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56. Thomas SL, Alam R, Lemke N, Schultz LR, Gutiérrez JA, Rempel SA: PTEN augments SPARC suppression of proliferation and inhibits SPARC-induced migration by suppressing SHC-RAF-ERK and AKT signaling. Neuro Oncol; 2010 Sep;12(9):941-55
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  • SPARC (secreted protein acidic and rich in cysteine) is expressed in all grades of astrocytoma, including glioblastoma (GBM).
  • SPARC suppresses glioma growth but promotes migration and invasion by mediating integrin and growth factor receptor-regulated kinases and their downstream effectors.
  • This study determined whether PTEN reconstitution in PTEN-mutant, SPARC-expressing U87MG cells could further suppress proliferation and tumor growth but inhibit migration and invasion in SPARC-expressing cells in vitro and in vivo, and thereby prolong survival in animals with xenograft tumors.
  • These findings demonstrate that PTEN reconstitution or inhibition of signaling pathways that are activated by the loss of PTEN provide potential therapeutic strategies to inhibit SPARC-induced invasion while enhancing the negative effect of SPARC on tumor growth.

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  • (PMID = 20472716.001).
  • [ISSN] 1523-5866
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA086997; United States / NCI NIH HHS / CA / R01CA86997
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Osteonectin; 0 / Shc Signaling Adaptor Proteins; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / raf Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC2940688
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57. Asano K, Miyamoto S, Kubo O, Kikkukawa T, Yagihashi A, Ohkuma H: A case of anaplastic pleomorphic xanthoastrocytoma presenting with tumor bleeding and cerebrospinal fluid dissemination. Brain Tumor Pathol; 2006 Apr;23(1):55-63
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  • [Title] A case of anaplastic pleomorphic xanthoastrocytoma presenting with tumor bleeding and cerebrospinal fluid dissemination.
  • Pleomorphic xanthoastrocytoma (PXA) has been considered an astrocytic tumor with a relatively favorable prognosis.
  • The present case was a 59-year-old woman who presented with tumor bleeding onset and cerebrospinal fluid dissemination.
  • After emergency surgery had removed the hematoma, postoperative contrast-enhanced CT scan revealed a left temporal tumor.
  • A second surgery was therefore performed for initial tumor removal 2 months later.
  • Histopathological findings showed that the tumor was typical PXA with strong pleomorphism and xanthomatous changes and contained an ependymoma-like component in the center area.
  • This case report is the first case in which PXA presented with tumor bleeding onset.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Carcinoma / pathology. Hematoma / pathology
  • [MeSH-minor] Biomarkers, Tumor. Fatal Outcome. Female. Humans. Image Processing, Computer-Assisted. Magnetic Resonance Imaging. Middle Aged. Mitosis / physiology. Neoplasm Recurrence, Local. Tomography, X-Ray Computed

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  • (PMID = 18095120.001).
  • [ISSN] 1433-7398
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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58. Aoyama T, Hida K, Ishii N, Seki T, Ikeda J, Iwasaki Y: Intramedullary spinal cord germinoma--2 case reports. Surg Neurol; 2007 Feb;67(2):177-83; discussion 183
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  • Astrocytic tumor was initially suspected, and partial removal was performed.
  • Because the lesion did not respond to steroid pulse therapy, spinal cord tumor was suspected and biopsy was performed.
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols. Biomarkers, Tumor / analysis. Biomarkers, Tumor / metabolism. Chorionic Gonadotropin, beta Subunit, Human / analysis. Chorionic Gonadotropin, beta Subunit, Human / metabolism. Female. Humans. Magnetic Resonance Imaging. Neurosurgical Procedures. Paraparesis / etiology. Radiotherapy. Treatment Outcome. Urination Disorders / etiology

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  • (PMID = 17254883.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chorionic Gonadotropin, beta Subunit, Human
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59. Papuashvili GSh, Gagua RO, Ninua NG: [Temozolomide--a new antitumor preparation in the treatment of central nervous system malignant tumors]. Georgian Med News; 2006 May;(134):31-4
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  • On the basis of the detailed analysis of both retrospective and prospective materials it has been shown that histological type of the tumor is of great importance for the remote treatment results.
  • Of all malignant tumors of central nervous system temozolomide is more effective in the treatment of astrocytomas in comparison with the tumors of other histological types.

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  • (PMID = 16783060.001).
  • [ISSN] 1512-0112
  • [Journal-full-title] Georgian medical news
  • [ISO-abbreviation] Georgian Med News
  • [Language] rus
  • [Publication-type] Controlled Clinical Trial; English Abstract; Journal Article
  • [Publication-country] Georgia (Republic)
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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60. Schichor C, Kerkau S, Visted T, Martini R, Bjerkvig R, Tonn JC, Goldbrunner R: The brain slice chamber, a novel variation of the Boyden Chamber Assay, allows time-dependent quantification of glioma invasion into mammalian brain in vitro. J Neurooncol; 2005 May;73(1):9-18
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  • [Title] The brain slice chamber, a novel variation of the Boyden Chamber Assay, allows time-dependent quantification of glioma invasion into mammalian brain in vitro.
  • Glioma cell invasion occurs in a complex micromilieu consisting of neural and glial cells, myelinated fiber tracts, blood vessels and extracellular matrix proteins.
  • The present work describes the brain slice chamber (BSC) as a novel experimental model for assessing invasion of glioma cells into adult mammalian white and gray matter on the basis of the well known Boyden chamber system.
  • As a matrix for invasive tumor cells we used freshly prepared brain tissue from adult pigs.
  • Human U-373 and U87 astrocytoma cells stably transfected with green fluorescent protein (GFP) were assessed for their invasiveness into the brain-slices during a 24 h period.
  • Two cytostatics (vincristin and paclitaxel) which both are known to affect the cytoskeleton, inhibited glioma cell invasion in a dose dependent manner, which makes the presented model system suitable for functional experiments.
  • In conclusion, the BSC represents a valid and rapid experimental model that may be used to describe the invasive behavior of glioma cells within the preserved three-dimensional structure of mammalian brain tissue in vitro.
  • [MeSH-major] Brain Neoplasms / pathology. Coculture Techniques / methods. Frontal Lobe / pathology. Glioma / pathology. Organ Culture Techniques / methods. Parietal Lobe / pathology
  • [MeSH-minor] Animals. Antineoplastic Agents, Phytogenic / administration & dosage. Astrocytes / drug effects. Astrocytes / pathology. Dose-Response Relationship, Drug. Extracellular Matrix / pathology. Neoplasm Invasiveness. Paclitaxel / administration & dosage. Swine. Vincristine / administration & dosage

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  • (PMID = 15933811.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 5J49Q6B70F / Vincristine; P88XT4IS4D / Paclitaxel
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61. Tirosh B, Iwakoshi NN, Lilley BN, Lee AH, Glimcher LH, Ploegh HL: Human cytomegalovirus protein US11 provokes an unfolded protein response that may facilitate the degradation of class I major histocompatibility complex products. J Virol; 2005 Mar;79(5):2768-79
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  • In the human astrocytoma cell line U373, turning on expression of US11, but not US2, is sufficient to induce a UPR, as manifested by upregulation of the ER chaperone Bip and by splicing of XBP-1 mRNA.

