-03; United States / NIDCD NIH HHS / DC / P30 DC005211-089002
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Phosphoproteins; 148294-77-3 / noggin protein
  • [Other-IDs] NLM/ NIHMS193803; NLM/ PMC2906132
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19. Lawandi J, Toumieux S, Seyer V, Campbell P, Thielges S, Juillerat-Jeanneret L, Moitessier N: Constrained peptidomimetics reveal detailed geometric requirements of covalent prolyl oligopeptidase inhibitors. J Med Chem; 2009 Nov 12;52(21):6672-84
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  • Prolyl oligopeptidases cleave peptides on the carboxy side of internal proline residues and their inhibition has potential in the treatment of human brain disorders.
  • Synthesis and biological assays using human brain-derived astrocytic cells and endothelial cells and human fibroblasts revealed that these compounds act as selective inhibitors of prolyl oligopeptidase activity compared to prolyl-dipeptidyl-aminopeptidase activity, are able to penetrate the cells and inhibit intracellular activities in intact living cells.
  • [MeSH-minor] Astrocytes / drug effects. Astrocytes / enzymology. Bicyclo Compounds / chemical synthesis. Bicyclo Compounds / chemistry. Bicyclo Compounds / pharmacology. Brain / blood supply. Brain / cytology. Catalytic Domain. Cell Line, Tumor. Cell Membrane Permeability. Dipeptidyl-Peptidase IV Inhibitors. Drug Design. Endothelial Cells / drug effects. Endothelial Cells / enzymology. Fibroblasts / drug effects. Fibroblasts / enzymology. Humans. Models, Molecular. Molecular Mimicry. Protein Binding. Stereoisomerism. Structure-Activity Relationship

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  • (PMID = 19888757.001).
  • [ISSN] 1520-4804
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1-aza-7-benzyloxycarbonylamino-8-oxo-4-thiabicyclo(3.3.0)octane-2-carbonitrile; 0 / Azabicyclo Compounds; 0 / Bicyclo Compounds; 0 / Carbamates; 0 / Dipeptidyl-Peptidase IV Inhibitors; 0 / Nitriles; 0 / Peptides; 0 / Pyrrolidines; 0 / Serine Proteinase Inhibitors; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.26 / prolyl oligopeptidase
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20. Comincini S, Chiarelli LR, Zelini P, Del Vecchio I, Azzalin A, Arias A, Ferrara V, Rognoni P, Dipoto A, Nano R, Valentini G, Ferretti L: Nuclear mRNA retention and aberrant doppel protein expression in human astrocytic tumor cells. Oncol Rep; 2006 Dec;16(6):1325-32
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  • [Title] Nuclear mRNA retention and aberrant doppel protein expression in human astrocytic tumor cells.
  • Recently, ectopic expression of doppel was found in two different tumor types, specifically in glial and haematological cancers.
  • In this study the doppel gene (PRND) mRNA and protein expression in PRT-HU2 and IPDDC-A2 astrocytoma-derived cell lines was investigated.
  • Northern blot analysis revealed two equally abundant PRND mRNA isoforms, while real-time PCR, on nuclear and cytoplasmic RNA fractions, and cRNA in situ hybridization, on astrocytoma cells and bioptical specimens, showed a nuclear retention of PRND transcripts.
  • Immunohistochemistry experiments demonstrated that Dpl was mainly localised in the cytoplasm of the astrocytic tumor cells, and that it failed to be GPI-anchored to the cell membrane.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Cell Nucleus / metabolism. Prions / biosynthesis. RNA, Messenger / metabolism
  • [MeSH-minor] Blotting, Northern. Blotting, Western. Cell Line, Tumor. Cytoplasm / metabolism. GPI-Linked Proteins. Gene Expression. Gene Expression Profiling. Humans. Immunohistochemistry. Protein Biosynthesis. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic. Transfection

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  • (PMID = 17089057.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / GPI-Linked Proteins; 0 / PRND protein, human; 0 / Prions; 0 / RNA, Messenger
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21. Wong TT, Ho DM, Chang KP, Yen SH, Guo WY, Chang FC, Liang ML, Pan HC, Chung WY: Primary pediatric brain tumors: statistics of Taipei VGH, Taiwan (1975-2004). Cancer; 2005 Nov 15;104(10):2156-67
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  • [Title] Primary pediatric brain tumors: statistics of Taipei VGH, Taiwan (1975-2004).
  • BACKGROUND: The purpose of the current study was to investigate a hospital series of 986 cases of primary pediatric brain tumors in Taiwan.
  • METHODS: The authors reviewed the database of primary pediatric brain tumors in patients < 18 years of age collected in Taipei Veterans General Hospital (Taipei VGH) from 1975 to May 2004.
  • Age and gender distribution, location, and classification of brain tumors were analyzed.
  • Intracranial tumors with diagnostic imaging were included.
  • In these series, 886 patients had either histologic diagnosis (842 patients) or clinical diagnosis (44 patients).
  • The most common 5 categories of tumors were astrocytic tumors (31.1%), germ cell tumors (14.0%), medulloblastomas (13.3%), craniopharyngiomas (8.3%), and ependymal tumors (5.8%).
  • Atypical teratoid/rhabdoid tumors (AT/RTs), a rare but highly malignant tumor, were 2.1%.
  • The high incidence of primary intracranial germ cell tumors correlated with reported series from Japan and Korea.
  • For the remaining 100 patients without diagnostic classifications, the majority were most likely astrocytic tumors in brain stem.
  • CONCLUSIONS: The authors analyzed a large hospital series of primary brain tumors in children.
  • Although it was not a study of a population-based brain tumor registry, it could still be representative of primary pediatric brain tumors in Taiwan.
  • [MeSH-major] Brain Neoplasms / classification. Brain Neoplasms / pathology

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  • [Copyright] Copyright 2005 American Cancer Society
  • (PMID = 16220552.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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22. da Cruz-Höfling MA, Rapôso C, Verinaud L, Zago GM: Neuroinflammation and astrocytic reaction in the course of Phoneutria nigriventer (armed-spider) blood-brain barrier (BBB) opening. Neurotoxicology; 2009 Jul;30(4):636-46
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  • [Title] Neuroinflammation and astrocytic reaction in the course of Phoneutria nigriventer (armed-spider) blood-brain barrier (BBB) opening.
  • Phoneutria nigriventer spider venom (PNV) causes uneven BBB permeability throughout different cerebral regions.
  • A clear explanation for this differential modulation is unclear, but likely result from regional differences in astrocytic/neuronal populations, BBB tightness, and/or extent/distribution of microvasculature and/or ion channels density/distribution.
  • [MeSH-major] Astrocytes / drug effects. Blood-Brain Barrier / drug effects. Cytokines / metabolism. Spider Venoms / toxicity
  • [MeSH-minor] Animals. Glial Fibrillary Acidic Protein / metabolism. Interferon-alpha / metabolism. Male. Neuroimmunomodulation / drug effects. Rats. Rats, Wistar. S100 Proteins / metabolism. Time Factors. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19393263.001).
  • [ISSN] 1872-9711
  • [Journal-full-title] Neurotoxicology
  • [ISO-abbreviation] Neurotoxicology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytokines; 0 / Glial Fibrillary Acidic Protein; 0 / Interferon-alpha; 0 / S100 Proteins; 0 / Spider Venoms; 0 / Tumor Necrosis Factor-alpha
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23. Lu Z, Cao Y, Wang Y, Zhang Q, Zhang X, Wang S, Li Y, Xie H, Jiao B, Zhang J: Polymorphisms in the matrix metalloproteinase-1, 3, and 9 promoters and susceptibility to adult astrocytoma in northern China. J Neurooncol; 2007 Oct;85(1):65-73
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  • [Title] Polymorphisms in the matrix metalloproteinase-1, 3, and 9 promoters and susceptibility to adult astrocytoma in northern China.
  • The single nucleotide polymorphisms (SNPs) in the promoter region of matrix metalloproteinase (MMP) genes may influence tumor occurrence and progression via modifying mRNA transcription and protein expression.
  • The study aims to explore the association of the SNPs in MMP-1, 3 and MMP-9 promoters with susceptibility to adult brain astrocytoma in northern China.
  • Genotyping for the MMP-1 -1607 2G/1G, MMP-3 -1171 5A/6A, and MMP-9 -1562 C/T SNPs were performed by PCR-RFLP methods among 236 adult astrocytoma patients and 366 healthy controls.
  • The results showed that the overall distribution of the MMP-1 allelotype and genotype among astrocytoma patients and healthy controls was significantly different (P = 0.002 and P < 0.001, respectively).
  • Compared with the 2G/2G genotype, the 1G/1G genotype significantly decreased the risk of astrocytoma development (adjusted OR = 0.58, 95% CI = 0.42-0.79).
  • The similar results were obtained when stratified by gender and age at tumor diagnosis (< or =45 or >45 years).
  • The association between MMP-3 -1171 5A/6A or MMP-9 -1562 C/T SNPs and susceptibility to astrocytoma was not observed in this study.
  • However, MMP-1 1G-MMP-3 6A haplotype significantly reduced the risk of astrocytoma development when using MMP-1 2G-MMP-3 6A haplotype as a reference (OR = 0.45, 95% CI = 0.29-0.67).
  • The present study suggested that, the MMP-1 -1607 1G/1G genotype and MMP-1 1G-MMP-3 6A haplotype may play protective role in the development of adult astrocytoma in northern Chinese, whereas the MMP-3 -1171 5A/6A and MMP-9 -1562 C/T polymorphisms may not be independent factors to influence susceptibility to adult astrocytoma in this population.
  • [MeSH-major] Astrocytoma / epidemiology. Astrocytoma / genetics. Brain Neoplasms / epidemiology. Brain Neoplasms / genetics. Matrix Metalloproteinase 1 / genetics. Matrix Metalloproteinase 3 / genetics. Matrix Metalloproteinase 9 / genetics. Polymorphism, Genetic / genetics. Promoter Regions, Genetic / genetics
  • [MeSH-minor] Adult. Case-Control Studies. China / epidemiology. DNA, Neoplasm / biosynthesis. DNA, Neoplasm / genetics. Genetic Linkage / genetics. Genotype. Haplotypes. Humans. Polymorphism, Single Nucleotide. Risk

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  • (PMID = 17502998.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 3.4.24.17 / Matrix Metalloproteinase 3; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.4.24.7 / Matrix Metalloproteinase 1
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24. Steiner J, Bernstein HG, Bogerts B, Gos T, Richter-Landsberg C, Wunderlich MT, Keilhoff G: S100B is expressed in, and released from, OLN-93 oligodendrocytes: Influence of serum and glucose deprivation. Neuroscience; 2008 Jun 23;154(2):496-503
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  • S100B (member of a family of proteins that are 100% soluble in ammonium sulfate at neutral pH) has been widely used as astrocyte marker in animal models and in human brain diseases.
  • To address this question, S100B expression and protein release were analyzed in a highly pure oligodendrocytic OLN-93 cell line (from rat), in the astrocytic C6 cell line (from rat) and primary astrocytes.
  • The experimental results provide further evidence for a production/release of S100B in/from oligodendrocytes, e.g. in metabolic stress conditions like cerebral ischemia.
  • [MeSH-minor] Animals. Animals, Newborn. Astrocytes / metabolism. Astrocytes / ultrastructure. Cell Line, Tumor. Cells, Cultured. Coloring Agents. Culture Media, Serum-Free. Fluoresceins. Glial Fibrillary Acidic Protein / metabolism. Immunohistochemistry. Rats. Reverse Transcriptase Polymerase Chain Reaction. S100 Calcium Binding Protein beta Subunit

