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1. Tehrani M, Friedman TM, Olson JJ, Brat DJ: Intravascular thrombosis in central nervous system malignancies: a potential role in astrocytoma progression to glioblastoma. Brain Pathol; 2008 Apr;18(2):164-71
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  • [Title] Intravascular thrombosis in central nervous system malignancies: a potential role in astrocytoma progression to glioblastoma.
  • The presence of necrosis within a diffuse glioma is a powerful predictor of poor prognosis, yet little is known of its origins.
  • Intravascular thrombosis is a frequent finding in glioblastoma [GBM; World Health Organization (WHO) grade IV] specimens and could potentially be involved in astrocytoma progression to GBM or represent a surrogate marker of GBM histology.
  • We investigated whether intravascular thrombosis was more frequent or prominent in GBM than other central nervous system (CNS) malignancies and considered its prognostic significance in anaplastic astrocytoma (AA; WHO grade III), which lacks necrosis.
  • Histologic sections were examined for thrombosis, necrosis and microvascular hyperplasia from each of 297 CNS tumors, including 103 GBMs, 46 AAs, 20 diffuse astrocytoma (DAs; WHO grade II), eight anaplastic oligodendrogliomas (AOs; WHO grade III), 20 oligodendrogliomas (ODs; WHO grade II), 49 metastatic carcinomas (METs), 31 primary central nervous system lymphomas (PCNSLs) and 20 medulloblastomas (MBs).

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  • (PMID = 18093251.001).
  • [ISSN] 1015-6305
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS053727-01; United States / NINDS NIH HHS / NS / R01 NS053727; United States / NINDS NIH HHS / NS / NS053727; United States / NINDS NIH HHS / NS / R01 NS053727-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Switzerland
  • [Other-IDs] NLM/ NIHMS82090; NLM/ PMC2610479
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2. Liu L, Bäcklund LM, Nilsson BR, Grandér D, Ichimura K, Goike HM, Collins VP: Clinical significance of EGFR amplification and the aberrant EGFRvIII transcript in conventionally treated astrocytic gliomas. J Mol Med (Berl); 2005 Nov;83(11):917-26
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  • [Title] Clinical significance of EGFR amplification and the aberrant EGFRvIII transcript in conventionally treated astrocytic gliomas.
  • The aim of this study was to evaluate the clinical value of assessing epidermal growth factor receptor (EGFR) amplification and the common 5' rearrangement of EGFR resulting in the EGFRvIII transcript in astrocytic gliomas.
  • Amplification of EGFR was found in 41% (65/160) of glioblastomas (GBs) and 10% (4/41) of anaplastic astrocytomas (AAs).
  • There were no abnormalities of the EFGR or its transcript in grade II astrocytoma (AII).
  • We noted a tendency towards decreased survival with any EGFR abnormality in the 41 patients with AAs.
  • [MeSH-major] Astrocytoma / genetics. Central Nervous System Neoplasms / genetics. Gene Amplification. Glioblastoma / genetics. Glioma / genetics. Receptor, Epidermal Growth Factor / genetics

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  • (PMID = 16133418.001).
  • [ISSN] 0946-2716
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6618
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers; 0 / epidermal growth factor receptor VIII; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC2815848; NLM/ UKMS2690
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3. Götze S, Wolter M, Reifenberger G, Müller O, Sievers S: Frequent promoter hypermethylation of Wnt pathway inhibitor genes in malignant astrocytic gliomas. Int J Cancer; 2010 Jun 1;126(11):2584-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent promoter hypermethylation of Wnt pathway inhibitor genes in malignant astrocytic gliomas.
  • Recent studies suggested a role of Wnt signaling in gliomas, the most common primary brain tumors.
  • We investigated 70 gliomas of different malignancy grades for promoter hypermethylation in 8 genes encoding members of the secreted frizzled-related protein (SFRP1, SFRP2, SFRP4, SFRP5), dickkopf (DKK1, DKK3) and naked (NKD1, NKD2) families of Wnt pathway inhibitors.
  • While none of the tumors carried CTNNB1 mutations, we found frequent promoter hypermethylation of Wnt pathway inhibitor genes, with at least one of these genes being hypermethylated in 6 of 16 diffuse astrocytomas (38%), 4 of 14 anaplastic astrocytomas (29%), 7 of 10 secondary glioblastomas (70%) and 23 of 30 primary glioblastomas (77%).
  • Furthermore, SFRP1-hypermethylated gliomas showed significantly lower expression of the respective transcripts when compared with unmethylated tumors.
  • Taken together, our results suggest an important role of epigenetic silencing of Wnt pathway inhibitor genes in astrocytic gliomas, in particular, in glioblastomas, with distinct patterns of hypermethylated genes distinguishing primary from secondary glioblastomas.
  • [MeSH-major] Astrocytoma / genetics. DNA Methylation / genetics. Promoter Regions, Genetic. Wnt Proteins / genetics
  • [MeSH-minor] Carrier Proteins / genetics. Cell Line, Tumor. DNA Mutational Analysis. DNA, Neoplasm / genetics. DNA, Neoplasm / isolation & purification. Exons. Eye Proteins / genetics. Glioblastoma / genetics. Glioblastoma / secondary. Glioma / genetics. Glioma / pathology. Humans. Intercellular Signaling Peptides and Proteins / genetics. Membrane Proteins / genetics. Mutation. Polymerase Chain Reaction. Proto-Oncogene Proteins / genetics. beta Catenin / genetics

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  • (PMID = 19847810.001).
  • [ISSN] 1097-0215
  • [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 / CTNNB1 protein, human; 0 / Carrier Proteins; 0 / DNA, Neoplasm; 0 / Eye Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / NKD1 protein, human; 0 / NKD2 protein, human; 0 / Proto-Oncogene Proteins; 0 / SFRP1 protein, human; 0 / SFRP2 protein, human; 0 / SFRP4 protein, human; 0 / SFRP5 protein, human; 0 / Wnt Proteins; 0 / beta Catenin
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4. Ritch PS, Carroll SL, Sontheimer H: Neuregulin-1 enhances survival of human astrocytic glioma cells. Glia; 2005 Aug 15;51(3):217-28
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuregulin-1 enhances survival of human astrocytic glioma cells.
  • Malignant astrocytic gliomas, referred to as astrocytomas, represent the most commonly diagnosed adult primary brain tumor.
  • Tumor expansion into the healthy surrounding brain tissue produces severe and often fatal consequences.
  • In this study, we examine the potential for the neuregulin-1/erbB receptor signaling cascade to contribute to this process by modulating glioma cell growth.
  • Using antibodies specific for the erbB receptors, we demonstrate the expression patterns for the erbB2, erbB3, and erbB4 receptors in human glioma biopsy samples.
  • We then verify receptor expression in a panel of human glioma cell lines.
  • Next, we investigate the status of the erbB2 and erbB3 receptors in the human glioma cell lines and find that they are constitutively tyrosine-phosphorylated and heterodimerized.
  • Furthermore, we show that exogenous activation of erbB2 and erbB3 receptors in U251 glioma cells by recombinant Nrg-1beta results in enhanced glioma cell growth under conditions of serum-deprivation.
  • Moreover, Nrg-1beta activates an inhibitor of apoptosis, Akt, implying a possible role for this kinase in mediating Nrg-1beta effects in gliomas.
  • This data suggests that glioma cells may use autocrine or paracrine neuregulin-1/erbB receptor signaling to enhance cell survival under conditions where growth would otherwise be limited.

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  • (PMID = 15812817.001).
  • [ISSN] 0894-1491
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA097247-010003; United States / NINDS NIH HHS / NS / R01 NS036692-05A1; United States / NCI NIH HHS / CA / CA097247-010003; United States / NCI NIH HHS / CA / P50 CA097247; United States / NCI NIH HHS / CA / P50CA97247; United States / NINDS NIH HHS / NS / NS036692-05A1; United States / NINDS NIH HHS / NS / R01 NS036692; United States / NINDS NIH HHS / NS / R01-NS36692; United States / NINDS NIH HHS / NS / R01 NS036692-06; United States / NINDS NIH HHS / NS / NS036692-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neuregulin-1; 0 / Protein Subunits; 0 / Proto-Oncogene Proteins; 0 / Recombinant Fusion Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / ERBB4 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.10.1 / Receptor, ErbB-3; EC 2.7.10.1 / Receptor, ErbB-4; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ NIHMS25075; NLM/ PMC2548407
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5. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • We previously explicated the expression and prognostic value of PAX6, PTEN, VEGF, and EGFR in these glioma tissues and established a comprehensive prognostic model (Zhou et al., 2003).
  • 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.
  • This finding suggests that the expression of IGFBP2 is associated with pathways activated specifically in GBMs that result in enhancing invasiveness and angiogenesis.
  • [MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / analysis. Brain Neoplasms / genetics. Models, Statistical

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  • (PMID = 16212813.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers; 0 / Insulin-Like Growth Factor Binding Protein 2; 0 / Ribosomal Proteins; 0 / ribosomal protein S9; EC 3.4.24.24 / Matrix Metalloproteinase 2
  • [Other-IDs] NLM/ PMC1871729
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6. Figarella-Branger D, Bouvier C: [Histological classification of human gliomas: state of art and controversies]. Bull Cancer; 2005 Apr;92(4):301-9
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  • [Title] [Histological classification of human gliomas: state of art and controversies].
  • [Transliterated title] Classification anatomopathologique des gliomes: faits et controverses.
  • The histological classification of human gliomas remains in 2005 a challenge.
  • The aim is to define the histological type of glioma (astrocytic, oligodendrocytic or mixed) and the grade in order to classify the patients and give them an accurate treatment.
  • Although the standard remains the WHO classification, this classification suffered from lack of reproducibility among pathologists.
  • In particular this classification does not take into account the intrinsic morphological heterogeneity of infiltrative gliomas and does not discriminate the tumour cells from the residual brain parenchyma.
  • According to the WHO classification, infiltrative gliomas encompass astrocytic gliomas (diffuse astrocytomas grade II, anaplastic astrocytomas grade III and glioblastomas grade IV), oligodendroglial tumours (oligodendrogliomas grade II, anaplastic oligodendrogliomas grade III) and mixed gliomas (oligoastrocytomas grade II and anaplastic oligoastrocytomas grade III).
  • Circumscribed gliomas mainly corresponds to pilocytic astrocytomas (grade I).
  • In contrast, the Sainte Anne classification takes into account the macroscopic informations provided by imaging techniques and the tumour growth patterns.
  • Three distinct tumour growth patterns may be seen in gliomas, type I: tumor tissue only, type II: tumour tissue and isolated tumor cells permeating the brain parenchyma (ITC) and type III: ITCs only and no tumor tissue.
  • According to the Sainte Anne classification, gliomas are divided into astrocytic gliomas (pilocytic astrocytomas, structure type I, glioblastomas structure type II) and oligodendrogliomas and mixed oligoastrocytomas (grade A: lack of contrast enhancement and lack of endothelial hyperplasia, structure type III; and grade B: contrast enhancement or endothelial hyperplasia, structure type II and III).
  • In the future the glioma classification has to be unique and should take into account clinical data, neuroradiological and histological features and results of molecular biology.
  • [MeSH-major] Brain Neoplasms / pathology. Glioma / pathology
  • [MeSH-minor] Astrocytoma / pathology. Humans. Neoplasms, Complex and Mixed / classification. Neoplasms, Complex and Mixed / pathology. Oligodendroglioma / pathology. Reproducibility of Results. World Health Organization

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  • (PMID = 15888386.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
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7. Uno M, Oba-Shinjo SM, Wakamatsu A, Huang N, Avancini Ferreira Alves V, Rosemberg S, Pires de Aguiar PH, Leite C, Miura F, Marino J R, Scaff M, Nagahashi-Marie SK: Association of TP53 mutation, p53 overexpression, and p53 codon 72 polymorphism with susceptibility to apoptosis in adult patients with diffuse astrocytomas. Int J Biol Markers; 2006 Jan - Mar;21(1):50-57

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of TP53 mutation, p53 overexpression, and p53 codon 72 polymorphism with susceptibility to apoptosis in adult patients with diffuse astrocytomas.
  • : Clarification of TP53 alterations is important to understand the mechanisms underlying the development of diffuse astrocytomas.
  • The aim of this study was to analyze the possible association of TP53 mutation, p53 overexpression, and p53 codon 72 polymorphism with susceptibility to apoptosis in adult Brazilian patients with diffuse astrocytomas.
  • We analyzed 56 surgical specimens of diffuse astrocytomas for alterations of TP53, using polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) direct sequencing. p53 and cleaved caspase 3 protein expression were assessed by immunohistochemistry.
  • We concluded that clarification of the TP53 alterations allows a better understanding of the mechanisms involved in the progression of diffuse astrocytomas, and the allele status at codon 72 was not associated with apoptosis in these tumors.

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  • (PMID = 28207094.001).
  • [ISSN] 1724-6008
  • [Journal-full-title] The International journal of biological markers
  • [ISO-abbreviation] Int. J. Biol. Markers
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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8. Komotar RJ, Carson BS, Rao C, Chaffee S, Goldthwaite PT, Tihan T: Pilomyxoid Astrocytoma of the Spinal Cord: Report of Three Cases. Neurosurgery; 2005 Jan 01;56(1):E206-E210

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  • [Title] Pilomyxoid Astrocytoma of the Spinal Cord: Report of Three Cases.

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  • (PMID = 28184642.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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9. Khattab AZ, Ahmed MI, Fouad MA, Essa WA: Significance of p53 and CD31 in astrogliomas. Med Oncol; 2009;26(1):86-92
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  • [Title] Significance of p53 and CD31 in astrogliomas.
  • BACKGROUND: Astrogliomas are the most common primary brain tumor.
  • Its progression is the result of activation of oncogenes, inactivation of tumor suppressor genes (TSGs), and expression of various growth factors.
  • The angiogenesis and p53 in astrogliomas play an important role in its grading, treatment strategies, and hence its clinical outcome.
  • OBJECTIVES: To analyze the frequency of presentation and the possible co-expression of p53 and angiogenesis marker (CD31) and their clinical implications in astrogliomas.
  • MATERIAL AND METHODS: This retrograde study included 45 cases with astrocytomas in the form of paraffin blocks.
  • Sections were stained with hematoxylin and eosin to determine the type and histological grade according to WHO (2007) classification of CNS tumors.
  • RESULTS: Both p53 and CD31 expressions were correlated well with the histopathological grades of different subtypes of astrogliomas with good discrimination between low and high grades.
  • Overall, a highly significant statistical correlation was observed between the grades of astrocytomas and the p53 and CD31 labeling indices.
  • Obviously, these observations demonstrate that the co-expression and increased levels of p53 and CD31 in astrogliomas are increasing as the tumor grade is increasing.
  • Thus, the two markers can be used as adjunct to the diagnosis and stratification of the high grade from the low-grade intrinsic brain astrogliomas.
  • [MeSH-major] Antigens, CD31 / biosynthesis. Astrocytoma / metabolism. Biomarkers, Tumor. Brain Neoplasms / metabolism. Tumor Suppressor Protein p53 / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Immunohistochemistry. Infant. Male. Middle Aged. Neoplasm Staging

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  • (PMID = 18821037.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Protein p53
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10. Mizoguchi M, Betensky RA, Batchelor TT, Bernay DC, Louis DN, Nutt CL: Activation of STAT3, MAPK, and AKT in malignant astrocytic gliomas: correlation with EGFR status, tumor grade, and survival. J Neuropathol Exp Neurol; 2006 Dec;65(12):1181-8
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  • [Title] Activation of STAT3, MAPK, and AKT in malignant astrocytic gliomas: correlation with EGFR status, tumor grade, and survival.
  • Diffuse astrocytic gliomas are the most common human glial tumors with glioblastoma being the most malignant form.
  • In this study, we investigated the activation status of these 3 signaling molecules as well as wild-type (EGFRwt) and mutant (EGFRvIII) EGFR in 82 malignant astrocytic gliomas (55 glioblastomas and 27 anaplastic astrocytomas) using immunohistochemistry.
  • The distribution of these 3 activated molecules varied significantly with tumor grade; although activation of STAT3 was essentially identical between anaplastic astrocytomas and glioblastomas, an increase in the activation of MAPK and AKT appeared to correlate with the progression of anaplastic astrocytoma to glioblastoma.
  • Taken together, these findings begin to elucidate the interrelationship between these signaling pathways in astrocytic gliomas in vivo.
  • [MeSH-major] Astrocytoma / enzymology. Brain Neoplasms / enzymology. Glioblastoma / enzymology. Mitogen-Activated Protein Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Epidermal Growth Factor / biosynthesis. STAT3 Transcription Factor / metabolism
  • [MeSH-minor] Biomarkers, Tumor / analysis. Biomarkers, Tumor / metabolism. Diagnosis, Differential. Disease Progression. Enzyme Activation / genetics. Genetic Predisposition to Disease / genetics. Humans. Immunohistochemistry. Mutation / genetics. Predictive Value of Tests. Prognosis. Signal Transduction / physiology. Survival Rate / trends. Transcriptional Activation / genetics

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  • (PMID = 17146292.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 57683; United States / NCI NIH HHS / CA / CA 95616
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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16. Karrasch M, Gillespie GY, Braz E, Liechty PG, Nabors LB, Lakeman AD, Palmer CA, Parker JN, Whitley RJ, Markert JM: Treatment of recurrent malignant glioma with G207, a genetically engineered herpes simplex virus-1, followed by irradiation: Phase I study results. J Clin Oncol; 2009 May 20;27(15_suppl):2042

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of recurrent malignant glioma with G207, a genetically engineered herpes simplex virus-1, followed by irradiation: Phase I study results.
  • Safety and efficacy of intracerebral inoculations of G207 to patients suffering from recurrent malignant gliomas have been demonstrated in previous clinical trials.
  • METHODS: In this phase I clinical trial, a total of 1 x 10<sup>9</sup> plaque forming units (pfu) G207 were administered by five stereotactic injections of 0.2 mL each into regions of recurrent malignant glioma defined by MRI, followed by focal radiation therapy 24 hours post injection.
  • Included patients suffered from inoperable pathologically proven recurrent glioblastoma multiforme (GBM) or anaplastic astrocytoma (AA) which was progressive despite radiotherapy or chemotherapy and failed external beam radiotherapy > 5 Gray prior to study enrolment.
  • The 2 patients with initial PR (1xGBM, 1xAA) were re-treated with G207/Irradiation at time point of tumor recurrence, showing PR one month after re-treatment again.
  • Within persistent areas of tumor, HSV staining was present by using a polyclonal antibody for HSV, indicating intratumoral G207 replication (proof of concept).