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  • (PMID = 15708995.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI32412; United States / NCI NIH HHS / CA / 1P50CA100707; United States / NIAID NIH HHS / AI / R37 AI033456; United States / NCI NIH HHS / CA / P50 CA100707; United States / NIAID NIH HHS / AI / 5R37-AI33456; United States / NIAID NIH HHS / AI / R01 AI032412
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Heat-Shock Proteins; 0 / Histocompatibility Antigens Class I; 0 / Membrane Glycoproteins; 0 / Molecular Chaperones; 0 / Nuclear Proteins; 0 / RNA-Binding Proteins; 0 / Transcription Factors; 0 / US11 protein, herpesvirus; 0 / US2 protein, Varicellovirus; 0 / Viral Envelope Proteins; 0 / Viral Proteins; 0 / molecular chaperone GRP78; 0 / regulatory factor X transcription factors
  • [Other-IDs] NLM/ PMC548438
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62. Witte HT, Jeibmann A, Klämbt C, Paulus W: Modeling glioma growth and invasion in Drosophila melanogaster. Neoplasia; 2009 Sep;11(9):882-8
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  • [Title] Modeling glioma growth and invasion in Drosophila melanogaster.
  • Glioblastoma is the most common and most malignant intrinsic human brain tumor, characterized by extensive invasion and proliferation of glial (astrocytic) tumor cells, frequent activation of tyrosine kinase receptor signaling pathways, relative resistance to chemotherapy and radiotherapy, and poor prognosis.
  • Using the Gal4-UAS system, we have produced glioma models in Drosophila by overexpressing homologs of human tyrosine kinase receptors under control of the glia-specific promoter reversed polarity (repo).
  • Glial overexpression of activated epidermal growth factor receptor (EGFR) resulted in enhanced proliferation and migration of larval glial cells with increased numbers in the eye imaginal disc, diffuse tumor-like enlargement of the optic stalk, and marked ectopic invasion of glial cells along the optic nerve.
  • We suggest that Drosophila models will be useful for deciphering signaling cascades underlying abnormal behavior of glioma cells for genetic screens to reveal interacting genes involved in gliomagenesis and for experimental therapy approaches.
  • [MeSH-major] Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Drosophila melanogaster / metabolism. Glioma / pathology
  • [MeSH-minor] Animals. Eye / cytology. Eye / metabolism. Humans. Immunoenzyme Techniques. Neoplasm Invasiveness. Phosphatidylinositol 3-Kinases / metabolism. Platelet-Derived Growth Factor / metabolism. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins c-akt / metabolism. Quinazolines / pharmacology. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism. Receptors, Platelet-Derived Growth Factor / metabolism. Receptors, Vascular Endothelial Growth Factor / metabolism. Tumor Cells, Cultured

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  • (PMID = 19724682.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Platelet-Derived Growth Factor; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; S65743JHBS / gefitinib
  • [Other-IDs] NLM/ PMC2735809
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63. Kumar R, Kalra SK: Pediatric brain stem lesions: introduction of a scoring system for clinical evaluation and their treatment analysis. Childs Nerv Syst; 2008 Apr;24(4):467-75
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  • [Title] Pediatric brain stem lesions: introduction of a scoring system for clinical evaluation and their treatment analysis.
  • INTRODUCTION: Brainstem lesions in pediatric age group include mainly gliomas.
  • RESULTS AND DISCUSSION: Twenty-seven had gliomas, and in nonglioma group, seven had brainstem tuberculosis (BSTB).
  • Most gliomas were pilocytic astrocytomas (n = 21).
  • CONCLUSION: Gliomas form majority of pediatric brainstem lesions, with high occurrence of BSTB in nongliomatous group.
  • [MeSH-minor] Age Factors. Brain Neoplasms / complications. Child. Child, Preschool. Decompression / methods. Female. Glioma / complications. Humans. Karnofsky Performance Status. Male. Outcome and Process Assessment (Health Care). Retrospective Studies

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  • (PMID = 17978821.001).
  • [ISSN] 0256-7040
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Germany
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6
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4. Chen CC, Cheng PW, Tseng HM, Young YH: Posterior cranial fossa tumors in young adults. Laryngoscope; 2006 Sep;116(9):1678-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: From 1991 to 2005, 16 (0.8%) of 2,091 young adults (range, 16-29 years) with dizziness/vertigo, hearing loss, or tinnitus were diagnosed with posterior fossa tumor.
  • Diagnoses consisted of vestibular schwannoma and neurofibromatosis II in eight patients (50%), glial neoplasm (including astrocytoma, ependymoma, glioma) in four patients (25%), epidermoid cyst in three patients, and glomus jugulare tumor in one patient.
  • At study close, excluding one lost patient, three patients died as a result of recurrent or residual tumor at the primary site.
  • CONCLUSIONS: Unlike predominant medulloblastoma in children, the most frequent posterior fossa tumor in young adults is vestibular schwannoma and neurofibroma.
  • However, the second most frequent one in young adults is glial neoplasm as opposed to meningioma in adults.

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  • (PMID = 16955003.001).
  • [ISSN] 0023-852X
  • [Journal-full-title] The Laryngoscope
  • [ISO-abbreviation] Laryngoscope
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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65. Hamke M, Herpfer I, Lieb K, Wandelt C, Fiebich BL: Substance P induces expression of the corticotropin-releasing factor receptor 1 by activation of the neurokinin-1 receptor. Brain Res; 2006 Aug 2;1102(1):135-44
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  • As a model system, we used the human astrocytoma cell line U373 MG as well as primary rat astroglial cells, which both are known to express functional neurokinin-1 receptors (NK-1-R) and to secret various cytokines upon stimulation with SP.
  • In conclusion, this study demonstrates that SP induces CRF1 receptor expression in cells of the CNS, which may be of potential interest for a better understanding of the interplay between SP and the stress hormone axis and, thus, diseases like affective or anxiety disorders.
  • [MeSH-minor] Animals. Animals, Newborn. Astrocytes / drug effects. Astrocytoma. Blotting, Western / methods. Cells, Cultured. Dose-Response Relationship, Drug. Drug Interactions. Enzyme Activation / drug effects. Enzyme Inhibitors / pharmacology. Humans. Imidazoles / pharmacology. Neurokinin-1 Receptor Antagonists. Oligonucleotide Array Sequence Analysis / methods. Piperidines / pharmacology. Pyridines / pharmacology. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction / methods. Time Factors

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  • (PMID = 16806114.001).
  • [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 / 4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole; 0 / CRF receptor type 1; 0 / Enzyme Inhibitors; 0 / Imidazoles; 0 / Neurokinin-1 Receptor Antagonists; 0 / Piperidines; 0 / Pyridines; 0 / RNA, Messenger; 0 / Receptors, Corticotropin-Releasing Hormone; 0 / Receptors, Neurokinin-1; 148700-85-0 / 3-((3,5-bis(trifluoromethyl)phenyl)methyloxy)-2-phenylpiperidine; 33507-63-0 / Substance P
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66. Ramos TC, Figueredo J, Catala M, González S, Selva JC, Cruz TM, Toledo C, Silva S, Pestano Y, Ramos M, Leonard I, Torres O, Marinello P, Pérez R, Lage A: Treatment of high-grade glioma patients with the humanized anti-epidermal growth factor receptor (EGFR) antibody h-R3: report from a phase I/II trial. Cancer Biol Ther; 2006 Apr;5(4):375-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of high-grade glioma patients with the humanized anti-epidermal growth factor receptor (EGFR) antibody h-R3: report from a phase I/II trial.
  • The poor prognosis of patients with high-grade glioma has led to the search for new therapeutic strategies.
  • In order to evaluate safety, immunogenicity and preliminary efficacy of h-R3 in newly diagnosed high-grade glioma patients, we conducted a Phase I/II trial.
  • Tumor types were: glioblastoma (GB) (16 patients), anaplastic astrocytoma (AA) (12 patients) and anaplastic oligodendroglioma (AO) (1 patient).
  • Objective response-rate was 37.9% (17.2% complete response, 20.7% partial response) while stable disease occurred in 41.4% of the patients.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Astrocytoma / therapy. Glioblastoma / therapy. Glioma / pathology. Glioma / therapy. Oligodendroglioma / therapy. Receptor, Epidermal Growth Factor / immunology