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  • (PMID = 18472341.001).
  • [ISSN] 0306-4522
  • [Journal-full-title] Neuroscience
  • [ISO-abbreviation] Neuroscience
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Coloring Agents; 0 / Culture Media, Serum-Free; 0 / Fluoresceins; 0 / Glial Fibrillary Acidic Protein; 0 / Nerve Growth Factors; 0 / S100 Calcium Binding Protein beta Subunit; 0 / S100 Proteins; 0 / S100B protein, human; 0 / S100b protein, rat; 596-09-8 / 3',6'-diacetylfluorescein; IY9XDZ35W2 / Glucose
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25. Laczko R, Szauter KM, Jansen MK, Hollosi P, Muranyi M, Molnar J, Fong KS, Hinek A, Csiszar K: Active lysyl oxidase (LOX) correlates with focal adhesion kinase (FAK)/paxillin activation and migration in invasive astrocytes. Neuropathol Appl Neurobiol; 2007 Dec;33(6):631-43
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  • The extracellular matrix (ECM) plays a critical role during the development and invasion of primary brain tumours.
  • We have recently reported the ECM enzyme, lysyl oxidase (LOX), in the central nervous system and observed up-regulation of LOX in anaplastic astrocytoma cells.
  • While the catalytic function of LOX is essential for cross-linking of ECM proteins, we also reported that LOX induced invasive and metastatic properties in breast tumour epithelial cells through hydrogen peroxide-mediated FAK/Src activation.
  • Results demonstrate that increased expression and activity of LOX positively correlated with invasive phenotype of malignant astrocytoma cell lines.
  • Immunohistochemistry detected increased LOX within tumour cells and ECM in grade I-IV astrocytic neoplasm compared with normal brain and coincidence of increased LOX with the loss of glial fibrillary acidic protein in higher-grade tumours.
  • These results demonstrate an important LOX-mediated mechanism that promotes migratory/invasive behaviour of malignant astrocytes.
  • [MeSH-major] Astrocytes / enzymology. Brain Neoplasms / enzymology. Enzyme Activation / physiology. Focal Adhesion Protein-Tyrosine Kinases / metabolism. Paxillin / metabolism. Protein-Lysine 6-Oxidase / metabolism
  • [MeSH-minor] Astrocytoma / enzymology. Blotting, Western. Cell Line, Tumor. Cell Movement / physiology. Humans. Immunohistochemistry. Neoplasm Invasiveness. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17931358.001).
  • [ISSN] 0305-1846
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / AR47713; United States / NCRR NIH HHS / RR / G12RR003096
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Paxillin; EC 1.4.3.13 / Protein-Lysine 6-Oxidase; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases
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26. Zhou YH, Hess KR, Liu L, Linskey ME, Yung WK: Modeling prognosis for patients with malignant astrocytic gliomas: quantifying the expression of multiple genetic markers and clinical variables. Neuro Oncol; 2005 Oct;7(4):485-94
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  • [Title] Modeling prognosis for patients with malignant astrocytic gliomas: quantifying the expression of multiple genetic markers and clinical variables.
  • The disparate lengths of survival among patients with malignant astrocytic gliomas (anaplastic astrocytomas [AAs] and glioblastoma multiforme [GBM]) cannot be adequately accounted for by clinical variables (patient age, histology, and recurrent status).
  • Using real-time quantitative reverse transcription-polymerase chain reaction, we quantified the expression of four genes that were putative prognostic markers (CDK4, IGFBP2, MMP2, and RPS9) in a set of 43 AAs, 41 GBMs, and seven adjacent normal brain tissues.
  • This study attempts to improve that model by including four additional genetic markers, which exhibited a differential expression (P < 0.001) among tumor grades and between tumor and normal tissues.
  • [MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / analysis. Brain Neoplasms / genetics. Models, Statistical


27. Sen S, Dong M, Kumar S: Isoform-specific contributions of alpha-actinin to glioma cell mechanobiology. PLoS One; 2009 Dec 23;4(12):e8427
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  • Glioblastoma Multiforme (GBM) is a malignant astrocytic tumor associated with low survival rates because of aggressive infiltration of tumor cells into the brain parenchyma.
  • To probe the cellular basis of this correlation, we have suppressed expression of the nonmuscle isoforms alpha-actinin-1 and alpha-actinin-4 and examined the contribution of each isoform to the structure, mechanics, and motility of human glioma tumor cells in culture.

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  • (PMID = 20037648.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NIH HHS / OD / DP2 OD004213; United States / NIH HHS / OD / 1DP2OD004213
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; 11003-00-2 / Actinin; 125361-02-6 / Vinculin; EC 3.6.4.1 / Myosins
  • [Other-IDs] NLM/ PMC2793025
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28. Whitmore RG, Krejza J, Kapoor GS, Huse J, Woo JH, Bloom S, Lopinto J, Wolf RL, Judy K, Rosenfeld MR, Biegel JA, Melhem ER, O'Rourke DM: Prediction of oligodendroglial tumor subtype and grade using perfusion weighted magnetic resonance imaging. J Neurosurg; 2007 Sep;107(3):600-9
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  • [Title] Prediction of oligodendroglial tumor subtype and grade using perfusion weighted magnetic resonance imaging.
  • Perfusion weighted magnetic resonance (MR) imaging allows for noninvasive determination of relative tumor blood volume (rTBV) and has been used to predict the grade of astrocytic neoplasms.
  • The aim of this study was to use perfusion weighted MR imaging to predict tumor grade and cytogenetic profile in oligodendroglial neoplasms.
  • Tumor blood volume was calculated in relation to contralateral white matter.
  • Multivariate logistic regression analysis was used to develop predictive models of cytogenetic profile and tumor grade.
  • CONCLUSIONS: Oligodendroglial classification models derived from advanced imaging will improve the accuracy of tumor grading, provide prognostic information, and have potential to influence treatment decisions.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Loss of Heterozygosity / genetics. Magnetic Resonance Angiography. Oligodendroglioma / genetics. Oligodendroglioma / pathology
  • [MeSH-minor] Adult. Aged. Blood Volume. Female. Humans. Male. Middle Aged. Predictive Value of Tests. Retrospective Studies. Tumor Burden

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  • (PMID = 17886561.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA-90586
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
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29. Hartmann C, Meyer J, Balss J, Capper D, Mueller W, Christians A, Felsberg J, Wolter M, Mawrin C, Wick W, Weller M, Herold-Mende C, Unterberg A, Jeuken JW, Wesseling P, Reifenberger G, von Deimling A: Type and frequency of IDH1 and IDH2 mutations are related to astrocytic and oligodendroglial differentiation and age: a study of 1,010 diffuse gliomas. Acta Neuropathol; 2009 Oct;118(4):469-74
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  • [Title] Type and frequency of IDH1 and IDH2 mutations are related to astrocytic and oligodendroglial differentiation and age: a study of 1,010 diffuse gliomas.
  • We report on an inverse association of IDH1 and IDH2 mutations in these gliomas and a non-random distribution of the mutation types within the tumor entities.
  • IDH1 mutations of the R132C type are strongly associated with astrocytoma, while IDH2 mutations predominantly occur in oligodendroglial tumors.
  • [MeSH-major] Brain Neoplasms / genetics. Glioma / genetics. Isocitrate Dehydrogenase / genetics
  • [MeSH-minor] Adult. Age Factors. Brain / pathology. Cell Differentiation. DNA Mutational Analysis. Female. Humans. Male. Middle Aged. Mutation. Prognosis. Tumor Cells, Cultured

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  • (PMID = 19554337.001).
  • [ISSN] 1432-0533
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 1.1.1.41 / Isocitrate Dehydrogenase
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30. Lefranc F, Rynkowski M, DeWitte O, Kiss R: Present and potential future adjuvant issues in high-grade astrocytic glioma treatment. Adv Tech Stand Neurosurg; 2009;34:3-35
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  • [Title] Present and potential future adjuvant issues in high-grade astrocytic glioma treatment.
  • Despite major advances in the management of malignant gliomas of which glioblastomas represent the ultimate grade of malignancy, they remain characterized by dismal prognoses.
  • Malignant gliomas are associated with such dismal prognoses because glioma cells can actively migrate through the narrow extra-cellular spaces in the brain, often travelling relatively long distances, making them elusive targets for effective surgical management.
  • Clinical and experimental data have demonstrated that invasive malignant glioma cells show a decrease in their proliferation rates and a relative resistance to apoptosis (type I programmed cell death) as compared to the highly cellular centre of the tumor, and this may contribute to their resistance to conventional pro-apoptotic chemotherapy and radiotherapy.
  • Components of these pathways are mutated or aberrantly expressed in human cancer, notably glioblastomas.
  • Monoclonal antibodies and low molecular-weight kinase inhibitors of these pathways are the most common classes of agents in targeted cancer treatment.
  • Despite resistance to apoptosis being closely linked to tumorigenesis, tumor cells can still be induced to die by non-apoptotic mechanisms such as necrosis, senescence, autophagy (type II programmed cell death) and mitotic catastrophe.
  • Another way to potentially overcome apoptosis resistance is to decrease the migration of malignant glioma cells in the brain, which then should restore a level of sensitivity to pro-apoptotic drugs.
  • Recent series of studies have supported the concept that malignant gliomas might be seen as an orchestration of cross-talks between cancer cells, microenvironment, vasculature and cancer stem cells.
  • The present chapter focuses on (i) the major signaling pathways making glioblastomas resistant to apoptosis, (ii) the signaling pathways distinctly activated by pro-autophagic drugs as compared to pro-apoptotic ones, (iii) autophagic cell death as an alternative to combat malignant gliomas, (iv) the major scientific data already obtained by researchers to prove that temozolomide is actually a pro-autophagic and pro-apoptotic drug, (v) the molecular and cellular therapies and local drug delivery which could be used to complement conventional treatments, and a review of some of the currently ongoing clinical trials, (vi) the fact that reducing the levels of malignant glioma cell motility can restore pro-apoptotic drug sensitivity, (vii) the observation that inhibiting the sodium pump activity reduces both glioma cell proliferation and migration, (viii) the brain tumor stem cells as a target to complement conventional treatment.
  • [MeSH-major] Astrocytoma / pathology. Astrocytoma / therapy. Brain Neoplasms / pathology. Brain Neoplasms / therapy


31. Reddy PH, Manczak M, Zhao W, Nakamura K, Bebbington C, Yarranton G, Mao P: Granulocyte-macrophage colony-stimulating factor antibody suppresses microglial activity: implications for anti-inflammatory effects in Alzheimer's disease and multiple sclerosis. J Neurochem; 2009 Dec;111(6):1514-28
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  • The objective of our study was to determine granulocyte-macrophage colony-stimulating factor (GM-CSF) activity in the brain following GM-CSF induction.
  • Using quantitative real-time RT-PCR, we assessed microglial, astrocytic, and neuronal activity by measuring mRNA expression of pro-inflammatory cytokines, GFAP, and the neuronal marker NeuN in the cerebral cortex tissues from C57BL6 mice.
  • We found increased mRNA expression of CD40 (9.75-fold), tumor necrosis factor-alpha (2.1-fold), CD45 (1.73-fold), and CD11c (1.70-fold) in the cerebral cortex of C57BL6 mice that were induced with recombinant GM-CSF, compared with control mice.

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  • (PMID = 19840215.001).
  • [ISSN] 1471-4159
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P51 RR000163; United States / NIA NIH HHS / AG / AG028072-02; United States / NIA NIH HHS / AG / R03 AG026051-02; United States / NCRR NIH HHS / RR / RR00163; United States / NIA NIH HHS / AG / AG026051; United States / NIA NIH HHS / AG / R01 AG028072-02; United States / NIA NIH HHS / AG / R01 AG028072; United States / NCRR NIH HHS / RR / K01 RR000163; United States / NIA NIH HHS / AG / R03 AG026051; United States / NIA NIH HHS / AG / AG028072
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, CD11c; 0 / Antigens, CD40; 0 / Cytokines; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger; 0 / glial fibrillary astrocytic protein, mouse; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 4.2.1.11 / Phosphopyruvate Hydratase
  • [Other-IDs] NLM/ NIHMS152428; NLM/ PMC2796704
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32. Ellert-Miklaszewska A, Grajkowska W, Gabrusiewicz K, Kaminska B, Konarska L: Distinctive pattern of cannabinoid receptor type II (CB2) expression in adult and pediatric brain tumors. Brain Res; 2007 Mar 16;1137(1):161-9
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  • [Title] Distinctive pattern of cannabinoid receptor type II (CB2) expression in adult and pediatric brain tumors.
  • The efficacy of cannabinoids against high-grade glioma in animal models, mediated by two specific receptors, CB1 and CB2, raised promises for targeted treatment of the most frequent and malignant primary brain tumors.
  • Unlike the abundantly expressed CB1, the CB2 receptor shows a restricted distribution in normal brain.
  • Although brain tumors constitute the second most common malignancy in children and the prevalence of histological types of brain tumors vary significantly between the adult and pediatric populations, cannabinoid receptor expression in pediatric tumors remains unknown.
  • In the present study, we compared the expression of the CB2 receptor in paraffin-embedded sections from primary brain tumors of adult and pediatric patients.
  • Most glioblastomas expressed very high levels of CB2 receptors and the expression correlated with tumor grade.
  • Interestingly, some benign pediatric astrocytic tumors, such as subependymal giant cell astrocytoma (SEGA), which may occasionally cause mortality owing to progressive growth, also displayed high CB2 immunoreactivity.
  • In contrast, all examined cases of embryonal tumors (medulloblastoma and S-PNET), the most frequently diagnosed malignant brain tumors in childhood, showed no or trace CB2 immunoreactivity.
  • Our results suggest that the CB2 receptor expression depends primarily on the histopathological origin of the brain tumor cells and differentiation state, reflecting the tumor grade.
  • [MeSH-major] Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic / physiology. Receptor, Cannabinoid, CB2 / metabolism
  • [MeSH-minor] Adolescent. Adult. Age Factors. Astrocytoma / metabolism. Child. Glioblastoma / metabolism. Histocompatibility Antigens / metabolism. Humans. Immunohistochemistry. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 17239827.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Histocompatibility Antigens; 0 / Receptor, Cannabinoid, CB2
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33. Preusser M, Hoischen A, Novak K, Czech T, Prayer D, Hainfellner JA, Baumgartner C, Woermann FG, Tuxhorn IE, Pannek HW, Bergmann M, Radlwimmer B, Villagrán R, Weber RG, Hans VH: Angiocentric glioma: report of clinico-pathologic and genetic findings in 8 cases. Am J Surg Pathol; 2007 Nov;31(11):1709-18
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  • Angiocentric glioma has recently been described as a novel epilepsy associated tumor with distinct clinico-pathologic features.
  • We report the clinical and pathologic findings in 8 additional cases of this rare tumor type and extend its characterization by genomic profiling.
  • Histologically, the tumors were characterized by diffuse growth and prominent perivascular tumor cell arrangements with features of astrocytic/ependymal differentiation, but lacking neoplastic neuronal features.
  • All patients are seizure free and without evidence of tumor recurrence at follow-up times ranging from 1/2 to 6.9 years.
  • Our findings support 2 previous reports proposing that angiocentric glioma is a novel glial tumor entity of low-grade malignancy.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / ultrastructure. Epilepsy / genetics. Gene Expression Regulation, Neoplastic. Glioma / genetics. Glioma / ultrastructure