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  • (PMID = 27964649.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Simonelli M, Banna G, Navarria P, Di Ieva A, Zucali P, De Vincenzo F, Gaetani P, Condorelli R, Rodriguez Y Baena R, Scorsetti M, Santoro A: Addition of temozolomide to radiotherapy for treatment of newly diagnosed anaplastic gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13037

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Addition of temozolomide to radiotherapy for treatment of newly diagnosed anaplastic gliomas.
  • : e13037 Background: Anaplastic astrocytoma (AA), oligodendroglioma (AOD), and oligoastrocytoma (AOA) are rare tumors showing variable outcome due to their histological heterogeneity and different chemo- and radio-sensitivity.
  • Currently, the addition of chemotherapy to radiotherapy (RT) for newly diagnosed anaplastic gliomas is not sustained by available data.
  • We evaluated the addition of temozolomide (TMZ) to radiotherapy for newly diagnosed anaplastic gliomas in terms of tolerability, progression-free survival (PFS), and overall survival (OS).
  • METHODS: Since September 2004, following initial surgery, patients (pts) with histologically confirmed anaplastic glioma, Karnofsky Performance Status (KPS) ≥40, adequate organ function, no prior chemotherapy, were treated with RT to limited fields once daily at 2 Gy per fraction, 5 days a week, for a total of 60 Gy with concomitant TMZ (75 mg/m<sup>2</sup> for 7 days a week) followed by 6 cycles of maintenance TMZ at 200 mg/m<sup>2</sup> on days 1-5 every 28 days.
  • Nine pts (32%) underwent tumor complete resection, 10 partial resection (36%), and 9 (32%) tumor biopsy.
  • CONCLUSIONS: The addition of temozolomide to radiation therapy for newly diagnosed anaplastic gliomas is well tolerated and seems active; efficacy needs confirmation in a randomized clinical trial.

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  • (PMID = 27962859.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Abacioglu MU, Caglar HB, Yumuk PF, Akgun Z, Atasoy BM, Sengoz M: Efficacy of protracted dose-dense temozolomide (TMZ) in patients with progressive high-grade glioma. J Clin Oncol; 2009 May 20;27(15_suppl):e13018

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Efficacy of protracted dose-dense temozolomide (TMZ) in patients with progressive high-grade glioma.
  • : e13018 Background: The study was aimed to evaluate the efficacy of TMZ on a protracted dose-dense schedule after standard 5-day TMZ regimen in patients with progressive high-grade glioma.
  • METHODS: In this phase II prospective study, patients who had progression on standard 5-day TMZ for recurrence (group 1) or recurrence after concurrent radiotherapy+TMZ and ≥ 2 cycles of adjuvant TMZ (group 2) for high-grade glioma received TMZ 100 mg/m2× 21 q28 days until progression according to MacDonald's criteria.
  • The histopathology was glioblastoma in 18 and grade 3 glioma (anaplastic astrocytoma, anaplastic oligoastrocytoma or anaplastic oligodendroglioma) in 7.
  • The best response during treatment was partial response in 2 (8%), stable disease in 9 (36%), and progression in 9 (36%) out of 20 patients assessed.
  • CONCLUSIONS: Protracted dose-dense TMZ after 5-day schedule for recurrent or progressive disease has modest efficacy with tolerable toxicity.

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  • (PMID = 27962826.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Franceschi E, Tosoni A, Ermani M, Spagnolli F, La Torre L, Galzio RJ, Pozzati E, Talacchi A, Benevento F, Brandes AA: Impact of MGMT methylation status on 1p/19q intact anaplastic gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13003

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of MGMT methylation status on 1p/19q intact anaplastic gliomas.
  • : e13003 Background: Chromosomes 1p/19q codeletion has been recognized as a prognostic and predictive factor in patients (pts) with grade 3 gliomas.
  • Non-codeleted (intact) anaplastic oligodendroglioma showed a survival comparable to that usually observed in pts with anaplastic astrocytomas; MGMT methylation status, moreover, has been found to be a prognostic factor in glioblastoma and anaplastic gliomas (AG).
  • Histology was anaplastic oligodendroglioma in 17 pts, anaplastic oligoastrocytoma in 20 pts, and anaplastic astrocytoma in 30 pts; all these pts were 1p19q intact and received surgery, RT, and CT.

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  • (PMID = 27962754.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Witt H, Korshunov A, Remke M, Janzarik WG, Gnekow A, Scheurlen W, Kulozik AE, Lichter P, Pfister S: DNA methylation pattern of brain stem pilocytic astrocytomas in children. J Clin Oncol; 2009 May 20;27(15_suppl):10021

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA methylation pattern of brain stem pilocytic astrocytomas in children.
  • : 10021 Background: Pilocytic astrocytoma (WHO grade I) comprises the most frequent brain tumor in childhood.
  • METHODS: To identify novel genes involved in astrocytoma pathogenesis, we performed a genome-wide DNA methylation analysis of 78 pilocytic astrocytoma samples from different tumor locations (diencephalic, cerebral, cerebellar, brain stem).
  • Two CpG sites were analyzed for each of a total of 14.000 promoters per sample.
  • Moreover, from 14 tumors clustering together with the brain stem tumors, 5 patients experienced disease recurrence (38%) as opposed to 20% in the remaining group.
  • Genes contained in the signature most interestingly included three homeobox family genes (HOXB1, HOXD3, and HOXD4), and NES, a tumor stem cell marker.
  • CONCLUSIONS: These data suggest that brain stem pilocytic astrocytomas display biologic features different from most tumors of other locations and share a methylation signature with tumors prone to disease recurrence from other locations.
  • We provide first evidence for a role of differentially methylated homeobox family genes in the pathogenesis of pilocytic astrocytoma.

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  • (PMID = 27962622.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Ochsenbein AF, Schubert AD, Vassella E, Mariani L: Quantitative analysis of 0&lt;sup&gt;6&lt;/sup&gt;-methylguanine-DNA methyltransferase (MGMT) promoter methylation in patients with low-grade gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):2069

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitative analysis of 0<sup>6</sup>-methylguanine-DNA methyltransferase (MGMT) promoter methylation in patients with low-grade gliomas.
  • : 2069 Background: Loss of heterozygosity (LOH) on the chromosomes 1p and 19q is associated with sensitivity to alkylating agents like temozolomide (TMZ) in patients with low-grade gliomas; whether methylation of the MGMT-promoter, a predictive factor in glioblastoma patients, also correlates with tumor response to TMZ in low-grade gliomas is unclear.
  • METHODS: We performed a retrospective analysis of patients with histologically verified low-grade gliomas (WHO Grade II) who were treated with TMZ for tumor progression at our hospital between November 1999 and November 2007.
  • Objective tumor response was assessed by MRI at 6-month intervals.
  • LOH of microsatellite markers on chromosomes 1p and 19q was determined by polymerase chain reaction (PCR) amplification of the matched pairs of blood and tumor DNA.
  • Seven patients had prior surgical resection of the tumor.
  • Histological classification revealed 10 oligodendrogliomas, 7 oligoastrocytomas, and 5 astrocytomas.
  • CONCLUSIONS: Quantitative methylation-specific PCR of the MGMT promoter correlates with radiological response to chemotherapy with temozolomide in WHO grade II gliomas.

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  • (PMID = 27964685.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Herndon J 2nd, Vredenburgh J, Reardon D, Desjardins A, Peters K, Gururangan S, Norfleet J, Friedman A, Bigner D, Friedman HS: Phase I trial of vendetanib and oral etoposide for recurrent malignant gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13016

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial of vendetanib and oral etoposide for recurrent malignant gliomas.
  • : e13016 Background: Recurrent malignant gliomas have a poor prognosis, with a median survival of 6-15 months, with grade 4 glioblastomas more aggressive than grade 3 anaplastic astrocytomas or oligodendrogliomas.
  • Vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF) are critically important in glioma biology.
  • We report a phase I trial of vandetanib in combination with oral etoposide for recurrent malignant glioma.
  • METHODS: Patients with histologically documented recurrent grade 3 or grade 4 malignant glioma were eligible.

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  • (PMID = 27962830.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Merrell RT, Lachance DH, Anderson SK: Seizures in patients with glioma treated with phenytoin and levetiracetam. J Clin Oncol; 2009 May 20;27(15_suppl):e13020

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Seizures in patients with glioma treated with phenytoin and levetiracetam.
  • : e13020 Background: Seizures are common in patients with glioma.
  • We compare seizure outcomes and side effects in patients with glioma treated with phenytoin and levetiracetam monotherapy.
  • METHODS: Retrospective analysis of consecutive patients with glioma.
  • RESULTS: 76 patients (34 female) with pathologically proven glioma and seizures were identified, 25 treated with phenytoin and 51 with levetiracetam.
  • 64% had grade 4 astrocytoma.
  • When adjusting for age, gender, type of seizure, type of glioma, and dosage using univariate and multivariate models there were no differences between the treatment groups and none of these covariates were statistically significant for explaining the second seizure rates between treatment groups (all p values >0.05).
  • CONCLUSIONS: In this study, glioma patients treated with levetiracetam had similar seizure control as patients treated with phenytoin.
  • Levetiracetam is a safe, effective, and preferred alternative for seizure management in patients with glioma.

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  • (PMID = 27962817.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Rudnick JD, Phuphanich S, Chu R, Mazer M, Wang H, Serrano N, Francisco M, Black KL, Wheeler C, Yu J: A phase I trial of surgical resection with biodegradable carmustine (BCNU) wafer placement followed by vaccination with dendritic cells pulsed with tumor lysate for patients with malignant glioma. J Clin Oncol; 2009 May 20;27(15_suppl):2033

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  • [Title] A phase I trial of surgical resection with biodegradable carmustine (BCNU) wafer placement followed by vaccination with dendritic cells pulsed with tumor lysate for patients with malignant glioma.
  • : 2033 Background: Our prior immunotherapy trials demonstrated efficacy in generating a tumor specific immune response in malignant glioma and the potential for high tumor-specific toxicity and sustained tumoricidal activity.
  • METHODS: We exploited this synergistic effect to maintain a cytotoxic environment around the tumor milieu.
  • Patients with high-grade glioma were eligible after maximal resection with biodegradable carmustine (BCNU) wafer placement.
  • Screening leukapheresis is used to isolate mononuclear cells which are differentiated into dendritic cells, pulsed with tumor lysate, and then 3 intradermal vaccines are administered at 2-week intervals.
  • The histology included 3 newly diagnosed glioblastoma multiforme (GBM), 8 recurrent GBM, 2 newly diagnosed anaplastic astrocytoma (AA), and 2 recurrent AA.
  • A stable disease interval of 13 to 90 weeks was observed for patients who received vaccine.
  • The 3 newly diagnosed GBM patients have stable disease (18 to 71 weeks).

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  • (PMID = 27964627.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Potthast L, Chowdhary S, Pan E, Yu D, Zhu W, Brem S: The infiltrative, diffuse pattern of recurrence in patients with malignant gliomas treated with bevacizumab. J Clin Oncol; 2009 May 20;27(15_suppl):2057

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The infiltrative, diffuse pattern of recurrence in patients with malignant gliomas treated with bevacizumab.
  • : 2057 Background: There is no standard of care for recurrent gliomas; however, bevacizumab is often used as a salvage chemotherapy regimen.
  • A diffuse, infiltrative pattern of recurrence, as evidenced by MR imaging, was seen manifesting as multifocal disease or presumed CSF dissemination with subependymal spread.
  • METHODS: We conducted a retrospective analysis of 40 recurrent glioma patients followed at Moffitt Cancer Center from September 2006 through December 2008 treated with bevacizumab alone or in combination with irinotecan.
  • Histologies included glioblastoma (GB), anaplastic astrocytomas (AA), anaplastic oligodendrogliomas (AO), anaplastic oligoastrocytomas (AOA), and low-grade astrocytomas.
  • CONCLUSIONS: There appears to be an increase in a diffuse, infiltrative pattern of recurrence among recurrent glioma patients treated with bevacizumab as a salvage regimen.
  • It is unclear why the disparity among this subset of patients occurs, however, we hypothesize that this may once again highlight the distinct tumor biology among young glioma patients.
  • The impact of this observation on clinical decision making on whether to utilize bevacizumab in young recurrent glioma patients warrants further investigation.

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  • (PMID = 27964663.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Korkolopoulou P, Perdiki M, Thymara I, Boviatsis E, Agrogiannis G, Kotsiakis X, Angelidakis D, Rologis D, Diamantopoulou K, Thomas-Tsagli E, Kaklamanis L, Gatter K, Patsouris E: Expression of hypoxia-related tissue factors in astrocytic gliomas. A multivariate survival study with emphasis upon carbonic anhydrase IX. Hum Pathol; 2007 Apr;38(4):629-38

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of hypoxia-related tissue factors in astrocytic gliomas. A multivariate survival study with emphasis upon carbonic anhydrase IX.
  • In the present study, we examined the expression of this enzyme in diffuse gliomas of astrocytic origin in relation to vascular endothelial growth factor (VEGF) and HIF-1alpha expression, proliferation rate (as assessed with Ki-67 antigen), microvessel morphology, and survival.
  • We conclude that CAIX may be used as a prognostic indicator in diffuse astrocytomas to refine the information provided by grade.
  • Given the role of CAIX in the acidification of tumor environment and its up-regulation by hypoxia, it is thought that CAIX expression may be linked to resistance of tumor cells to radiotherapy by allowing them to acclimatize to a hypoxic and acidic microenvironment.
  • [MeSH-major] Antigens, Neoplasm / biosynthesis. Astrocytoma / metabolism. Astrocytoma / pathology. Carbonic Anhydrases / biosynthesis

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  • (PMID = 17367605.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Ki-67 Antigen; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
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27. Katsetos CD, Reddy G, Dráberová E, Smejkalová B, Del Valle L, Ashraf Q, Tadevosyan A, Yelin K, Maraziotis T, Mishra OP, Mörk S, Legido A, Nissanov J, Baas PW, de Chadarévian JP, Dráber P: Altered cellular distribution and subcellular sorting of gamma-tubulin in diffuse astrocytic gliomas and human glioblastoma cell lines. J Neuropathol Exp Neurol; 2006 May;65(5):465-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Altered cellular distribution and subcellular sorting of gamma-tubulin in diffuse astrocytic gliomas and human glioblastoma cell lines.
  • Centrosome amplification is a pivotal mechanism underlying tumorigenesis but its role in gliomas is underinvestigated.
  • The present study specifically examines the expression and distribution of the centrosome-associated cytoskeletal protein gamma-tubulin in 56 primary diffuse astrocytic gliomas (grades II-IV) and in 4 human glioblastoma cell lines (U87MG, U118MG, U138MG, and T98G).
  • In tumors in adults (n = 46), varying degrees of localization were detected in all tumor grades, but immunoreactivity was significantly increased in high-grade anaplastic astrocytomas and glioblastomas multiforme as compared to low-grade diffuse astrocytomas (p = 0.0001).
  • A similar trend was noted in diffuse gliomas in children but the sample of cases was too small as to be statistically meaningful.
  • Our results indicate that overexpression and ectopic cellular distribution of gamma-tubulin in astrocytic gliomas may be significant in the context of centrosome protein amplification and may be linked to tumor progression and anaplastic potential.
  • [MeSH-minor] Antigens / metabolism. Blotting, Northern / methods. Cell Line, Tumor. Humans. Immunohistochemistry / methods

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  • (PMID = 16772870.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens; 0 / Tubulin; 0 / pericentrin
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28. Dong L, Pu PY, Wang H, Wang GX, Kang CS, Jiao DR: [Study on the expression of epidermal growth factor receptor and p53 in astrocytic gliomas: evidence for a distinct genetic pathway]. Zhonghua Bing Li Xue Za Zhi; 2006 Apr;35(4):232-6
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  • [Title] [Study on the expression of epidermal growth factor receptor and p53 in astrocytic gliomas: evidence for a distinct genetic pathway].
  • OBJECTIVE: To study further the most important and frequent genetic alterations of p53 and epidermal growth factor receptor (EGFR) in astrocytic gliomas. METHODS:.
  • (1) EGFR expression was examined in samples collected from 37 astrocytic gliomas and 6 normal brain tissue using reverse transcriptase polymerase chain reaction and immunohistochemical staining. (2) p53 gene mutation and accumulation were detected simultaneously in the same specimens using PCR-SSCP, DNA sequencing and immunohistochemical staining.
  • RESULTS: The frequency of p53 mutation in diffuse astrocytomas, anaplastic astrocytomas, primary glioblastomas and secondary glioblastomas was 1/10, 4/19 (21.1%), 4/6 and 2/2, respectively and the frequency of EGFR overexpression was 5/10, 10/19 (52.6%), 5/6 and 2/2, respectively.
  • Both p53 accumulation and EGFR overexpression increased accompanied by a successive increase of degree of the glioma malignancy.
  • CONCLUSIONS: EGFR overexpression is not infrequently seen, however, p53 mutation is rarely seen in the low grade gliomas.
  • Consequently, EGFR overexpression and p53 gene mutation are not mutually exclusive in astrocytic gliomagenesis but synergistically to promote the glioma progression.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Receptor, Epidermal Growth Factor / genetics. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 16776982.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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29. Elsir T, Eriksson A, Orrego A, Lindström MS, Nistér M: Expression of PROX1 Is a common feature of high-grade malignant astrocytic gliomas. J Neuropathol Exp Neurol; 2010 Feb;69(2):129-38
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  • [Title] Expression of PROX1 Is a common feature of high-grade malignant astrocytic gliomas.
  • PROX1 is a prospero-related transcription factor that plays a critical role in the development of various organs including the mammalian lymphatic and central nervous systems; it controls cell proliferation and differentiation through different transcription pathwaysand has both oncogenic and tumor-suppressive functions.
  • We investigated PROX1 expression patterns in 56 human astrocytic gliomas of different grades using immunohistochemistry.
  • An average of 79% of cells in World Health Organization Grade IV (glioblastoma, n = 15) and 57% of cells in World Health Organization Grade III (anaplastic astrocytoma, n = 13) were strongly PROX1 positive; low-grade diffuse astrocytomas (Grade II, n = 13) had 21% of cells that were strongly positive; Grade I tumors (n = 15) had 1.5%; and non-neoplastic brain tissue (n = 15) had 3.7% of cells that were PROX1 positive.
  • Analyses of coexpression with proliferation markers suggest that PROX1+ cells have a marginally lower rate of proliferation than other tumor cells but are still mitotically active.
  • We conclude that PROX1 may constitute a useful tool for the diagnosis and grading ofastrocytic gliomas and for distinguishing Grade III and Grade IV tumors from Grade I and Grade II tumors.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Homeodomain Proteins / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Antigens, Nuclear / metabolism. Biomarkers / metabolism. Brain Diseases / metabolism. Cell Proliferation. Humans. Immunohistochemistry. Microtubule-Associated Proteins / metabolism. Microvessels / metabolism. Mitosis. Nerve Tissue Proteins / metabolism. Tubulin / metabolism