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  • (PMID = 16575203.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 99mTc-hR3 monoclonal antibody; 0 / Antibodies; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Organotechnetium Compounds; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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67. Debono B, Derrey S, Rabehenoina C, Proust F, Freger P, Laquerrière A: Primary diffuse multinodular leptomeningeal gliomatosis: case report and review of the literature. Surg Neurol; 2006 Mar;65(3):273-82; discussion 282
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Primary diffuse leptomeningeal gliomatosis is an exceptional neoplasm, and only 30 cases have been reported in the literature.
  • METHODS: A 50-year-old man was admitted to the neurosurgery department for a previous 4-month history of headache, associated with nonspecific neurological signs.
  • Histological examination revealed an anaplastic astrocytoma.
  • RESULTS: Complete neuraxis postmortem examination revealed no intraparenchymatous glioma and was conclusive for the diagnosis of primary leptomeningeal gliomatosis (astrocytic, World Health Organization grade III), with a multinodular pattern in the spinal cord, the brainstem, and the brain base with diffuse extension into the cerebellar subarachnoid spaces.
  • [MeSH-major] Astrocytoma / surgery. Meningeal Neoplasms / surgery. Neoplasms, Neuroepithelial / surgery. Peripheral Nervous System Neoplasms / surgery. Spinal Nerve Roots / surgery
  • [MeSH-minor] Brain / pathology. Cerebellum / pathology. Diagnosis, Differential. Fatal Outcome. Humans. Intracranial Pressure / physiology. Male. Meninges / pathology. Middle Aged. Neoplasm Invasiveness / pathology. Neurologic Examination. Prognosis

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  • (PMID = 16488248.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 39
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68. Kalluri SR, Illes Z, Srivastava R, Cree B, Menge T, Bennett JL, Berthele A, Hemmer B: Quantification and functional characterization of antibodies to native aquaporin 4 in neuromyelitis optica. Arch Neurol; 2010 Oct;67(10):1201-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Antibodies targeting membrane proteins play an important role in various autoimmune diseases of the nervous system.
  • DESIGN, SETTING, AND PARTICIPANTS: We developed a novel bioassay for quantification and characterization of human anti-AQP4 antibodies based on high-level expression of native AQP4 (nAQP4) protein on the surface of human astroglioma cells.
  • The test was validated in 2 independent cohorts of patients with NMO spectrum disease.
  • RESULTS: We detected anti-nAQP4-IgG with a sensitivity of 57.9% and specificity of 100% in patients with NMO spectrum diseases, suggesting that our bioassay is at least as sensitive and specific as the gold-standard NMO-IgG assay.
  • Our findings demonstrate the potential of bioassays to characterize biologically relevant antibodies in human autoimmune diseases.
  • [MeSH-minor] Adult. Aged. Biological Assay / methods. Cell Line, Tumor. Cohort Studies. Cytotoxicity Tests, Immunologic / methods. Female. Flow Cytometry / methods. Gene Expression Regulation, Neoplastic / physiology. Glioma / pathology. Humans. Male. Middle Aged. Transfection / methods. Young Adult

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  • (PMID = 20937947.001).
  • [ISSN] 1538-3687
  • [Journal-full-title] Archives of neurology
  • [ISO-abbreviation] Arch. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AQP4 protein, human; 0 / Aquaporin 4; 0 / Immunoglobulin G
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69. Kyprianou N, Murphy E, Lee P, Hargreaves I: Assessment of mitochondrial respiratory chain function in hyperphenylalaninaemia. J Inherit Metab Dis; 2009 Apr;32(2):289-96
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  • Phenylketonuria (PKU) is an autosomal recessive disorder resulting in neurological and intellectual disability when untreated.
  • Human 1321N1 astrocytoma cells were exposed to hyperphenylalaninaemia by the addition of 300 or 900 micromol/L of Phe to the cell culture medium.
  • [MeSH-major] Amino Acid Metabolism, Inborn Errors / metabolism. Electron Transport / physiology. Mitochondrial Diseases / metabolism. Phenylalanine / blood
  • [MeSH-minor] Adult. Cell Line, Tumor. Cells, Cultured. Culture Media. Female. Humans. Lactic Acid / metabolism. Male. Middle Aged. Phenylketonurias / blood. Phenylketonurias / metabolism. Pyruvic Acid / metabolism. Tremor / blood. Tremor / etiology. Tyrosine / blood. Ubiquinone / analogs & derivatives. Ubiquinone / blood. Young Adult

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  • (PMID = 19277893.001).
  • [ISSN] 1573-2665
  • [Journal-full-title] Journal of inherited metabolic disease
  • [ISO-abbreviation] J. Inherit. Metab. Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Culture Media; 1339-63-5 / Ubiquinone; 33X04XA5AT / Lactic Acid; 42HK56048U / Tyrosine; 47E5O17Y3R / Phenylalanine; 8558G7RUTR / Pyruvic Acid; EJ27X76M46 / coenzyme Q10
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70. Michalowski MB, de Fraipont F, Michelland S, Entz-Werle N, Grill J, Pasquier B, Favrot MC, Plantaz D: Methylation of RASSF1A and TRAIL pathway-related genes is frequent in childhood intracranial ependymomas and benign choroid plexus papilloma. Cancer Genet Cytogenet; 2006 Apr 1;166(1):74-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Ependymomas (EP) represent the third most frequent type of central nervous system (CNS) tumor of childhood, after astrocytomas and medulloblastomas.
  • The present objective was, for a sample of 27 children with intracranial EP and 7 with CPP, to describe and compare the methylation status of 19 genes (with current HUGO symbol, if any): p15INK4a (CDKN2B), p16INK4a and p14ARF (both CDKN2A), APC, RB1, RASSF1A (RASSF1), BLU (ZMYND10) FHIT, RARB, MGMT, DAPK (DAPK1), ECAD (CDH1), CASP8, TNFRSF10C, TNFRSF10D, FLIP (CFLAR), INI1 (SMARCB1), TIMP3, and NF2.
  • Although we did not observe a statistical relationship between methylation and clinical outcome, the methylation pattern does not appear to be randomly distributed in ependymoma and may represent a mechanism of tumor development and evolution.
  • [MeSH-major] Apoptosis Regulatory Proteins / genetics. Brain Neoplasms / genetics. DNA Methylation. Ependymoma / genetics. Membrane Glycoproteins / genetics. Papilloma, Choroid Plexus / genetics. Tumor Necrosis Factor-alpha / genetics. Tumor Suppressor Proteins / genetics


71. Hong C, Maunakea A, Jun P, Bollen AW, Hodgson JG, Goldenberg DD, Weiss WA, Costello JF: Shared epigenetic mechanisms in human and mouse gliomas inactivate expression of the growth suppressor SLC5A8. Cancer Res; 2005 May 1;65(9):3617-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Shared epigenetic mechanisms in human and mouse gliomas inactivate expression of the growth suppressor SLC5A8.
  • Using an integrated approach for genome-wide methylation and copy number analyses, we identified SLC5A8 on chromosome 12q23.1 that was affected frequently by aberrant methylation in human astrocytomas and oligodendrogliomas.
  • SLC5A8 encodes a sodium monocarboxylate cotransporter that was highly expressed in normal brain but was significant down-regulated in primary gliomas.
  • Bisulfite sequencing analysis showed that the CpG island was unmethylated in normal brain but frequently localized methylated in brain tumors, consistent with the tumor-specific loss of gene expression.
  • In glioma cell lines, SLC5A8 expression was also suppressed but could be reactivated with a methylation inhibitor.
  • Expression of exogenous SLC5A8 in LN229 and LN443 glioma cells inhibited colony formation, suggesting that it may function as a growth suppressor in normal brain cells.
  • Remarkably, 9 of 10 murine oligodendroglial tumors (from p53+/- or ink4a/arf+/- animals transgenic for S100beta-v-erbB) showed a similar tumor-specific down-regulation of mSLC5A8, the highly conserved mouse homologue.
  • Taken together, these data suggest that SLC5A8 functions as a growth suppressor gene in vitro and that it is silenced frequently by epigenetic mechanisms in primary gliomas.
  • The shared epigenetic inactivation of mSLC5A8 in mouse gliomas indicates an additional degree of commonality in the origin and/or pathway to tumorigenesis between primary human tumors and these mouse models of gliomas.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Cation Transport Proteins / genetics. Gene Silencing. Genes, Tumor Suppressor. Oligodendroglioma / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. CpG Islands / genetics. DNA Methylation. Disease Models, Animal. Down-Regulation. Gene Expression Regulation, Neoplastic. Genetic Vectors / genetics. Humans. Mice. Mice, Inbred DBA. Mice, Transgenic. Retroviridae / genetics


