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1. Katoh N, Shirato H, Aoyama H, Onimaru R, Suzuki K, Hida K, Miyasaka K, Iwasaki Y: Hypofractionated radiotherapy boost for dose escalation as a treatment option for high-grade spinal cord astrocytic tumor. J Neurooncol; 2006 May;78(1):63-9
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  • [Title] Hypofractionated radiotherapy boost for dose escalation as a treatment option for high-grade spinal cord astrocytic tumor.
  • PURPOSE: To retrospectively analyze the outcome of post-operative radiotherapy for spinal cord glioma with the emphasis on the hypofractionated radiotherapy boost for dose escalation as a treatment option for high-grade spinal cord astrocytic tumors.
  • There were 12 low-grade astrocytic tumors, 11 high-grade astrocytic tumors, 16 low-grade ependymal tumors and 2 high-grade ependymal tumors.
  • Among 11 patients with high-grade astrocytic tumors, 5 with anaplastic astrocytoma and 1 with glioblastoma received hypofractionated radiotherapy boost for dose escalation.
  • RESULTS: The Kaplan-Meier survival rates at 10 years from the date of the first surgery were 64% for the entire group, 47% for the astrocytic tumors and 84% for the ependymal tumors, respectively (P=0.009).
  • Among 11 patients with high-grade astrocytic tumors, the actuarial survival rate at 10 years was 35%.
  • DISCUSSION: The results for ependymal tumors and low-grade astrocytic tumors were comparable to those reported in the literature.
  • Hypofractionated radiotherapy boost for dose escalation may help to prolong the survival of patients with high-grade astrocytic tumors.
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Male. Middle Aged. Survival Analysis

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  • (PMID = 16314938.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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2. Ono A, Kanno H, Hayashi A, Nishimura S, Kyuma Y, Sato H, Ito S, Shimizu N, Chang CC, Gondo G, Yamamoto I, Sasaki T, Tanaka M: Collagen gel matrix assay as an in vitro chemosensitivity test for malignant astrocytic tumors. Int J Clin Oncol; 2007 Apr;12(2):125-30
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  • [Title] Collagen gel matrix assay as an in vitro chemosensitivity test for malignant astrocytic tumors.
  • METHODS: We examined the chemosensitivites for four anticancer agents - 1-(4-amino-2-methyl-5-pyrimidinyl) methyl-3 (2-chloroethyl)-3-nitrosourea hydrochloride (ACNU), carboplatin, cisplatin, and etoposide - of 43 malignant astrocytic tumors (21 anaplastic astrocytomas and 22 glioblastomas) by using a collagen gel matrix assay, and we also determined the survival periods of the tumor-bearing patients.
  • Individual chemotherapy for malignant astrocytic tumors, based on chemosensitivity data, could contribute to longer survival, particularly in anaplastic astrocytoma-bearing patients.
  • [MeSH-minor] Adult. Aged. Central Nervous System Neoplasms / drug therapy. Disease Progression. Disease-Free Survival. Drug Screening Assays, Antitumor. Female. Fibrin Foam. Follow-Up Studies. Glioblastoma / drug therapy. Glioblastoma / pathology. Humans. Japan. Karnofsky Performance Status. Male. Middle Aged. Sensitivity and Specificity. Survival Analysis. Tissue Adhesives. Treatment Outcome. Tumor Burden / drug effects. Tumor Cells, Cultured / drug effects

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  • (PMID = 17443280.001).
  • [ISSN] 1341-9625
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Fibrin Foam; 0 / Tissue Adhesives; 0S726V972K / Nimustine; 6PLQ3CP4P3 / Etoposide; 9007-34-5 / Collagen; BG3F62OND5 / Carboplatin; Q20Q21Q62J / Cisplatin
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3. Miwa T, Hirose Y, Sasaki H, Ikeda E, Yoshida K, Kawase T: Genetic characterization of adult infratentorial gliomas. J Neurooncol; 2009 Feb;91(3):251-5
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  • [Title] Genetic characterization of adult infratentorial gliomas.
  • Adult infratentorial gliomas are rare and have not been well studied.
  • We therefore conducted genetic analysis of those tumors to see if there was any characteristic that could be relevant in clinical management and understanding of tumorigenesis.
  • Nineteen adult infratentorial gliomas were analyzed for chromosomal aberration by comparative genomic hybridization, and for expression of p53 and epidermal growth factor receptor (EGFR) by immunohistochemistry.
  • However, the gain of 7q, the characteristic abnormality of supratentorial astrocytomas commonly associated with the gaining of 7p, was observed only in 1 of 11 adult infratentorial astrocytic tumors.
  • Our findings might suggest the presence of distinct tumorigenic pathway in adult infratentorial gliomas.
  • [MeSH-major] Brain Neoplasms / genetics. Frontal Lobe / pathology. Glioma / genetics. Receptor, Epidermal Growth Factor / genetics. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Adult. Aged. Chromosome Aberrations. Chromosome Deletion. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Chromosomes, Human, Pair 7 / genetics. Comparative Genomic Hybridization. Female. Humans. Loss of Heterozygosity. Male. Middle Aged. Young Adult