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  • (PMID = 18059228.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Membrane Glycoproteins; 0 / Mucin-1; 0 / Nerve Growth Factors; 0 / PDPN protein, human; 0 / S100 Calcium Binding Protein beta Subunit; 0 / S100 Proteins; 0 / S100B protein, human; 0 / Vimentin; EC 3.1.3.48 / PTPRJ protein, human; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 3
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34. Sugita Y, Ono T, Ohshima K, Niino D, Ito M, Toda K, Baba H: Brain surface spindle cell glioma in a patient with medically intractable partial epilepsy: a variant of monomorphous angiocentric glioma? Neuropathology; 2008 Oct;28(5):516-20
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  • [Title] Brain surface spindle cell glioma in a patient with medically intractable partial epilepsy: a variant of monomorphous angiocentric glioma?
  • We report a case of brain surface angiocentric glioma in a 6-year-old Japanese boy with medically intractable partial epilepsy.
  • At surgery, a yellowish tumor was localized in the superficial cortex.
  • Histologically, the tumor was predominantly composed of elongated astrocytic cells forming rings around blood vessels.
  • Tumor cells circumferential to vessels predominanted in low cellurarity areas, whereas radial alignment with perivascular pseudorosettes was observed in more cellular regions.
  • The tumor cells showed variable cytoplasmic immunoreactivity with GFAP.
  • However, in our case the tumor had a small foci of polymorphous appearance and a comparatively high MIB-1 labeling index (8%).
  • It remains to be determined whether the behavior of monomorphous angiocentric glioma is an example of benign biological characteristics or whether it more closely resembles a low-grade malignant tumor.
  • [MeSH-major] Brain Neoplasms / complications. Brain Neoplasms / pathology. Epilepsies, Partial / etiology. Glioma / complications. Glioma / pathology
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Malformations of Cortical Development / pathology. Neurosurgical Procedures

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  • (PMID = 18179412.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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35. Kanamori M, Kawaguchi T, Nigro JM, Feuerstein BG, Berger MS, Miele L, Pieper RO: Contribution of Notch signaling activation to human glioblastoma multiforme. J Neurosurg; 2007 Mar;106(3):417-27
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  • OBJECT: Because activation of Notch receptors has been suggested to be critical for Ras-mediated transformation, and because many gliomas exhibit deregulated Ras signaling, the authors measured Notch levels and activation in primary samples and cell lines derived from glioblastoma multiforme (GBM) as well as the contribution of Notch pathway activation to astrocytic transformation and growth.
  • Expansion of these studies to assess mRNA expression of components of the Notch signaling pathway by cDNA expression array showed that cDNAs encoding components of the Notch signaling pathway, including the Notch ligand Jagged-1, Notch 3, and the downstream targets of Notch (HES1 and HES2), were also overexpressed relative to non-neoplastic brain controls in 23, 71, and 51% of 35 primary GBMs, respectively.
  • [MeSH-major] Brain Neoplasms / metabolism. Glioblastoma / metabolism. Receptors, Notch / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Astrocytes / metabolism. Case-Control Studies. Cell Line, Tumor. Humans. RNA, Messenger / metabolism

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  • [CommentIn] J Neurosurg. 2007 Nov;107(5):1060-1; author reply 1061-2 [17977283.001]
  • (PMID = 17367064.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 100011; United States / NCI NIH HHS / CA / CA94989; United States / NCI NIH HHS / CA / CA97257
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Notch
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36. Kashimura H, Inoue T, Beppu T, Ogasawara K, Ogawa A: Diffusion tensor imaging for differentiation of recurrent brain tumor and radiation necrosis after radiotherapy--three case reports. Clin Neurol Neurosurg; 2007 Jan;109(1):106-10
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  • [Title] Diffusion tensor imaging for differentiation of recurrent brain tumor and radiation necrosis after radiotherapy--three case reports.
  • Fractional anisotropy (FA) is influenced by histological data such as cellularity, vascularity and/or fiber structure in astrocytic tumors.
  • We describe two patients with tumor recurrence and one patient with radiation necrosis who were diagnosed using assessment of FA value.
  • The assessment of FA value in enhanced lesions after radiotherapy may be able to differentiate radiation necrosis from tumor recurrence.
  • [MeSH-major] Brain / pathology. Brain Neoplasms / pathology. Diffusion Magnetic Resonance Imaging. Glioblastoma / pathology. Neoplasm Recurrence, Local / pathology. Radiation Injuries / pathology

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  • (PMID = 16793199.001).
  • [ISSN] 0303-8467
  • [Journal-full-title] Clinical neurology and neurosurgery
  • [ISO-abbreviation] Clin Neurol Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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37. Felsberg J, Wolter M, Seul H, Friedensdorf B, Göppert M, Sabel MC, Reifenberger G: Rapid and sensitive assessment of the IDH1 and IDH2 mutation status in cerebral gliomas based on DNA pyrosequencing. Acta Neuropathol; 2010 Apr;119(4):501-7
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  • [Title] Rapid and sensitive assessment of the IDH1 and IDH2 mutation status in cerebral gliomas based on DNA pyrosequencing.
  • Diffusely infiltrating cerebral gliomas frequently carry point mutations in codon 132 of the isocitrate dehydrogenase 1 (IDH1) gene or in codon 172 of the IDH2 gene, which are both clinically important as diagnostic and prognostic markers.
  • Due to its high sensitivity, the technique may also be used for the diagnostic assessment of IDH1 or IDH2 mutation in tissue samples with low tumor cell content, such as the infiltration zone of diffuse gliomas.
  • Using pyrosequencing and/or conventional cycle sequencing of IDH1 and IDH2 in 262 gliomas, we confirm frequent mutations in diffuse astrocytic and oligodendroglial gliomas, corroborate a prognostic role for IDH1 mutation in primary glioblastomas and show that pleomorphic xanthoastrocytomas generally lack mutations in these genes.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. DNA Mutational Analysis / methods. Isocitrate Dehydrogenase / genetics. Mutation. Oligodendroglioma / genetics

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  • (PMID = 20131059.001).
  • [ISSN] 1432-0533
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human
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38. Balss J, Meyer J, Mueller W, Korshunov A, Hartmann C, von Deimling A: Analysis of the IDH1 codon 132 mutation in brain tumors. Acta Neuropathol; 2008 Dec;116(6):597-602
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  • [Title] Analysis of the IDH1 codon 132 mutation in brain tumors.
  • We analyzed the genomic region spanning wild type R132 of IDH1 by direct sequencing in 685 brain tumors including 41 pilocytic astrocytomas, 12 subependymal giant cell astrocytomas, 7 pleomorphic xanthoastrocytomas, 93 diffuse astrocytomas, 120 adult glioblastomas, 14 pediatric glioblastomas, 105 oligodendrogliomas, 83 oligoastrocytomas, 31 ependymomas, 58 medulloblastomas, 9 supratentorial primitive neuroectodermal tumors, 17 schwannomas, 72 meningiomas and 23 pituitary adenomas.
  • The very high frequency of IDH1 mutations in WHO grade II astrocytic and oligodendroglial gliomas suggests a role in early tumor development.
  • [MeSH-major] Brain Neoplasms / genetics. Isocitrate Dehydrogenase / genetics. Mutation
  • [MeSH-minor] Astrocytoma / genetics. Astrocytoma / pathology. Base Sequence. DNA Mutational Analysis. Disease Progression. Gene Frequency. Glioblastoma / genetics. Glioblastoma / pathology. Glioma / etiology. Glioma / pathology. Humans. Oligodendroglioma / genetics. Oligodendroglioma / pathology. Polymerase Chain Reaction

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  • (PMID = 18985363.001).
  • [ISSN] 1432-0533
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 1.1.1.41 / Isocitrate Dehydrogenase
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39. Shahi MH, Afzal M, Sinha S, Eberhart CG, Rey JA, Fan X, Castresana JS: Regulation of sonic hedgehog-GLI1 downstream target genes PTCH1, Cyclin D2, Plakoglobin, PAX6 and NKX2.2 and their epigenetic status in medulloblastoma and astrocytoma. BMC Cancer; 2010;10:614
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  • [Title] Regulation of sonic hedgehog-GLI1 downstream target genes PTCH1, Cyclin D2, Plakoglobin, PAX6 and NKX2.2 and their epigenetic status in medulloblastoma and astrocytoma.
  • Impairment of this pathway can result in both birth defects and cancer.
  • Despite its importance in cancer development, the Shh pathway has not been thoroughly investigated in tumorigenesis of brain tumors.
  • In this study, we sought to understand the regulatory roles of GLI1, the immediate downstream activator of the Shh signaling pathway on its downstream target genes PTCH1, Cyclin D2, Plakoglobin, NKX2.2 and PAX6 in medulloblastoma and astrocytic tumors.
  • METHODS: We silenced GLI1 expression in medulloblastoma and astrocytic cell lines by transfection of siRNA against GLI1.
  • We also attempted to correlate the pattern of expression of GLI1 and its regulated genes in 14 cell lines and 41 primary medulloblastoma and astrocytoma tumor samples.
  • We also assessed the methylation status of the Cyclin D2 and PTCH1 promoters in these 14 cell lines and 58 primary tumor samples.
  • RESULTS: Silencing expression of GLI1 resulted up-regulation of all target genes in the medulloblastoma cell line, while only PTCH1 was up-regulated in astrocytoma.
  • We also observed methylation of the cyclin D2 promoter in a significant number of astrocytoma cell lines (63%) and primary astrocytoma tumor samples (32%), but not at all in any medulloblastoma samples.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Cyclin D2 / biosynthesis. Epigenesis, Genetic. Eye Proteins / biosynthesis. Gene Expression Regulation, Neoplastic. Hedgehog Proteins / biosynthesis. Homeodomain Proteins / biosynthesis. Medulloblastoma / metabolism. Paired Box Transcription Factors / biosynthesis. Receptors, Cell Surface / biosynthesis. Repressor Proteins / biosynthesis. Transcription Factors / biosynthesis. gamma Catenin / biosynthesis

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  • (PMID = 21059263.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin D2; 0 / Eye Proteins; 0 / GLI1 protein, human; 0 / Hedgehog Proteins; 0 / Homeodomain Proteins; 0 / Nkx-2.2 homedomain protein; 0 / PAX6 protein; 0 / Paired Box Transcription Factors; 0 / RNA, Small Interfering; 0 / Receptors, Cell Surface; 0 / Repressor Proteins; 0 / SHH protein, human; 0 / Transcription Factors; 0 / gamma Catenin; 0 / patched receptors
  • [Other-IDs] NLM/ PMC2989332
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40. Emdad L, Sarkar D, Lee SG, Su ZZ, Yoo BK, Dash R, Yacoub A, Fuller CE, Shah K, Dent P, Bruce JN, Fisher PB: Astrocyte elevated gene-1: a novel target for human glioma therapy. Mol Cancer Ther; 2010 Jan;9(1):79-88
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  • Malignant gliomas including glioblastoma multiforme (GBM) and anaplastic astrocytomas are the most common primary brain tumors.
  • In the present study, we investigated the potential contribution of astrocyte elevated gene-1 (AEG-1) in gliomagenesis and explored the possibility of AEG-1 as a therapeutic target for malignant glioma.
  • We analyzed the expression levels of AEG-1 in 9 normal brain tissues and 98 brain tumor patient samples by Western blot analysis and immunohistochemistry.
  • AEG-1 expression was significantly elevated in >90% of diverse human brain tumor samples including GBMs and astrocytic tumors, and also in human glioma cell lines compared with normal brain tissues and normal astrocytes.
  • In an orthotopic nude mouse brain tumor model using primary human GBM12 tumor cells, AEG-1 small interfering RNA significantly suppressed glioma cell growth in vivo.
  • Taken together, these provocative results indicate that AEG-1 may play a crucial role in the pathogenesis of glioma and that AEG-1 could represent a viable potential target for malignant glioma therapy.