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  • (PMID = 20084020.001).
  • [ISSN] 1554-6578
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Biomarkers; 0 / Homeodomain Proteins; 0 / MAP2 protein, human; 0 / Microtubule-Associated Proteins; 0 / Nerve Tissue Proteins; 0 / Tubulin; 0 / Tumor Suppressor Proteins; 0 / neuronal nuclear antigen NeuN, human; 0 / prospero-related homeobox 1 protein
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30. Aguilar Moliner I, Costa Orvay JA, Juma K, Costa Clara JM, Cruz Martínez O, Pou Fernández J: [Optic pathway astrocytoma: an unusual cause of failure to thrive in infants]. An Pediatr (Barc); 2007 Jun;66(6):622-4
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  • [Title] [Optic pathway astrocytoma: an unusual cause of failure to thrive in infants].
  • [Transliterated title] Astrocitoma de vías ópticas: una causa infrecuente de retraso ponderal en el lactante.
  • We report a case of low-grade astrocytoma of the optic pathway in a 2-month-old child whose main symptoms at diagnosis were failure to thrive and anorexia.
  • Unfortunately, despite therapeutic efforts, the tumor showed local and metastatic progression refractory to chemotherapy.
  • [MeSH-major] Brain Neoplasms / diagnosis. Failure to Thrive / etiology. Optic Nerve Glioma / diagnosis

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  • (PMID = 17583627.001).
  • [ISSN] 1695-4033
  • [Journal-full-title] Anales de pediatría (Barcelona, Spain : 2003)
  • [ISO-abbreviation] An Pediatr (Barc)
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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31. Pareés I, Alonso J, Rovira A, Martínez E, Montalban X: [Diffuse astrocytoma presenting as an optic-spinal syndrome]. Rev Neurol; 2009 Apr 1-15;48(7):354-6
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  • [Title] [Diffuse astrocytoma presenting as an optic-spinal syndrome].
  • [Transliterated title] Síndrome opticomedular como forma de presentación de un astrocitoma difuso.
  • INTRODUCTION: Spinal cord involvement is a rare presentation of grade II astrocytomas.
  • Nevertheless, differentiation from inflammatory demyelinating diseases of the central nervous system can be challenging in some clinical situations.
  • A patient with an optic-spinal syndrome due to a fibrillary astrocytoma is described.
  • CASE REPORT: A 32 years-old man was admitted to the hospital because of a subacute spinal cord syndrome.
  • A new MRI with spectroscopy revealed an infiltrative lesion involving the right frontal lobe, optic chiasm, internal capsule, brainstem and cervical spinal cord, which was suggestive of low-grade astrocytoma.
  • Brain biopsy confirmed the diagnosis of diffuse fibrillary astrocytoma.
  • Brain biopsy is often necessary for a definite diagnosis.
  • [MeSH-major] Astrocytoma. Demyelinating Diseases. Optic Neuritis. Spinal Cord / pathology

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  • (PMID = 19319816.001).
  • [ISSN] 1576-6578
  • [Journal-full-title] Revista de neurologia
  • [ISO-abbreviation] Rev Neurol
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Oligoclonal Bands
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32. 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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33. Furnari FB, Fenton T, Bachoo RM, Mukasa A, Stommel JM, Stegh A, Hahn WC, Ligon KL, Louis DN, Brennan C, Chin L, DePinho RA, Cavenee WK: Malignant astrocytic glioma: genetics, biology, and paths to treatment. Genes Dev; 2007 Nov 1;21(21):2683-710
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Malignant astrocytic glioma: genetics, biology, and paths to treatment.
  • Malignant astrocytic gliomas such as glioblastoma are the most common and lethal intracranial tumors.
  • This progress is fueling new opportunities for understanding the fundamental basis for development of this devastating disease and also novel therapies that, for the first time, portend meaningful clinical responses.
  • [MeSH-major] Astrocytoma / genetics. Astrocytoma / pathology. Astrocytoma / therapy. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Brain Neoplasms / therapy
  • [MeSH-minor] Animals. Animals, Genetically Modified. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease Models, Animal. Gene Regulatory Networks. Humans. Models, Biological. Necrosis / chemically induced. Neoplasm Invasiveness. Neoplasm Staging. Neovascularization, Pathologic / drug therapy

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  • (PMID = 17974913.001).
  • [ISSN] 0890-9369
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA099041; United States / NCI NIH HHS / CA / CA95616
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 306
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34. Perdiki M, Korkolopoulou P, Thymara I, Agrogiannis G, Piperi C, Boviatsis E, Kotsiakis X, Angelidakis D, Diamantopoulou K, Thomas-Tsagli E, Patsouris E: Cyclooxygenase-2 expression in astrocytomas. Relationship with microvascular parameters, angiogenic factors expression and survival. Mol Cell Biochem; 2007 Jan;295(1-2):75-83

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyclooxygenase-2 expression in astrocytomas. Relationship with microvascular parameters, angiogenic factors expression and survival.
  • The role of the up-regulation of COX-2 in the formation and progression of gliomas has been dealt with in earlier reports, which describe increased levels of PGs within gliomas.
  • In the present study, we examined the expression of COX-2 in diffuse gliomas of astrocytic origin in relation to microvascular parameters, angiogenic factors and survival.
  • MATERIALS AND METHODS: A total of 83 cases of diffuse astrocytomas (grade II-IV) were analyzed by immunohistochemistry for the presence of COX-2.
  • CONCLUSION: These results implicate COX-2 in the angiogenesis and biological aggressiveness of diffuse astrocytomas, and suggest that it would be worthwhile to examine how the inhibition of COX-2 expression may influence astrocytoma patients' survival.
  • [MeSH-major] Angiogenesis Inducing Agents / metabolism. Astrocytoma / blood supply. Astrocytoma / enzymology. Cyclooxygenase 2 / metabolism. Glioma / blood supply. Glioma / enzymology. Membrane Proteins / metabolism

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  • (PMID = 16868662.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inducing Agents; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Ki-67 Antigen; 0 / Membrane Proteins; 0 / Vascular Endothelial Growth Factor A; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
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35. van den Boom J, Wolter M, Blaschke B, Knobbe CB, Reifenberger G: Identification of novel genes associated with astrocytoma progression using suppression subtractive hybridization and real-time reverse transcription-polymerase chain reaction. Int J Cancer; 2006 Nov 15;119(10):2330-8
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  • [Title] Identification of novel genes associated with astrocytoma progression using suppression subtractive hybridization and real-time reverse transcription-polymerase chain reaction.
  • To identify novel genes involved in glioma progression we performed suppression subtractive hybridization combined with cDNA array analysis on 4 patients with primary low-grade gliomas of World Health Organization (WHO) grade II that recurred as secondary glioblastomas (WHO grade IV).
  • Eight genes showing differential expression between primary and recurrent tumors in 3 of the 4 patients were selected for further analysis using real-time reverse transcription-PCR on a series of 10 pairs of primary low-grade and recurrent high-grade gliomas as well as 42 astrocytic gliomas of different WHO grades.
  • These analyses revealed that 5 genes, i.e., AMOG (ATP1B2, 17p13.1), APOD (3q26.2-qter), DMXL1 (5q23.1) DRR1 (TU3A, 3p14.2) and PSD3 (KIAA09428/HCA67/EFA6R, 8p22), were expressed at significantly lower levels in secondary glioblastomas as compared to diffuse astrocytomas of WHO grade II.
  • In addition, AMOG, DRR1 and PSD3 transcript levels were significantly lower in primary glioblastomas than in diffuse astrocytomas.
  • Treatment of glioma cell lines with 5-aza-2'-deoxycytidine and trichostatin A resulted in increased expression of AMOG and APOD transcripts.
  • Sequencing of sodium bisulfite-modified DNA demonstrated AMOG promoter hypermethylation in the glioma cell lines and 1 primary anaplastic astrocytoma with low AMOG expression.
  • Taken together, we identified interesting novel candidate genes that likely contribute to glioma progression and provide first evidence for a role of epigenetic silencing of AMOG in malignant glioma cells.
  • [MeSH-major] Adenosine Triphosphatases / genetics. Astrocytoma / genetics. Brain Neoplasms / genetics. Cation Transport Proteins / genetics. Cell Adhesion Molecules, Neuronal / genetics. Gene Silencing. Nucleic Acid Hybridization. Reverse Transcriptase Polymerase Chain Reaction
  • [MeSH-minor] Antimetabolites, Antineoplastic / pharmacology. Apolipoproteins / genetics. Apolipoproteins D. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Biomarkers, Tumor / genetics. DNA Methylation. Disease Progression. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Glycoproteins / genetics. Histone Deacetylases / genetics. Humans. Hydroxamic Acids / pharmacology. Membrane Transport Proteins / genetics. Nerve Tissue Proteins / genetics. Nuclear Proteins / genetics. Oligonucleotide Array Sequence Analysis. Protein Synthesis Inhibitors / pharmacology. Proteins / genetics

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  • (PMID = 16865689.001).
  • [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 / APOD protein, human; 0 / ATP1B2 protein, human; 0 / Antimetabolites, Antineoplastic; 0 / Apolipoproteins; 0 / Apolipoproteins D; 0 / Biomarkers, Tumor; 0 / Cation Transport Proteins; 0 / Cell Adhesion Molecules, Neuronal; 0 / DMXL1 protein, human; 0 / FAM107A protein, human; 0 / Glycoproteins; 0 / Hydroxamic Acids; 0 / Membrane Transport Proteins; 0 / Nerve Tissue Proteins; 0 / Nuclear Proteins; 0 / PSD protein, human; 0 / Protein Synthesis Inhibitors; 0 / Proteins; 3X2S926L3Z / trichostatin A; 776B62CQ27 / decitabine; EC 3.5.1.98 / Histone Deacetylases; EC 3.5.1.98 / histone deacetylase 3; EC 3.6.1.- / Adenosine Triphosphatases; M801H13NRU / Azacitidine
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36. Xu P, Qiu M, Zhang Z, Kang C, Jiang R, Jia Z, Wang G, Jiang H, Pu P: The oncogenic roles of Notch1 in astrocytic gliomas in vitro and in vivo. J Neurooncol; 2010 Mar;97(1):41-51
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  • [Title] The oncogenic roles of Notch1 in astrocytic gliomas in vitro and in vivo.
  • Deregulation of Notch signaling has been implicated in some genetic diseases and tumorigenesis.
  • The function of Notch signaling in a variety of tumors can be either oncogenic or tumor-suppressive, depending on the cellular context.
  • In this study, Notch1 overexpression was observed in the majority of 45 astrocytic gliomas with different grades and in U251MG glioma cells.
  • Meanwhile, tumor growth was delayed in established subcutaneous gliomas in nude mice treated with Notch1 siRNA in vivo.
  • These results suggest that Notch1 plays an important oncogenic role in the development and progression of astrocytic gliomas.
  • [MeSH-major] Astrocytoma / genetics. Gene Expression Regulation, Neoplastic / physiology. Receptor, Notch1 / genetics
  • [MeSH-minor] Animals. Annexin A5 / metabolism. Apoptosis / drug effects. Apoptosis / physiology. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin D1 / metabolism. Disease Models, Animal. Flow Cytometry / methods. Humans. In Situ Nick-End Labeling / methods. Matrix Metalloproteinase 9 / metabolism. Mice. Oncogene Protein v-akt / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proliferating Cell Nuclear Antigen / metabolism. Proto-Oncogene Proteins p21(ras) / metabolism. RNA, Small Interfering / pharmacology. RNA, Small Interfering / therapeutic use. Receptor, Epidermal Growth Factor / metabolism. Signal Transduction / drug effects. Signal Transduction / genetics. Transfection / methods

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  • (PMID = 19771395.001).
  • [ISSN] 1573-7373
  • [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 / Annexin A5; 0 / Proliferating Cell Nuclear Antigen; 0 / RNA, Small Interfering; 0 / Receptor, Notch1; 136601-57-5 / Cyclin D1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Oncogene Protein v-akt; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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37. Freitas MR, de Muzio SD, Pessoa RC, Stávale JN, Borges LR, Malheiros SM: [Diffuse bone marrow metastasis in cerebellar high-grade astrocytoma. A case report]. Rev Neurol; 2009 Mar 1-15;48(5):242-4
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  • [Title] [Diffuse bone marrow metastasis in cerebellar high-grade astrocytoma. A case report].
  • [Transliterated title] Metastasis difusa de la medula osea en un astrocitoma cerebeloso de alto grado. Un caso clinico.
  • INTRODUCTION: Cerebellar high-grade astrocytoma is uncommon.
  • Although more prone to present cerebrospinal fluid dissemination, the cerebellar location is not particularly related to the occurrence of extra-cranial metastases, which are also unusual in supratentorial malignant gliomas.
  • CASE REPORT: A 46 year-old man with cerebellar anaplastic astrocytoma who developed pancytopenia due to extensive bone marrow metastases.
  • CONCLUSION: Extraneural metastases of brain gliomas are rare and the spread to the bone marrow confers an extremely poor prognosis for these patients.
  • The expected improvement in glioma patients' survival due to the combination of more efficient therapies may lead to an increased incidence of this uncommon presentation, justifying a more rigorous follow-up of systemic manifestations.
  • [MeSH-major] Astrocytoma / pathology. Bone Marrow Neoplasms / secondary. Cerebellar Neoplasms / pathology

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  • (PMID = 19263392.001).
  • [ISSN] 1576-6578
  • [Journal-full-title] Revista de neurologia
  • [ISO-abbreviation] Rev Neurol
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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38. Fisher PG, Tihan T, Goldthwaite PT, Wharam MD, Carson BS, Weingart JD, Repka MX, Cohen KJ, Burger PC: Outcome analysis of childhood low-grade astrocytomas. Pediatr Blood Cancer; 2008 Aug;51(2):245-50
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  • [Title] Outcome analysis of childhood low-grade astrocytomas.
  • BACKGROUND: We aimed to determine the long-term natural history of low-grade astrocytomas (LGA) in children, with respect to pathology, and to evaluate influence of treatment on survival.
  • RESULTS: Two hundred seventy-eight children (160 males; mean age 9.1 years; tumor location: 77 cerebrum, 62 cerebellum, 51 hypothalamic, 30 thalamus, 9 ventricle, 40 brainstem, and 9 spine) were assessed.
  • Among 246 specimens reviewed, diagnoses were 135 pilocytic astrocytoma (PA), 27 diffuse astrocytoma (DA), 75 unclassifiable well-differentiated astrocytoma (NOS), and 9 subependymal giant cell astrocytoma.
  • Reviewed diagnoses were highly associated with OS (P < 0.0001), with 5-year OS for PA 96%, DA 48%, and NOS 86%; these differences remained significant when stratified by location or extent of resection.
  • Among patients with residual tumor after surgery, 5-year PFS was 48% with observation alone (n = 114), no different (P = 0.32) from that achieved with immediate irradiation (n = 86).
  • While tumor location and resection extent affect outcome, pathologic diagnosis when carefully interpreted significantly influences long-term survival.
  • [MeSH-major] Astrocytoma / mortality. Brain Neoplasms / mortality

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  • (PMID = 18386785.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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39. Haapasalo J, Hilvo M, Nordfors K, Haapasalo H, Parkkila S, Hyrskyluoto A, Rantala I, Waheed A, Sly WS, Pastorekova S, Pastorek J, Parkkila AK: Identification of an alternatively spliced isoform of carbonic anhydrase XII in diffusely infiltrating astrocytic gliomas. Neuro Oncol; 2008 Apr;10(2):131-8
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  • [Title] Identification of an alternatively spliced isoform of carbonic anhydrase XII in diffusely infiltrating astrocytic gliomas.
  • CA XII has been proposed to be involved in acidification of the extracellular milieu, creating an appropriate microenvironment for rapid tumor growth.
  • Because RNA sequence databases have indicated that two isoforms of CA XII might exist in human tissues, and because alternatively spliced protein forms have been linked to aggressive behavior of cancer cells, we designed a study to evaluate the presence of the two forms of CA XII in diffuse astrocytomas, a tumor type known for its aggressive and often noncurable behavior.
  • Reverse transcription PCR of tumor samples surprisingly revealed that CA XII present in diffuse astrocytomas is mainly encoded by a shorter mRNA variant.
  • We further showed by Western blotting that anti-CA XII antibody recognized both isoforms in the glioblastoma cell lines, and we then evaluated the expression of CA XII in astrocytomas using immunohistochemistry and correlated the results with various clinicopathological and molecular factors.
  • Of 370 diffusely infiltrating astrocytomas, 363 cases (98%) showed immunoreactions for CA XII.
  • From these results, we conclude that CA XII is commonly expressed in diffuse astrocytomas and that it might be used as a biomarker of poor prognosis.
  • The absence of 11 amino acids in the shorter isoform, which seems to be common in astrocytomas, may affect the normal quaternary structure and biological function of CA XII.
  • [MeSH-major] Astrocytoma / enzymology. Biomarkers, Tumor / analysis. Brain Neoplasms / enzymology. Carbonic Anhydrases / genetics. Carbonic Anhydrases / metabolism