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  • (PMID = 18941867.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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4. Yao Y, Tang X, Li S, Mao Y, Zhou L: Brain tumor stem cells: view from cell proliferation. Surg Neurol; 2009 Mar;71(3):274-9
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  • [Title] Brain tumor stem cells: view from cell proliferation.
  • A small population of TSCs, which form neurospheres and possess the capacity for self-renewal, has been recently identified in adult and pediatric brain tumors.
  • They differentiate into phenotypically diverse populations, including neuronal, astrocytic, and oligodendroglial cells in vitro and recapitulate original tumors in vivo.
  • The understanding of brain TSCs has been greatly advanced by the knowledge of cell proliferation, which contributes to initiate and sustain the malignant phenotype.
  • In this article, the authors summarized the evidence of the presence of TSCs in human brain tumors and emphasized the significance of the proliferative status of TSCs.
  • Finally, the preliminary evidence that TSCs in malignant brain tumors have more proliferative capacity than stem/progenitor cells in benign brain tumors was discussed.
  • [MeSH-major] Adult Stem Cells / pathology. Brain Neoplasms / pathology. Neoplastic Stem Cells / pathology

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  • (PMID = 19249579.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 40
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5. Balss J, Meyer J, Mueller W, Korshunov A, Hartmann C, von Deimling A: Analysis of the IDH1 codon 132 mutation in brain tumors. Acta Neuropathol; 2008 Dec;116(6):597-602
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  • [Title] Analysis of the IDH1 codon 132 mutation in brain tumors.
  • We analyzed the genomic region spanning wild type R132 of IDH1 by direct sequencing in 685 brain tumors including 41 pilocytic astrocytomas, 12 subependymal giant cell astrocytomas, 7 pleomorphic xanthoastrocytomas, 93 diffuse astrocytomas, 120 adult glioblastomas, 14 pediatric glioblastomas, 105 oligodendrogliomas, 83 oligoastrocytomas, 31 ependymomas, 58 medulloblastomas, 9 supratentorial primitive neuroectodermal tumors, 17 schwannomas, 72 meningiomas and 23 pituitary adenomas.
  • The very high frequency of IDH1 mutations in WHO grade II astrocytic and oligodendroglial gliomas suggests a role in early tumor development.
  • [MeSH-major] Brain Neoplasms / genetics. Isocitrate Dehydrogenase / genetics. Mutation

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  • (PMID = 18985363.001).
  • [ISSN] 1432-0533
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 1.1.1.41 / Isocitrate Dehydrogenase
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6. Rodriguez FJ, Scheithauer BW, Jenkins R, Burger PC, Rudzinskiy P, Vlodavsky E, Schooley A, Landolfi J: Gliosarcoma arising in oligodendroglial tumors ("oligosarcoma"): a clinicopathologic study. Am J Surg Pathol; 2007 Mar;31(3):351-62
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  • [Title] Gliosarcoma arising in oligodendroglial tumors ("oligosarcoma"): a clinicopathologic study.
  • Gliosarcomas are morphologically biphasic tumors composed of glial and sarcomatous elements.
  • Seven patients with oligodendroglial tumors and a sarcomatous component were identified.
  • At first resection, the tumors included grade II oligodendroglioma (n=3), grade III oligodendroglioma (n=1), grade II oligoastrocytoma (n=1), and grade III oligoastrocytoma (n=2).
  • The sarcomatous component developed in recurrent/progressive tumors in 6 cases but was a focal finding at first tumor resection in 1 and included fibrosarcoma (n=5), leiomyosarcoma (n=1), or pleomorphic myogenic sarcoma (n=1).
  • Rhabdoid change was a focal finding in the sarcomatous component of 1 tumor.
  • The relatively frequent presence of 1p/19q codeletion in both glial and sarcomatous components supports the notion that the sarcomatous component represents a metaplastic change occurring in the glial element, the same mechanism active in classic astrocytic gliosarcomas.
  • [MeSH-major] Brain Neoplasms / pathology. Gliosarcoma / pathology. Neoplasms, Second Primary / pathology. Oligodendroglioma / pathology
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Brain / surgery. Chromosome Deletion. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Combined Modality Therapy. Fatal Outcome. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasm Recurrence, Local. Neoplasm Staging

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  • (PMID = 17325476.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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7. Yan B, Chour HH, Peh BK, Lim C, Salto-Tellez M: RhoA protein expression correlates positively with degree of malignancy in astrocytomas. Neurosci Lett; 2006 Oct 23;407(2):124-6
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  • Astrocytic tumors are the most common intracranial neoplasms.
  • A molecular marker that provides an objective reference for classification and prognostication of astrocytic tumors would be useful in diagnostic pathology.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. rhoA GTP-Binding Protein / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Immunohistochemistry. Infant. Male. Middle Aged. Neoplasm Invasiveness / pathology. Paraffin Embedding. Tissue Fixation. Up-Regulation