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  • (PMID = 20053777.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA134721-02; United States / NCI NIH HHS / CA / P01 CA104177-04; United States / NCI NIH HHS / CA / R01 CA134721-01A1; United States / NCI NIH HHS / CA / CA134721-01A1; United States / NCI NIH HHS / CA / R01 CA134721; United States / NCI NIH HHS / CA / R01 CA134721-02; United States / NCI NIH HHS / CA / R01 CA134721-03; United States / NCI NIH HHS / CA / P01 CA104177
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Antineoplastic Agents; 0 / Cell Adhesion Molecules; 0 / MTDH protein, human; 0 / RNA, Small Interfering; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ NIHMS162017; NLM/ PMC3165052
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41. Xu GW, Mymryk JS, Cairncross JG: Pharmaceutical-mediated inactivation of p53 sensitizes U87MG glioma cells to BCNU and temozolomide. Int J Cancer; 2005 Aug 20;116(2):187-92
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  • We examined the effect of PFTalpha on the chemosensitivity of a human cancer in which cell cycle arrest, not apoptosis, is the principle cellular consequence of p53 activation.
  • This was of interest because E6 silencing of p53 sensitizes U87MG astrocytic glioma cells to BCNU and temozolomide (TMZ), cytotoxic drugs that are modestly helpful in the treatment of aggressive astrocytic gliomas.
  • [MeSH-major] Antineoplastic Agents, Alkylating / pharmacology. Brain Neoplasms / pathology. Carmustine / pharmacology. Dacarbazine / analogs & derivatives. Dacarbazine / pharmacology. Glioma / pathology. Thiazoles / pharmacology. Toluene / analogs & derivatives. Toluene / pharmacology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Benzothiazoles. DNA Damage. Drug Interactions. Humans. Tumor Cells, Cultured

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15800902.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Benzothiazoles; 0 / Thiazoles; 0 / Tumor Suppressor Protein p53; 0 / pifithrin; 3FPU23BG52 / Toluene; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; U68WG3173Y / Carmustine
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42. Hagemann C, Gloger J, Anacker J, Said HM, Gerngras S, Kühnel S, Meyer C, Rapp UR, Kämmerer U, Vordermark D, Flentje M, Roosen K, Vince GH: RAF expression in human astrocytic tumors. Int J Mol Med; 2009 Jan;23(1):17-31
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  • [Title] RAF expression in human astrocytic tumors.
  • Alterations of C-RAF expression are discussed to play a role in lung cancer.
  • Malignant gliomas are the most prevalent primary brain tumors of adults.
  • Although a role of the mitogenic Ras-RAF-MEK-ERK signalling cascade in brain tumor development is well established, there are only few reports available addressing alterations in RAF sequence or protein expression and function in human gliomas.
  • Then we checked for RAF gene amplification by dot blot hybridization and examined RAF mRNA and protein expression patterns in human astrocytic gliomas of WHO grade II (LGA) and IV (GBM) by semiquantitative RT-PCR and Western blotting, respectively.
  • A-raf gene amplification was more often detected and overexpression of all three RAF proteins on mRNA and protein level was regularly found in human malignant gliomas.
  • [MeSH-major] Astrocytoma / genetics. Glioblastoma / genetics. Proto-Oncogene Proteins A-raf / genetics. Proto-Oncogene Proteins B-raf / genetics. Proto-Oncogene Proteins c-raf / genetics
  • [MeSH-minor] Cell Line, Tumor. Cell Movement. Cell Proliferation. Gene Expression Regulation. Humans. Mutant Proteins / genetics. Prognosis. RNA, Messenger / genetics. Sequence Analysis, DNA

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  • (PMID = 19082503.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Mutant Proteins; 0 / RNA, Messenger; EC 2.7.11.1 / Proto-Oncogene Proteins A-raf; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf
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43. Beetz C, Bergner S, Brodoehl S, Brodhun M, Ewald C, Kalff R, Krüger J, Patt S, Kiehntopf M, Deufel T: Outcome-based profiling of astrocytic tumours identifies prognostic gene expression signatures which link molecular and morphology-based pathology. Int J Oncol; 2006 Nov;29(5):1183-91
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  • [Title] Outcome-based profiling of astrocytic tumours identifies prognostic gene expression signatures which link molecular and morphology-based pathology.
  • Astrocytomas are intracranial malignancies for which invasive growth and high motility of tumour cells preclude total resection; the tumours usually recur in a more aggressive and, eventually, lethal form.
  • In order to identify novel molecular markers for prognosis we obtained expression profiles of: i) tumours associated with particularly long recurrence-free intervals, ii) tumours which led to rapid patient death, and iii) tumour-free control brain.
  • Our finding of cell-specificity for some of these outcome-determining genes relates global expression data to the presence of morphological correlates of tumour behaviour and, thus, provides a link between morphology-based and molecular pathology.
  • Our identification of expression signatures that are associated individually with clinical outcome confirms the prognostic relevance of gene expression data and, thus, represents a step towards eventually implementing molecular diagnosis into clinical practice in neuro-oncology.
  • [MeSH-major] Astrocytoma / mortality. Biomarkers, Tumor / analysis. Brain Neoplasms / mortality. Gene Expression Profiling. Genes, Neoplasm / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Prognosis. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17016650.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Neoplasm
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44. Lavon I, Zrihan D, Zelikovitch B, Fellig Y, Fuchs D, Soffer D, Siegal T: Longitudinal assessment of genetic and epigenetic markers in oligodendrogliomas. Clin Cancer Res; 2007 Mar 1;13(5):1429-37
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  • PURPOSE: Because little is known about the evolution of genetic and epigenetic changes that occur during tumor progression in oligodendrogliomas, we evaluated these changes in paired early and progressive oligodendrogliomas.
  • Of 17 early tumors described as pure oligodendrogliomas, 76.5% remained in this lineage, regardless of their grade, whereas others changed to astrocytic tumors.
  • Oligoastrocytic tumors had a significantly higher tendency to transform to astrocytic tumors.
  • Of tumors with early 1p deletion, 80% remained oligodendroglial at progression, whereas 75% of tumors with an intact 1p changed to astrocytic phenotype.
  • MGMT promoter methylation is more pronounced at tumor progression, particularly in tumors with an intact 1p.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. DNA Methylation. Epigenesis, Genetic. Oligodendroglioma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Female. Humans. Immunohistochemistry. Male. Microsatellite Repeats. Middle Aged. Phenotype. Polymerase Chain Reaction. Promoter Regions, Genetic. Tumor Suppressor Proteins / genetics

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  • (PMID = 17332285.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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45. Conley L, Geurs TL, Levin LA: Transcriptional regulation of ceruloplasmin by an IL-6 response element pathway. Brain Res Mol Brain Res; 2005 Oct 3;139(2):235-41
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  • Based on the fact that peripheral nerve injury induces interleukin-6 (IL-6) expression and that there are three IL-6 response elements in the upstream region of the Cp gene, we studied their role in transcriptional regulation of Cp in astrocytic C6 glioma cells, using transfection of a rat Cp-luciferase construct, followed by sequential and simultaneous mutation of the IL-6 response elements.
  • [MeSH-minor] Animals. Cell Line, Tumor. Dose-Response Relationship, Drug. Electrophoretic Mobility Shift Assay / methods. Glioma. Luciferases / metabolism. Mutagenesis / physiology. Promoter Regions, Genetic / physiology. Rats. Transcriptional Activation / drug effects. Transcriptional Activation / physiology. Transfection / methods

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  • (PMID = 15979198.001).
  • [ISSN] 0169-328X
  • [Journal-full-title] Brain research. Molecular brain research
  • [ISO-abbreviation] Brain Res. Mol. Brain Res.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / R01 EY12492
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Transcription Factors; EC 1.13.12.- / Luciferases; EC 1.16.3.1 / Ceruloplasmin
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46. Arvanitis DL, Arvanitis LD, Panourias IG, Kitsoulis P, Kanavaros P: The expression of the epitope H recognized by the monoclonal antibody H is higher in astrocytomas compared to anaplastic astrocytomas and glioblastomas. Histol Histopathol; 2005 10;20(4):1057-63
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  • In the present study we used the mAbH to investigate the immunohistochemical expression of the epitope H in 41 cases of astrocytic tumors including 19 cases of astrocytomas, 8 cases of anaplastic astrocytomas and 14 cases of glioblastomas.
  • These results indicate that the expression of the epitope H decreases in parallel with the increase of the grade of astrocytic tumors from low to higher grade neoplasms.
  • This could be of interest for predicting the progression of an astrocytic tumor since it is documented that astrocytomas progress to tumors of higher grade of malignancy.
  • Further investigation of the antigens bearing the epitope H might help to gain further insight into the mechanisms which regulate the progression of astrocytic tumors and to examine the relevance of the mAbH staining with respect to the prognosis of these neoplasms.
  • [MeSH-major] Antibodies, Monoclonal / metabolism. Astrocytoma / immunology. Epitopes / biosynthesis. Glioblastoma / immunology
  • [MeSH-minor] Animals. Brain Neoplasms / immunology. Brain Neoplasms / pathology. Glial Fibrillary Acidic Protein / analysis. Humans. Immunohistochemistry. Rabbits

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  • (PMID = 16136487.001).
  • [ISSN] 0213-3911
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Epitopes; 0 / Glial Fibrillary Acidic Protein
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47. Park SH, Min HS, Kim B, Myung J, Paek SH: Galectin-3: a useful biomarker for differential diagnosis of brain tumors. Neuropathology; 2008 Oct;28(5):497-506
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  • [Title] Galectin-3: a useful biomarker for differential diagnosis of brain tumors.
  • Gal-3's expression in and significance to brain tumors has not been fully addressed.
  • Here, we investigated its immunohistochemical expression in 409 cases of surgically resected primary brain tumors, including various glioneuronal tumors, pituitary adenomas, meningiomas and Schwannomas, among others.
  • In normal brain tissues, gal-3 was robustly expressed in normal astrocytes, endothelial cells and macrophages.
  • Focal positivity for gal-3 was also found in dysembryoplastic neuroepithelial tumors (DNTs) and gangliogliomas, in which the positive cells were the astrocytic component.
  • On the basis of our immunohistochemical data in conjunction with previous reports, we therefore conclude that gal-3 is differentially expressed in various brain tumors, and thereby, is a helpful biomarker in making differential diagnoses, especially in cases where a morphological diagnosis is controversial.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / diagnosis. Brain Neoplasms / metabolism. Galectin 3 / biosynthesis
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunohistochemistry

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  • (PMID = 18384511.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Galectin 3
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48. Qu M, Olofsson T, Sigurdardottir S, You C, Kalimo H, Nistér M, Smits A, Ren ZP: Genetically distinct astrocytic and oligodendroglial components in oligoastrocytomas. Acta Neuropathol; 2007 Feb;113(2):129-36
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  • [Title] Genetically distinct astrocytic and oligodendroglial components in oligoastrocytomas.
  • Oligoastrocytomas are glial tumours consisting of a mixture of neoplastic astrocytic and oligodendroglial cells.
  • To investigate whether these neoplastic cell types in oligoastrocytomas have different genetic profiles, we examined the two different components of oligoastrocytomas in comparison with the histological diagnosis of the specific tumour area for LOH 1p/19q and TP53 mutations by using microdissection technique.
  • We found a variety of lost markers for 1p and 19q, and the presence of two different TP53 mutations in the tumour samples.
  • In the majority of cases (9/11), the oligodendroglial and astrocytic components of an individual oligoastrocytoma displayed the same genotype.
  • We present two cases of biphasic oligoastrocytomas with aberrant findings, suggesting the coexistence of genetically and morphologically distinct tumour cell clones in these tumours.
  • In one case, the oligodendroglial part of the tumour showed LOH19q, whereas the astrocytic part showed TP53 mutation (codon 273).
  • In another case, we found LOH 1p/19q in the oligodendroglial component, but two retained areas on chromosome 1p in the astrocytic component of the tumour.
  • No evidence was found for the coexistence of tumour cells with the two genotypical changes within the same morphological region of one individual tumour.
  • The two cases of biphasic oligoastrocytomas in our sample that display a different genotype in the astrocytic and oligodendroglial part of the tumour show that different components of an oligoastrocytoma may be derived from different cell clones during neoplastic transformation.
  • [MeSH-major] Astrocytoma / classification. Astrocytoma / genetics. Brain Neoplasms / classification. Brain Neoplasms / genetics. Oligodendroglioma / genetics
  • [MeSH-minor] Adult. Aged. Chromosomes, Human, Pair 1 / genetics. Female. Humans. Male. Microsatellite Repeats. Middle Aged. Mutation. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 17031656.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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49. Phulwani NK, Esen N, Syed MM, Kielian T: TLR2 expression in astrocytes is induced by TNF-alpha- and NF-kappa B-dependent pathways. J Immunol; 2008 Sep 15;181(6):3841-9
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  • Since TLR2 is critical for signaling astrocytic cytokine production in response to S. aureus, we evaluated the effect of TNF-alpha loss on proinflammatory mediator release.
  • Similar results were obtained following LPS treatment, suggesting that TNF-alpha is an important regulator of astrocytic TLR2 expression and NO release in response to diverse microbial stimuli.