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  • (PMID = 18322268.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Isoenzymes; EC 4.2.1.1 / CA13 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
  • [Other-IDs] NLM/ PMC2613815
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40. Hartmann C, Hentschel B, Wick W, Capper D, Felsberg J, Simon M, Westphal M, Schackert G, Meyermann R, Pietsch T, Reifenberger G, Weller M, Loeffler M, von Deimling A: Patients with IDH1 wild type anaplastic astrocytomas exhibit worse prognosis than IDH1-mutated glioblastomas, and IDH1 mutation status accounts for the unfavorable prognostic effect of higher age: implications for classification of gliomas. Acta Neuropathol; 2010 Dec;120(6):707-18
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  • [Title] Patients with IDH1 wild type anaplastic astrocytomas exhibit worse prognosis than IDH1-mutated glioblastomas, and IDH1 mutation status accounts for the unfavorable prognostic effect of higher age: implications for classification of gliomas.
  • WHO grading of human brain tumors extends beyond a strictly histological grading system by providing a basis predictive for the clinical behavior of the respective neoplasm.
  • For example, patients with glioblastoma WHO grade IV usually show a less favorable clinical course and receive more aggressive first-line treatment than patients with anaplastic astrocytoma WHO grade III.
  • Here we provide evidence that the IDH1 status is more prognostic for overall survival than standard histological criteria that differentiate high-grade astrocytomas.
  • We sequenced the isocitrate dehydrogenase 1 gene (IDH1) at codon 132 in 382 patients with anaplastic astrocytoma and glioblastoma from the NOA-04 trial and from a prospective translational cohort study of the German Glioma Network.
  • Patients with anaplastic astrocytomas carried IDH1 mutations in 60%, and patients with glioblastomas in 7.2%.
  • The sequence from more favorable to poorer outcome was (1) anaplastic astrocytoma with IDH1 mutation, (2) glioblastoma with IDH1 mutation, (3) anaplastic astrocytoma without IDH1 mutation and (4) glioblastoma without IDH1 mutation (p < 0.0001).
  • In this combined set of anaplastic astrocytomas and glioblastomas both, IDH1 mutation and IDH1 expression status were of greater prognostic relevance than histological diagnosis according to the current WHO classification system.
  • We propose to complement the current WHO classification and grading of high-grade astrocytic gliomas by the IDH1 mutation status and to use this combined histological and molecular classification in future clinical trials.
  • [MeSH-major] Brain Neoplasms / genetics. Glioblastoma / genetics. Glioma / classification. Glioma / genetics. Isocitrate Dehydrogenase / genetics. Mutation / genetics
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Astrocytoma / diagnosis. Astrocytoma / genetics. Astrocytoma / pathology. Cohort Studies. Female. Humans. Male. Middle Aged. Prognosis. Prospective Studies. Young Adult


41. Hlobilkova A, Ehrmann J, Sedlakova E, Krejci V, Knizetova P, Fiuraskova M, Kala M, Kalita O, Kolar Z: Could changes in the regulation of the PI3K/PKB/Akt signaling pathway and cell cycle be involved in astrocytic tumor pathogenesis and progression? Neoplasma; 2007;54(4):334-41
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  • [Title] Could changes in the regulation of the PI3K/PKB/Akt signaling pathway and cell cycle be involved in astrocytic tumor pathogenesis and progression?
  • The most frequent alterations found in astrocytomas are two major groups of signaling proteins: the cell cycle and the growth factor-regulated signaling pathways.
  • The aim of our study was to detect changes in expression of the following proteins: the tumor suppressors PTEN, p53, and p21Waf1/Cip1, glial fibrillary acidic protein (GFAP, as a marker of astroglial differentiation), the phosphorylated form of protein kinase B/Akt (PKB/Akt), which is downstream to the epidermal growth factor receptor (EGFR), and MDM2, which degrades p53.
  • Paraffin-embedded astrocytoma tissue samples from 89 patients were divided into low grade (grade I-II; 42 samples) and high grade astrocytomas (grade III-IV; 47 samples).
  • EGFR protein was detected in 29 % of low grade and in 60 % of high grade astrocytomas.
  • The expression of phosphorylated PKB/Akt was found in roughly the same proportions: in 86% of low grade and in 79% of high grade astrocytomas.
  • PTEN was not found in most of astrocytomas, 64% of low grade and 74% of high grade tumors showed no PTEN staining.
  • Overexpression of the mutated form of p53 or loss of p53 expression, however, was found in about 63% in both groups of astrocytomas with no differences between them.
  • GFAP expression was decreased in tumor astrocytes compared to normal astrocytes and this decreased with grading.
  • GFAP positive tumor cells were detected in only 50% of low grade, and 32% of high grade astrocytomas.
  • We conclude that EGFR expression increases with astrocytoma grading.
  • PTEN defects may also participate in aggressive tumor behaviour through activation of the PKB/Akt pathway.
  • The alteration of p53 supports the finding that the cell cycle regulation is also disrupted during development of astrocytomas.
  • EGFR is one of the factors, which drives the progression of astrocytomas from low to high grade stage.
  • [MeSH-major] Astrocytoma / metabolism. Cell Cycle. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Disease Progression. Female. Gene Expression Regulation, Neoplastic. Glial Fibrillary Acidic Protein / metabolism. Humans. Male. Middle Aged. Mutation / genetics. Oligodendroglioma / metabolism. Oligodendroglioma / pathology. PTEN Phosphohydrolase / metabolism. Phosphorylation. Proto-Oncogene Proteins c-mdm2 / metabolism. Receptor, Epidermal Growth Factor / metabolism. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 17822324.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Glial Fibrillary Acidic Protein; 0 / Tumor Suppressor Protein p53; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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42. O'Callaghan FJ, Martyn CN, Renowden S, Noakes M, Presdee D, Osborne JP: Subependymal nodules, giant cell astrocytomas and the tuberous sclerosis complex: a population-based study. Arch Dis Child; 2008 Sep;93(9):751-4
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  • [Title] Subependymal nodules, giant cell astrocytomas and the tuberous sclerosis complex: a population-based study.
  • OBJECTIVES:. (1) In a population-based study of tuberous sclerosis (TSC), to identify the number of patients presenting with symptomatic giant cell astrocytomas (GCAs);.
  • A subset were invited to have a cranial MRI if they did not have a history of a symptomatic GCA and if they were likely to tolerate cranial imaging without a general anaesthetic.
  • Ten of these had a history of treatment for a symptomatic GCA.
  • This finding leads us to recommend that screening should not be undertaken.
  • [MeSH-major] Astrocytoma / epidemiology. Brain Neoplasms / epidemiology. Tuberous Sclerosis / epidemiology
  • [MeSH-minor] Adolescent. Adult. Child. Cross-Sectional Studies. Female. Humans. Intracranial Hypertension / etiology. Intracranial Hypertension / surgery. Magnetic Resonance Imaging. Male. Mental Disorders / etiology. Tomography, X-Ray Computed. Tumor Suppressor Proteins / metabolism

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  • [CommentIn] Arch Dis Child. 2009 Jan;94(1):75-6 [19103791.001]
  • (PMID = 18456692.001).
  • [ISSN] 1468-2044
  • [Journal-full-title] Archives of disease in childhood
  • [ISO-abbreviation] Arch. Dis. Child.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Suppressor Proteins
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43. Landriscina M, Schinzari G, Di Leonardo G, Quirino M, Cassano A, D'Argento E, Lauriola L, Scerrati M, Prudovsky I, Barone C: S100A13, a new marker of angiogenesis in human astrocytic gliomas. J Neurooncol; 2006 Dec;80(3):251-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] S100A13, a new marker of angiogenesis in human astrocytic gliomas.
  • Indeed, S100A13 is a copper binding protein able to enhance the export of FGF1 in response to stress in vitro and to induce the formation of a multiprotein aggregate responsible for FGF1 release.
  • We investigated the expression of S100A13 in human astrocytic gliomas in relation to tumour grading and vascularization.
  • A series of 26 astrocytic gliomas was studied to evaluate microvessel density and to assess FGF1, S100A13 and VEGF-A expression.
  • FGF1 was equally expressed in the vast majority of tumours, whereas S100A13 and VEGF-A were significantly up-regulated in high-grade vascularized gliomas.
  • These data suggest that the up-regulation of S100A13 and VEGF-A expression correlates with the activation of angiogenesis in high-grade human astrocytic gliomas.
  • [MeSH-major] Astrocytoma / blood supply. Biomarkers, Tumor / metabolism. Brain Neoplasms / blood supply. Neovascularization, Pathologic / metabolism. S100 Proteins / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16773219.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL32348; United States / NHLBI NIH HHS / HL / HL35627; United States / NCRR NIH HHS / RR / RR1555
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / S100 Proteins; 0 / S100A13 protein, human; 0 / Vascular Endothelial Growth Factor A; 62031-54-3 / Fibroblast Growth Factors
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44. Giannopoulou E, Ravazoula P, Kalofonos H, Makatsoris T, Kardamakis D: Expression of HIF-1alpha and iNOS in astrocytic gliomas: a clinicopathological study. In Vivo; 2006 May-Jun;20(3):421-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of HIF-1alpha and iNOS in astrocytic gliomas: a clinicopathological study.
  • BACKGROUND: Hypoxia-inducible-factor-1 (HIF-1) is present at high levels in human tumors and plays a crucial role in tumor promotion by up-regulating several target genes.
  • PATIENTS AND METHODS: Sixty-three human astrocytic gliomas were analyzed by immunohistochemistry for HIF-1alpha and iNOS using formalin-fixed paraffin-embedded material.
  • RESULTS: HIF-1alpha was detected only in astrocytic gliomas grades III and IV, both in the nucleus and in the cytoplasm.
  • The iNOS expression was increased in astrocytic gliomas grades I, II and III and was statistically significantly decreased in astrocytic gliomas grade IV. iNOS was localized round the capillary vessels as well.
  • CONCLUSION: We believe that HIF-1alpha and iNOS expressions merit further investigations in order to understand the biology of astrocytic gliomas.
  • [MeSH-major] Astrocytoma / enzymology. Astrocytoma / metabolism. Biomarkers, Tumor / analysis. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Nitric Oxide Synthase Type II / biosynthesis

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  • (PMID = 16724682.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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45. Martins DC, Malheiros SM, Santiago LH, Stávale JN: Gemistocytes in astrocytomas: are they a significant prognostic factor? J Neurooncol; 2006 Oct;80(1):49-55
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  • [Title] Gemistocytes in astrocytomas: are they a significant prognostic factor?
  • Our aim was to retrospectively evaluate the influence of gemistocytic astrocytes, cellular proliferation indices, immunoexpression of proteins p53 and bcl-2 in the clinical outcome of 39 patients with WHO grade II and III astrocytomas with the presence of gemistocytes.
  • Out of 24 who presented clinical and neuroimaging worsening, characterized as tumor progression or recurrence, 16 had histological confirmation and were also analyzed.
  • Our finding confirms recent reports that question the role of gemistocytes as a prognostic factor in diffuse astrocytomas.
  • The significance and role of gemistocytes in astrocytomas has yet to be defined and warrants further study.
  • [MeSH-major] Astrocytoma / mortality. Astrocytoma / pathology. Brain Neoplasms / mortality. Brain Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Cell Proliferation. Disease-Free Survival. Female. Humans. Immunohistochemistry. Ki-67 Antigen / metabolism. Male. Middle Aged. Prognosis. Proto-Oncogene Proteins c-bcl-2 / metabolism. Retrospective Studies. Survival Analysis. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 16645716.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53
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46. Knizetova P, Darling JL, Bartek J: Vascular endothelial growth factor in astroglioma stem cell biology and response to therapy. J Cell Mol Med; 2008 Jan-Feb;12(1):111-25
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  • [Title] Vascular endothelial growth factor in astroglioma stem cell biology and response to therapy.
  • Malignant astrogliomas are among the most aggressive, highly vascular and infiltrating tumours bearing a dismal prognosis, mainly due to their resistance to current radiation treatment and chemotherapy.
  • Efforts to identify and target the mechanisms that underlie astroglioma resistance have recently focused on candidate cancer stem cells, their biological properties, interplay with their local microenvironment or 'niche', and their role in tumour progression and recurrence.
  • Both paracrine and autocrine regulation of astroglioma cell behaviour by locally produced cytokines such as the vascular endothelial growth factor (VEGF) are emerging as key factors that determine astroglioma cell fate.
  • Here, we review these recent rapid advances in astroglioma research, with emphasis on the significance of VEGF in astroglioma stem-like cell biology.
  • Furthermore, we highlight the unique DNA damage checkpoint properties of the CD133-marker-positive astroglioma stem-like cells, discuss their potential involvement in astroglioma radioresistance, and consider the implications of this new knowledge for designing combinatorial, more efficient therapeutic strategies.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / therapy. Brain Neoplasms / metabolism. Brain Neoplasms / therapy. Neoplastic Stem Cells / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 18031298.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Peptides; 0 / Vascular Endothelial Growth Factor A
  • [Number-of-references] 129
  • [Other-IDs] NLM/ PMC3823475
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47. Hamlat A, Saikali S, Diabira S, Messerer M, Riffaud L: Diagnosis of childhood astrocytomas. Expert Opin Med Diagn; 2009 Sep;3(5):501-22

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  • [Title] Diagnosis of childhood astrocytomas.
  • BACKGROUND: Astrocytomas are the most common brain tumours, accounting for 28 - 50% of all primary CNS tumours.
  • Objectives/method: The clinical presentations of CNS astrocytomas vary with their sites of location; therefore, a period of uncertainty often precedes diagnosis, and approximately 42% of patients with an intracranial process make several visits to various physicians between the onset and diagnosis.
  • However, on clinical suspicion of a brain tumour, a wide range of neuroimaging techniques may be used to assess the diagnosis of paediatric brain lesions.
  • In this review the authors, for ease of presentation, describe the clinical presentations of supratentorial, infratentorial and spinal cord astrocytomas as well as their radiological and pathological features, and discuss their differential diagnoses.
  • RESULTS/CONCLUSIONS: Understanding and mastering the numerous imaging features of several subtypes of primary brain tumours affecting children, in addition to radiological features of non-tumoural disorders, remains a significant challenge and demands increased awareness of the paediatric brain diseases.

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  • (PMID = 23495981.001).
  • [ISSN] 1753-0059
  • [Journal-full-title] Expert opinion on medical diagnostics
  • [ISO-abbreviation] Expert Opin Med Diagn
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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48. Nakamura M, Tsuji O, Fujiyoshi K, Watanabe K, Tsuji T, Ishii K, Matsumoto M, Toyama Y, Chiba K: Cordotomy for patients with thoracic malignant astrocytoma. J Neurosurg Spine; 2010 Oct;13(4):418-23

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  • [Title] Cordotomy for patients with thoracic malignant astrocytoma.
  • OBJECT: The optimal management of malignant astrocytomas remains controversial, and the prognosis of these lesions has been dismal regardless of the administered treatment.
  • In this study the authors investigated the surgical outcomes of cordotomy in patients with thoracic malignant astrocytomas to determine the effectiveness of this procedure.
  • METHODS: Cordotomy was performed in 5 patients with glioblastoma multiforme (GBM) and 2 with anaplastic astrocytoma (AA).
  • In the 2 patients with GBM, cordotomy was performed 2 and 3 weeks after a partial tumor resection.
  • In the 2 patients with AA, the initial treatment consisted of partial tumor resection and subtotal resection combined with radiotherapy, and rostral tumor growth and progressive paralysis necessitated cordotomy 2 and 28 months later.
  • One patient with a secondary GBM underwent cordotomy; the GBM developed 1 year after subtotal resection and radiotherapy for a WHO Grade II astrocytoma.
  • In patients with thoracic GBM, even if paralysis is incomplete, cordotomy should be performed before the tumor disseminates through the CSF.
  • If the tumor persists, radiotherapy and chemotherapy are indicated, and cordotomy should be reserved for lesions growing progressively after such second-line treatments.
  • [MeSH-major] Astrocytoma / surgery. Cordotomy. Thoracic Neoplasms / surgery
  • [MeSH-minor] Adolescent. Adult. Disease Progression. Encephalitis / etiology. Female. Glioblastoma / complications. Glioblastoma / pathology. Glioblastoma / surgery. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Staging. Pain, Postoperative. Paraplegia / etiology. Paraplegia / surgery. Prognosis. Radiotherapy, Adjuvant. Treatment Outcome. Young Adult

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  • (PMID = 20887138.001).
  • [ISSN] 1547-5646
  • [Journal-full-title] Journal of neurosurgery. Spine
  • [ISO-abbreviation] J Neurosurg Spine
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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49. 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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50. Maris C, Rorive S, Sandras F, D'Haene N, Sadeghi N, Bièche I, Vidaud M, Decaestecker C, Salmon I: Tenascin-C expression relates to clinicopathological features in pilocytic and diffuse astrocytomas. Neuropathol Appl Neurobiol; 2008 Jun;34(3):316-29
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  • [Title] Tenascin-C expression relates to clinicopathological features in pilocytic and diffuse astrocytomas.
  • AIMS: Tenascin-C (TN-C) is an extracellular matrix brain glycoprotein for which conflicting in vitro and in vivo results are reported in the literature dealing with its involvement in astrocytoma aggressiveness, in particular astrocytoma invasion.
  • In view of these conflicting results and the lack of data available on low-grade astrocytomas, the present study focuses on pilocytic World Health Organization (WHO) grade I, and diffuse WHO grade II astrocytomas, that is, two histological entities associated with very different invasive abilities.
  • METHODS: Using real-time reverse transcription polymerase chain reaction and immunohistochemistry, we analysed the TN-C expression in normal brain tissue as well as in a series of 54 pilocytic and 53 grade II astrocytomas.
  • Paralleling these observations, we showed that TN-C expression in low-grade astrocytomas similarly varies according to tumour site.
  • Cox regression analysis evidenced that TN-C provided an independent prognostic value which is enhanced in the case of grade II astrocytomas for which positive TN-C expression is associated with a higher risk of recurrence.
  • We also analysed TN-C expression specifically in vascular areas of low-grade astrocytomas without demonstrating any prognostic value for this additional feature.
  • RESULTS: Similarly to normal brain, low-grade astrocytomas exhibit variations in TN-C expression with site, and this expression is associated with an independent prognostic value in terms of recurrence.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Tenascin / biosynthesis
  • [MeSH-minor] Adult. Age Factors. Biomarkers, Tumor / analysis. Child. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Neoplasm Recurrence, Local / pathology. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Spinal Cord Neoplasms / metabolism. Spinal Cord Neoplasms / mortality. Spinal Cord Neoplasms / pathology