72. Kondyli M, Gatzounis G, Kyritsis A, Varakis J, Assimakopoulou M: Immunohistochemical detection of phosphorylated JAK-2 and STAT-5 proteins and correlation with erythropoietin receptor (EpoR) expression status in human brain tumors. J Neurooncol; 2010 Nov;100(2):157-64
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  • Using specific antibodies and immunohistochemistry on formalin-fixed, paraffin-embedded semi-serial tissue sections a total of 87 human brain tumors and samples from normal brain tissue were studied. pJAK-2/pSTAT-5 nuclear co-expression was detected in 39% of astrocytomas, 43% of oligodendrogliomas, 50% of ependymomas, and in all (100%) of the medulloblastomas examined.
  • EpoR/pJAK-2/pSTAT-5 co-expression was detected in a small percentage of astrocytomas (18%) and ependymomas (33%).
  • Tumor vessels exhibited EpoR, pJAK-2, and pSTAT-5 immunoreactivity.

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  • (PMID = 20336349.001).
  • [ISSN] 1573-7373
  • [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 / Receptors, Erythropoietin; 0 / STAT5 Transcription Factor; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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73. 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

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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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74. Reznik TE, Sang Y, Ma Y, Abounader R, Rosen EM, Xia S, Laterra J: Transcription-dependent epidermal growth factor receptor activation by hepatocyte growth factor. Mol Cancer Res; 2008 Jan;6(1):139-50
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  • Epidermal growth factor receptor (EGFR) and c-Met are frequently coexpressed in cancers, including those associated with hepatocyte growth factor (HGF) overexpression, such as malignant astrocytoma.
  • In a previous analysis of the HGF-induced transcriptome, we found that two EGFR agonists, transforming growth factor-alpha and heparin-binding epidermal growth factor-like growth factor (HB-EGF), are prominently up-regulated by HGF in human glioma cells.

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  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS032148; United States / NINDS NIH HHS / NS / R01 NS043987; United States / NINDS NIH HHS / NS / NS043987-03; United States / NIEHS NIH HHS / ES / ES 09169; United States / NIEHS NIH HHS / ES / R01 ES009169; United States / NINDS NIH HHS / NS / NS 43987; United States / NINDS NIH HHS / NS / NS 32148; United States / NINDS NIH HHS / NS / R01 NS032148-13; United States / NINDS NIH HHS / NS / R01 NS043987-03; United States / NINDS NIH HHS / NS / NS032148-13
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / HBEGF protein, human; 0 / Heparin-binding EGF-like Growth Factor; 0 / Intercellular Signaling Peptides and Proteins; 0 / Ligands; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Transforming Growth Factor alpha; 21820-51-9 / Phosphotyrosine; 67256-21-7 / Hepatocyte Growth Factor; 92092-36-9 / CRM197 (non-toxic variant of diphtheria toxin); EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS135584; NLM/ PMC2839502
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75. Edwards LA, Thiessen B, Dragowska WH, Daynard T, Bally MB, Dedhar S: Inhibition of ILK in PTEN-mutant human glioblastomas inhibits PKB/Akt activation, induces apoptosis, and delays tumor growth. Oncogene; 2005 May 19;24(22):3596-605
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  • [Title] Inhibition of ILK in PTEN-mutant human glioblastomas inhibits PKB/Akt activation, induces apoptosis, and delays tumor growth.
  • The tumor suppressor gene phosphatase and tensin homologue (PTEN) regulates the phosphatidylinositol-3'-kinase (PI3K) signaling pathway and has been shown to correlate with poor prognosis in high-grade astrocytomas when mutational inactivation or loss of the PTEN gene occurs.
  • 5 mg/kg), exhibited stable disease with < or =7% increase in tumor volume over the 3-week course of treatment.
  • In contrast, animals treated with an oligonucleotide control or saline exhibited a >100% increase in tumor volume over the same time period.
  • [MeSH-minor] 3-Phosphoinositide-Dependent Protein Kinases. Animals. Apoptosis / physiology. Blotting, Western. Cell Line, Tumor. Enzyme Activation / physiology. Flow Cytometry. Humans. Immunohistochemistry. Male. Mice. Mutation. PTEN Phosphohydrolase. Phosphoric Monoester Hydrolases / genetics. Proto-Oncogene Proteins c-akt. Tumor Suppressor Proteins / genetics


76. Hsieh JC, Lesniak MS: Surgical management of high-grade gliomas. Expert Rev Neurother; 2005 Nov;5(6 Suppl):S33-9
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  • [Title] Surgical management of high-grade gliomas.
  • High-grade gliomas, in particular anaplastic astrocytoma and glioblastoma multiforme, represent two of the most devastating forms of brain cancer.
  • In spite of the poor prognosis, new treatments and emerging therapies are making an impact on this disease.
  • This review discusses the role of the surgical management of high-grade gliomas and provides an overview of the currently available therapies which depend on surgical intervention.
  • [MeSH-major] Brain Neoplasms / surgery. Glioma / surgery. Neurosurgical Procedures / methods
  • [MeSH-minor] Brachytherapy / methods. Craniotomy / methods. Diagnostic Imaging / methods. Disease Progression. Drug Delivery Systems / methods. Drug Therapy / methods. Expert Testimony. Humans

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  • [CommentIn] Expert Rev Neurother. 2005 Nov;5(6 Suppl):1-2 [16274264.001]
  • (PMID = 16274269.001).
  • [ISSN] 1744-8360
  • [Journal-full-title] Expert review of neurotherapeutics
  • [ISO-abbreviation] Expert Rev Neurother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 40
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77. Minehan KJ, Brown PD, Scheithauer BW, Krauss WE, Wright MP: Prognosis and treatment of spinal cord astrocytoma. Int J Radiat Oncol Biol Phys; 2009 Mar 1;73(3):727-33
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  • [Title] Prognosis and treatment of spinal cord astrocytoma.
  • PURPOSE: To identify the prognostic factors for spinal cord astrocytoma and determine the effects of surgery and radiotherapy on outcome.
  • METHODS AND MATERIALS: This retrospective study reviewed the cases of consecutive patients with spinal cord astrocytoma treated at Mayo Clinic Rochester between 1962 and 2005.
  • Of these 136 patients, 69 had pilocytic and 67 had infiltrative astrocytoma.
  • Patients with pilocytic tumors survived significantly longer than those with infiltrative astrocytomas (median overall survival, 39.9 vs. 1.85 years; p < 0.001).
  • Postoperative radiotherapy, delivered in 75% of cases, gave no significant survival benefit for those with pilocytic tumors (39.9 vs. 18.1 years, p = 0.33) but did for those with infiltrative astrocytomas (24 vs. 3 months; Wilcoxon p = 0.006).
  • CONCLUSION: The results of our study have shown that histologic type is the most important prognostic variable affecting the outcome of spinal cord astrocytomas.
  • Postoperative radiotherapy significantly improved survival for patients with infiltrative astrocytomas but not for those with pilocytic tumors.
  • [MeSH-major] Astrocytoma / radiotherapy. Astrocytoma / surgery. Spinal Cord Neoplasms / radiotherapy. Spinal Cord Neoplasms / surgery

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  • (PMID = 18687533.001).
  • [ISSN] 1879-355X
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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78. Hargrave DR, Zacharoulis S: Pediatric CNS tumors: current treatment and future directions. Expert Rev Neurother; 2007 Aug;7(8):1029-42
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  • Pediatric CNS tumors are the most common solid tumor of childhood and are the leading cause of cancer-related death in this age group.
  • This article will discuss current treatment standards for the most common pediatric CNS tumors: astrocytomas (low- and high-grade glioma), ependymoma and primitive neuroectodermal tumors (medulloblastoma), as well as future biological-based novel therapies.