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  • (PMID = 18768838.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / R01 MH065297; United States / NINDS NIH HHS / NS / NS055385-05A2; United States / NINDS NIH HHS / NS / P30 NS047546-04; United States / NIMH NIH HHS / MH / R01 MH65297; United States / NINDS NIH HHS / NS / NS055385-06; United States / NINDS NIH HHS / NS / P30 NS047546; United States / NINDS NIH HHS / NS / R01 NS055385-06; United States / NINDS NIH HHS / NS / R01 NS055385-05A2; United States / NINDS NIH HHS / NS / NS047546-04; United States / NINDS NIH HHS / NS / R01 NS055385
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Inflammation Mediators; 0 / NF-kappa B; 0 / Tlr2 protein, mouse; 0 / Toll-Like Receptor 2; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide
  • [Other-IDs] NLM/ NIHMS93624; NLM/ PMC2649826
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50. Sawada T, Kato Y, Kobayashi M: Expression of aquaporine-4 in central nervous system tumors. Brain Tumor Pathol; 2007;24(2):81-4
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  • Cerebral edema is associated with common brain tumors.
  • Aquaporine-4 (AQP4) is a member of the water channel protein family, which is thought to be a major factor regulating cerebral edema.
  • Brain tumors and nontumorous cerebral tissue for control were evaluated by immunohistochemical staining using anti-AQP4, VEGF, CD34, and MIB-1.
  • In tumor cells, only glial tumor cells showed a positive reaction for AQP4.
  • Although endothelial cells were negative and/or weakly positive for AQP4, the positive relationship suggested the expression of VEGF in endothelial cells in neovasculature and that of AQP 4 in tumor cells.
  • APQ4 expression increased in human astrocytic tumors and edematous cerebral tissue.
  • Upregulation of APQ4 by tumor cells and reactive astroglia were major factors of cerebral edema.
  • [MeSH-major] Aquaporin 4 / biosynthesis. Brain Neoplasms / metabolism. Brain Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Astrocytes / metabolism. Brain Edema / etiology. Brain Edema / metabolism. Female. Gene Expression. Humans. Immunohistochemistry. Male. Middle Aged. Receptors, Vascular Endothelial Growth Factor / biosynthesis. Up-Regulation. Vascular Endothelial Growth Factor A / biosynthesis

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  • (PMID = 18095136.001).
  • [ISSN] 1433-7398
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / AQP4 protein, human; 0 / Aquaporin 4; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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51. Balosso S, Ravizza T, Perego C, Peschon J, Campbell IL, De Simoni MG, Vezzani A: Tumor necrosis factor-alpha inhibits seizures in mice via p75 receptors. Ann Neurol; 2005 Jun;57(6):804-12
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  • [Title] Tumor necrosis factor-alpha inhibits seizures in mice via p75 receptors.
  • Brain inflammatory reactions have been described in various neurological disorders, including epilepsy.
  • Although there is clear evidence that cytokines affect neuroglial functions and blood-brain barrier permeability, scarce information is available on the functional consequences of brain inflammation on seizures.
  • We studied the role of tumor necrosis factor-alpha (TNF)-alpha and its p55 and p75 receptors in seizure modulation.
  • Transgenic mice with a perturbed TNF-alpha system showed profound alterations in seizure susceptibility: astrocytic overexpression of TNF-alpha was associated with reduced seizures, whereas mice lacking TNF-alpha p75 or both p55 and p75, receptors showed prolonged seizures.
  • Our findings show that increased brain levels of TNF-alpha result in significant inhibition of seizures in mice, and this action is mediated by neuronal p75 receptors.
  • This evidence highlights a novel function of TNF-alpha in brain and indicates a new system for anticonvulsive intervention.
  • [MeSH-major] Anticonvulsants / pharmacology. Epilepsy / drug therapy. Epilepsy / physiopathology. Receptors, Tumor Necrosis Factor, Type II / genetics. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Electroencephalography. Excitatory Amino Acid Agonists. Gene Expression. Hippocampus / physiology. Kainic Acid. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Receptors, Tumor Necrosis Factor, Type I / genetics. Receptors, Tumor Necrosis Factor, Type I / metabolism

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  • (PMID = 15852477.001).
  • [ISSN] 0364-5134
  • [Journal-full-title] Annals of neurology
  • [ISO-abbreviation] Ann. Neurol.
  • [Language] eng
  • [Grant] Italy / Telethon / / GP0285Y01; United States / NIDA NIH HHS / DA / DA12444
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / Excitatory Amino Acid Agonists; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Tumor Necrosis Factor-alpha; SIV03811UC / Kainic Acid
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52. Alaraj A, Chan M, Oh S, Michals E, Valyi-Nagy T, Hersonsky T: Astroblastoma presenting with intracerebral hemorrhage misdiagnosed as dural arteriovenous fistula: review of a rare entity. Surg Neurol; 2007 Mar;67(3):308-13
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  • Immunohistochemically, the tumor cells show diffuse strong positivity for GFAP, S-100 protein, vimentin, as well as neuron-specific enolase and focal positivity for EMA.
  • A 4-vessel cerebral angiogram revealed a dural AVF in the left posterior temporal area.
  • Because of its high degree of proliferation, the presence of astroblastic pseudorosettes, prominent perivascular hyalinization, regional hyaline changes, and pushing borders with regard to the adjacent brain, the tumor was considered anaplastic.
  • CONCLUSIONS: Astroblastoma is a rare pure pathologic entity--a distinct form of astrocytic gliomas.
  • The diagnosis of astroblastoma is often difficult because of the astroblastic aspects that can be found in astrocytic tumors, in ependymomas, and in nonneuroepithelial tumors.
  • [MeSH-major] Central Nervous System Vascular Malformations / diagnosis. Cerebral Hemorrhage. Diagnostic Errors. Neoplasms, Neuroepithelial
  • [MeSH-minor] Adult. Cerebral Angiography. Diagnosis, Differential. Humans. Magnetic Resonance Imaging. Male. Neoplasm Staging

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  • (PMID = 17320647.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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53. Janardhanan R, Banik NL, Ray SK: N-(4-Hydroxyphenyl)retinamide induced differentiation with repression of telomerase and cell cycle to increase interferon-gamma sensitivity for apoptosis in human glioblastoma cells. Cancer Lett; 2008 Mar 8;261(1):26-36
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  • Glioblastoma is the most malignant and prevalent brain tumor in humans.
  • N-(4-Hydroxyphenyl)retinamide (4-HPR) induced astrocytic differentiation and increased sensitivity to interferon-gamma (IFN-gamma) for apoptosis in human glioblastoma A172, LN18, and SNB19 cells.

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  • (PMID = 18164543.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS057811-03; United States / NCI NIH HHS / CA / CA091460-04; United States / NCI NIH HHS / CA / R01 CA-91460; United States / NCI NIH HHS / CA / R01 CA091460-04; United States / NCI NIH HHS / CA / R01 CA091460; United States / NINDS NIH HHS / NS / R01 NS057811-03; United States / NINDS NIH HHS / NS / R01 NS-57811; United States / NINDS NIH HHS / NS / R01 NS057811
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Ireland
  • [Chemical-registry-number] 187EJ7QEXL / Fenretinide; 82115-62-6 / Interferon-gamma; EC 2.7.7.49 / Telomerase; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ NIHMS43293; NLM/ PMC3103940
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54. Bannykh SI, Stolt CC, Kim J, Perry A, Wegner M: Oligodendroglial-specific transcriptional factor SOX10 is ubiquitously expressed in human gliomas. J Neurooncol; 2006 Jan;76(2):115-27
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  • The two most common types of gliomas: astrocytoma and oligodendroglioma are distinguished based on their morphologic similarities to mature astrocytes and oligodendroglia.
  • We applied immunohistochemistry to analyze whether the expression of SOX10 can differentiate astrocytoma and oligodendroglioma.
  • High levels of expression were also found in pilocytic astrocytoma, consistent with recent studies suggesting that pilocytic astrocytomas have greater overlap with oligodendroglial than astrocytic tumors.
  • [MeSH-major] Brain Neoplasms / metabolism. DNA-Binding Proteins / biosynthesis. Glioma / metabolism. High Mobility Group Proteins / biosynthesis. Oligodendroglia / metabolism. Transcription Factors / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Astrocytes / metabolism. Astrocytoma / metabolism. Basic Helix-Loop-Helix Transcription Factors / metabolism. Biomarkers, Tumor / metabolism. Blotting, Western. Child. Child, Preschool. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Nerve Tissue Proteins / metabolism. SOXE Transcription Factors

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  • (PMID = 16205963.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / High Mobility Group Proteins; 0 / Nerve Tissue Proteins; 0 / OLIG1 protein, human; 0 / OLIG2 protein, human; 0 / SOX10 protein, human; 0 / SOXE Transcription Factors; 0 / Transcription Factors
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55. Froger N, Orellana JA, Cohen-Salmon M, Ezan P, Amigou E, Sáez JC, Giaume C: Cannabinoids prevent the opposite regulation of astroglial connexin43 hemichannels and gap junction channels induced by pro-inflammatory treatments. J Neurochem; 2009 Dec;111(6):1383-97
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  • Brain injuries as well as neurodegenerative diseases, are associated with neuro-inflammation characterized by astroglial and microglial activation and/or proliferation.
  • This opposite regulation is mediated by two pro-inflammatory cytokines, interleukin-1 beta and tumor necrosis factor-alpha, released from activated microglia.
  • We observed that CBs inhibited the LPS-induced release of interleukin-1 beta and tumor necrosis factor-alpha from microglia.
  • Pharmacological characterizations of CB actions on astrocytic connexin43 channels revealed that these effects were mainly mediated through CB1 receptors activation, although non-CB1/CB2 receptors seemed to mediate the action of the methanandamide.
  • [MeSH-minor] Analgesics / pharmacology. Animals. Animals, Newborn. Arachidonic Acids / pharmacology. Benzoxazines / pharmacology. Cells, Cultured. Cerebral Cortex / cytology. Culture Media, Conditioned / pharmacology. Cyclohexanols / pharmacology. Drug Interactions. Enzyme-Linked Immunosorbent Assay / methods. Ethidium / metabolism. Gene Expression Regulation / drug effects. Interleukin-1beta / metabolism. Maximum Tolerated Dose. Mice. Microglia / chemistry. Morpholines / pharmacology. Naphthalenes / pharmacology. Piperidines / pharmacology. Pyrazoles / pharmacology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 20050288.001).
  • [ISSN] 1471-4159
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Analgesics; 0 / Arachidonic Acids; 0 / Benzoxazines; 0 / Cannabinoids; 0 / Connexin 43; 0 / Connexins; 0 / Culture Media, Conditioned; 0 / Cyclohexanols; 0 / Interleukin-1beta; 0 / Lipopolysaccharides; 0 / Morpholines; 0 / Naphthalenes; 0 / Piperidines; 0 / Pyrazoles; 0 / Tumor Necrosis Factor-alpha; 134959-51-6 / Win 55212-2; 150314-39-9 / methanandamide; 158681-13-1 / rimonabant; 83003-12-7 / 3-(2-hydroxy-4-(1,1-dimethylheptyl)phenyl)-4-(3-hydroxypropyl)cyclohexanol; EN464416SI / Ethidium
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56. Li M, Jia ZZ, Gu HM, Zhou XJ, Tang LM: [Application of apparent diffusion coefficient and fractional anisotropy in identification of tumor component and grading of brain astrocytoma]. Zhonghua Yi Xue Za Zhi; 2008 Dec 23;88(47):3352-5
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  • [Title] [Application of apparent diffusion coefficient and fractional anisotropy in identification of tumor component and grading of brain astrocytoma].
  • OBJECTIVE: To evaluate the value of apparent diffusion coefficient (ADC) and fractional anisotropy (FA) in identification of tumor element and grading of brain astrocytoma.
  • METHODS: Thirty-three patients with histologically confirmed astrocytoma underwent diffusion weighted imaging (DWI), diffusion tensor imaging (DTI), and conventional MRI before operation.
  • The values of ADC and FA of different regions in the same tumor and of astrocytoma of different grades were measured and compared.
  • RESULTS: The ADC values of the tumor parenchyma, necrotic region, peritumoral edema region were (1.28 +/- 0.44), (1.97 +/- 0.53), and (1.74 +/- 0.47) respectively, all significantly higher than that of the corresponding normal brain tissues [(0.80 +/- 0.18), P = 0.009, P = 0.000, P = 0.000] with significantly differences between the tumor parenchyma and necrotic region and peritumoral edema region (both P < 0.05), however, there was not significant difference between the necrotic region and peritumoral edema region.
  • The FA values of the tumor parenchyma, necrotic region, and peritumoral edema region were (0.18 +/- 0.07), (0.14 +/- 0.05), and (0.16 +/- 0.05) respectively, all significantly higher than that of the corresponding normal brain tissues [(0.58 +/- 0.10), all P = 0.000], without significant differences among the former 3 groups.
  • There were no significant differences in the ADC and FA values among the tumors at different grades, however, there was a tendency of ADC to decrease and of FA to increase along the increase of grade of tumor, although not significantly.
  • CONCLUSION: ADC value plays an important part in distinguishing tumor components and determining tumor boundary, and plays a certain role in judging the grade of astrocytomas.
  • FA value is vital to determine the tumor boundary, and has certain value in differentiating high-grade from low-grade astrocytomas.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Diffusion Magnetic Resonance Imaging / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Anisotropy. Female. Humans. Male. Middle Aged. Neoplasm Staging