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  • (PMID = 17983425.001).
  • [ISSN] 1365-2990
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Tenascin
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51. Matsuda K, Sakurada K, Mouri W, Saino M, Sato S, Saito S, Kayama T, Nakazato Y: [Operative case of isomorphic astrocytoma]. Brain Nerve; 2007 Aug;59(8):881-6
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  • [Title] [Operative case of isomorphic astrocytoma].
  • Diffuse astrocytomas are classified as WHO Grade II tumors.
  • Recently, a subtype presenting with better prognosis has been proposed, and it is known as "isomorphic astrocytoma."
  • A clinical case that we encountered was believed to be categorized as this subtype; it has been presented in this report.
  • The tumor was resected under awake surgery.
  • The pathological diagnosis was diffuse astrocytoma, but this tumor was considered to be the isomorphic subtype.
  • Some parts of the tumor showed a relatively high MIB-1 labeling index (LI) of 9.2%, and additional 50-Gy radiotherapy was performed.
  • Isomorphic astrocytoma is characterized by prolonged epileptic seizures, a low MIB-1 LI, and better prognosis.
  • In our case, since the MIB-1 LI was higher in some parts of the tumor, the appropriate therapy for WHO Grade II tumors was performed.
  • However, this case was considered representative of isomorphic astrocytoma.
  • No reports of this tumor subtype have been previously described in Japan.
  • Therefore, this report is the first case of isomorphic astrocytoma reported to Japanese literature.
  • [MeSH-major] Astrocytoma / surgery. Brain Neoplasms / surgery

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  • (PMID = 17713125.001).
  • [ISSN] 1881-6096
  • [Journal-full-title] Brain and nerve = Shinkei kenkyū no shinpo
  • [ISO-abbreviation] Brain Nerve
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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52. Yu J, Deshmukh H, Gutmann RJ, Emnett RJ, Rodriguez FJ, Watson MA, Nagarajan R, Gutmann DH: Alterations of BRAF and HIPK2 loci predominate in sporadic pilocytic astrocytoma. Neurology; 2009 Nov 10;73(19):1526-31
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  • [Title] Alterations of BRAF and HIPK2 loci predominate in sporadic pilocytic astrocytoma.
  • OBJECTIVE: Independent studies have previously demonstrated that both the HIPK2 and BRAF genes are amplified and rearranged, respectively, in pilocytic astrocytomas (PAs).
  • CONCLUSIONS: BRAF rearrangement represents the most common genetic alteration in sporadic, but not neurofibromatosis type 1-associated, pilocytic astrocytomas (PAs).
  • These findings implicate BRAF in the pathogenesis of these common low-grade astrocytomas in children, and suggest that PAs arise either from NF1 inactivation or BRAF gain of function.

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  • (PMID = 19794125.001).
  • [ISSN] 1526-632X
  • [Journal-full-title] Neurology
  • [ISO-abbreviation] Neurology
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / UL1 RR024992; United States / NCI NIH HHS / CA / P30 CA91842
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / DNA, Neoplasm; 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
  • [Other-IDs] NLM/ PMC2777068
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53. Gaiser T, Becker MR, Meyer J, Habel A, Siegelin MD: p53-mediated inhibition of angiogenesis in diffuse low-grade astrocytomas. Neurochem Int; 2009 Jun;54(7):458-63
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  • [Title] p53-mediated inhibition of angiogenesis in diffuse low-grade astrocytomas.
  • In this study we evaluated the associations of p53 status and vessel density (angiogenesis) in a set of diffuse low-grade astrocytomas.
  • Immunohistochemistry was performed on 23 diffuse low-grade astrocytomas for CD31 and p53.
  • We found that 9/23 (39%) of the astrocytomas stained positive for p53 in the immunohistochemistry.
  • We identified TP53 mutations in 11/23 (47%) of the astrocytomas.
  • However, the MVD was significantly increased in p53 mutated low-grade astrocytomas.
  • Furthermore, the absolute vessel number was significantly higher in p53 mutated than in p53 wild-type low-grade astrocytomas.
  • To analyse the molecular background for that epiphenomenon LN229 glioma cells which harbour a TP53 mutation were transfected with a plasmid encoding p53 wild-type and an angiogenesis protein array was performed.
  • The higher microvessel density and the increased absolute vessel number in p53 mutated tumours supports the importance of p53 for tumour angiogenesis in diffuse low-grade astrocytomas.
  • Our results support the hypothesis that p53 regulates angiogenesis in low-grade astrocytomas.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Neovascularization, Pathologic / pathology. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Blotting, Western. Capillaries / pathology. Cell Line, Tumor. DNA Mutational Analysis. Humans. Immunohistochemistry. Matrix Metalloproteinase 9 / biosynthesis. Matrix Metalloproteinase 9 / genetics. Protein Array Analysis. Proteomics. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 19428789.001).
  • [ISSN] 1872-9754
  • [Journal-full-title] Neurochemistry international
  • [ISO-abbreviation] Neurochem. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; EC 3.4.24.35 / Matrix Metalloproteinase 9
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54. Zajdel A, Wilczok A, Slowinski J, Orchel J, Mazurek U: Aldehydic lipid peroxidation products in human brain astrocytomas. J Neurooncol; 2007 Sep;84(2):167-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aldehydic lipid peroxidation products in human brain astrocytomas.
  • We explored whether these aldehydes and histone H3 mRNA levels could serve as biomarkers of malignancy and predictive factor in human brain astrocytomas.
  • Aldehydic lipid peroxidation products were determined as their dinitrophenylhydrazone derivatives in specimens obtained from 26 adult patients with brain astrocytomas.
  • H3 mRNA, 2-hydroxyhexanal, and 4-hydroxynonenal levels were higher in high-grade astrocytomas compared to low-grade astrocytomas and showed negative correlation with survival.
  • Higher levels of 2-hydroxyhexanal and 4-hydroxynonenal, and lower levels of n-hexanal were associated with poorer patient prognosis.
  • Our data suggest that tissue concentrations of aldehydic lipid peroxidation products can assist grading and predicting the clinical outcome in patients with astrocytic brain tumors.
  • Possibly, this parameter will enhance optimal selection of patients for individualized treatment protocols, tailored to unique biochemical and molecular profile of the tumor.
  • [MeSH-major] Aldehydes / analysis. Astrocytoma / metabolism. Brain Chemistry / physiology. Brain Neoplasms / metabolism. Lipid Peroxidation / physiology

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  • (PMID = 17487452.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Aldehydes; 0 / Histones; 0 / RNA, Messenger
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55. Foehr ED, Lorente G, Vincent V, Nikolich K, Urfer R: FAS associated phosphatase (FAP-1) blocks apoptosis of astrocytomas through dephosphorylation of FAS. J Neurooncol; 2005 Sep;74(3):241-8
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  • [Title] FAS associated phosphatase (FAP-1) blocks apoptosis of astrocytomas through dephosphorylation of FAS.
  • Astrocytomas are the most common primary tumor of the adult human central nervous system.
  • Despite efforts to develop more effective clinical treatment strategies, median survival time for patients with the most severe form of astrocytoma, glioblastoma multiforme (GBM), remains about one year.
  • Astrocytomas are resistant to cytotoxic therapy in general and radiation therapy in particular, greatly limiting treatment options.
  • We have characterized the role of the tyrosine phosphatase FAP-1 (FAS-associated phosphatase 1) in astrocytomas.
  • Our studies demonstrate that FAP-1 is overexpressed in astrocytomas and this contributes to the resistance of the tumor cells to FAS-mediated apoptosis.
  • We demonstrate that knockdown of FAP-1 by RNA interference leads to increased apoptosis and increased sensitivity of astrocytoma cells to FAS-induced cell death.
  • FAP-1 binds to FAS in a ligand-dependent manner and forms a signaling complex that modulates the ability of astrocytoma cells to undergo FAS ligand (FASL)-mediated cell death.
  • In astrocytoma cells, FASL treatment induces tyrosine phosphorylation of FAS.
  • This is the first direct evidence that FAS activity can be regulated by reversible phosphorylation and suggests a mechanism for astrocytoma resistance to apoptosis.
  • [MeSH-major] Antigens, CD95 / metabolism. Apoptosis / physiology. Astrocytoma / pathology. Brain Neoplasms / pathology. Protein Tyrosine Phosphatases / metabolism
  • [MeSH-minor] Cell Line, Tumor. Gene Expression. Gene Expression Profiling. Humans. Immunoblotting. Immunohistochemistry. Phosphorylation. Protein Phosphatase 1. Protein Tyrosine Phosphatase, Non-Receptor Type 13. RNA Interference. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16187021.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / RNA, Messenger; EC 3.1.3.16 / Protein Phosphatase 1; EC 3.1.3.48 / PTPN13 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 13; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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56. Azad S, Kudesia S, Chawla N, Azad R, Singhal M, Rai SM, Arora P: Pilomyxoid astrocytoma. Indian J Pathol Microbiol; 2010 Apr-Jun;53(2):294-6
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  • [Title] Pilomyxoid astrocytoma.
  • Pilomyxoid astrocytoma (PMA) is a recently described brain tumor.
  • PMA shares similar features with pilocytic astrocytoma (PA), the most common central nervous system (CNS) tumor in the pediatric population, yet displays subtle histologic differences.
  • The histological findings revealed a tumor composed of a monotonous population of loosely arranged cells with delicate piloid like processes, within a prominent myxoid background.
  • The tumor lacked biphasic appearance, Rosenthal fibers, eosinophilic granular bodies and calcification that are commonly observed in classical PA.
  • [MeSH-major] Astrocytoma / diagnosis. Astrocytoma / pathology. Brain Neoplasms / diagnosis. Brain Neoplasms / pathology

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  • (PMID = 20551536.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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57. Rodríguez-Francia P, Sánchez-Tocino H, García-Cantera M, Martín-Castillo J: [Optic nerve pilocytic astrocytoma with retinal involvement]. Arch Soc Esp Oftalmol; 2005 Dec;80(12):733-6
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  • [Title] [Optic nerve pilocytic astrocytoma with retinal involvement].
  • [Transliterated title] Astrocitoma pilocítico de nervio óptico con afectación de retina.
  • INTRODUCTION: This is an atypical case of a pilocytic astrocytoma that involved the optic nerve (ON) and the retina.
  • CLINICAL CASE: The patient was a 30-year-old male, who had attended ONCE since his early childhood because of the suspicion of an intraocular tumor.
  • The ophthalmology exploration showed an ON and retinal coloboma in the right eye and microphthalmy, shutting of the pupil, retinal detachment and proof of an intraocular tumor in the left eye.
  • The MR revealed an ON tumor that involved the retina.
  • The histopathological study after enucleation was pilocytic astrocytoma.
  • [MeSH-major] Optic Nerve Glioma / secondary. Optic Nerve Neoplasms / pathology. Retinal Neoplasms / secondary

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  • (PMID = 16372218.001).
  • [ISSN] 0365-6691
  • [Journal-full-title] Archivos de la Sociedad Española de Oftalmología
  • [ISO-abbreviation] Arch Soc Esp Oftalmol
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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58. Brehar FM, Ciurea AV, Zarnescu O, Bleotu C, Gorgan RM, Dragu D, Matei L: Infiltrating growing pattern xenografts induced by glioblastoma and anaplastic astrocytoma derived tumor stem cells. Chirurgia (Bucur); 2010 Sep-Oct;105(5):685-94
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  • [Title] Infiltrating growing pattern xenografts induced by glioblastoma and anaplastic astrocytoma derived tumor stem cells.
  • OBJECTIVE: The number of evidences regarding the role of tumor stem cells (TSC) in the initiation and progression of high-grade astrocytomas became more and more numerous in the last years.
  • This issue has been intensively tested in glioblastoma, but little attention has been paid for anaplastic astrocytoma.
  • The main objective of this paper was to study the morphological characteristics of the xenografts developed from glioblastoma and anaplastic astrocytoma derived cancer stem cells.
  • METHODS: The authors of this study successfully isolated and partial characterized primary cultures of glioblastoma and anaplastic astrocytoma derived TSC.
  • RESULTS: The tumor xenografts which have been established in nude mice using TSC had different characteristics when compared with U87 xenografts previously developed by our group, and depend of the origin type of the tumors (glioblastoma versus anaplastic astrocytoma).
  • The diffuse growing pattern and cells infiltration have been more pronounced in both anaplastic astrocytoma and glioblastoma derived TSC xenografts compared with U87 line xenografts.
  • CONCLUSION: Our results support the hypothesis regarding the role of TSC in the infiltration process of glioblastoma and anaplastic astrocytoma.
  • The extensive infiltration growing patterns of these types of xenografts make them useful models for studying the invasion mechanisms in gliomas.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Glioblastoma / pathology. Neoplastic Stem Cells / pathology. Transplantation, Heterologous

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  • (PMID = 21141095.001).
  • [ISSN] 1221-9118
  • [Journal-full-title] Chirurgia (Bucharest, Romania : 1990)
  • [ISO-abbreviation] Chirurgia (Bucur)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Romania
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59. Rao SA, Santosh V, Somasundaram K: Genome-wide expression profiling identifies deregulated miRNAs in malignant astrocytoma. Mod Pathol; 2010 Oct;23(10):1404-17
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  • [Title] Genome-wide expression profiling identifies deregulated miRNAs in malignant astrocytoma.
  • Malignant astrocytoma includes anaplastic astrocytoma (grade III) and glioblastoma (grade IV).
  • Among them, glioblastoma is the most common primary brain tumor with dismal responses to all therapeutic modalities.
  • We performed a large-scale, genome-wide microRNA (miRNA) (n=756) expression profiling of 26 glioblastoma, 13 anaplastic astrocytoma and 7 normal brain samples with an aim to find deregulated miRNA in malignant astrocytoma.
  • We identified several differentially regulated miRNAs between these groups, which could differentiate glioma grades and normal brain as recognized by PCA.
  • More importantly, we identified a most discriminatory 23-miRNA expression signature, by using PAM, which precisely distinguished glioblastoma from anaplastic astrocytoma with an accuracy of 95%.
  • The differential expression pattern of nine miRNAs was further validated by real-time RT-PCR on an independent set of malignant astrocytomas (n=72) and normal samples (n=7).
  • Thus we have identified the miRNA expression signature for malignant astrocytoma, in particular glioblastoma, and showed the miRNA involvement and their importance in astrocytoma development.
  • [MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. MicroRNAs / genetics

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  • (PMID = 20711171.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MicroRNAs
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60. Bender AM, Collier LS, Rodriguez FJ, Tieu C, Larson JD, Halder C, Mahlum E, Kollmeyer TM, Akagi K, Sarkar G, Largaespada DA, Jenkins RB: Sleeping beauty-mediated somatic mutagenesis implicates CSF1 in the formation of high-grade astrocytomas. Cancer Res; 2010 May 1;70(9):3557-65
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  • [Title] Sleeping beauty-mediated somatic mutagenesis implicates CSF1 in the formation of high-grade astrocytomas.
  • To identify glioma-associated genes, we evaluated tumor formation in the brain tissue from 117 transgenic mice that had undergone constitutive SB-mediated transposition.
  • Upon analysis, 21 samples (18%) contained neoplastic tissue with features of high-grade astrocytomas.
  • These tumors expressed glial markers and were histologically similar to human glioma.
  • Genomic DNA from SB-induced astrocytoma tissue was extracted and transposon insertion sites were identified.
  • Using reverse transcription-PCR, we documented increased Csf1 RNAs in tumor versus adjacent normal tissue, with the identification of transposon-terminated Csf1 mRNAs in astrocytomas with SB insertions in intron 8.
  • Together, these results indicate that SB-insertional mutagenesis can identify high-grade astrocytoma-associated genes and they imply an important role for CSF1 in the development of these tumors.