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  • (PMID = 16978776.001).
  • [ISSN] 0304-3940
  • [Journal-full-title] Neuroscience letters
  • [ISO-abbreviation] Neurosci. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] EC 3.6.5.2 / rhoA GTP-Binding Protein
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8. Scrideli CA, Carlotti CG Jr, Mata JF, Neder L, Machado HR, Oba-Sinjo SM, Rosemberg S, Marie SK, Tone LG: Prognostic significance of co-overexpression of the EGFR/IGFBP-2/HIF-2A genes in astrocytomas. J Neurooncol; 2007 Jul;83(3):233-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This study aimed to define the profile of their expressions, interactions and correlation with clinical features and prognostic significance in microdissected tumor samples from 84 patients with astrocytomas of different grades and from 6 white matter non-neoplasic brain tissue sample.
  • EGFR, IGFBP-2 and HIF-2A gene expression levels were analyzed by quantitative real-time PCR and differed significantly between grades I-IV astrocytic tumors (P < 0.0001, P < 0.0001 and P: 0.0013, respectively) when analyzed by the Kruskal-Wallis test.
  • Grade I astrocytomas presented gene expression levels similar to those encountered in samples of microdissected white matter of non-neoplastic brain tissue Overexpression of the EGFR, IGFBP-2 and HIF-2A genes was significantly associated with lower 2-year survival (P: 0.009, P: 0.0002 and P: 0.008, respectively).
  • [MeSH-major] Astrocytoma / genetics. Basic Helix-Loop-Helix Transcription Factors / genetics. Brain Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Insulin-Like Growth Factor Binding Protein 2 / genetics. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adult. Child. Female. Humans. Male. Microdissection. Middle Aged. Neoplasm Staging. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17285230.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Insulin-Like Growth Factor Binding Protein 2; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / endothelial PAS domain-containing protein 1; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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9. Kashimura H, Inoue T, Beppu T, Ogasawara K, Ogawa A: Diffusion tensor imaging for differentiation of recurrent brain tumor and radiation necrosis after radiotherapy--three case reports. Clin Neurol Neurosurg; 2007 Jan;109(1):106-10
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  • [Title] Diffusion tensor imaging for differentiation of recurrent brain tumor and radiation necrosis after radiotherapy--three case reports.
  • Fractional anisotropy (FA) is influenced by histological data such as cellularity, vascularity and/or fiber structure in astrocytic tumors.
  • We describe two patients with tumor recurrence and one patient with radiation necrosis who were diagnosed using assessment of FA value.
  • The assessment of FA value in enhanced lesions after radiotherapy may be able to differentiate radiation necrosis from tumor recurrence.
  • [MeSH-major] Brain / pathology. Brain Neoplasms / pathology. Diffusion Magnetic Resonance Imaging. Glioblastoma / pathology. Neoplasm Recurrence, Local / pathology. Radiation Injuries / pathology
  • [MeSH-minor] Adult. Aged. Anisotropy. Female. Humans. Middle Aged. Necrosis. Radiotherapy / adverse effects

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  • (PMID = 16793199.001).
  • [ISSN] 0303-8467
  • [Journal-full-title] Clinical neurology and neurosurgery
  • [ISO-abbreviation] Clin Neurol Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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10. Fountzilas G, Karkavelas G, Kalogera-Fountzila A, Karina M, Ignatiadis M, Koukoulis G, Plataniotis G, Misailidou D, Bobos M, Pectasides D, Razis E, Karavelis A, Selviaridis P: Post-operative combined radiation and chemotherapy with temozolomide and irinotecan in patients with high-grade astrocytic tumors. A phase II study with biomarker evaluation. Anticancer Res; 2006 Nov-Dec;26(6C):4675-86
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  • [Title] Post-operative combined radiation and chemotherapy with temozolomide and irinotecan in patients with high-grade astrocytic tumors. A phase II study with biomarker evaluation.
  • BACKGROUND: Clinical studies have shown that temozolomide (TMZ) and irinotecan demonstrate activity in high grade astrocytic tumors (HGAT).
  • Two out of the five biomarkers studied, epidermal growth factor receptor (EGFR) and vascular endothelial growth factor-C (VEGF-C), were found to be overexpressed in 74% of the tumors, however they had no predictive value for progression-free or overall survival.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / metabolism. Astrocytoma / therapy. Biomarkers, Tumor / biosynthesis. Brain Neoplasms / metabolism. Brain Neoplasms / therapy. Glioblastoma / metabolism. Glioblastoma / therapy
  • [MeSH-minor] Adult. Aged. Camptothecin / administration & dosage. Camptothecin / adverse effects. Camptothecin / analogs & derivatives. Combined Modality Therapy. Cyclooxygenase 2 / biosynthesis. Dacarbazine / administration & dosage. Dacarbazine / adverse effects. Dacarbazine / analogs & derivatives. Feasibility Studies. Female. Humans. Ki-67 Antigen / biosynthesis. Male. Middle Aged. PTEN Phosphohydrolase / biosynthesis. Patient Compliance. Postoperative Care. Vascular Endothelial Growth Factor C / biosynthesis

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  • (PMID = 17214326.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Vascular Endothelial Growth Factor C; 7673326042 / irinotecan; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; XT3Z54Z28A / Camptothecin
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11. 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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  • Astrocytomas are the most common form of primary brain tumors.
  • 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.
  • 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.
  • [MeSH-minor] Adolescent. Adult. Base Sequence. Blotting, Western. DNA Primers. Female. Humans. Immunohistochemistry. Male. Middle Aged. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Young Adult