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  • (PMID = 19257968.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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57. Mortazavi H, Abedini R, Sadri F, Soori T, Vasheghani-Farahani A: Crusted scabies in a patient with brain astrocytoma: report of a case. Int J Infect Dis; 2010 Jun;14(6):e526-7
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  • [Title] Crusted scabies in a patient with brain astrocytoma: report of a case.
  • He suffered from a brain tumor (astrocytoma) and was immunosuppressed because he was receiving systemic steroids and chemo-radiation therapy.
  • He also had psychomotor retardation and behavior changes due to the pressure effect of his brain tumor.
  • The diagnosis of crusted scabies was established based on direct positive skin smears from the lesions.
  • [MeSH-major] Astrocytoma / complications. Brain Neoplasms / complications. Sarcoptes scabiei. Scabies / diagnosis
  • [MeSH-minor] Adult. Animals. Diagnosis, Differential. Fatal Outcome. Humans. Immunocompromised Host. Male. Pruritus / pathology

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  • [Copyright] Copyright 2009 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.
  • (PMID = 19700360.001).
  • [ISSN] 1878-3511
  • [Journal-full-title] International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases
  • [ISO-abbreviation] Int. J. Infect. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Canada
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58. Monnet-Tschudi F, Hazekamp A, Perret N, Zurich MG, Mangin P, Giroud C, Honegger P: Delta-9-tetrahydrocannabinol accumulation, metabolism and cell-type-specific adverse effects in aggregating brain cell cultures. Toxicol Appl Pharmacol; 2008 Apr 1;228(1):8-16
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  • [Title] Delta-9-tetrahydrocannabinol accumulation, metabolism and cell-type-specific adverse effects in aggregating brain cell cultures.
  • The quantification of 11-OH-THC and of THC-COOH showed that brain aggregates were capable of THC metabolism.
  • Only the GABAergic marker was affected after the single treatment, whereas the GABAergic, cholinergic and astrocytic markers were decreased after the repeated treatments.
  • [MeSH-major] Brain / pathology. Dronabinol / metabolism. Dronabinol / toxicity
  • [MeSH-minor] Animals. Cannabinoids / metabolism. Cell Aggregation / drug effects. Cells, Cultured. Choline O-Acetyltransferase / metabolism. Chromatography, High Pressure Liquid. Female. GTP Phosphohydrolases / metabolism. Glutamate Decarboxylase / metabolism. Interleukin-6 / biosynthesis. L-Lactate Dehydrogenase / metabolism. Mass Spectrometry. Neuroglia / drug effects. Neurons / drug effects. Pregnancy. Rats. Receptor, Cannabinoid, CB1 / agonists. Receptor, Cannabinoid, CB2 / agonists. Reference Standards. Reverse Transcriptase Polymerase Chain Reaction. Solvents. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 18083204.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cannabinoids; 0 / Interleukin-6; 0 / Receptor, Cannabinoid, CB1; 0 / Receptor, Cannabinoid, CB2; 0 / Solvents; 0 / Tumor Necrosis Factor-alpha; 7J8897W37S / Dronabinol; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 2.3.1.6 / Choline O-Acetyltransferase; EC 3.6.1.- / GTP Phosphohydrolases; EC 4.1.1.15 / Glutamate Decarboxylase
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59. Anan'eva II, Malkarov MS, Korsakova NA, Balkanov AS, Dorofeev AE, Kachkov IA, Suchkov SV: [Glial tumors of the brain: current aspects of their classification and bases for genetic predisposition]. Arkh Patol; 2007 Jan-Feb;69(1):54-60
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  • [Title] [Glial tumors of the brain: current aspects of their classification and bases for genetic predisposition].
  • Malignant astrocytic gliomas account for 50% of all primary brain tumors.
  • Cells of origin are unknown for the majority of brain tumors: CNS tumors have frequently in their content many histological forms and their classification will depend on what the parts of neoplasm that will be clearly identified at the material taking and further investigation.
  • Current immunohistochemical studies may determine the antigenic structure of a tumor cell, compare it with the antigens expressed by a certain cell type and, thus, classify the tumor by its origin, but there are no antibodies which would correctly identify different types of tumors.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / classification. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Genetic Predisposition to Disease
  • [MeSH-minor] Antigens, Neoplasm / biosynthesis. Antigens, Neoplasm / genetics. Antigens, Neoplasm / immunology. Gene Expression Regulation, Neoplastic / genetics. Humans

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  • (PMID = 19385137.001).
  • [ISSN] 0004-1955
  • [Journal-full-title] Arkhiv patologii
  • [ISO-abbreviation] Arkh. Patol.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antigens, Neoplasm
  • [Number-of-references] 45
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60. Riemenschneider MJ, Reifenberger G: Astrocytic tumors. Recent Results Cancer Res; 2009;171:3-24
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  • [Title] Astrocytic tumors.
  • Astrocytic gliomas are the most common primary brain tumors and account for up to two thirds of all tumors of glial origin.
  • In this review we outline the basic histological and epidemiological aspects of the different astrocytoma subtypes in adults.
  • In addition, we summarize the key genetic alterations that have been attributed to astrocytoma patho-genesis and progression.
  • Also, the first steps have been taken in refining classical histopathological diagnosis by use of molecular predictive markers, for example, MGMT promoter hypermethylation in glioblastomas.
  • Finally, the tumor stem cell hypothesis has challenged our way of understanding astrocytoma biology by emphasizing intratumoral heterogeneity.
  • [MeSH-major] Brain Neoplasms / genetics
  • [MeSH-minor] Animals. Astrocytoma / chemistry. Astrocytoma / diagnosis. Astrocytoma / genetics. Astrocytoma / pathology. Disease Models, Animal. Humans. Immunohistochemistry. Neoplasm Invasiveness. Signal Transduction

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  • (PMID = 19322535.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 109
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61. Santel T, Pflug G, Hemdan NY, Schäfer A, Hollenbach M, Buchold M, Hintersdorf A, Lindner I, Otto A, Bigl M, Oerlecke I, Hutschenreuther A, Sack U, Huse K, Groth M, Birkemeyer C, Schellenberger W, Gebhardt R, Platzer M, Weiss T, Vijayalakshmi MA, Krüger M, Birkenmeier G: Curcumin inhibits glyoxalase 1: a possible link to its anti-inflammatory and anti-tumor activity. PLoS One; 2008;3(10):e3508
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  • [Title] Curcumin inhibits glyoxalase 1: a possible link to its anti-inflammatory and anti-tumor activity.
  • METHODOLOGY/PRINCIPAL FINDINGS: Cultures of whole blood cells and tumor cell lines (PC-3, JIM-1, MDA-MD 231 and 1321N1) were set up to investigate the effect of selected polyphenols, including curcumin, on the LPS-induced cytokine production (cytometric bead-based array), cell proliferation (WST-1 assay), cytosolic Glo1 and Glo2 enzymatic activity, apoptosis/necrosis (annexin V-FITC/propidium iodide staining; flow cytometric analysis) as well as GSH and ATP content.
  • Moreover, whereas curcumin was found to hamper the growth of breast cancer (JIMT-1, MDA-MB-231), prostate cancer PC-3 and brain astrocytoma 1321N1 cells, no effect on growth or vitality of human primary hepatocytes was elucidated.
  • Curcumin decreased D-lactate release by tumor cells, another clue for inhibition of intracellular Glo1.
  • This may account for curcumin's potency as an anti-inflammatory and anti-tumor agent.

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  • [ErratumIn] PLoS One. 2011;6(7). doi:10.1371/annotation/0eb2b9f3-1006-4dcd-ad61-367310a2686a. Hutschenreuter, Antje [corrected to Hutschenreuther, Antje]
  • (PMID = 18946510.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Interleukin-1beta; 0 / Lipopolysaccharides; 0 / Phenols; 0 / Polyphenols; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 4.4.1.5 / Lactoylglutathione Lyase; IT942ZTH98 / Curcumin
  • [Other-IDs] NLM/ PMC2567432
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62. Brozzi F, Arcuri C, Giambanco I, Donato R: S100B Protein Regulates Astrocyte Shape and Migration via Interaction with Src Kinase: IMPLICATIONS FOR ASTROCYTE DEVELOPMENT, ACTIVATION, AND TUMOR GROWTH. J Biol Chem; 2009 Mar 27;284(13):8797-811
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  • [Title] S100B Protein Regulates Astrocyte Shape and Migration via Interaction with Src Kinase: IMPLICATIONS FOR ASTROCYTE DEVELOPMENT, ACTIVATION, AND TUMOR GROWTH.
  • We show here that reducing S100B levels in the astrocytoma cell line GL15 and the Müller cell line MIO-M1 by small interference RNA technique results in a rapid disassembly of stress fibers, collapse of F-actin onto the plasma membrane and reduced migration, and acquisition of a stellate shape.
  • These results suggest that S100B might contribute to reduce the differentiation potential of cells of the astrocytic lineage and participate in the astrocyte activation process in the case of brain insult and in invasive properties of glioma cells.
  • [MeSH-major] Astrocytes / metabolism. Astrocytoma / metabolism. Cell Movement. Cell Shape. Nerve Growth Factors / metabolism. S100 Proteins / metabolism. src-Family Kinases / metabolism
  • [MeSH-minor] Animals. Bucladesine / pharmacology. Cell Line, Tumor. Glycogen Synthase Kinase 3 / genetics. Glycogen Synthase Kinase 3 / metabolism. Humans. Phosphatidylinositol 3-Kinases / genetics. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / genetics. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / genetics. Rats. S100 Calcium Binding Protein beta Subunit. Stress Fibers / genetics. Stress Fibers / metabolism. Stroke / genetics. Stroke / metabolism. rac1 GTP-Binding Protein / genetics. rac1 GTP-Binding Protein / metabolism. rhoA GTP-Binding Protein / genetics. rhoA GTP-Binding Protein / metabolism

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • (PMID = 19147496.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nerve Growth Factors; 0 / RAC1 protein, human; 0 / RNA, Small Interfering; 0 / S100 Calcium Binding Protein beta Subunit; 0 / S100 Proteins; 0 / S100B protein, human; 0 / S100b protein, rat; 124671-05-2 / RHOA protein, human; 63X7MBT2LQ / Bucladesine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 3.6.1.- / Rac1 protein, rat; EC 3.6.5.2 / rac1 GTP-Binding Protein; EC 3.6.5.2 / rhoA GTP-Binding Protein
  • [Other-IDs] NLM/ PMC2659238
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63. Nakamura M, Ishida E, Shimada K, Kishi M, Nakase H, Sakaki T, Konishi N: Frequent LOH on 22q12.3 and TIMP-3 inactivation occur in the progression to secondary glioblastomas. Lab Invest; 2005 Feb;85(2):165-75
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  • Frequent allelic losses on the long arm of chromosome 22 (22q) in gliomas indicate the presence of tumor suppressor gene (TSG) at this location.
  • However, the target gene(s) residing in this chromosome are still unknown and their putative roles in the development of astrocytic tumors, especially in secondary glioblastoma, have not yet been defined.
  • To compile a precise physical map for the region of common deletions in astrocytic tumors, we performed a high-density loss of heterozygosity (LOH) analysis using 31 polymorphic microsatellite markers spanning 22q in a series of grade II diffuse astrocytomas, anaplastic astrocytomas, primary glioblastomas, and secondary glioblastomas that had evolved from lower grade astrocytomas.
  • This epigenetic change was significantly correlated to poor survival in eight patients with grade II diffuse astrocytoma.
  • Our results suggest that a 957 kb locus, located at 22q12.3, may contain the putative TSG, TIMP-3, that appears to be relevant to progression to secondary glioblastoma and subsequently to the prognosis of grade II diffuse astrocytoma.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 22. Glioblastoma / genetics. Loss of Heterozygosity. Tissue Inhibitor of Metalloproteinase-3 / genetics
  • [MeSH-minor] Adult. Alleles. DNA Methylation. Disease Progression. Epigenesis, Genetic. Gene Deletion. Gene Expression Regulation, Neoplastic. Genetic Markers. Humans. Immunohistochemistry. Microsatellite Repeats. Neoplasm Metastasis. Neoplasm Staging. Physical Chromosome Mapping. Polymorphism, Genetic. Prognosis. Promoter Regions, Genetic. Survival Analysis

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  • (PMID = 15592495.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; 0 / Tissue Inhibitor of Metalloproteinase-3
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64. Hayashi S, Yamamoto M, Tachibana K, Ueno Y, Bu G, Fukushima T: Mechanism of photofrin-enhanced ultrasound-induced human glioma cell death. Anticancer Res; 2009 Mar;29(3):897-905
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  • BACKGROUND: Low-intensity ultrasound showed tumor cell killing by a non-thermal effect in human leukemia cells.
  • The aim of our study was to investigate the efficacy of low-intensity ultrasound on malignant astrocytic tumor cells with the photosensitizer, Photofrin, which is taken up by the cell surface receptor, low density lipoprotein receptor-related protein/alpha2-macroglobulin receptor (LRP/alpha2MR).
  • RESULTS: Ultrasound alone induced instant cell killing immediately after sonication in both U251MG and U105MG malignant gliomas cells.
  • CONCLUSION: This is the first report to demonstrate the usefulness of low-intensity ultrasound for the cell killing of malignant glioma cells.
  • [MeSH-major] Brain Neoplasms / therapy. Cell Survival / drug effects. Dihematoporphyrin Ether / therapeutic use. Glioma / therapy. Photosensitizing Agents / therapeutic use. Ultrasonic Therapy
  • [MeSH-minor] Combined Modality Therapy. Humans. Low Density Lipoprotein Receptor-Related Protein-1 / genetics. Low Density Lipoprotein Receptor-Related Protein-1 / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured. alpha-Macroglobulins / genetics. alpha-Macroglobulins / metabolism