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  • [Copyright] (c)2010 AACR.
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  • (PMID = 20388773.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA113636-02; United States / NCI NIH HHS / CA / CA113636-03; United States / NCI NIH HHS / CA / R01CA113636; United States / NCI NIH HHS / CA / R01 CA113636-03; United States / NCI NIH HHS / CA / K01CA122183; United States / NCI NIH HHS / CA / T32 CA009138; United States / NCI NIH HHS / CA / R01 CA113636-05; United States / NCI NIH HHS / CA / R01 CA113636-01A1; United States / NCI NIH HHS / CA / CA113636-01A1; United States / NCI NIH HHS / CA / R01 CA113636; United States / NCI NIH HHS / CA / CA113636-05; United States / NCI NIH HHS / CA / R01 CA113636-04; United States / NCI NIH HHS / CA / CA113636-02; United States / NCI NIH HHS / CA / K01 CA122183; United States / NCI NIH HHS / CA / CA113636-04
  • [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 / DNA Transposable Elements; 0 / RNA, Messenger; 81627-83-0 / Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor; EC 2.7.7.- / Transposases
  • [Other-IDs] NLM/ NIHMS185042; NLM/ PMC2862088
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61. Akaishi K, Nakayama J, Sakai K, Kobayashi T, Rutka JT: Antigen p57/Kip2 as a potential negative regulator of human astrocytoma growth. J Clin Neurosci; 2009 Dec;16(12):1615-8
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  • [Title] Antigen p57/Kip2 as a potential negative regulator of human astrocytoma growth.
  • This study was performed to determine the relationship between p57/Kip2 and the growth of human astrocytomas.
  • Immunohistochemical staining for p57/Kip2, p53, p16, and Ki67 antigen was performed on paraffin-embedded tissue specimens obtained from 36 patients with astrocytoma.
  • Expression of p57/Kip2, p53, p16, and Ki67 antigen was generally increased in association with the astrocytoma tumor grade.
  • Expression of p16 was higher in patients whose tumors express p57/Kip2 in greater than 10% of tumor cells (p<0.05).
  • Expression of p53 also tended to be higher, but not to a statistically significant extent, in patients whose tumors express p57/Kip2 in greater than 10% of tumor cells.
  • These findings suggest that p57/Kip2 inhibits the growth of human astrocytomas, and may function in parallel with p16 and p53.
  • However, p57/Kip2 is, by itself, insufficient to arrest the cellular proliferation of human astrocytomas.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Cyclin-Dependent Kinase Inhibitor p57 / metabolism. Gene Expression Regulation, Neoplastic / physiology
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Female. Humans. Ki-67 Antigen / metabolism. Male. Middle Aged. Neoplasm Proteins / metabolism. Retrospective Studies. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 19822429.001).
  • [ISSN] 1532-2653
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CDKN1C protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p57; 0 / Ki-67 Antigen; 0 / Neoplasm Proteins; 0 / P16 protein, human; 0 / Tumor Suppressor Protein p53
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62. Sareddy GR, Panigrahi M, Challa S, Mahadevan A, Babu PP: Activation of Wnt/beta-catenin/Tcf signaling pathway in human astrocytomas. Neurochem Int; 2009 Sep;55(5):307-17
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  • [Title] Activation of Wnt/beta-catenin/Tcf signaling pathway in human astrocytomas.
  • Astrocytomas are the most common form of primary brain tumors.
  • Understanding the molecular basis of development and progression of astrocytomas is required to develop more effective therapies.
  • Although, over activation of Wnt/beta-catenin/Tcf pathway is a hallmark of several forms of cancer, little is known about its role in human astrocytomas.
  • Here, we report the evidence that Wnt/beta-catenin/Tcf signaling pathway is constitutively activated in astrocytic tumors.
  • In the present study, human astrocytic tumors with different clinical grades were analyzed for mRNA expression of Dvl-1, Dvl-2, Dvl-3, beta-catenin, c-myc and cyclin D1 and protein levels of beta-catenin, Lef1, Tcf4, c-Myc, N-Myc, c-jun and cyclin D1.
  • RT-PCR analysis demonstrated the overexpression of Dvl-3, beta-catenin, c-myc and cyclin D1 in astrocytomas.
  • Western blotting revealed upregulation of beta-catenin, Lef1, Tcf4 and their target proteins in the core tumor tissues in comparison to peritumor and normal brain tissues.
  • Our studies tend to suggest that Wnt/beta-catenin/Tcf signaling pathway is implicated in malignancy of astrocytomas.
  • [MeSH-major] Astrocytoma / metabolism. Signal Transduction. TCF Transcription Factors / metabolism. Wnt Proteins / metabolism. beta Catenin / metabolism


63. Lemire J, Mailloux R, Puiseux-Dao S, Appanna VD: Aluminum-induced defective mitochondrial metabolism perturbs cytoskeletal dynamics in human astrocytoma cells. J Neurosci Res; 2009 May 1;87(6):1474-83
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  • [Title] Aluminum-induced defective mitochondrial metabolism perturbs cytoskeletal dynamics in human astrocytoma cells.
  • Whereas the control cells had well-defined structures, the Al-exposed astrocytoma cells appeared as globular structures.
  • Creatine kinase (CK) and profilin-2, two critical modulators of cellular morphology, were markedly diminished in the astrocytoma cells treated with Al.
  • Taken together, these data reveal an intricate link between ATP metabolism and astrocytic dysfunction and provide molecular insights into the pathogenesis of Al-induced neurological diseases.
  • [MeSH-minor] Acetylcysteine / administration & dosage. Adenosine Triphosphate / metabolism. Antioxidants / administration & dosage. Cell Line, Tumor. Creatine Kinase / metabolism. Electrophoresis, Polyacrylamide Gel. Humans. Immunoblotting. Ketoglutaric Acids / administration & dosage. Microscopy, Fluorescence. Profilins / metabolism

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  • (PMID = 19084901.001).
  • [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 / Antioxidants; 0 / Ketoglutaric Acids; 0 / Profilins; 328-50-7 / alpha-ketoglutaric acid; 8L70Q75FXE / Adenosine Triphosphate; CPD4NFA903 / Aluminum; EC 2.7.3.2 / Creatine Kinase; WYQ7N0BPYC / Acetylcysteine
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64. Omura T, Nawashiro H, Osada H, Shima K, Tsuda H, Shinsuke A: Pilomyxoid astrocytoma of the fourth ventricle in an adult. Acta Neurochir (Wien); 2008 Nov;150(11):1203-6; discussion 1206

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pilomyxoid astrocytoma of the fourth ventricle in an adult.
  • Pilomyxoid astrocytomas have been identified as a variant of pilocytic astrocytoma.
  • They are listed as a novel clinico-pathological entity in the 2007 World Health Organisation (WHO) classification of tumours of the central nervous system.
  • This tumour corresponds to a WHO grade II neoplasm whereas pilocytic astrocytoma corresponds to WHO grade I.
  • Pilomyxoid astrocytomas are not limited to the hypothalamic/chiasmatic region in children.
  • Additional knowledge and recognition of this entity is necessary to improve treatment of pilomyxoid astrocytoma.
  • [MeSH-major] Astrocytoma / pathology. Cerebral Ventricle Neoplasms / pathology. Fourth Ventricle / pathology
  • [MeSH-minor] Adult. Age Distribution. Biomarkers, Tumor / analysis. Biomarkers, Tumor / metabolism. Cranial Nerve Diseases / etiology. Cranial Nerve Diseases / physiopathology. Humans. Hyperacusis / etiology. Magnetic Resonance Imaging. Male. Neurosurgical Procedures. Postoperative Complications / etiology. Postoperative Complications / physiopathology. Tinnitus / etiology. Treatment Outcome

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  • (PMID = 18958385.001).
  • [ISSN] 0942-0940
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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65. Chamberlain MC, Johnston S: Salvage chemotherapy with bevacizumab for recurrent alkylator-refractory anaplastic astrocytoma. J Neurooncol; 2009 Feb;91(3):359-67
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  • [Title] Salvage chemotherapy with bevacizumab for recurrent alkylator-refractory anaplastic astrocytoma.
  • A retrospective study of bevacizumab only in adults with recurrent temozolomide (TMZ)-refractory anaplastic astrocytoma (AA) with a primary objective of determining progression free survival (PFS).
  • Sixteen patients (64%) demonstrated a partial radiographic response, 2 (8.0%) stable disease and 7 (28%) progressive disease following two cycles of bevacizumab.
  • Time to tumor progression ranged from 1 to 20 months (median: 7).
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antibodies, Monoclonal / therapeutic use. Astrocytoma / drug therapy. Astrocytoma / mortality. Brain Neoplasms / drug therapy. Brain Neoplasms / mortality. Neoplasm Recurrence, Local
  • [MeSH-minor] Adult. Antibodies, Monoclonal, Humanized. Bevacizumab. Disease Progression. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Male. Middle Aged. Retrospective Studies

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  • (PMID = 18953491.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab
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66. Koenig MK, Butler IJ, Northrup H: Regression of subependymal giant cell astrocytoma with rapamycin in tuberous sclerosis complex. J Child Neurol; 2008 Oct;23(10):1238-9
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  • [Title] Regression of subependymal giant cell astrocytoma with rapamycin in tuberous sclerosis complex.
  • The authors present a 21-year-old woman who has been receiving rapamycin for 5 months for bilateral subependymal giant cell astrocytomas.
  • Magnetic resonance imaging of the brain 2(1/2) months after initiating rapamycin demonstrated a decrease in size of both astrocytomas (11 to 7.5 mm on the right and 8 to 5 mm on the left).

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  • [Cites] Pediatr Res. 2005 Jan;57(1):67-75 [15557109.001]
  • [Cites] BMC Dermatol. 2008;8:1 [18226258.001]
  • [Cites] N Engl J Med. 2008 Jan 10;358(2):140-51 [18184959.001]
  • [Cites] Ann Neurol. 2006 Mar;59(3):490-8 [16453317.001]
  • (PMID = 18952591.001).
  • [ISSN] 1708-8283
  • [Journal-full-title] Journal of child neurology
  • [ISO-abbreviation] J. Child Neurol.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / KL2 RR024149; United States / NCRR NIH HHS / RR / RR024149-05S1; United States / NCRR NIH HHS / RR / KL2 RR024149-05S1
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ NIHMS282750; NLM/ PMC3072698
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67. Ulu MO, Tanriöver N, Biçeroğlu H, Oz B, Canbaz B: A case report: a noninfantile desmoplastic astrocytoma. Turk Neurosurg; 2008 Jan;18(1):42-6
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  • [Title] A case report: a noninfantile desmoplastic astrocytoma.
  • INTRODUCTION AND CASE DESCRIPTION: Desmoplastic infantile astrocytomas (DIA) are rare intracranial tumors of infancy with distinctive clinical and radiological features.
  • CONCLUSION: Although accepted as a tumor of infancy, DIA can also be encountered in older patients.
  • Careful diagnosis and differentiation of DIA cases with other tumors, particularly malignant astrocytomas is important since the therapeutic strategies may differ.
  • [MeSH-major] Astrocytoma / pathology. Astrocytoma / surgery. Brain Neoplasms / pathology. Brain Neoplasms / surgery. Magnetic Resonance Imaging

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  • (PMID = 18382977.001).
  • [ISSN] 1019-5149
  • [Journal-full-title] Turkish neurosurgery
  • [ISO-abbreviation] Turk Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Turkey
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68. Tanaka Y, Sasaki A, Ishiuchi S, Nakazato Y: Diversity of glial cell components in pilocytic astrocytoma. Neuropathology; 2008 Aug;28(4):399-407
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  • [Title] Diversity of glial cell components in pilocytic astrocytoma.
  • To characterize the cellular density and proliferative activity of GFAP-negative cells in pilocytic astrocytoma (PA), surgically excised tissues of PAs (n=37) and diffuse astrocytomas (DAs) (n=11) were examined morphologically and immunohistochemically using antibodies against GFAP, Olig2, Iba1 and Ki-67 (MIB-1).
  • [MeSH-major] Astrocytoma / metabolism. Basic Helix-Loop-Helix Transcription Factors / biosynthesis. Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Nerve Tissue Proteins / biosynthesis. Neuroglia / metabolism

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  • (PMID = 18312545.001).
  • [ISSN] 0919-6544
  • [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 / AIF1 protein, human; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Glial Fibrillary Acidic Protein; 0 / Ki-67 Antigen; 0 / Nerve Tissue Proteins; 0 / OLIG2 protein, human
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69. Watanabe T, Katayama Y, Yoshino A, Yachi K, Ohta T, Ogino A, Komine C, Fukushima T: Aberrant hypermethylation of p14ARF and O6-methylguanine-DNA methyltransferase genes in astrocytoma progression. Brain Pathol; 2007 Jan;17(1):5-10
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  • [Title] Aberrant hypermethylation of p14ARF and O6-methylguanine-DNA methyltransferase genes in astrocytoma progression.
  • The aim of the present study was to elucidate genetic alterations that are critically involved in astrocytoma progression.
  • We characterized 27 World Health Organization grade II fibrillary astrocytomas which later underwent recurrence or progression, paying specific attention to the CpG island methylation status of critical growth regulatory genes. p14(ARF) and O(6)-methylguanine-DNA methyltransferase (MGMT) hypermethylation represented frequent events (26% and 63%, respectively), which were mutually exclusive except in one case, with alternate or simultaneous methylation of these two genes occurring in 85% of our tumor series.
  • Our findings suggest that p14(ARF) hypermethylation and MGMT hypermethylation constitute distinct molecular pathways of astrocytoma progression, which could differ in biological behavior and clinical outcome.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. CpG Islands / physiology. Neoplasm Recurrence, Local / metabolism. O(6)-Methylguanine-DNA Methyltransferase / metabolism. Tumor Suppressor Protein p14ARF / metabolism
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Methylation. Middle Aged. Mutation / genetics. Promoter Regions, Genetic / physiology. Survival Analysis. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 17493032.001).
  • [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 / Tumor Suppressor Protein p14ARF; 0 / Tumor Suppressor Protein p53; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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70. Arifin MT, Hama S, Kajiwara Y, Sugiyama K, Saito T, Matsuura S, Yamasaki F, Arita K, Kurisu K: Cytoplasmic, but not nuclear, p16 expression may signal poor prognosis in high-grade astrocytomas. J Neurooncol; 2006 May;77(3):273-7
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  • [Title] Cytoplasmic, but not nuclear, p16 expression may signal poor prognosis in high-grade astrocytomas.
  • BACKGROUND: The negative consequences of the cytoplasmic localization of p16 in patients with high-grade astrocytomas, on their prognosis, was investigated.
  • METHODS: p16 Expression was examined in 20 anaplastic astrocytoma and 42 glioblastoma patients by immunohistochemical analysis, and the relationship between both cytoplasmic and nuclear p16 expression and prognosis analyzed.
  • CONCLUSION: The cytoplasmic immunoreactivity of p16 appears to be an unfavorable prognostic indicator in high-grade astrocytoma patients.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Glioblastoma / metabolism
  • [MeSH-minor] Adolescent. Aged. Cell Nucleus / metabolism. Cytoplasm / metabolism. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Survival Analysis. Tumor Cells, Cultured

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  • (PMID = 16614947.001).
  • [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] Netherlands
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16
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71. Nowak-Sadzikowska J, Gliński B, Szpytma T, Pluta E: Postoperative irradiation of incompletely excised gemistocytic astrocytomas. Clinical outcome and prognostic factors. Strahlenther Onkol; 2005 Apr;181(4):246-50
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  • [Title] Postoperative irradiation of incompletely excised gemistocytic astrocytomas. Clinical outcome and prognostic factors.
  • BACKGROUND AND PURPOSE: Although gemistocytic astrocytomas are considered slow-growing tumors, they often behave aggressively and carry the least favorable prognosis among low-grade astrocytomas.
  • The aim of this study is to evaluate the outcomes and prognostic factors of patients with incompletely excised gemistocytic astrocytomas irradiated postoperatively.
  • PATIENTS AND METHODS: Records of 48 patients with incompletely excised gemistocytic astrocytoma, irradiated between 1976 and 1998 at the Department of Radiation Oncology, Maria Skłodowska-Curie Memorial Cancer Center, Cracow, Poland, were reviewed.
  • The treatment volume covered the residual tumor with a margin of 1-2 cm.
  • CONCLUSION: In most patients with gemistocytic astrocytoma, combined surgery and postoperative radiotherapy result in only short-term survival.
  • Older age is the most important unfavorable prognostic factor in patients with gemistocytic astrocytoma.
  • [MeSH-major] Astrocytoma / radiotherapy. Astrocytoma / surgery. Brain Neoplasms / radiotherapy. Brain Neoplasms / surgery

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  • (PMID = 15827694.001).
  • [ISSN] 0179-7158
  • [Journal-full-title] Strahlentherapie und Onkologie : Organ der Deutschen Röntgengesellschaft ... [et al]
  • [ISO-abbreviation] Strahlenther Onkol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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72. Zscharnack K, Kessler R, Bleichert F, Warnke JP, Eschrich K: The PFKFB3 splice variant UBI2K4 is downregulated in high-grade astrocytomas and impedes the growth of U87 glioblastoma cells. Neuropathol Appl Neurobiol; 2009 Dec;35(6):566-78
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  • [Title] The PFKFB3 splice variant UBI2K4 is downregulated in high-grade astrocytomas and impedes the growth of U87 glioblastoma cells.
  • Here, we studied the role of the PFKFB3 splice variants in human astrocytic gliomas.
  • METHODS: We analysed the PFKFB3 splice variants in 48 astrocytic gliomas by RT-PCR and real-time PCR.
  • RESULTS: UBI2K5 and UBI2K6 are the predominant splice variants in rapidly proliferating high-grade astrocytomas while the expression of UBI2K3 and UBI2K4 is mainly restricted to low-grade astrocytomas and nonneoplastic brain tissue.
  • The UBI2K4 mRNA level is downregulated in astrocytic gliomas with increasing malignancy grade.
  • CONCLUSIONS: Our results demonstrate that the splice variant UBI2K4 impedes the tumour cell growth and might serve as a tumour suppressor in astrocytic tumours.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Glioblastoma / metabolism. Phosphofructokinase-2 / metabolism
  • [MeSH-minor] Brain / metabolism. Cell Count. Cell Line, Tumor. Cell Proliferation. Cell Survival. Down-Regulation. Humans. Neoplasm Staging. Polymerase Chain Reaction. Protein Isoforms / genetics. Protein Isoforms / metabolism. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Transfection

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  • (PMID = 19490427.001).
  • [ISSN] 1365-2990
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / RNA, Messenger; EC 2.7.1.105 / PFKFB3 protein, human; EC 2.7.1.105 / Phosphofructokinase-2
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73. Takata K, Gasparetto EL, Leite Cda C, Lucato LT, Reed UC, Matushita H, Aguiar PH, Rosemberg S: [Subependymal giant cell astrocytoma in patients with tuberous sclerosis: magnetic resonance imaging findings in ten cases]. Arq Neuropsiquiatr; 2007 Jun;65(2A):313-6
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  • [Title] [Subependymal giant cell astrocytoma in patients with tuberous sclerosis: magnetic resonance imaging findings in ten cases].
  • [Transliterated title] Astrocitoma subependimário de células gigantes em pacientes com esclerose tuberosa: achados em ressonância magnética de dez casos.
  • OBJECTIVE: To report the magnetic resonance imaging (MRI) findings in 10 patients with subependimal giant cell astrocytoma (SGCA) and tuberous sclerosis (TS).
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Cerebral Ventricles / pathology. Tuberous Sclerosis / pathology


74. Li H, Wang Q, Gao F, Zhu F, Wang X, Zhou C, Liu C, Chen Y, Ma C, Sun W, Zhang L: Reduced expression of PDCD5 is associated with high-grade astrocytic gliomas. Oncol Rep; 2008 Sep;20(3):573-9
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  • [Title] Reduced expression of PDCD5 is associated with high-grade astrocytic gliomas.
  • However, the expression level of PDCD5 in human gliomas has not been investigated.
  • In the present study, we examined the expression of PDCD5 in 88 human glioma samples at both mRNA and protein levels by RT-PCR, Western blotting and immunohistochemistry.
  • We found that 53.3% (16/30) of the glioma samples had a reduced expression of PDCD5 mRNA and 70.5% (62/88) had a reduced expression of the PDCD5 protein as compared to normal brain tissue.
  • Furthermore, we studied the correlation of the expression level of PDCD5 with the clinicopathological grade and survival of patients with astrocytomas.
  • Although longitudinal studies of a cohort of patients with astrocytoma revealed that PDCD5 expression was not able to predict clinical outcome (p>0.05), a decreased expression of PDCD5 correlated significantly with high-grade astrocytomas (p<0.001).
  • In conclusion, our data suggest that reduced PDCD5 expression may contribute to the pathogenesis of human gliomas.
  • [MeSH-major] Apoptosis Regulatory Proteins / metabolism. Astrocytoma / metabolism. Brain Neoplasms / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Adult. Blotting, Western. Female. Humans. Immunoenzyme Techniques. Male. Neoplasm Staging. Prognosis. RNA, Messenger. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Tumor Cells, Cultured

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  • (PMID = 18695908.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Neoplasm Proteins; 0 / PDCD5 protein, human; 0 / RNA, Messenger
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75. Zakrzewski K, Biernat W, Liberski PP, Polis L, Nowoslawska E: Pilocytic astrocytoma as a predominant component of a recurrent complex type DNT. Folia Neuropathol; 2009;47(3):284-8
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  • [Title] Pilocytic astrocytoma as a predominant component of a recurrent complex type DNT.
  • We report an unusual case of a 7-year-old girl with a temporal lobe DNT, which recurred four years after subtotal resection of the tumour.
  • In the recurrent lesion we identified pilocytic astrocytoma (PA) as a predominant component of the tumour.
  • In rare cases development of a secondary, histologically different neoplasm may also occur.