12. Barbashina V, Salazar P, Holland EC, Rosenblum MK, Ladanyi M: Allelic losses at 1p36 and 19q13 in gliomas: correlation with histologic classification, definition of a 150-kb minimal deleted region on 1p36, and evaluation of CAMTA1 as a candidate tumor suppressor gene. Clin Cancer Res; 2005 Feb 1;11(3):1119-28
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  • [Title] Allelic losses at 1p36 and 19q13 in gliomas: correlation with histologic classification, definition of a 150-kb minimal deleted region on 1p36, and evaluation of CAMTA1 as a candidate tumor suppressor gene.
  • Because most 1p deletions in gliomas involve almost the entire chromosome arm, narrowing the region of the putative tumor suppressor gene has been difficult.
  • EXPERIMENTAL DESIGN: Among 205 consecutive cases of glioma studied for 1p loss of heterozygosity (LOH), 112 tumors were evaluated for both 1p and 19q LOH using at least three polymorphic markers on 1p and 19q each.
  • The latter group included both low-grade tumors (oligodendroglioma, diffuse astrocytoma, and "oligoastrocytoma") and high-grade tumors (anaplastic oligodendrogliomas, anaplastic astrocytomas, anaplastic oligoastrocytomas).
  • Tumors with small segmental 1p losses (defined as LOH at some loci with retention of heterozygosity at other loci) were studied using a more extensive panel of markers to define the 1p MDR.
  • In contrast, no astrocytomas and only 6 of 30 (20%) oligoastrocytic tumors had combined 1p/19q loss.
  • Eleven tumors (6 oligodendrogliomas or having oligodendroglial components, 5 purely astrocytic) with small segmental 1p losses underwent further detailed LOH mapping.
  • All informative tumors in the oligodendroglial group and 2 of 3 informative astrocytomas showed LOH at 1p36.23, with a 150-kb MDR located between D1S2694 and D1S2666, entirely within the CAMTA1 transcription factor gene.
  • CAMTA1 is normally expressed predominantly in non-neoplastic adult brain tissue.
  • Relative to the latter, the expression level of CAMTA1 was low in oligodendroglial tumors and was further halved in cases with 1p deletion compared with those without 1p deletion (Mann-Whitney, P = 0.03).
  • CONCLUSIONS: Our data confirm the strong association of combined 1p/19q loss with classic oligodendroglioma histology and identify a very small segment of 1p36 located within CAMTA1 that was deleted in all oligodendroglial tumors with 1p LOH.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Glioma / genetics. Loss of Heterozygosity
  • [MeSH-minor] Adult. Astrocytoma / genetics. Astrocytoma / pathology. Calcium-Binding Proteins / genetics. Chromosome Deletion. Chromosome Mapping. Expressed Sequence Tags. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Humans. Microsatellite Repeats. Mutation. Oligodendroglioma / genetics. Oligodendroglioma / pathology. Reverse Transcriptase Polymerase Chain Reaction. Trans-Activators / genetics

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  • (PMID = 15709179.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CAMTA1 protein, human; 0 / Calcium-Binding Proteins; 0 / Trans-Activators
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13. Jing R, Pizzolato G, Robson RM, Gabbiani G, Skalli O: Intermediate filament protein synemin is present in human reactive and malignant astrocytes and associates with ruffled membranes in astrocytoma cells. Glia; 2005 Apr 15;50(2):107-20
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  • Western blotting shows that astrocytic tumors contain greater amounts of alpha-synemin than do normal brain tissues.
  • These tumors also contain beta-synemin, which is not detectable in normal brain.
  • Immunohistochemistry demonstrates that, while synemin is present in normal adult brain only in vascular smooth muscle cells, it is newly synthesized by reactive and neoplastic astrocytes.
  • [MeSH-major] Astrocytes / metabolism. Astrocytoma / metabolism. Brain Neoplasms / metabolism. Intermediate Filament Proteins / metabolism. Muscle Proteins / metabolism
  • [MeSH-minor] Actinin / metabolism. Antibodies, Neoplasm / biosynthesis. Antibodies, Neoplasm / isolation & purification. Blotting, Western. Brain Chemistry. Cell Membrane / metabolism. Cell Movement. Fluorescent Antibody Technique. Humans. Immunoenzyme Techniques. Immunoprecipitation. Reverse Transcriptase Polymerase Chain Reaction. Vimentin / metabolism

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15657940.001).
  • [ISSN] 0894-1491
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS-35317
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Intermediate Filament Proteins; 0 / Muscle Proteins; 0 / Vimentin; 0 / desmuslin; 11003-00-2 / Actinin
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14. 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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  • 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.
  • 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


15. Nakamura M, Shimada K, Ishida E, Higuchi T, Nakase H, Sakaki T, Konishi N: Molecular pathogenesis of pediatric astrocytic tumors. Neuro Oncol; 2007 Apr;9(2):113-23
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  • [Title] Molecular pathogenesis of pediatric astrocytic tumors.
  • Astrocytomas are the most common pediatric brain tumors, accounting for 7%-8% of all childhood cancers.
  • Relatively few studies have been performed on their molecular properties; therefore, classification of pediatric astrocytic tumors into genetic subtypes similar to that of adult tumors remains to be defined.
  • Here, we report an extensive characterization of 44 pediatric astrocytomas--16 diffuse astrocytomas (WHO grade II), 10 anaplastic astrocytomas (WHO grade III), and 18 glioblastomas (WHO grade IV)--in terms of genetic alterations frequently observed in adult astrocytomas.
  • Loss of heterozygosity (LOH) on 1p/19q and 10p/10q was less common in pediatric astrocytic tumors than in those seen in adults, but the frequency of LOH on 22q was comparable, occurring in 44% of diffuse astrocytomas, 40% of anaplastic astrocytomas, and 61% of glioblastomas.
  • Interestingly, a higher frequency of p53 mutations and LOH on 19q and 22q in tumors from children six or more years of age at diagnosis was found, compared with those from younger children.
  • Our results suggest some differences in children compared to adults in the genetic pathways leading to the formation of de novo astrocytic tumors.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics

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  • (PMID = 17327574.001).
  • [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] EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC1871665
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16. Zhang LY, Ye J, Zhang F, Li FF, Li H, Gu Y, Liu F, Chen GS, Li Q: Axin induces cell death and reduces cell proliferation in astrocytoma by activating the p53 pathway. Int J Oncol; 2009 Jul;35(1):25-32
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  • Astrocytic tumors are the most common brain tumors with various genetic defects.
  • As a tumor suppressor gene, Axin could control cell death and growth.
  • [MeSH-major] Apoptosis. Astrocytoma / metabolism. Brain Neoplasms / metabolism. Cell Proliferation. Glioblastoma / metabolism. Repressor Proteins / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Animals. Axin Protein. Benzothiazoles / pharmacology. Cell Line, Tumor. Child. Child, Preschool. Cyclin D1 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. RNA Interference. Rats. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Toluene / analogs & derivatives. Toluene / pharmacology. Transfection. Young Adult