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  • (PMID = 19414325.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Low Density Lipoprotein Receptor-Related Protein-1; 0 / Photosensitizing Agents; 0 / RNA, Messenger; 0 / alpha-Macroglobulins; 97067-70-4 / Dihematoporphyrin Ether
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65. Lee FY, Jan YJ, Wen MC, Li MC, Wang J, Wen-Hsien C: A 32-year-old man with a fourth ventricular mass. Brain Pathol; 2009 Apr;19(2):333-6
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  • Our case is in the fourth ventricle of a 32 year-old man.Many areas showed tumor cells with a signet-ring appearance and focally formed perivascular arrangements.
  • There was strong positive immunoreactivity to GFAP and S-100 protein, even in those vacuolated tumor cells.The proliferation index was less than 10%.
  • These findings confirm that the vacuoles were lipid droplets in astrocytic tumor cells.
  • The features noted are suggestive of a probable better prognosis in this variant of low-grade astrocytoma.
  • [MeSH-major] Astrocytoma / pathology. Cerebral Ventricle Neoplasms / pathology

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  • (PMID = 19291000.001).
  • [ISSN] 1750-3639
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / S100 Proteins
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66. Zarkovic K, Juric G, Waeg G, Kolenc D, Zarkovic N: Immunohistochemical appearance of HNE-protein conjugates in human astrocytomas. Biofactors; 2005;24(1-4):33-40
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  • Those of astrocytic origin are the most widespread of primary brain tumors and account for more then 60% of all CNS neoplasms.
  • The current state of knowledge on the associations between tumor etiology and oxidative stress suggests that environmental factors that cause oxidative stress could also induce and promote cancer, especially in case of hereditary predisposition.
  • The aim of present study was to investigate by immunohistochemistry the presence of HNE-modified proteins in different types of astrocytoma.
  • Our study comprised 45 astrocytic tumors.
  • Slides of paraffin-embedded tumor tissue were stained with hematoxylin-eosin or were prepared for immunohistochemistry with monoclonal antibodies to HNE-histidine conjugate.
  • Lowest intensity of HNE immunopositivity was present in tumor cells of almost all DA, predominantly around blood vessels.
  • In malignant variants of astrocytoma, AA and GB, HNE positivity was moderate to strong, and diffusely distributed in all tumors.
  • [MeSH-major] Aldehydes / analysis. Aldehydes / metabolism. Astrocytoma / chemistry. Immunohistochemistry. Proteins / analysis. Proteins / metabolism
  • [MeSH-minor] Antibodies, Monoclonal. Blood Vessels / chemistry. Brain Neoplasms / blood supply. Brain Neoplasms / chemistry. Brain Neoplasms / pathology. Endothelium, Vascular / chemistry. Humans

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  • (PMID = 16403961.001).
  • [ISSN] 0951-6433
  • [Journal-full-title] BioFactors (Oxford, England)
  • [ISO-abbreviation] Biofactors
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Aldehydes; 0 / Antibodies, Monoclonal; 0 / Proteins; 29343-52-0 / 4-hydroxy-2-nonenal
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67. Crespo-Rodríguez AM, Smirniotopoulos JG, Rushing EJ: MR and CT imaging of 24 pleomorphic xanthoastrocytomas (PXA) and a review of the literature. Neuroradiology; 2007 Apr;49(4):307-15
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  • INTRODUCTION: The aim of our study was to review the imaging appearance of PXA, a rare and usually low-grade, astrocytic tumor that typically occurs in young adults.
  • [MeSH-major] Astrocytoma / diagnosis. Magnetic Resonance Imaging / methods. Supratentorial Neoplasms / diagnosis. Tomography, X-Ray Computed / methods

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  • (PMID = 17205313.001).
  • [ISSN] 0028-3940
  • [Journal-full-title] Neuroradiology
  • [ISO-abbreviation] Neuroradiology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 44
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68. Bisland SK, Goebel EA, Hassanali NS, Johnson C, Wilson BC: Increased expression of mitochondrial benzodiazepine receptors following low-level light treatment facilitates enhanced protoporphyrin IX production in glioma-derived cells in vitro. Lasers Surg Med; 2007 Sep;39(8):678-84
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  • BACKGROUND AND OBJECTIVES: This study investigates whether low-level light treatment (LLLT) can enhance the expression of peripheral-type mitochondrial benzodiazepine receptors (PBRs) on glioma-derived tumor cells, and by doing so promote the synthesis of protoporphyrin IX (PpIX) and increase the photodynamic therapy (PDT)-induced cell kill using 5-aminolevulinic acid (ALA).
  • Cells of astrocytic derivation within the brain express PBRs, while neurons express the central-type of benzodiazepine receptor.
  • STUDY DESIGN: Astrocytoma-derived CNS-1 cells were exposed to a range of differing low-level light protocols immediately prior to PDT.
  • CONCLUSIONS: These data suggest that by selectively increasing PBR expression in tumor cells, LLLT facilitates enhanced tumor cell kill using ALA-PDT.
  • This may further improve the selectivity and efficacy of PDT treatment of brain tumors.
  • [MeSH-minor] Astrocytoma. Cell Cycle. Cell Survival. In Vitro Techniques. Microscopy, Confocal. Spectrometry, Fluorescence

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  • [Copyright] 2007 Wiley-Liss, Inc
  • (PMID = 17886284.001).
  • [ISSN] 0196-8092
  • [Journal-full-title] Lasers in surgery and medicine
  • [ISO-abbreviation] Lasers Surg Med
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-43892
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protoporphyrins; 0 / Receptors, GABA; 0 / TSPO protein, human; 553-12-8 / protoporphyrin IX
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69. Dim DC, Lingamfelter DC, Taboada EM, Fiorella RM: Papillary glioneuronal tumor: a case report and review of the literature. Hum Pathol; 2006 Jul;37(7):914-8
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  • [Title] Papillary glioneuronal tumor: a case report and review of the literature.
  • Papillary glioneuronal tumor is a recently described central nervous system neoplasm that almost always occurs adjacent to the lateral ventricle.
  • We present a case of this rare entity, representing the 21st case of this lesion, which exhibits a mixed astrocytic and neuronal differentiation.
  • Histologic evaluation after surgical removal showed a cystic tumor consisting of 2 distinct components: a unique pseudopapillary architecture admixed with foci of solid areas.
  • The combination of cytologic benignity, lack of necrosis, and low proliferative index as evidenced by immunohistochemistry using antibody to Ki-67 confirmed the low malignant potential of this tumor.
  • [MeSH-major] Brain Neoplasms / pathology. Carcinoma, Papillary / pathology. Ganglioglioma / pathology

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  • (PMID = 16784993.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Chromogranins; 0 / Glial Fibrillary Acidic Protein; 0 / Ki-67 Antigen; 0 / Neurofilament Proteins; 0 / S100 Proteins; 0 / Synaptophysin
  • [Number-of-references] 12
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70. Anan M, Inoue R, Ishii K, Abe T, Fujiki M, Kobayashi H, Goya T, Nakazato Y: A rosette-forming glioneuronal tumor of the spinal cord: the first case of a rosette-forming glioneuronal tumor originating from the spinal cord. Hum Pathol; 2009 Jun;40(6):898-901
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  • [Title] A rosette-forming glioneuronal tumor of the spinal cord: the first case of a rosette-forming glioneuronal tumor originating from the spinal cord.
  • Rosette-forming glioneuronal tumors of the fourth ventricle are rare brain tumors, and only 19 such lesions have been previously reported.
  • Magnetic resonance imaging demonstrated a mass in the cervicothoracic spinal cord that suggested an intramedullary spinal tumor.
  • A total gross resection of the tumor was performed.
  • As is typical of rosette-forming glioneuronal tumors of the fourth ventricle, this spinal cord example manifested neurocytic and astrocytic components.
  • The astrocytic component showed characteristic features of a pilocytic astrocytoma, as is often the case in the fourth ventricle examples.
  • [MeSH-major] Cerebral Ventricle Neoplasms / pathology. Fourth Ventricle / pathology. Spinal Cord / pathology. Spinal Cord Neoplasms / pathology
  • [MeSH-minor] Adult. Astrocytoma / pathology. Female. Humans. Rosette Formation

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  • [CommentIn] Hum Pathol. 2009 Oct;40(10):1510; author reply 1510 [19616823.001]
  • (PMID = 19269010.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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71. Takenaga K, Nygren J, Zelenina M, Ohira M, Iuchi T, Lukanidin E, Sjöquist M, Kozlova EN: Modified expression of Mts1/S100A4 protein in C6 glioma cells or surrounding astrocytes affects migration of tumor cells in vitro and in vivo. Neurobiol Dis; 2007 Mar;25(3):455-63
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  • [Title] Modified expression of Mts1/S100A4 protein in C6 glioma cells or surrounding astrocytes affects migration of tumor cells in vitro and in vivo.
  • The calcium-binding Mts1/S100A4 protein plays an important role in motility and metastatic activity of tumor cells.
  • To investigate if Mts1/S100A4 has a significant role on brain tumor progression, we made quantitative RT-PCR analysis for the expression of S100A4/Mts1 in various grades of astrocytic tumors.
  • Our data showed that high-grade glioblastomas express higher amount of S100A4/Mts1 than low-grade astrocytic tumors.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Cell Movement. S100 Proteins / metabolism
  • [MeSH-minor] Animals. Astrocytes / metabolism. Astrocytes / pathology. Cell Communication. Cell Line, Tumor. Corpus Callosum / metabolism. Corpus Callosum / pathology. Glioblastoma / metabolism. Glioblastoma / pathology. Humans. Immunohistochemistry. In Vitro Techniques. Metalloproteases / metabolism. Neoplasm Invasiveness. Neoplasm Transplantation. Nerve Fibers, Myelinated / metabolism. Nerve Fibers, Myelinated / pathology. RNA, Small Interfering. Rats

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  • (PMID = 17223348.001).
  • [ISSN] 0969-9961
  • [Journal-full-title] Neurobiology of disease
  • [ISO-abbreviation] Neurobiol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0 / S100 Proteins; 0 / S100a4 protein, rat; 142662-27-9 / S100A4 protein, human; EC 3.4.- / Metalloproteases
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72. Stremenova J, Krepela E, Mares V, Trim J, Dbaly V, Marek J, Vanickova Z, Lisa V, Yea C, Sedo A: Expression and enzymatic activity of dipeptidyl peptidase-IV in human astrocytic tumours are associated with tumour grade. Int J Oncol; 2007 Oct;31(4):785-92
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  • [Title] Expression and enzymatic activity of dipeptidyl peptidase-IV in human astrocytic tumours are associated with tumour grade.
  • Alterations in dipeptidyl peptidase-IV (DPP-IV) enzymatic activity are characteristic of malignant transformation.
  • This study was set up to address the relative representation and enzymatic activity of plasma membrane localized DPP-IV/CD26 and FAP-alpha in human brain and astrocytic tumours.
  • This is the first report showing that non-malignant brain tissue contains a DPP-IV-like enzymatic activity attributable mostly to DPP-8/9, while the substantial part of the activity in glioma is due to increased DPP-IV/CD26, localized in both the vascular and parenchymal compartments.
  • DPP-IV enzymatic activity increased dramatically with tumour grade severity.
  • [MeSH-major] Astrocytoma / enzymology. Astrocytoma / genetics. Dipeptidyl Peptidase 4 / genetics. Dipeptidyl Peptidase 4 / metabolism. Gene Expression Regulation, Enzymologic / physiology
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm / genetics. Antigens, Neoplasm / metabolism. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Brain Neoplasms / enzymology. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Cell Membrane / metabolism. Female. Gelatinases. Humans. Immunoenzyme Techniques. Male. Membrane Proteins. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Receptors, CXCR4 / genetics. Receptors, CXCR4 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Serine Endopeptidases / genetics. Serine Endopeptidases / metabolism. Tumor Cells, Cultured

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  • (PMID = 17786309.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, CXCR4; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
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73. Tan G, Sun SQ, Yuan DL: Expression of Kir 4.1 in human astrocytic tumors: correlation with pathologic grade. Biochem Biophys Res Commun; 2008 Mar 21;367(4):743-7
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  • [Title] Expression of Kir 4.1 in human astrocytic tumors: correlation with pathologic grade.
  • In this study, we investigated the expression of Kir 4.1 mRNA and protein in 80 cases of human astrocytic tumors by reverse transcription polymerase chain reaction, Western blot and immunohistochemistry, respectively.
  • The correlation between Kir 4.1 expression and pathologic grade of astrocytic tumors was further analyzed.
  • Therefore, Kir 4.1 may be a new biomarker for astrocytic tumors.
  • It may also be an attractive therapy target for human astrocytic tumors.
  • [MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Neoplasm Proteins / metabolism. Potassium Channels, Inwardly Rectifying / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Male. Middle Aged. Statistics as Topic. Tumor Cells, Cultured

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  • (PMID = 18191638.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Kcnj10 (channel); 0 / Neoplasm Proteins; 0 / Potassium Channels, Inwardly Rectifying
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74. Jin YH, Jung S, Jin SG, Jung TY, Moon KS, Kim IY: GRIM-19 Expression and Function in Human Gliomas. J Korean Neurosurg Soc; 2010 Jul;48(1):20-30
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  • OBJECTIVE: We determined whether the expression of GRIM-19 is correlated with pathologic types and malignant grades in gliomas, and determined the function of GRIM-19 in human gliomas.
  • METHODS: Tumor tissues were isolated and frozen at -80 just after surgery.
  • The tissues consisted of normal brain tissue (4), astrocytomas (2), anaplastic astrocytomas (2), oligodendrogliomas (13), anaplastic oligodendrogliomas (11), and glioblastomas (16).
  • To profile tumor-related genes, we applied RNA differential display using a Genefishing DEG kit, and validated the tumor-related genes by reverse transcription polymerase chain reaction (RT-PCR).
  • RESULTS: Based on RT-PCR analysis, the expression of GRIM-19 was higher in astrocytic tumors than oligodendroglial tumors.
  • The expression of GRIM-19 was higher in high-grade tumors than low-grade tumors or normal brain tissue; glioblastomas showed the highest expression.