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  • (PMID = 19813149.001).
  • [ISSN] 1641-4640
  • [Journal-full-title] Folia neuropathologica
  • [ISO-abbreviation] Folia Neuropathol
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Poland
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76. Ooba H, Abe T, Kamida T, Anan M, Momii Y, Tokuuye K, Fujiki M: Malignant fibrous histiocytosis after high-dose proton radiation therapy for anaplastic astrocytoma. J Clin Neurosci; 2009 Dec;16(12):1641-3
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  • [Title] Malignant fibrous histiocytosis after high-dose proton radiation therapy for anaplastic astrocytoma.
  • This report presents a 70-year-old male who presented with a rare malignant fibrous histiocytosis after high-dose proton radiation therapy for anaplastic astrocytoma.
  • [MeSH-minor] Aged. Astrocytoma / radiotherapy. Brain Neoplasms / radiotherapy. Humans. Magnetic Resonance Imaging / methods. Male

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  • (PMID = 19766005.001).
  • [ISSN] 1532-2653
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
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77. Bence M, Kereszturi E, Mozes V, Sasvari-Szekely M, Keszler G: Hypoxia-induced transcription of dopamine D3 and D4 receptors in human neuroblastoma and astrocytoma cells. BMC Neurosci; 2009;10:92
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  • [Title] Hypoxia-induced transcription of dopamine D3 and D4 receptors in human neuroblastoma and astrocytoma cells.
  • In order to clarify the hypoxic sensitivity of key dopaminergic genes, we aimed to study their transcriptional regulation in the context of neuroblastoma and astrocytoma cell lines exposed to 1% hypoxia.
  • [MeSH-minor] Astrocytoma. Blotting, Western. Cell Line, Tumor. Gene Transfer Techniques. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Immunohistochemistry. Neuroblastoma. Reverse Transcriptase Polymerase Chain Reaction. Transcriptional Activation

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  • (PMID = 19653907.001).
  • [ISSN] 1471-2202
  • [Journal-full-title] BMC neuroscience
  • [ISO-abbreviation] BMC Neurosci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DRD3 protein, human; 0 / DRD4 protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Receptors, Dopamine D3; 137750-34-6 / Receptors, Dopamine D4
  • [Other-IDs] NLM/ PMC3224682
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78. Arvanitis LD, Koukoulis GK, Kanavaros P: The expression of the O-linked N-acetylglucosamine containing epitope H in the gemistocytic, pilocytic and subependymal giant cell astrocytomas. Oncol Rep; 2009 Sep;22(3):521-4
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  • [Title] The expression of the O-linked N-acetylglucosamine containing epitope H in the gemistocytic, pilocytic and subependymal giant cell astrocytomas.
  • In normal human brains the epitope H is present mostly to a minority of fibrous astrocytes, whereas it is greatly up-regulated in reactive astrocytes and is increased in well differentiated fibrillary astrocytomas compared to anaplastic astrocytomas and glioblastomas.
  • In this study the expression of the epitope H was investigated in thirty cases of gemistocytic (WHO grade II), pilocytic (WHO grade I), and subependymal giant cell (WHO grade I) astrocytomas using the mAbH with the indirect immunoperoxidase method.
  • The ten cases of gemistocytic astrocytomas revealed an overall high expression pattern.
  • The ten cases of pilocytic astrocytomas revealed a biphasic pattern of epitope H expression.
  • The dense tumor areas composed of elongated pilocytic cells revealed high expression of the epitope H.
  • The loose cystic tumor areas composed of stellate cells revealed low expression of the epitope H.
  • The ten cases of subependynal giant cell astrocytomas occurring in tuberous sclerosis revealed an overall high expression pattern.
  • This study shows that there is high expression of the epitope H in gemistocytic, pilocytic and subependymal giant cell astrocytomas.
  • Collectively considering, the present and our previous data, it appears that there is a spectrum of the expression levels of the epitope H ranging from the high expression in the reactive astrocytes and low grade astrocytomas to the low/null expression in the normal astrocytes and glioblastomas.
  • [MeSH-major] Acetylglucosamine / analysis. Astrocytoma / chemistry. Brain Neoplasms / chemistry. Epitopes

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  • (PMID = 19639198.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Epitopes; V956696549 / Acetylglucosamine
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79. Hidaka T, Hama S, Shrestha P, Saito T, Kajiwara Y, Yamasaki F, Sugiyama K, Kurisu K: The combination of low cytoplasmic and high nuclear expression of p27 predicts a better prognosis in high-grade astrocytoma. Anticancer Res; 2009 Feb;29(2):597-603
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  • [Title] The combination of low cytoplasmic and high nuclear expression of p27 predicts a better prognosis in high-grade astrocytoma.
  • No previous reports have examined the subcellular localization of p27 in glioma which was evaluated here regarding the prognosis in high-grade astrocytomas.
  • PATIENTS AND METHODS: The pattern of subcellular localization of p27 expression was examined immunohistochemically in 49 patients with high-grade astrocytoma who were over 20 years of age.
  • Cox multiple regression analysis showed the combination of high nuclear and low cytoplasmic p27 expression associated with a significantly better prognosis in high-grade astrocytoma.
  • CONCLUSION: A combination of low cytoplasmic and high nuclear expression of p27 predicts a better prognosis in high-grade astrocytomas and thus the subcellular localization of p27 expression is useful for predicting the prognosis for these patients.
  • [MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor / biosynthesis. Brain Neoplasms / metabolism. Cyclin-Dependent Kinase Inhibitor p27 / biosynthesis

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  • (PMID = 19331209.001).
  • [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 / Biomarkers, Tumor; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
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80. Hassan F, Paluzzi A, Kayello R, Bradey N, Strachan RD: Hydrocephalus as presenting feature of spinal astrocytoma in a adolescent patient. Br J Neurosurg; 2008 Jun;22(3):433-5
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  • [Title] Hydrocephalus as presenting feature of spinal astrocytoma in a adolescent patient.
  • We report the case of an adolescent with a thoracic spine astrocytoma whose initial presentation was communicating hydrocephalus.
  • [MeSH-major] Astrocytoma / complications. Hydrocephalus / etiology. Spinal Cord Neoplasms / complications

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  • (PMID = 18568734.001).
  • [ISSN] 0268-8697
  • [Journal-full-title] British journal of neurosurgery
  • [ISO-abbreviation] Br J Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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81. Hirai T, Murakami R, Nakamura H, Kitajima M, Fukuoka H, Sasao A, Akter M, Hayashida Y, Toya R, Oya N, Awai K, Iyama K, Kuratsu JI, Yamashita Y: Prognostic value of perfusion MR imaging of high-grade astrocytomas: long-term follow-up study. AJNR Am J Neuroradiol; 2008 Sep;29(8):1505-10
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  • [Title] Prognostic value of perfusion MR imaging of high-grade astrocytomas: long-term follow-up study.
  • BACKGROUND AND PURPOSE: Although the prognostic value of perfusion MR imaging in various gliomas has been investigated, that in high-grade astrocytomas alone has not been fully evaluated.
  • The purpose of this study was to evaluate retrospectively whether the tumor maximum relative cerebral blood volume (rCBV) on pretreatment perfusion MR imaging is of prognostic value in patients with high-grade astrocytoma.
  • MATERIALS AND METHODS: Between January 1999 and December 2002, 49 patients (30 men, 19 women; age range, 23-76 years) with supratentorial high-grade astrocytoma underwent MR imaging before the inception of treatment.
  • The patient age, sex, symptom duration, neurologic function, mental status, Karnofsky Performance Scale, extent of surgery, histopathologic diagnosis, tumor component enhancement, and maximum rCBV were assessed to identify factors affecting survival.
  • RESULTS: The maximum rCBV was significantly higher in the 31 patients with glioblastoma multiforme than in the 18 with anaplastic astrocytoma (P < .03).
  • CONCLUSION: The maximum rCBV at pretreatment perfusion MR imaging is a useful clinical prognostic biomarker for survival in patients with high-grade astrocytoma.
  • [MeSH-major] Astrocytoma / diagnosis. Astrocytoma / mortality. Brain Neoplasms / diagnosis. Brain Neoplasms / mortality. Magnetic Resonance Imaging / methods

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  • (PMID = 18556364.001).
  • [ISSN] 1936-959X
  • [Journal-full-title] AJNR. American journal of neuroradiology
  • [ISO-abbreviation] AJNR Am J Neuroradiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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82. Vaquero E, Gómez CM, Quintero EA, González-Rosa JJ, Márquez J: Differential prefrontal-like deficit in children after cerebellar astrocytoma and medulloblastoma tumor. Behav Brain Funct; 2008;4:18
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  • [Title] Differential prefrontal-like deficit in children after cerebellar astrocytoma and medulloblastoma tumor.
  • The astrocytoma group (CE, n = 13) did not receive additional treatments.
  • The performances of the clinical groups with respect to controls were compared considering the tumor's localization (vermis or hemisphere) and the affectation (or not) of the dentate nucleus.
  • The Astrocytoma group also showed executive deficits in digits span, semantic fluency (animal category) and moderate to slight deficit in Stroop (word and colour) tests.
  • In the astrocytoma group, the tumor's localization and dentate affectation showed different profile and level of impairment: moderate to slight for vermal and hemispheric patients respectively.
  • CONCLUSION: Results suggest a differential prefrontal-like deficit due to cerebellar lesions and/or cerebellar-frontal diaschisis, as indicate the results in astrocytoma group (without treatments), that also can be generated and/or increased by treatments in the medulloblastoma group.

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  • (PMID = 18412947.001).
  • [ISSN] 1744-9081
  • [Journal-full-title] Behavioral and brain functions : BBF
  • [ISO-abbreviation] Behav Brain Funct
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2362115
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83. Beppu T, Sato Y, Uesugi N, Kuzu Y, Ogasawara K, Ogawa A: Desmoplastic infantile astrocytoma and characteristics of the accompanying cyst. Case report. J Neurosurg Pediatr; 2008 Feb;1(2):148-51
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  • [Title] Desmoplastic infantile astrocytoma and characteristics of the accompanying cyst. Case report.
  • A desmoplastic infantile astrocytoma (DIA) is an extremely rare tumor that comprises a solid astrocytic tumor accompanied by a large cyst and involves the superficial cerebral cortex and leptomeninges in infants.
  • The solid part of this type of tumor has been well described in various reports and books, but characteristics of the cystic portion have remained unclear.
  • The authors report on the clinical and histological features of the cyst in a case of a DIA.
  • Contrast-enhanced magnetic resonance imaging revealed a strongly enhancing single-lobed large cyst located in the deep white matter, under the solid part of the tumor attached to the dura mater of the left frontal lobe.
  • Both the solid and cystic portions of the tumor were surgically removed.
  • Histologically, the cyst wall was composed of gliosis representing a rough accumulation of reactive astrocytes, lymphocytes, and small capillary vessels in edematous parenchyma, but no tumor cells.
  • The present case and previous reports suggest that the cyst does not contain tumor cells, even if strongly depicted on contrast-enhanced neuroimaging, and that a thickly enhancing cyst wall indicates gliosis with accumulation of numerous small vessels.
  • [MeSH-major] Astrocytoma / diagnosis. Brain Diseases / diagnosis. Brain Neoplasms / diagnosis. Cysts / diagnosis

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  • (PMID = 18352787.001).
  • [ISSN] 1933-0707
  • [Journal-full-title] Journal of neurosurgery. Pediatrics
  • [ISO-abbreviation] J Neurosurg Pediatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
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84. Stosić-Opinćal T, Gavrilov M, Stosić S, Lavrnić S, Perić V, Grujicić D: [FLAIR MR sequence in the diagnosis and follow-up of low-grade astrocytomas]. Vojnosanit Pregl; 2005 Jul-Aug;62(7-8):525-8
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  • [Title] [FLAIR MR sequence in the diagnosis and follow-up of low-grade astrocytomas].
  • AIM: To evaluate the sensitivity of fluid-attenuated inversion recovery (FLAIR) sequence in the diagnosis and follow-up of the patients with low-grade astrocytomas compared with T2-weighted (T2W) sequence.
  • METHODS: Twenty-four patients with biopsy-confirmed low-grade astrocytoma (age range, 15-66 years) underwent T1-weighted (T1W), T2W and FLAIR imaging with a superconducting unit 1.0 T.
  • To evaluate the diagnostic value of FLAIR, the neuroradiologists individually assessed the possibilities of the detection of lesions, as well as the possibilities of the differentiation of tumor from the surrounding edema on FLAIR vs. T2W images.
  • The comparison of images with regard to the differentiation of tumor boundaries vs. surrounding edema showed that 92.5% of FLAIR studies were superior, 7.5% were of similar diagnostic value, and none was inferior to the T2W images.
  • CONCLUSION: Our results were similar to the previous studies' results concerning the advantages of FLAIR sequence in the diagnosis of low grade astrocytomas over T2W sequence.
  • FLAIR was better at showing different tumor components, and at distinguishing CSF from the cystic component, and the postoperative cavity, compared with T2W images.
  • Our conclusion was that FLAIR could be routinely used in the evaluation and follow-up of low-grade astrocytomas.
  • [MeSH-major] Astrocytoma / diagnosis. Brain Neoplasms / diagnosis. Magnetic Resonance Imaging

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  • (PMID = 16171014.001).
  • [ISSN] 0042-8450
  • [Journal-full-title] Vojnosanitetski pregled
  • [ISO-abbreviation] Vojnosanit Pregl
  • [Language] srp
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Serbia and Montenegro
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85. You H, Kim YI, Im SY, Suh-Kim H, Paek SH, Park SH, Kim DG, Jung HW: Immunohistochemical study of central neurocytoma, subependymoma, and subependymal giant cell astrocytoma. J Neurooncol; 2005 Aug;74(1):1-8
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  • [Title] Immunohistochemical study of central neurocytoma, subependymoma, and subependymal giant cell astrocytoma.
  • For investigation of histogenesis of central neurocytomas (CNs), subependymoma (SEs), subependymal giant cell astrocytomas (SEGAs), we studied expression of various neuronal and glial biomarkers by immunohistochemical (IHC) study and reverse transcriptase-polymerase chain reaction (RT-PCR).
  • Control group was five ependymomas (EPs) and four pilocytic astrocytomas (PAs).
  • Conclusively, coexpression of neuronal and glial markers and expression of nestin in CNs, SEGAs and SEs suggested the origin of these tumor cells might be the stem cells being able to differentiate into both neuronal and glial phenotypes.
  • [MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Glioma, Subependymal / metabolism. Neurocytoma / metabolism


86. Ebinger M, Senf L, Wachowski O, Scheurlen W: No aberrant methylation of neurofibromatosis 1 gene (NF1) promoter in pilocytic astrocytoma in childhood. Pediatr Hematol Oncol; 2005 Jan-Feb;22(1):83-7
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  • [Title] No aberrant methylation of neurofibromatosis 1 gene (NF1) promoter in pilocytic astrocytoma in childhood.
  • With 30-40% of this heterogenous group, low-grade astrocytomas represent the most common subtype.
  • Neurofibromatosis type 1 (NF1) is strongly associated with the development of pilocytic astrocytoma (PA), frequently appearing as optic glioma.
  • Neurofibromatosis 1 gene (NF1 ) fulfills the criteria of a tumor suppressor gene and is deleted or mutated heterozygously in patients with NF1.
  • To clarify whether silencing of NF1 by promoter methylation plays a role in PA and especially in optic glioma, the authors investigated the methylation status in 30 PA, 6 of which had optic glioma.
  • To rule out that silencing of NF1 by promoter methylation is restricted to higher-grade astrocytomas, 15 pediatric WHO II degree and IV degree astrocytomas were analyzed: 12 astrocytomas II and 3 glioblastomas displayed no NF1 promoter methylation.
  • The authors conclude that NF1 silencing by methylation plays no role in low-grade astrocytoma.