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  • (PMID = 19513548.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Axin Protein; 0 / Benzothiazoles; 0 / Ccnd1 protein, rat; 0 / Cdkn1a protein, rat; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Repressor Proteins; 0 / Tumor Suppressor Protein p53; 0 / pifithrin; 136601-57-5 / Cyclin D1; 3FPU23BG52 / Toluene
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17. Kaloshi G, Mokhtari K, Carpentier C, Taillibert S, Lejeune J, Marie Y, Delattre JY, Godbout R, Sanson M: FABP7 expression in glioblastomas: relation to prognosis, invasion and EGFR status. J Neurooncol; 2007 Sep;84(3):245-8
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  • Nuclear expression of FABP7 was more specifically related to EGFR amplification and more invasive tumors.
  • These data, although they need to be confirmed by further studies, support the relation between FABP7, astrocytic features, invasion and poor prognosis and suggests that EGFR amplification is associated with nuclear translocation of FABP7.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / pathology. Carrier Proteins / biosynthesis. Glioblastoma / pathology. Receptor, Epidermal Growth Factor / metabolism. Tumor Suppressor Proteins / biosynthesis
  • [MeSH-minor] Adult. Aged. Cell Nucleus / metabolism. Cytoplasm / metabolism. Fatty Acid-Binding Protein 7. Female. Gene Amplification. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Invasiveness / pathology. Prognosis. Protein Transport / physiology

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  • (PMID = 17415524.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / FABP7 protein, human; 0 / Fatty Acid-Binding Protein 7; 0 / Tumor Suppressor Proteins; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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18. Mahzouni P, Mohammadizadeh F, Mougouei K, Moghaddam NA, Chehrei A, Mesbah A: Determining the relationship between "microvessel density" and different grades of astrocytoma based on immunohistochemistry for "factor VIII-related antigen" (von Willebrand factor) expression in tumor microvessels. Indian J Pathol Microbiol; 2010 Oct-Dec;53(4):605-10
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  • [Title] Determining the relationship between "microvessel density" and different grades of astrocytoma based on immunohistochemistry for "factor VIII-related antigen" (von Willebrand factor) expression in tumor microvessels.
  • BACKGROUND: Astrocytic brain tumors are the most common primary central nervous system tumors, which are classified into four grades.
  • Because tumor angiogenesis is a necessary factor for growth and invasiveness of malignancies, microvessel density (MVD) and intensity of angiogenesis may be used to determine the grade of astrocytomas and plan therapy accordingly.
  • The intensity of microvessel stain increases in parallel with increasing tumor grade.
  • [MeSH-minor] Adult. Child. Female. Formaldehyde. Humans. Immunohistochemistry / methods. Male. Microscopy. Middle Aged. Paraffin Embedding. Pathology / methods. Statistics as Topic. Tissue Fixation

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  • (PMID = 21045378.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / von Willebrand Factor; 1HG84L3525 / Formaldehyde
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19. Hirose T, Ishizawa K, Shimada S: Utility of in situ demonstration of 1p loss and p53 overexpression in pathologic diagnosis of oligodendroglial tumors. Neuropathology; 2010 Dec;30(6):586-96
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  • [Title] Utility of in situ demonstration of 1p loss and p53 overexpression in pathologic diagnosis of oligodendroglial tumors.
  • To improve the diagnostic accuracy of oligodendroglial tumors and to find more convenient parameters that could predict the cytogenetic status, oligodendroglial and astrocytic tumors were cytogenetically and immunohistochemically investigated.
  • Materials included 22 oligodendroglial tumors (15 oligodendrogliomas and 7 oligoastrocytomas) and 20 astrocytic tumors.
  • Furthermore, TP53 mutation analyses were carried out on three oligodendroglial tumors showing p53 protein overexpression with a direct sequence analysis.
  • Our FISH studies demonstrated 1p loss in 73% of oligodendroglial tumors (80% oligodendrogliomas and 57% oligoastrocytomas) and in only 10% of astrocytic tumors.
  • There were no clear-cut morphologic differences between 1p-deleted and 1p-intact oligodendroglial tumors.
  • GFAP and Olig2 were expressed in most oligodendroglial and astrocytic tumors, and their cellular localization was almost independent of each other.
  • Overexpression of p53 was observed in five oligodendroglial tumors, all of which were 1p-intact.
  • In comparison, 16 oligodendroglial tumors with 1p deletion showed no overexpression of p53.
  • TP53 missense mutations were detected in three of the p53 overexpressed oligodendroglial tumors studied.
  • Our results suggest that 1p loss is almost specific to oligodendroglial tumors.
  • Although the prediction of 1p status based solely on the morphologic features seems to be difficult, the immunohistochemistry for p53 is a useful tool in that p53 overexpression is closely related to the 1p-intact status in oligodendroglial tumors.
  • [MeSH-major] Astrocytoma / diagnosis. Brain Neoplasms / diagnosis. Chromosomes, Human, Pair 1 / genetics. Oligodendroglioma / diagnosis. Tumor Suppressor Protein p53 / biosynthesis
  • [MeSH-minor] Adult. Aged. Basic Helix-Loop-Helix Transcription Factors / biosynthesis. Female. Gene Deletion. Glial Fibrillary Acidic Protein / biosynthesis. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mutation. Nerve Tissue Proteins / biosynthesis