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  • (PMID = 17678498.001).
  • [ISSN] 1744-8360
  • [Journal-full-title] Expert review of neurotherapeutics
  • [ISO-abbreviation] Expert Rev Neurother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 147
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79. Sadanari H, Tanaka J, Li Z, Yamada R, Matsubara K, Murayama T: Proteasome inhibitor differentially regulates expression of the major immediate early genes of human cytomegalovirus in human central nervous system-derived cell lines. Virus Res; 2009 Jun;142(1-2):68-77
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  • Treatment of HCMV-infected 118MGC glioma and U373-MG astrocytoma cells with three proteasome inhibitors, MG132, clasto-lactacystin beta-lactone, and epoxomicin, suppressed MIE protein expression.

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  • (PMID = 19201384.001).
  • [ISSN] 0168-1702
  • [Journal-full-title] Virus research
  • [ISO-abbreviation] Virus Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Activating Transcription Factor 2; 0 / Immediate-Early Proteins; 0 / Lactones; 0 / Leupeptins; 0 / Oligopeptides; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Proto-Oncogene Proteins c-jun; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 134381-21-8 / epoxomicin; 155975-72-7 / clasto-lactacystin beta-lactone
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80. Chosdol K, Misra A, Puri S, Srivastava T, Chattopadhyay P, Sarkar C, Mahapatra AK, Sinha S: Frequent loss of heterozygosity and altered expression of the candidate tumor suppressor gene 'FAT' in human astrocytic tumors. BMC Cancer; 2009;9:5
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  • [Title] Frequent loss of heterozygosity and altered expression of the candidate tumor suppressor gene 'FAT' in human astrocytic tumors.
  • BACKGROUND: We had earlier used the comparison of RAPD (Random Amplification of Polymorphic DNA) DNA fingerprinting profiles of tumor and corresponding normal DNA to identify genetic alterations in primary human glial tumors.
  • METHODS: In this study we used RAPD-PCR to identify novel genomic alterations in the astrocytic tumors of WHO grade II (Low Grade Diffuse Astrocytoma) and WHO Grade IV (Glioblastoma Multiforme).
  • RESULTS: Bands consistently altered in the RAPD profile of tumor DNA in a significant proportion of tumors were identified.
  • One such 500 bp band, that was absent in the RAPD profile of 33% (4/12) of the grade II astrocytic tumors, was selected for further study.
  • Its sequence corresponded with a region of FAT, a putative tumor suppressor gene initially identified in Drosophila.
  • Fifty percent of a set of 40 tumors, both grade II and IV, were shown to have Loss of Heterozygosity (LOH) at this locus by microsatellite (intragenic) and by SNP markers.
  • CONCLUSION: These results point to a role of the FAT in astrocytic tumorigenesis and demonstrate the use of RAPD analysis in identifying specific alterations in astrocytic tumors.
  • [MeSH-major] Astrocytoma / genetics. Cadherins / genetics. Central Nervous System Neoplasms / genetics. Genes, Tumor Suppressor. Loss of Heterozygosity

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  • (PMID = 19126244.001).
  • [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 / Cadherins; 0 / DNA Primers; 0 / FAT1 protein, human
  • [Other-IDs] NLM/ PMC2631005
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81. Kamnasaran D, Hawkins C, Guha A: Characterization and transformation potential of "Synthetic" astrocytes differentiated from murine embryonic stem cells. Glia; 2008 Mar;56(4):457-70
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  • In contrast, retroviral transduction of either wt or p53+/- synthetic astrocytes and not the postnatal somatic astrocytes, with relevant oncogenes found in human malignant astrocytomas (MDM2, myr-AKT, V12H-RAS), led to intracranial high-grade undifferentiated gliomas.
  • [MeSH-minor] Animals. Animals, Newborn. Brain / cytology. Brain / embryology. Cell Lineage. Cells, Cultured. Embryo, Mammalian. Fibroblast Growth Factor 2 / pharmacology. Gangliosides / metabolism. Gene Expression Regulation, Developmental / drug effects. Glial Fibrillary Acidic Protein / metabolism. Humans. In Situ Nick-End Labeling. Mice. Mice, Knockout. Oligonucleotide Array Sequence Analysis / methods. Transduction, Genetic / methods. Tumor Suppressor Protein p53 / deficiency

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  • [Copyright] (Copyright) 2008 Wiley-Liss, Inc.
  • (PMID = 18205175.001).
  • [ISSN] 0894-1491
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] eng
  • [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 / Gangliosides; 0 / Glial Fibrillary Acidic Protein; 0 / Tumor Suppressor Protein p53; 0 / ganglioside A2B5; 103107-01-3 / Fibroblast Growth Factor 2
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82. McLendon RE, Turner K, Perkinson K, Rich J: Second messenger systems in human gliomas. Arch Pathol Lab Med; 2007 Oct;131(10):1585-90
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  • [Title] Second messenger systems in human gliomas.
  • CONTEXT: Patients with glioblastoma (astrocytoma, World Health Organization grade IV) exhibit 2-year survival rates of less than 20% despite significant advances in therapeutic options available to patients.
  • Epidermal growth factor receptor (EGFR) hyperexpression is one of the most commonly encountered abnormalities in this tumor.
  • OBJECTIVE: It is important to both gain some understanding of the functional significance of these pathways and to understand the role the pathologist might play in characterizing the activation status of certain downstream messenger proteins that are targeted in these brain tumor therapies.
  • [MeSH-major] Central Nervous System Neoplasms / metabolism. Glioma / metabolism. Receptor, Epidermal Growth Factor / metabolism. Second Messenger Systems / physiology

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  • (PMID = 17922598.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / epidermal growth factor receptor VIII; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Number-of-references] 35
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83. Revert Ventura AJ, Sanz-Requena R, Martí-Bonmatí L, Jornet J, Piquer J, Cremades A, Carot JM: [Nosological analysis of MRI tissue perfusion parameters obtained using the unicompartmental and pharmacokinetic models in cerebral glioblastomas]. Radiologia; 2010 Sep-Oct;52(5):432-41
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  • [Transliterated title] Análisis nosológico con parámetros de perfusión tisular de RM obtenidos mediante los modelos monocompartimental y farmacocinético en los glioblastomas cerebrales.
  • OBJECTIVES: To classify the tumor areas in patients with grade IV astrocytoma by calculating and statistically analyzing quantitative MRI perfusion parameters.
  • MATERIAL AND METHODS: We applied two models of MRI perfusion, the unicompartmental and the pharmacokinetic models, in 15 patients diagnosed with grade IV astrocytoma.
  • For each parameter, histograms were obtained for the total tumor area, for the peritumoral area, and for the healthy tissue.
  • CONCLUSION: When parameters are considered individually, CBV is the one that best enables differentiation between tumor, peritumoral, and healthy tissue.
  • The classificatory function generated from CBV and K(trans) results in improved classification by areas.