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  • (PMID = 15770836.001).
  • [ISSN] 0888-0018
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neurofibromin 1
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87. Misra A, Chattopadhyay P, Chosdol K, Sarkar C, Mahapatra AK, Sinha S: Clonal mutations in primary human glial tumors: evidence in support of the mutator hypothesis. BMC Cancer; 2007;7:190
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  • BACKGROUND: A verifiable consequence of the mutator hypothesis is that even low grade neoplasms would accumulate a large number of mutations that do not influence the tumor phenotype (clonal mutations).
  • In this study, we have attempted to quantify the number of clonal mutations in primary human gliomas of astrocytic cell origin.
  • These alterations were identified in tumor tissue, microscopically confirmed to have over 70% neoplastic cells.
  • METHODS: Random Amplified Polymorphic DNA (RAPD) analysis was performed using a set of fifteen 10-mer primers of arbitrary but definite sequences in 17 WHO grade II astrocytomas (low grade diffuse astrocytoma or DA) and 16 WHO grade IV astrocytomas (Glioblastoma Multiforme or GBM).
  • The RAPD profile of the tumor tissue was compared with that of the leucocyte DNA of the same patient and alteration(s) scored.
  • CONCLUSION: This study demonstrates the presence of extensive clonal mutations in gliomas, more in lower grade.
  • This is consistent with our earlier work demonstrating that technique like RAPD analysis, unbiased for locus, is able to demonstrate more intra-tumor genetic heterogeneity in lower grade gliomas compared to higher grade.
  • [MeSH-minor] Cell Line, Tumor. Cloning, Molecular. DNA / metabolism. DNA Primers / chemistry. Data Interpretation, Statistical. Glioma / genetics. Humans. Leukocytes / metabolism. Models, Genetic. Models, Theoretical. Polymerase Chain Reaction. Polymorphism, Genetic. Reproducibility of Results

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  • (PMID = 17925012.001).
  • [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 / DNA Primers; 9007-49-2 / DNA
  • [Other-IDs] NLM/ PMC2190769
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88. Faria AV, Azevedo GC, Zanardi VA, Ghizoni E, Queiroz LS: Dissemination patterns of pilocytic astrocytoma. Clin Neurol Neurosurg; 2006 Sep;108(6):568-72
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  • [Title] Dissemination patterns of pilocytic astrocytoma.
  • Two patients with multifocal pilocytic astrocytoma diagnosed by magnetic resonance imaging (MRI) and confirmed by histopathological examination are reported.
  • They presented distinct sites and mechanisms of metastasis: to distant ventricles through the cerebral spinal fluid (CSF) in patient 1 and to contralateral parenchyma, possibly through white matter tracts, in patient 2, a pathway not so far reported in pilocytic astrocytoma.
  • Early detection of multifocal pilocytic astrocytoma by MRI may change treatment strategies and improve prognosis.
  • [MeSH-major] Astrocytoma / secondary. Brain Neoplasms / pathology


89. Hernández M, Martín R, García-Cubillas MD, Maeso-Hernández P, Nieto ML: Secreted PLA2 induces proliferation in astrocytoma through the EGF receptor: another inflammation-cancer link. Neuro Oncol; 2010 Oct;12(10):1014-23
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  • [Title] Secreted PLA2 induces proliferation in astrocytoma through the EGF receptor: another inflammation-cancer link.
  • Previously, we reported the mitogenic properties of this sPLA(2) in the human astrocytoma cell line 1321N1.
  • Therefore, this mechanism could contribute to worsen the prognosis of a tumor in an inflammatory microenvironment.
  • We also present more links of the tumor chain possibly susceptible to targeting.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Group II Phospholipases A2 / metabolism. Inflammation / metabolism. Receptor, Epidermal Growth Factor / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Enzyme Activation / physiology. Fluorescent Antibody Technique. Humans. Immunoblotting. Immunoprecipitation. Transcriptional Activation

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  • (PMID = 20639215.001).
  • [ISSN] 1523-5866
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.1.4 / Group II Phospholipases A2; EC 3.1.1.4 / PLA2G2A protein, human
  • [Other-IDs] NLM/ PMC3018927
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90. 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.
  • [MeSH-major] Astrocytoma / complications. Brain Neoplasms / complications. Sarcoptes scabiei. Scabies / diagnosis

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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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91. Honma S, Saito M, Kikuchi H, Saito Y, Oshima Y, Nakahata N, Yoshida M: A reduction of epidermal growth factor receptor is involved in brefelamide-induced inhibition of phosphorylation of ERK in human astrocytoma cells. Eur J Pharmacol; 2009 Aug 15;616(1-3):38-42
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  • [Title] A reduction of epidermal growth factor receptor is involved in brefelamide-induced inhibition of phosphorylation of ERK in human astrocytoma cells.
  • We found that brefelamide has a potent inhibitory growth effect measured by MTT assay in 1321N1 human astrocytoma cells.
  • These results suggest that one of the mechanisms of action of brefelamide is assumed to be inhibition of phosphorylation of ERK through a reduction of EGF receptor activity in 1321N1 human astrocytoma cells.
  • [MeSH-major] Amides / pharmacology. Antineoplastic Agents / pharmacology. Astrocytoma / metabolism. Astrocytoma / pathology. Phenols / pharmacology. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Epidermal Growth Factor / pharmacology. Extracellular Signal-Regulated MAP Kinases / metabolism. Gene Expression Regulation, Neoplastic / drug effects. Humans. Phosphorylation / drug effects. Signal Transduction / drug effects. Tyrosine / metabolism

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  • (PMID = 19559020.001).
  • [ISSN] 1879-0712
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Amides; 0 / Antineoplastic Agents; 0 / Phenols; 0 / brefelamide; 42HK56048U / Tyrosine; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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92. Samaras V, Piperi C, Levidou G, Zisakis A, Kavantzas N, Themistocleous MS, Boviatsis EI, Barbatis C, Lea RW, Kalofoutis A, Korkolopoulou P: Analysis of interleukin (IL)-8 expression in human astrocytomas: associations with IL-6, cyclooxygenase-2, vascular endothelial growth factor, and microvessel morphometry. Hum Immunol; 2009 Jun;70(6):391-7
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  • [Title] Analysis of interleukin (IL)-8 expression in human astrocytomas: associations with IL-6, cyclooxygenase-2, vascular endothelial growth factor, and microvessel morphometry.
  • Malignant astrocytomas are highly vascular neoplasms with potent angiogenic activity.
  • The present study aimed to investigate peripheral and local expression of interleukin (IL)-8 in astrocytomas with possible associations to IL-6, cyclooxygenase-2 (COX-2), vascular endothelial growth factor (VEGF) expression, and microvessel morphometry.
  • IL-6- and IL-8-secreting peripheral blood monocytes (PBMCs) were evaluated in 17 glioblastoma (WHO grade IV), 5 anaplastic astrocytoma (WHO grade III), and 6 diffuse astrocytoma patients (WHO grade II), in parallel with 23 healthy controls using enzyme-linked immunosorbent spot (ELISPOT) assay.
  • The IL-8 expression was assessed immunohistochemically in patients' tumor tissue sections and correlated with the expression of COX-2, VEGF, IL-6, and microvessel morphometry (assessed using CD34 antibody).
  • IL-6 and IL-8 were highly secreted in the PBMCs of glioma patients compared with controls (p = 0.0001, p < 0.0001, respectively), with a positive correlation between IL-8 expression and secretion levels (p = 0.001).
  • IL-8 immunoreactivity was detected in malignant cells or macrophages in perivascular areas and in pseudopalisading cells around necrosis and was positively correlated with histological grade (p = 0.0175) and tumor necrosis (p = 0.0793).
  • The coordinate expression and topographical relationship of IL-6, IL-8, COX-2, and VEGF in the same tumor areas (e.g., perinecrotic areas) attest to their intimate liaison in terms of cancer-induced angiogenesis, which is probably secondary to the induction of multiple interdependent molecular pathways.
  • Moreover, our study seems to be the first attempt to link IL-8 expression by tumor cells with histological grade, implicating its potent role in gliomagenesis.
  • [MeSH-major] Astrocytoma / immunology. Brain Neoplasms / immunology. Cyclooxygenase 2 / immunology. Microvessels / immunology. Vascular Endothelial Growth Factor A / immunology

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  • (PMID = 19332096.001).
  • [ISSN] 1879-1166
  • [Journal-full-title] Human immunology
  • [ISO-abbreviation] Hum. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Interleukin-6; 0 / Interleukin-8; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 1.14.99.1 / Cyclooxygenase 2
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93. Arulrajah S, Huisman TA: Pilomyxoid astrocytoma of the spinal cord with cerebrospinal fluid and peritoneal metastasis. Neuropediatrics; 2008 Aug;39(4):243-5
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  • [Title] Pilomyxoid astrocytoma of the spinal cord with cerebrospinal fluid and peritoneal metastasis.
  • Pilomyxoid astrocytoma (PMA) is a recently described rare tumor which is a variant of pilocytic astrocytoma (PA).
  • Two years later she presented with peritoneal carcinomatoses which was consistent with metastatic tumor via a ventriculoperitoneal (VP) shunt.
  • [MeSH-major] Astrocytoma / cerebrospinal fluid. Astrocytoma / pathology. Carcinoma / secondary. Peritoneal Neoplasms / secondary. Spinal Cord Neoplasms / cerebrospinal fluid. Spinal Cord Neoplasms / pathology

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  • (PMID = 19165714.001).
  • [ISSN] 0174-304X
  • [Journal-full-title] Neuropediatrics
  • [ISO-abbreviation] Neuropediatrics
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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94. Guo XL, Zhong YF, Sun YH, Liu HH, Jin B, Liang W, Li XS: [Muscle atrophy of hand as an initial sign in a patient with protoplasmic astrocytoma: a case report and literature review]. Beijing Da Xue Xue Bao; 2008 Dec 18;40(6):649-51
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  • [Title] [Muscle atrophy of hand as an initial sign in a patient with protoplasmic astrocytoma: a case report and literature review].
  • We reported a rare case of protoplasmic astrocytoma presenting small muscle atrophy of the right hand as an initial sign.
  • CT and MRI revealed multiply expansive intracranial lesion in left hemisphere, which was highly suspected of cerebral echinococcus or Balo disease.
  • The patient underwent surgical excision and pathological report was protoplasmic astrocytoma, with glial fibrillary acidic protein (GFAP, +++) of immunohistochemical method.
  • We reviewed clinical features, radiological manifestations and pathology of protoplasmic astrocytoma with medical literature documents.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Muscular Atrophy / complications

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  • (PMID = 19088841.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
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95. Barbosa KC, Oba-Shinjo SM, Uno M, Carvalho PO, Rosemberg S, Aguiar PH, Carlotti CG, Malheiros SM, Toledo S, Lotufo P, Marie SK: Association of EGFR c.2073A&gt;T polymorphism with decreased risk of diffusely infiltrating astrocytoma in a Brazilian case-control study. Int J Biol Markers; 2008 Jul-Sep;23(3):140-6
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  • [Title] Association of EGFR c.2073A>T polymorphism with decreased risk of diffusely infiltrating astrocytoma in a Brazilian case-control study.
  • Epidermal growth factor receptor (EGFR) gene overexpression has been implicated in the development of many types of tumors, including glioblastomas, the most frequent diffusely infiltrating astrocytomas.
  • However, little is known about the influence of the polymorphisms of EGFR on EGFR production and/or activity, possibly modulating the susceptibility to astrocytomas.
  • This study aimed to examine the association of two EGFR promoter polymorphisms (c.-191C>A and c.-216G>T) and the c.2073A>T polymorphism located in exon 16 with susceptibility to astrocytomas, EGFR gene expression and survival in a case-control study of 193 astrocytoma patients and 200 cancer-free controls.
  • We found that the variant TT genotype of the EGFR c.2073A>T polymorphism was associated with a significantly decreased risk of astrocytoma when compared with the AA genotype [sex- and age-adjusted odds ratio 0.51, 95% confidence interval 0.26-0.98].
  • No association of the two promoter EGFR polymorphisms (or combinations of these polymorphisms) and risk of astrocytomas, EGFR expression or survival was found.
  • Our findings suggest that modulation of the EGFR c.2073A>T polymorphism could play a role in future therapeutic approaches to astrocytoma.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Polymorphism, Genetic. Receptor, Epidermal Growth Factor / genetics

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  • (PMID = 18949739.001).
  • [ISSN] 0393-6155
  • [Journal-full-title] The International journal of biological markers
  • [ISO-abbreviation] Int. J. Biol. Markers
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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96. Tirabosco R, De Maglio G, Skrap M, Falconieri G, Pizzolitto S: Expression of the Polycomb-Group protein BMI1 and correlation with p16 in astrocytomas an immunohistochemical study on 80 cases. Pathol Res Pract; 2008;204(9):625-31
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  • [Title] Expression of the Polycomb-Group protein BMI1 and correlation with p16 in astrocytomas an immunohistochemical study on 80 cases.
  • To gain a new insight, we tested 80 primary brain astrocytomas for BMI1 expression using immunohistochemistry and established a correlation with the expression of p16, a negatively regulated target of BMI1 function.
  • Slight non-significant differences were noted in the expression profile between grades II, III, and IV astrocytomas.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Cyclin-Dependent Kinase Inhibitor p16 / biosynthesis. Nuclear Proteins / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Repressor Proteins / biosynthesis
  • [MeSH-minor] Biomarkers, Tumor / analysis. Gene Expression. Humans. Immunohistochemistry. Polycomb Repressive Complex 1. Prognosis

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  • (PMID = 18450386.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / BMI1 protein, human; 0 / Biomarkers, Tumor; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; EC 6.3.2.19 / Polycomb Repressive Complex 1
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97. Walker DG, Laherty R, Tomlinson FH, Chuah T, Schmidt C: Results of a phase I dendritic cell vaccine trial for malignant astrocytoma: potential interaction with adjuvant chemotherapy. J Clin Neurosci; 2008 Feb;15(2):114-21
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  • [Title] Results of a phase I dendritic cell vaccine trial for malignant astrocytoma: potential interaction with adjuvant chemotherapy.
  • Dendritic cell vaccination has been applied to the treatment of a variety of cancers, including malignant astrocytoma.
  • We have treated 13 patients with malignant astrocytoma using dendritic cell vaccination and have shown that this treatment is safe and is likely to be effective in combination with standard adjuvant therapy.
  • [MeSH-major] Astrocytoma / therapy. Brain Neoplasms / therapy. Cancer Vaccines / therapeutic use. Chemotherapy, Adjuvant / methods. Dendritic Cells / immunology. Immunotherapy, Active / methods

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  • (PMID = 18083572.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antigens, CD8; 0 / Cancer Vaccines; EC 3.1.3.48 / Antigens, CD45
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98. Amos S, Mut M, diPierro CG, Carpenter JE, Xiao A, Kohutek ZA, Redpath GT, Zhao Y, Wang J, Shaffrey ME, Hussaini IM: Protein kinase C-alpha-mediated regulation of low-density lipoprotein receptor related protein and urokinase increases astrocytoma invasion. Cancer Res; 2007 Nov 1;67(21):10241-51
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  • [Title] Protein kinase C-alpha-mediated regulation of low-density lipoprotein receptor related protein and urokinase increases astrocytoma invasion.
  • Low-density lipoprotein receptor-related protein (LRP) is expressed by glioblastoma, but the role of this receptor in astrocytic tumor invasion remains poorly understood.
  • Pretreatment of tumor cells with PKC inhibitors, phosphoinositide 3-kinase (PI3K) inhibitor, PKC-alpha small interfering RNA (siRNA), and short hairpin RNA abrogated phorbol 12-myristate 13-acetate-induced down-regulation of LRP and inhibited astrocytic tumor invasion in vitro.
  • Taken together, our results strongly suggest the involvement of PKC-alpha/PI3K signaling pathways in the regulation of LRP-mediated astrocytoma invasion.

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  • (PMID = 17974965.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS035122; United States / NHLBI NIH HHS / HL / P01HL48807; United States / NCI NIH HHS / CA / CA090851; United States / NCI NIH HHS / CA / R01 CA090851; United States / NINDS NIH HHS / NS / R29 NS035122; United States / NINDS NIH HHS / NS / NS035122-10; United States / NINDS NIH HHS / NS / R01 NS035122-10; United States / NINDS NIH HHS / NS / NS035122; United States / NHLBI NIH HHS / HL / P01 HL048807
  • [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 / Low Density Lipoprotein Receptor-Related Protein-1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.13 / Protein Kinase C-alpha; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; NI40JAQ945 / Tetradecanoylphorbol Acetate
  • [Other-IDs] NLM/ NIHMS48323; NLM/ PMC2386949
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99. Salhia B, Hwang JH, Smith CA, Nakada M, Rutka F, Symons M, Rutka JT: Role of myosin II activity and the regulation of myosin light chain phosphorylation in astrocytomas. Cell Motil Cytoskeleton; 2008 Jan;65(1):12-24
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  • [Title] Role of myosin II activity and the regulation of myosin light chain phosphorylation in astrocytomas.
  • Accordingly, in this study we examined the effects of ROCK and Rac1 inhibition on MLC phosphorylation in astrocytoma cells.
  • We also observed that astrocytoma migration is stimulated by low concentrations of the myosin II inhibitor blebbistatin.
  • Taken together, our data show that modulation of myosin II activity is important in determining optimal astrocytoma migration.
  • [MeSH-major] Astrocytoma / metabolism. Myosin Light Chains / metabolism. Myosin Type II / physiology
  • [MeSH-minor] Cell Line, Tumor. Cell Movement / physiology. Humans. Phosphorylation. rac1 GTP-Binding Protein / physiology. rho-Associated Kinases / physiology

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  • (PMID = 17896341.001).
  • [ISSN] 0886-1544
  • [Journal-full-title] Cell motility and the cytoskeleton
  • [ISO-abbreviation] Cell Motil. Cytoskeleton
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA87567
  • [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 / Myosin Light Chains; 0 / RAC1 protein, human; EC 2.7.11.1 / rho-Associated Kinases; EC 3.6.1.- / Myosin Type II; EC 3.6.5.2 / rac1 GTP-Binding Protein
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100. Sharma MK, Mansur DB, Reifenberger G, Perry A, Leonard JR, Aldape KD, Albin MG, Emnett RJ, Loeser S, Watson MA, Nagarajan R, Gutmann DH: Distinct genetic signatures among pilocytic astrocytomas relate to their brain region origin. Cancer Res; 2007 Feb 1;67(3):890-900
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinct genetic signatures among pilocytic astrocytomas relate to their brain region origin.
  • Pilocytic astrocytomas (PAs) are the most common glioma in children.
  • Whereas many PAs are slow-growing or clinically indolent, others exhibit more aggressive features with tumor recurrence and death.
  • Lastly, we also identified a gene expression pattern common to PAs and normal mouse astrocytes and neural stem cells from these distinct brain regions as well as a gene expression pattern shared between PAs and another human glial tumor (ependymoma) arising supratentorially compared with those originating in the posterior fossa.
  • [MeSH-major] Astrocytoma / genetics. Infratentorial Neoplasms / genetics. Supratentorial Neoplasms / genetics

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  • (PMID = 17283119.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE5582/ GSE5675
  • [Grant] United States / NCI NIH HHS / CA / P30 CA 91842
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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