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  • [Copyright] © 2010 Japanese Society of Neuropathology.
  • (PMID = 20408960.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Glial Fibrillary Acidic Protein; 0 / Nerve Tissue Proteins; 0 / OLIG2 protein, human; 0 / Tumor Suppressor Protein p53
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20. 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 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.
  • PTEN was not found in most of astrocytomas, 64% of low grade and 74% of high grade tumors showed no PTEN staining.
  • 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.
  • Loss of p21Waf1/Cip1 expression was shown in 20% of low and in 45% of high grade tumors.
  • In the subgroup of high grade tumors with wild type p53, 86% showed p21Waf1/Cip1 expression, whereas in the subgroup of high grade tumors with altered p53, only 35% displayed p21Waf1/Cip1.
  • PTEN defects may also participate in aggressive tumor behaviour through activation of the PKB/Akt pathway.
  • [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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21. Jha P, Agarwal S, Pathak P, Srivastava A, Suri V, Sharma MC, Chosdol K, Srivastava T, Gupta D, Gupta A, Suri A, Sarkar C: Heterozygosity status of 1p and 19q and its correlation with p53 protein expression and EGFR amplification in patients with astrocytic tumors: novel series from India. Cancer Genet Cytogenet; 2010 Apr 15;198(2):126-34
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  • [Title] Heterozygosity status of 1p and 19q and its correlation with p53 protein expression and EGFR amplification in patients with astrocytic tumors: novel series from India.
  • There are few reports of loss of heterozygosity (LOH) of 1p and 19q in astrocytic tumors, especially glioblastoma multiforme (GBM).
  • Thus, 1p and 19q LOH can occur in astrocytic tumors, most commonly in secondary GBMs without morphological correlation with an oligodendroglial histology.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Gene Amplification. Genes, erbB-1. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Case-Control Studies. Child. Female. Heterozygote. Humans. India. Loss of Heterozygosity. Male. Middle Aged. Young Adult

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20362227.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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22. Avninder S, Sharma MC, Deb P, Mehta VS, Karak AK, Mahapatra AK, Sarkar C: Gemistocytic astrocytomas: histomorphology, proliferative potential and genetic alterations--a study of 32 cases. J Neurooncol; 2006 Jun;78(2):123-7
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  • Immunoreactivity for CD3 (T-cells), CD20 (B-cells) and CD68 (macrophages) were evaluated to characterize the perivascular inflammatory infiltrates, while p53, epidermal growth factor receptor (EGFR), cyclin D1 and p27-immunolabeling were studied to analyze the tumor biology.Overall, the mean gemistocytic index in the study was 39.6% (range, 12.2-80.8%), with multinucleation in gemistocytes and mitosis being present in 56.2% and 15.6% respectively.
  • Similar type of inflammatory infiltrates was also present within the tumor parenchyma.
  • MIB-1 labeling was restricted to the small astrocytic cells, similar to p27 and cyclin D1 immunoreactivity, both of which were present in 71.5% cases.
  • Gemistocytes lack proliferative activity possibly indicating terminal differentiation, while small cells are the proliferating cells and their overall percentage may reflect the biological aggressiveness of these tumors and help to identify GAs of higher grade undergoing malignant progression.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Giant Cells / pathology. Ki-67 Antigen / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adolescent. Adult. Antigens, CD / metabolism. Antigens, CD20 / metabolism. Antigens, CD3 / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Cell Proliferation. DNA Mutational Analysis. Female. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis

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  • (PMID = 16614946.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD20; 0 / Antigens, CD3; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD68 antigen, human; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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23. Shen CF, Yuan XR, Qin ZQ: [Clinical significance of the expression of the RCAS1 mRNA and protein in astrocytic tumors]. Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2007 Oct;32(5):836-9
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  • [Title] [Clinical significance of the expression of the RCAS1 mRNA and protein in astrocytic tumors].
  • OBJECTIVE: To determine the mRNA and protein expressions of RCAS1 in human astrocytic tumors, and to explore the relation between their expression and the genesis and development of tumor.
  • METHODS: The RCAS1 mRNA expression in human astrocytic tumors was evaluated by RT-PCR, and the RCAS1 protein expression was studied by immunohistochemical staining.
  • RCAS1 protein expression was positively correlated with the tumor grade (r=0.573,P<0.001).
  • The RCAS1 protein was not detected in normal brain tissues by immunohistochemical staining.
  • CONCLUSION: The RCAS1 expression is related to the histological grade of astrocytic tumor.
  • In astrocytic tumors, the RCAS1 expression is regulated transcriptionally and posttranscriptionally.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Astrocytoma / metabolism. Brain Neoplasms / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Male. Middle Aged. RNA, Messenger / genetics. Young Adult

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  • (PMID = 18007080.001).
  • [ISSN] 1672-7347
  • [Journal-full-title] Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
  • [ISO-abbreviation] Zhong Nan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] Controlled Clinical Trial; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / EBAG9 protein, human; 0 / RNA, Messenger
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24. Shrestha P, Saito T, Hama S, Arifin MT, Kajiwara Y, Yamasaki F, Hidaka T, Sugiyama K, Kurisu K: Geminin: a good prognostic factor in high-grade astrocytic brain tumors. Cancer; 2007 Mar 1;109(5):949-56
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  • [Title] Geminin: a good prognostic factor in high-grade astrocytic brain tumors.
  • For this study, the authors investigated geminin expression in high-grade astrocytic tumors, including anaplastic astrocytoma (AA) and glioblastoma multiforme (GBM), with a view to predicting clinical outcomes on this basis in patients with these malignant brain tumors.
  • METHODS: Immunohistochemistry was used to detect geminin expression in 51 patients with high-grade astrocytic tumors (19 AA and 32 GBM).
  • The relation of geminin expression to clinical outcome in these malignant brain tumors was analyzed by using the Kaplan-Meier method and a Cox proportional hazards regression model.
  • CONCLUSIONS: Although it is an inhibitor of DNA proliferation and, thus, is a cell cycle inhibitor, geminin expression was found in all malignant astrocytic tumors.
  • [MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Cell Cycle Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Child. Female. Geminin. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Survival Analysis