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  • [Copyright] Copyright © 2009 SERAM. Published by Elsevier Espana. All rights reserved.
  • (PMID = 20655078.001).
  • [ISSN] 0033-8338
  • [Journal-full-title] Radiología
  • [ISO-abbreviation] Radiologia
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
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84. Alexiou GA, Fotopoulos AD, Papadopoulos A, Kyritsis AP, Polyzoidis KS, Tsiouris S: Evaluation of brain tumor recurrence by (99m)Tc-tetrofosmin SPECT: a prospective pilot study. Ann Nucl Med; 2007 Jul;21(5):293-8
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  • [Title] Evaluation of brain tumor recurrence by (99m)Tc-tetrofosmin SPECT: a prospective pilot study.
  • OBJECTIVE: The differentiation between brain tumor recurrence and post-irradiation injury remains an imaging challenge.
  • Although glioma cell line studies substantiated a plausible imaging superiority of (99m)Tc-tetrofosmin ((99m)Tc-TF) over other radiopharmaceuticals, little has been reported on its in vivo imaging properties.
  • We assessed (99m)Tc-TF single-photon emission CT (SPECT) in cases where morphologic brain imaging was inconclusive between recurrence and radionecrosis.
  • The initial diagnosis was glioblastoma multiforme (4), anaplastic astrocytoma (1), anaplastic oligodendroglioma (3), grade-II astrocytoma (2), and low-grade oligodendroglioma (1).
  • [MeSH-major] Brain Neoplasms / diagnosis. Brain Neoplasms / pathology. Glioma / radionuclide imaging. Organophosphorus Compounds / pharmacology. Organotechnetium Compounds / pharmacology. Radiopharmaceuticals / pharmacology. Recurrence. Tomography, Emission-Computed, Single-Photon / methods
  • [MeSH-minor] Adult. Brain / pathology. Brain / radionuclide imaging. Cell Line, Tumor. Female. Humans. Magnetic Resonance Imaging / methods. Male. Middle Aged. Pilot Projects. Tomography, X-Ray Computed / methods

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  • (PMID = 17634847.001).
  • [ISSN] 0914-7187
  • [Journal-full-title] Annals of nuclear medicine
  • [ISO-abbreviation] Ann Nucl Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Organophosphorus Compounds; 0 / Organotechnetium Compounds; 0 / Radiopharmaceuticals; 0 / technetium Tc 99m 1,2-bis(bis(2-ethoxyethyl)phosphino)ethane
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85. Broniscer A, Chintagumpala M, Fouladi M, Krasin MJ, Kocak M, Bowers DC, Iacono LC, Merchant TE, Stewart CF, Houghton PJ, Kun LE, Ledet D, Gajjar A: Temozolomide after radiotherapy for newly diagnosed high-grade glioma and unfavorable low-grade glioma in children. J Neurooncol; 2006 Feb;76(3):313-9
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  • [Title] Temozolomide after radiotherapy for newly diagnosed high-grade glioma and unfavorable low-grade glioma in children.
  • Chemotherapy is commonly used in the treatment of children with high-grade glioma, although its usefulness is uncertain.
  • We conducted a multi-institutional study to evaluate the efficacy of temozolomide given after radiotherapy in children with newly diagnosed high-grade glioma and unfavorable low-grade glioma (gliomatosis cerebri or bithalamic involvement).
  • The 5-day schedule of temozolomide (200 mg/m2 per day) started 4 weeks after the completion of radiotherapy and continued for a total of 6 cycles.
  • The predominant histologic diagnoses were glioblastoma multiforme (n = 15, 48%) and anaplastic astrocytoma (n = 10, 32%).
  • Two patients had bithalamic grade II astrocytoma.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Glioma / drug therapy

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  • (PMID = 16200343.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA21765
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 0H43101T0J / irinotecan; 7GR28W0FJI / Dacarbazine; XT3Z54Z28A / Camptothecin; YF1K15M17Y / temozolomide
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86. Henderson MA, Fakiris AJ, Timmerman RD, Worth RM, Lo SS, Witt TC: Gamma knife stereotactic radiosurgery for low-grade astrocytomas. Stereotact Funct Neurosurg; 2009;87(3):161-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gamma knife stereotactic radiosurgery for low-grade astrocytomas.
  • Patients with low-grade astrocytoma (LGA; 8 pilocytic astrocytomas, 2 subependymal giant cell astrocytomas, 2 fibrillary astrocytomas) were selected for treatment with gamma knife stereotactic radiosurgery (GKSRS) based on having a demarcated appearance on CT or MRI and the possibility of dose sparing of adjacent eloquent structures.
  • A median dose of 13 Gy was prescribed to the 50% isodose line, which covered the gross tumor.
  • With a median follow-up of 48.2 months, 4-year tumor control and overall survival were 77 and 83%, respectively.
  • [MeSH-major] Astrocytoma / surgery. Brain Neoplasms / surgery. Radiosurgery / methods

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  • [Copyright] 2009 S. Karger AG, Basel.
  • (PMID = 19321969.001).
  • [ISSN] 1423-0372
  • [Journal-full-title] Stereotactic and functional neurosurgery
  • [ISO-abbreviation] Stereotact Funct Neurosurg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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87. Niculescu CE, Stănescu L, Popescu M, Niculescu D: Supratentorial pilocytic astrocytoma in children. Rom J Morphol Embryol; 2010;51(3):577-80
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  • [Title] Supratentorial pilocytic astrocytoma in children.
  • The authors describe the case of a child aged 2 years and 4 months with increased intracranial pressure, symptomatology accompanied by rapid deterioration of general condition.
  • Histopathological examination revealed the typical grade I pilocytic astrocytoma.
  • [MeSH-major] Astrocytoma / pathology. Supratentorial Neoplasms / pathology

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  • (PMID = 20809042.001).
  • [ISSN] 1220-0522
  • [Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
  • [ISO-abbreviation] Rom J Morphol Embryol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Romania
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88. Zhou W, Jiang Z, Song X, Liu Y, Wen P, Guo Y, Xu F, Kong L, Zhang P, Han A, Yu J: Promoter hypermethylation-mediated down-regulation of CXCL12 in human astrocytoma. J Neurosci Res; 2008 Oct;86(13):3002-10
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  • [Title] Promoter hypermethylation-mediated down-regulation of CXCL12 in human astrocytoma.
  • However, the role of CXCL12/CXCR4 axis, especially CXCL12, in the regulation of tumor invasiveness is largely still unknown.
  • Using real-time quantitative RT-PCR assays, we observed that CXCR4 expression increased with increasing WHO grade in astrocytoma, suggesting that CXCR4 may be a marker of aggressive biological behavior of astrocytoma.
  • Methylation of CXCL12 was detected in 34.2% (26/76) of astrocytomas by methylation-specific PCR.
  • Epigenetic inactivation of CXCL12 was implicated mainly in low-grade astrocytomas, via DNA hypermethylation by DNMT1, -3A, and -3B; 21.1% (16/76) of the astrocytomas showed reduced or lack of CXCL12 expression, in line with epigenetic silencing of gene transcripts.
  • However, it is interesting to note that 61.8% (47/76) of tumors, mainly high-grade astrocytomas, displayed elevated transcription of CXCL12.
  • In summary, our data show that CXCL12 promoter hypermethylation is an early event in astrocytoma development.
  • However, the high expressions of CXCR4 and CXCL12 in glioblastomas, the more invasive astrocytomas, suggest a different role of CXCL12/CXCR4 signaling axis in astrocytoma progression.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Chemokine CXCL12 / genetics. DNA Methylation. Promoter Regions, Genetic

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18512766.001).
  • [ISSN] 1097-4547
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CXCL12 protein, human; 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / RNA, Messenger; 0 / Receptors, CXCR4
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89. Palmieri C, Brock C, Newlands ES: Maintenance of fertility following treatment with temozolomide for a high grade astrocytoma. J Neurooncol; 2005 Jun;73(2):185
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  • [Title] Maintenance of fertility following treatment with temozolomide for a high grade astrocytoma.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Fertility / drug effects. Infertility, Male / chemically induced. Infertility, Male / prevention & control

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90. Arrieta O, Pineda-Olvera B, Guevara-Salazar P, Hernández-Pedro N, Morales-Espinosa D, Cerón-Lizarraga TL, González-De la Rosa CH, Rembao D, Segura-Pacheco B, Sotelo J: Expression of AT1 and AT2 angiotensin receptors in astrocytomas is associated with poor prognosis. Br J Cancer; 2008 Jul 8;99(1):160-6
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  • [Title] Expression of AT1 and AT2 angiotensin receptors in astrocytomas is associated with poor prognosis.
  • Astrocytomas develop intense vascular proliferation, essential for tumour growth and invasiveness.
  • We studied 133 tumours from patients with diagnosis of astrocytoma who underwent surgery from 1997 to 2002.
  • Ten per cent of low-grade astrocytomas were positive for AT1, whereas grade III and IV astrocytomas were positive in 67% (P<0.001).
  • AT2 receptors were positive in 17% of low-grade astrocytomas and in 53% of high-grade astrocytomas (P=0.01).
  • These findings suggest that ANGII receptors might be potential therapeutic targets for high-grade astrocytomas.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Receptor, Angiotensin, Type 1 / biosynthesis. Receptor, Angiotensin, Type 2 / biosynthesis