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  • (PMID = 20717508.001).
  • [ISSN] 1598-7876
  • [Journal-full-title] Journal of Korean Neurosurgical Society
  • [ISO-abbreviation] J Korean Neurosurg Soc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2916144
  • [Keywords] NOTNLM ; Cell line / GRIM-19 / Gene Fishing / Glioblastoma / Human glioma
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75. Martínez C, Molina JA, Alonso-Navarro H, Jiménez-Jiménez FJ, Agúndez JA, García-Martín E: Two common nonsynonymous paraoxonase 1 (PON1) gene polymorphisms and brain astrocytoma and meningioma. BMC Neurol; 2010;10:71
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  • [Title] Two common nonsynonymous paraoxonase 1 (PON1) gene polymorphisms and brain astrocytoma and meningioma.
  • Aiming to identify genetic variations related to the risk of developing brain tumors, we investigated the putative association between common nonsynonymous PON1 polymorphisms and the risk of developing astrocytoma and meningioma.
  • METHODS: Seventy one consecutive patients with brain tumors (43 with astrocytoma grade II/III and 28 with meningioma) with ages ranging 21 to 76 years, and 220 healthy controls subjects were analyzed for the frequency of the nonsynonymous PON1 genotypes L55M rs854560 and Q192R rs662.
  • RESULTS: The frequencies of the PON1 genotypes and allelic variants of the polymorphisms PON1 L55M and PON1 Q192R did not differ significantly between patients with astrocytoma and meningioma and controls.
  • The minor allele frequencies were as follows: PON1 55L, 0.398, 0.328 and 0.286 for patients with astrocytoma, meningioma and control individuals, respectively; PON1 192R, 0.341, 0.362 and 0.302 for patients with astrocytoma, meningioma and control individuals, respectively.
  • Haplotype association analyses did not identify any significant association with the risk of developing astrocytoma or meningioma.
  • CONCLUSIONS: Common nonsynonymous PON1 polymorphisms are not related with the risk of developing astrocytoma and meningioma.
  • [MeSH-major] Aryldialkylphosphatase / genetics. Astrocytoma / genetics. Brain Neoplasms / genetics. Meningeal Neoplasms / genetics. Meningioma / genetics

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  • (PMID = 20723250.001).
  • [ISSN] 1471-2377
  • [Journal-full-title] BMC neurology
  • [ISO-abbreviation] BMC Neurol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.1.8.1 / Aryldialkylphosphatase; EC 3.1.8.1 / PON1 protein, human
  • [Other-IDs] NLM/ PMC2936881
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76. Hsuchou H, Pan W, Barnes MJ, Kastin AJ: Leptin receptor mRNA in rat brain astrocytes. Peptides; 2009 Dec;30(12):2275-80
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  • [Title] Leptin receptor mRNA in rat brain astrocytes.
  • We recently reported that mouse astrocytes express leptin receptors (ObR), and that obesity induces upregulation of astrocytic ObR.
  • To provide further evidence of the importance of astrocytic ObR expression, we performed double-labeling fluorescent in situ hybridization (FISH) and immunohistochemistry in the rat hypothalamus.
  • Laser confocal microscopic image analysis showed that ObR mRNA was present in glial fibrillary acidic protein (+) cells that show distinctive astrocytic morphology as well as in neurons.
  • In cultured rat C6 astrocytoma cells treated with different doses of lipopolysaccharide for 6h, the mRNA for ObRa or ObRb did not show significant changes, as measured by quantitative RT-PCR.
  • However, the protein expression of both ObRa and ObRb, determined by Western blotting, was increased after the C6 cells were treated with either lipopolysaccharide or tumor necrosis factor-alpha.
  • The results indicate that astrocytic ObR expression is present in rats as well as mice, and that it probably plays a role in the neuroinflammatory response.

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  • (PMID = 19747514.001).
  • [ISSN] 1873-5169
  • [Journal-full-title] Peptides
  • [ISO-abbreviation] Peptides
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS045751-06; United States / NIDDK NIH HHS / DK / DK54880; United States / NINDS NIH HHS / NS / R01 NS062291-02; United States / NINDS NIH HHS / NS / NS062291-02; United States / NINDS NIH HHS / NS / R01 NS045751; United States / NINDS NIH HHS / NS / R01 NS062291; United States / NINDS NIH HHS / NS / NS045751-06; United States / NIDDK NIH HHS / DK / R01 DK054880; United States / NINDS NIH HHS / NS / NS62291; United States / NINDS NIH HHS / NS / NS45751; United States / NIDDK NIH HHS / DK / R56 DK054880
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lipopolysaccharides; 0 / RNA, Messenger; 0 / Receptors, Leptin; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ NIHMS144773; NLM/ PMC2787995
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77. Bellavance MA, Blanchette M, Fortin D: Recent advances in blood-brain barrier disruption as a CNS delivery strategy. AAPS J; 2008;10(1):166-77
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  • [Title] Recent advances in blood-brain barrier disruption as a CNS delivery strategy.
  • The blood-brain barrier (BBB) is a complex functional barrier composed of endothelial cells, pericytes, astrocytic endfeets and neuronal cells.
  • We also summarize recent clinical series highlighting promising results in the application of this procedure to maximize delivery of chemotherapy in the treatment of brain tumor patients.
  • [MeSH-major] Blood-Brain Barrier / metabolism. Central Nervous System / metabolism. Pharmaceutical Preparations / administration & dosage. Pharmaceutical Preparations / metabolism

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  • (PMID = 18446517.001).
  • [ISSN] 1550-7416
  • [Journal-full-title] The AAPS journal
  • [ISO-abbreviation] AAPS J
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pharmaceutical Preparations
  • [Number-of-references] 64
  • [Other-IDs] NLM/ PMC2751463
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78. Wegrzynowicz M, Hilgier W, Dybel A, Oja SS, Saransaari P, Albrecht J: Upregulation of cerebral cortical glutathione synthesis by ammonia in vivo and in cultured glial cells: the role of cystine uptake. Neurochem Int; 2007 Jun;50(7-8):883-9
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  • [Title] Upregulation of cerebral cortical glutathione synthesis by ammonia in vivo and in cultured glial cells: the role of cystine uptake.
  • Glutathione (GSH) is a major antioxidant in the brain and ammonia neurotoxicity is associated with oxidative stress.
  • In this study, we show that intracerebral administration of ammonium chloride ("ammonia", final concentration 5mM) via a microdialysis probe, increases by 80% the glutathione content in cerebral cortical microdialysates, and tends to increase its content in striatal microdialysates.
  • Treatment with ammonia in vitro dose-dependently increased the glutathione content in cultured cerebral cortical astrocytes and a C6 glioma cell line.
  • In our hands, cystine, the precursor for astrocytic glutathione synthesis, was transported to astrocytes almost exclusively by system X(AG)-, while in C6 cells the transport engaged both system x(c)- (approximately 60% of uptake) and X(AG)- (approximately 40% of uptake).
  • The results are consistent with the concept of increased astrocytic glutathione synthesis as an adaptive response of the brain to ammonia challenge, and emphasize upregulation of cystine uptake as a factor contributing to this response.
  • [MeSH-major] Ammonia / pharmacology. Cerebral Cortex / metabolism. Cystine / metabolism. Glutathione / biosynthesis. Neuroglia / metabolism
  • [MeSH-minor] Animals. Animals, Newborn. Biological Transport. Bucladesine / pharmacology. Cell Differentiation / drug effects. Cell Line, Tumor. Cells, Cultured. Corpus Striatum / drug effects. Corpus Striatum / metabolism. Glioma. Male. Microdialysis. Prefrontal Cortex / drug effects. Prefrontal Cortex / metabolism. Rats. Rats, Sprague-Dawley. Rats, Wistar

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  • (PMID = 17239489.001).
  • [ISSN] 0197-0186
  • [Journal-full-title] Neurochemistry international
  • [ISO-abbreviation] Neurochem. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 48TCX9A1VT / Cystine; 63X7MBT2LQ / Bucladesine; 7664-41-7 / Ammonia; GAN16C9B8O / Glutathione
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79. Stukel JM, Caplan MR: Targeted drug delivery for treatment and imaging of glioblastoma multiforme. Expert Opin Drug Deliv; 2009 Jul;6(7):705-18
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  • Glioblastoma multiforme is a grade IV astrocytic tumor with a very high mortality rate.
  • Although current treatment often includes surgical resection, this rarely removes all primary tumor cells, so is usually followed by radiation and/or chemotherapy.
  • Remaining migratory tumor cells invade surrounding healthy tissue and contribute to secondary and tertiary tumor recurrence; therefore, despite significant research into glioma removal and treatment, prognosis remains poor.
  • As systemic delivery is limited by molecules larger than approximately 500 Da being unable to cross the blood-brain barrier (BBB), therapeutic concentrations are difficult to attain; thus, localized delivery options relying on diffusion and CED have been used to circumvent the BBB.
  • [MeSH-minor] Animals. Blood-Brain Barrier / metabolism. Combined Modality Therapy. Humans. Models, Theoretical. Tissue Distribution

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  • (PMID = 19538036.001).
  • [ISSN] 1744-7593
  • [Journal-full-title] Expert opinion on drug delivery
  • [ISO-abbreviation] Expert Opin Drug Deliv
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 118
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80. Banerjee HN, Zhang L: Deciphering the finger prints of brain cancer astrocytoma in comparison to astrocytes by using near infrared Raman spectroscopy. Mol Cell Biochem; 2007 Jan;295(1-2):237-40
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  • [Title] Deciphering the finger prints of brain cancer astrocytoma in comparison to astrocytes by using near infrared Raman spectroscopy.
  • To explore the biochemical differences between brain cancer cells Astrocytoma and normal cells Astrocyte, we investigated the Raman spectra of single cell from these two cell types and analyzed the difference in spectra and intensity.
  • The Raman spectra of brain cancer cells was similar to those of normal cells, but the Raman intensity of cancer cells was much higher than that of normal cells.
  • The Raman spectra of brain cancer Astrocytoma shows that the structural changes of cancer cells happen so that many biological functions of these cells are lost.
  • The results indicate that Raman spectra can offer the experimental basis for the cancer diagnosis and treatment.
  • [MeSH-major] Astrocytes / chemistry. Astrocytoma / chemistry. Brain Neoplasms / chemistry. Spectroscopy, Near-Infrared. Spectrum Analysis, Raman

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  • (PMID = 16924417.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / G11HD 34280-05
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
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81. Akimoto J, Fukami S, Tsutsumi M, Hashimoto T, Miki T, Haraoka J, Kudo M: Radiopathological characteristics of cerebellar malignant glioma in adults. Brain Tumor Pathol; 2009;26(2):59-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiopathological characteristics of cerebellar malignant glioma in adults.
  • Our aim was to extract the radiopathological features of cerebellar malignant glioma in adults from the four cases we encountered.
  • Initially, these patients were given a diagnosis of cerebellar infarction or cavernous angioma, or had faint abnormalities in the cerebellum that were overlooked.
  • These patients were followed up for 2-14 months (mean, 6 months), and the tumor was detected when their clinical symptoms deteriorated.
  • The tumor was located in the hemisphere in one patient and in the vermis in three patients.
  • All patients underwent subtotal tumor resection, followed by postoperative radiochemotherapy.
  • The pathological features were typical of malignant glioma, partially presenting the features of low-grade glioma, such as pilocytic, astrocytic, or oligodendroglial components.
  • At the onset of cerebellar malignant glioma, diagnostic imaging shows few signs of brain tumor.
  • Because cerebellar malignant glioma is a rare disease, it is difficult to differentiate it from metastatic brain tumors and primary central nervous system lymphoma by preoperative imaging.
  • Some patho logical features suggesting malignant transformation from low-grade glioma were detected.
  • [MeSH-minor] Aged. Aged, 80 and over. Fatal Outcome. Female. Humans. Image Processing, Computer-Assisted. Immunohistochemistry. Ki-67 Antigen / metabolism. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Recurrence, Local / pathology. Staining and Labeling. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 19856216.001).
  • [ISSN] 1861-387X
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-c