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  • (PMID = 17262828.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / GMNN protein, human; 0 / Geminin
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25. Jacobs JF, Grauer OM, Brasseur F, Hoogerbrugge PM, Wesseling P, Gidding CE, van de Rakt MW, Figdor CG, Coulie PG, de Vries IJ, Adema GJ: Selective cancer-germline gene expression in pediatric brain tumors. J Neurooncol; 2008 Jul;88(3):273-80
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  • [Title] Selective cancer-germline gene expression in pediatric brain tumors.
  • Cancer-germline genes (CGGs) code for immunogenic antigens that are present in various human tumors and can be targeted by immunotherapy.
  • Their expression has been studied in a wide range of human tumors in adults.
  • We measured the expression of 12 CGGs in pediatric brain tumors, to identify targets for therapeutic cancer vaccines.
  • Real Time PCR was used to quantify the expression of genes MAGE-A1, MAGE-A2, MAGE-A3, MAGE-A4, MAGE-A6, MAGE-A10, MAGE-A12, MAGE-C2, NY-ESO-1 and GAGE-1,2,8 in 50 pediatric brain tumors of different histological subtypes.
  • Fifty-five percent of the medulloblastomas (n = 11), 86% of the ependymomas (n = 7), 40% of the choroid plexus tumors (n = 5) and 67% of astrocytic tumors (n = 27) expressed one or more CGGs.
  • With exception of a minority of tumors, the overall level of CGG expression in pediatric brain tumors was low.
  • CGG-encoded antigens are therefore suitable targets in a very selected group of pediatric patients with a brain tumor.
  • Interestingly, glioblastomas from adult patients expressed CGGs more often and at significantly higher levels compared to pediatric glioblastomas.
  • This observation is in line with the notion that pediatric and adult glioblastomas develop along different genetic pathways.
  • [MeSH-major] Brain Neoplasms / genetics. Gene Expression. Genes, Neoplasm
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Humans. Immunohistochemistry. Infant. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18398575.001).
  • [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
  • [Other-IDs] NLM/ PMC2440921
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26. Moskowitz SI, Jin T, Prayson RA: Role of MIB1 in predicting survival in patients with glioblastomas. J Neurooncol; 2006 Jan;76(2):193-200
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  • BACKGROUND: Histologic immunomarkers of cell cycle proteins have been utilized for prognosis in high-grade astrocytic tumors.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Glioblastoma / metabolism. Ki-67 Antigen / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Combined Modality Therapy. Female. Humans. Immunohistochemistry. Karnofsky Performance Status. Male. Middle Aged. Predictive Value of Tests. Retrospective Studies. Survival Analysis

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  • (PMID = 16234986.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen
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27. Guo D, Nilsson J, Haapasalo H, Raheem O, Bergenheim T, Hedman H, Henriksson R: Perinuclear leucine-rich repeats and immunoglobulin-like domain proteins (LRIG1-3) as prognostic indicators in astrocytic tumors. Acta Neuropathol; 2006 Mar;111(3):238-46
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  • [Title] Perinuclear leucine-rich repeats and immunoglobulin-like domain proteins (LRIG1-3) as prognostic indicators in astrocytic tumors.
  • We have previously characterized three human leucine-rich repeats and immunoglobulin-like domains (LRIG) genes and proteins, named LRIG1-3 and proposed that they may act as suppressors of tumor growth.
  • In this study, we evaluated the mRNA expression level of LRIG1-3 in human glioma cell lines and control-matched glioma tissues, characterized the sub-cellular localization of an LRIG3-GFP fusion protein, and analyzed the relationship between sub-cellular localization of LRIG1-3 and clinical parameters in 404 astrocytic tumors by immunohistochemistry.
  • Perinuclear staining of LRIG3 was associated with a lower proliferation index and was in addition to tumor grade, an independent prognostic factor.
  • Furthermore, within the groups of grade III and grade IV tumors, perinuclear staining of LRIG3 significantly correlated with better survival.
  • These results indicate that expression and sub-cellular localization of LRIG1-3 might be of importance in the pathogenesis and prognosis of astrocytic tumors.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Membrane Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Line, Tumor. Cell Proliferation. Child. Child, Preschool. Female. Gene Expression Regulation, Neoplastic. Humans. Infant. Infant, Newborn. Male. Middle Aged. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Survival Rate


28. Burgoyne AM, Palomo JM, Phillips-Mason PJ, Burden-Gulley SM, Major DL, Zaremba A, Robinson S, Sloan AE, Vogelbaum MA, Miller RH, Brady-Kalnay SM: PTPmu suppresses glioma cell migration and dispersal. Neuro Oncol; 2009 Dec;11(6):767-78
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  • Glioblastomas (GBMs) are the highest grade of primary brain tumors with astrocytic similarity and are characterized by marked dispersal of tumor cells.
  • PTPmu expression was examined in human GBM, low-grade astrocytoma, and normal brain tissue.
  • These studies revealed a striking loss of PTPmu protein expression in highly dispersive GBMs compared to less dispersive low-grade astrocytomas and normal brain.
  • The migration of brain tumor cells was assessed in vitro using a scratch wound assay.
  • Next, a brain slice assay replicating the three-dimensional environment of the brain was used.
  • To assess migration, labeled U-87 MG glioma cells were injected into adult rat brain slices, and their movement was followed over time.
  • However, PTPmu shRNA induced migration and dispersal of U-87 MG cells in the brain slice.
  • Together, these data suggest that loss of PTPmu in human GBMs contributes to tumor cell migration and dispersal, implicating loss of PTPmu in glioma progression.