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  • (PMID = 18594540.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptor, Angiotensin, Type 1; 0 / Receptor, Angiotensin, Type 2
  • [Other-IDs] NLM/ PMC2453037
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91. Jacob K, Albrecht S, Sollier C, Faury D, Sader E, Montpetit A, Serre D, Hauser P, Garami M, Bognar L, Hanzely Z, Montes JL, Atkinson J, Farmer JP, Bouffet E, Hawkins C, Tabori U, Jabado N: Duplication of 7q34 is specific to juvenile pilocytic astrocytomas and a hallmark of cerebellar and optic pathway tumours. Br J Cancer; 2009 Aug 18;101(4):722-33
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  • [Title] Duplication of 7q34 is specific to juvenile pilocytic astrocytomas and a hallmark of cerebellar and optic pathway tumours.
  • BACKGROUND: Juvenile pilocytic astrocytomas (JPA), a subgroup of low-grade astrocytomas (LGA), are common, heterogeneous and poorly understood subset of brain tumours in children.
  • [MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Chromosomes, Human, Pair 7 / genetics

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  • (PMID = 19603027.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carrier Proteins; EC 2.7.1.- / HIPK2 protein, human; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC2736806
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92. Reynolds GM, Peet AC, Arvanitis TN: Generating prior probabilities for classifiers of brain tumours using belief networks. BMC Med Inform Decis Mak; 2007 Sep 18;7:27
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  • To verify the usefulness of the networks, an application of the method is presented in which prior probabilities were generated and combined with a classification of tumours based solely on MRS data.
  • Networks are presented for astrocytoma grades I and II, astrocytoma grades III and IV, ependymoma, pineoblastoma, primitive neuroectodermal tumour (PNET), germinoma, medulloblastoma, craniopharyngioma and a group representing rare tumours, "other".
  • Using the network to generate prior probabilities for classification improves the accuracy when compared with generating prior probabilities based on class prevalence.
  • CONCLUSION: Bayesian belief networks are a simple way of using discrete clinical information to generate probabilities usable in classification.
  • Inclusion of a priori knowledge is an effective way of improving classification of brain tumours by non-invasive methods.
  • [MeSH-major] Bayes Theorem. Brain Neoplasms / classification. Decision Support Techniques. Diagnosis, Computer-Assisted. Germinoma / classification. Neuroectodermal Tumors / classification
  • [MeSH-minor] Child. Databases, Factual. Diagnosis, Differential. Humans. Magnetic Resonance Spectroscopy. Neoplasm Staging. Probability

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  • (PMID = 17877822.001).
  • [ISSN] 1472-6947
  • [Journal-full-title] BMC medical informatics and decision making
  • [ISO-abbreviation] BMC Med Inform Decis Mak
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0601327
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2040142
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93. Cassoni P, Senetta R, Castellano I, Ortolan E, Bosco M, Magnani I, Ducati A: Caveolin-1 expression is variably displayed in astroglial-derived tumors and absent in oligodendrogliomas: concrete premises for a new reliable diagnostic marker in gliomas. Am J Surg Pathol; 2007 May;31(5):760-9
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  • [Title] Caveolin-1 expression is variably displayed in astroglial-derived tumors and absent in oligodendrogliomas: concrete premises for a new reliable diagnostic marker in gliomas.
  • All studied astrocitomas of any grade (from II to IV) were cav-1 positive, displaying staining patterns and intensity specifically associated to the different tumor grades.
  • In anaplastic astrocytomas, a less intense membrane staining or a cytoplasmic dotlike immunoreactivity were present, the latter being almost the exclusive pattern observed in diffuse astrocitomas grade II.
  • Interestingly, a cav-1 distribution overlapping the pattern described in tissues was observed also in primary cell cultures of human glioblastomas and astrocytomas, and also in one established glioblastoma cell line (U251 MG), analyzed by means of confocal microscopy and flow cytometry.
  • In conclusion, among astroglial tumors cav-1 expression varies in distribution, pattern, and intensity specifically according to tumor types and grades.
  • The association between tumor progression and a more structured membranous pattern of cav-1 expression could suggest the hypothesis of a neoplastic shift towards a mesenchymal phenotype, whose behavioral and biologic significance worth further studies.
  • [MeSH-major] Astrocytes / metabolism. Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Caveolin 1 / metabolism. Glioblastoma / metabolism. Oligodendroglioma / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Count. Cell Line, Tumor. Cell Separation. Chromosome Deletion. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Disease Progression. Flow Cytometry. Humans. Immunohistochemistry. Middle Aged. Neoplasm Staging

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  • (PMID = 17460461.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Caveolin 1
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94. Ohgaki H, Kleihues P: Genetic pathways to primary and secondary glioblastoma. Am J Pathol; 2007 May;170(5):1445-53
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  • Glioblastoma is the most frequent and most malignant human brain tumor.
  • Primary and secondary glioblastoma constitute distinct disease subtypes, affecting patients of different age and developing through different genetic pathways.
  • The majority of cases (>90%) are primary glioblastomas that develop rapidly de novo, without clinical or histological evidence of a less malignant precursor lesion.
  • Secondary glioblastomas develop through progression from low-grade diffuse astrocytoma or anaplastic astrocytoma and manifest in younger patients.
  • In the pathway to secondary glioblastoma, TP53 mutations are the most frequent and earliest detectable genetic alteration, already present in 60% of precursor low-grade astrocytomas.
  • [MeSH-minor] Chromosomes, Human, Pair 10 / genetics. Humans. Loss of Heterozygosity / genetics. Mutation. PTEN Phosphohydrolase / genetics. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 17456751.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Number-of-references] 85
  • [Other-IDs] NLM/ PMC1854940
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95. Lamoral-Theys D, Le Mercier M, Le Calvé B, Rynkowski MA, Bruyère C, Decaestecker C, Haibe-Kains B, Bontempi G, Dubois J, Lefranc F, Kiss R: Long-term temozolomide treatment induces marked amino metabolism modifications and an increase in TMZ sensitivity in Hs683 oligodendroglioma cells. Neoplasia; 2010 Jan;12(1):69-79
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  • Gliomas account for more than 50% of all primary brain tumors.
  • The worst prognosis is associated with gliomas of astrocytic origin, whereas gliomas with an oligodendroglial origin offer higher sensitivity to chemotherapy, especially when oligodendroglioma cells display 1p19q deletions.
  • Temozolomide (TMZ) provides therapeutic benefits and is commonly used with radiotherapy in highly malignant astrocytic tumors, including glioblastomas.
  • [MeSH-minor] Animals. Antineoplastic Agents, Alkylating / pharmacology. Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Gene Expression Regulation, Neoplastic / drug effects. Genomics / methods. HT29 Cells. Humans. Mice. Mice, Nude. Neoplasm Invasiveness. Neoplastic Stem Cells / drug effects. Neoplastic Stem Cells / metabolism. Neoplastic Stem Cells / pathology. Proteomics / methods. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Xenograft Model Antitumor Assays

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  • (PMID = 20072655.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Amino Acids; 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
  • [Other-IDs] NLM/ PMC2805885
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96. McGirt MJ, Chaichana KL, Gathinji M, Attenello F, Than K, Ruiz AJ, Olivi A, Quiñones-Hinojosa A: Persistent outpatient hyperglycemia is independently associated with decreased survival after primary resection of malignant brain astrocytomas. Neurosurgery; 2008 Aug;63(2):286-91; discussion 291
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  • [Title] Persistent outpatient hyperglycemia is independently associated with decreased survival after primary resection of malignant brain astrocytomas.
  • OBJECTIVE: Patients with malignant brain astrocytomas are at high risk for developing hyperglycemia secondary to frequent corticosteroid administration.
  • Several clinical studies have shown that hyperglycemia is associated with poor outcome in multiple disease states.
  • Furthermore, hyperglycemia augments in vitro astrocytoma growth, whereas hypoglycemia attenuates in vitro astrocytoma cell growth.
  • We hypothesized that persistent hyperglycemic states in the outpatient setting may serve as a prognostic marker of decreased survival in patients with malignant brain astrocytomas.
  • METHODS: We retrospectively reviewed 367 cases of craniotomy for malignant brain astrocytomas (World Health Organization Grade III or IV).
  • RESULTS: A total of 367 craniotomies (209 primary, 158 secondary) were performed for malignant brain astrocytomas (glioblastoma multiforme, 297; anaplastic astrocytomas, 70); 68 (19%) and 28 (8%) of the patients experienced isolated or persistent outpatient hyperglycemia, respectively.
  • Adjusting for intergroup differences and variables associated with survival in this model, age (P = 0.001), Karnofsky Performance Scale score (P = 0.001), tumor grade (P = 0.001), primary versus secondary resection (P = 0.008), temozolomide (P = 0.007), subsequent resection (P = 0.07), and continued outpatient dexamethasone therapy, persistent outpatient hyperglycemia (relative risk, 1.79; 95% confidence interval, 1.05-3.05, P = 0.03) remained independently associated with decreased survival.
  • CONCLUSION: In our experience, persistent outpatient hyperglycemia was associated with decreased survival in patients undergoing surgical resection for malignant astro- cytomas and was independent of the degree of disability, tumor grade, diabetes, prolonged dexamethasone use, or subsequent treatment modalities.
  • Increased glucose control is warranted in this patient population and may contribute to improved outcomes in the treatment of malignant brain astrocytomas.
  • [MeSH-major] Ambulatory Care / trends. Astrocytoma / mortality. Astrocytoma / surgery. Brain Neoplasms / mortality. Brain Neoplasms / surgery. Hyperglycemia / mortality

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  • (PMID = 18797358.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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97. Rodriguez y Baena R, Di Ieva A, Colombo P, Collini P, Navarria P, Scorsetti M, Gaetani P, Santoro A: Intramedullary astrocytoma with granular cell differentiation. Neurosurg Rev; 2007 Oct;30(4):339-43; discussion 343
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  • [Title] Intramedullary astrocytoma with granular cell differentiation.
  • Granular cell astrocytomas are uncommon tumors of the central nervous system (CNS) of which no cases have been documented in the spinal cord.
  • This variant of glioma should not be confused with benign granular cell tumor which, although rare, has been well characterized in the spinal cord.
  • We describe here the clinical, pathological, and radiological features of such an astrocytoma arising within the spinal cord at the dorsal level.
  • Magnetic resonance imaging (MRI) studies showed a 2-cm contrast-enhanced mass in the spinal cord at T6-T7, which had the appearance of an astrocytoma.
  • At surgery, the tumor was found to be infiltrating a posterior column with no dural attachment.
  • The histological diagnosis was astrocytoma with granular cell differentiation.
  • In addition to documenting a unique example of intramedullary granular cell astrocytoma, we review the literature to investigate differences from other tumors with granular changes described in the spinal cord.
  • [MeSH-major] Astrocytoma / diagnostic imaging. Astrocytoma / pathology. Spinal Cord Neoplasms / diagnostic imaging. Spinal Cord Neoplasms / pathology

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98. Boda-Heggemann J, Régnier-Vigouroux A, Franke WW: Beyond vessels: occurrence and regional clustering of vascular endothelial (VE-)cadherin-containing junctions in non-endothelial cells. Cell Tissue Res; 2009 Jan;335(1):49-65
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  • Such cells include mammalian astrocytes and glioma, probably mostly astrocytoma cells growing in culture, and a specific subtype of astrocytoma in situ.
  • [MeSH-minor] Animals. Astrocytoma / metabolism. Astrocytoma / pathology. Calcium / metabolism. Humans. Neoplasm Metastasis

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  • (PMID = 19002500.001).
  • [ISSN] 1432-0878
  • [Journal-full-title] Cell and tissue research
  • [ISO-abbreviation] Cell Tissue Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CDH2 protein, human; 0 / Cadherins; 0 / cadherin 5; 156621-71-5 / osteoblast cadherin; SY7Q814VUP / Calcium
  • [Number-of-references] 114
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99. Jiang L, Saetre P, Jazin E, Carlström EL: Haloperidol changes mRNA expression of a QKI splice variant in human astrocytoma cells. BMC Pharmacol; 2009;9:6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Haloperidol changes mRNA expression of a QKI splice variant in human astrocytoma cells.
  • Disturbed QKI mRNA expression is observed in the prefrontal cortex of patients, and some of these changes correlate to treatment with antipsychotic drugs.To test if low doses of antipsychotic drugs can modify QKI mRNA expression, human astrocytoma (U343) and oligodendroglioma (HOG) cell lines were treated with five different antipsychotic drugs including Haloperidol, Aripiprazole, Clozapine, Olanzapine and Risperidone.
  • [MeSH-minor] Alternative Splicing. Antipsychotic Agents / pharmacology. Aripiprazole. Astrocytoma / genetics. Astrocytoma / pathology. Benzodiazepines / pharmacology. Cell Line, Tumor. Clozapine / pharmacology. Dose-Response Relationship, Drug. Humans. Piperazines / pharmacology. Quinolones / pharmacology. Receptors, Dopamine D2 / genetics. Reverse Transcriptase Polymerase Chain Reaction. Risperidone / pharmacology. Time Factors

  • Hazardous Substances Data Bank. RISPERIDONE .
  • Hazardous Substances Data Bank. Olanzapine .
  • Hazardous Substances Data Bank. HALOPERIDOL .
  • Hazardous Substances Data Bank. CLOZAPINE .
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  • (PMID = 19335891.001).
  • [ISSN] 1471-2210
  • [Journal-full-title] BMC pharmacology
  • [ISO-abbreviation] BMC Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antipsychotic Agents; 0 / Piperazines; 0 / QKI protein, human; 0 / Quinolones; 0 / RNA, Messenger; 0 / RNA-Binding Proteins; 0 / Receptors, Dopamine D2; 12794-10-4 / Benzodiazepines; 132539-06-1 / olanzapine; 82VFR53I78 / Aripiprazole; J60AR2IKIC / Clozapine; J6292F8L3D / Haloperidol; L6UH7ZF8HC / Risperidone
  • [Other-IDs] NLM/ PMC2676266
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100. Roach JD Jr, Aguinaldo GT, Jonnalagadda K, Hughes FM Jr, Spangelo BL: Gamma-aminobutyric acid inhibits synergistic interleukin-6 release but not transcriptional activation in astrocytoma cells. Neuroimmunomodulation; 2008;15(2):117-24
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  • [Title] Gamma-aminobutyric acid inhibits synergistic interleukin-6 release but not transcriptional activation in astrocytoma cells.
  • OBJECTIVE: A decline in the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) may enhance cytokine release in Alzheimer's disease (AD) resulting in neuroinflammation.
  • We investigated the GABA-mediated suppression of the synergistic release of interleukin (IL)-6 due to interleukin 1-beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha).
  • METHODS: Rat C6 astrocytoma cells were treated with IL-1 beta and TNF-alpha in the absence and presence of GABA.

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  • [Copyright] (c) 2008 S. Karger AG, Basel.
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  • (PMID = 18679050.001).
  • [ISSN] 1423-0216
  • [Journal-full-title] Neuroimmunomodulation
  • [ISO-abbreviation] Neuroimmunomodulation
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS051198-01A1; United States / NINDS NIH HHS / NS / R15 NS051198; United States / NINDS NIH HHS / NS / 1R15NS051198-01A; United States / NINDS NIH HHS / NS / R15 NS051198-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / I-kappa B Proteins; 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 139874-52-5 / NF-kappaB inhibitor alpha; 56-12-2 / gamma-Aminobutyric Acid; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS194281; NLM/ PMC2859952
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