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  • (PMID = 19304959.001).
  • [ISSN] 1523-5866
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS051520-04; United States / NEI NIH HHS / EY / P30 EY011373; United States / NINDS NIH HHS / NS / R01 NS051520; United States / NINDS NIH HHS / NS / R01-NS051520; United States / NCI NIH HHS / CA / K08 CA101954; United States / NINDS NIH HHS / NS / NS051520-04; United States / NEI NIH HHS / EY / P30 EY011373-119002; United States / NCI NIH HHS / CA / P20 CA103736; United States / NEI NIH HHS / EY / P30 EY011373-129002; United States / NCI NIH HHS / CA / P30 CA043703; United States / NEI NIH HHS / EY / P30 EY011373-139002; United States / NCI NIH HHS / CA / T32 CA059366; United States / NINDS NIH HHS / NS / NS051520-02; United States / NINDS NIH HHS / NS / NS051520-01A1; United States / NEI NIH HHS / EY / EY011373-139002; United States / NIGMS NIH HHS / GM / T32-GM007250; United States / NEI NIH HHS / EY / P30-EY11373; United States / NEI NIH HHS / EY / EY011373-119002; United States / NINDS NIH HHS / NS / NS051520-03; United States / NINDS NIH HHS / NS / R01 NS051520-02; United States / NINDS NIH HHS / NS / R01 NS051520-01A1; United States / NEI NIH HHS / EY / EY011373-129002; United States / NCI NIH HHS / CA / K08-CA101954; United States / NCI NIH HHS / CA / R01-CA116257; United States / NCI NIH HHS / CA / P30-CA043703; United States / NCI NIH HHS / CA / T32-CA059366; United States / NCI NIH HHS / CA / R01 CA116257; United States / NIGMS NIH HHS / GM / T32 GM007250; United States / NINDS NIH HHS / NS / R01 NS051520-03; United States / NCI NIH HHS / CA / P20-CA103736
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / RNA, Small Interfering; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 2
  • [Other-IDs] NLM/ PMC2802397
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29. Parafiniuk D, Jezewski D, Nowacki P: [Malignant astrocytoma as a recurrance of astrocytoma II WHO after 13 years. Case report and literature review]. Ann Acad Med Stetin; 2010;56(2):45-50
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  • Astrocytomas--neroepithelial originated tumors that belong to the big, differential group of tumors, which derive from astrocytic glial.
  • They include slow growing tumors such as fibillary astrocytoma or very malignant glioblastoma multiforme.
  • Due to this adverse event MRI was ordered and suspicion of tumor recurrence was put forward.
  • According to literature, the factors regarding remission time, tumor malignancy and therapeutic aim were analyzed.
  • [MeSH-major] Brain Neoplasms / radiotherapy. Brain Neoplasms / surgery. Neoplasm Recurrence, Local / diagnosis
  • [MeSH-minor] Adult. Astrocytoma. Female. Frontal Lobe. Humans. Reoperation. Seizures / etiology

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  • (PMID = 21473001.001).
  • [ISSN] 1427-440X
  • [Journal-full-title] Annales Academiae Medicae Stetinensis
  • [ISO-abbreviation] Ann Acad Med Stetin
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Poland
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30. Rorive S, Maris C, Debeir O, Sandras F, Vidaud M, Bièche I, Salmon I, Decaestecker C: Exploring the distinctive biological characteristics of pilocytic and low-grade diffuse astrocytomas using microarray gene expression profiles. J Neuropathol Exp Neurol; 2006 Aug;65(8):794-807
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  • Although more than 50 microarray-related studies have been carried out to characterize the molecular profiles of astrocytic tumors, we have identified only 11 that provide sound data on low-grade astrocytomas.
  • Interestingly, a group of 6 genes (TIMP4, C1NH, CHAD, THBS4, IGFBP2, and TLE2) constitute an expression profile characteristic of grade I astrocytomas as compared with all other categories of tissue (normal brain, grade II, and high-grade astrocytomas).
  • The end products (proteins) of these genes act as antimigratory compounds, a fact that could explain why pilocytic astrocytomas behave as compact (well-circumscribed) tumors as opposed to all the other astrocytic tumor types that diffusely invade the brain parenchyma.
  • [MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Gene Expression Profiling / methods. Gene Expression Regulation, Neoplastic / genetics. Genetic Predisposition to Disease / genetics
  • [MeSH-minor] Adult. Cell Adhesion / genetics. Cell Movement / genetics. Child. Extracellular Matrix Proteins / genetics. Extracellular Matrix Proteins / metabolism. Humans. Models, Neurological. Neoplasm Invasiveness / genetics. Neoplasm Invasiveness / physiopathology. Oligonucleotide Array Sequence Analysis / methods. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16896313.001).
  • [ISSN] 0022-3069
  • [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 / Biomarkers, Tumor; 0 / Extracellular Matrix Proteins
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31. Liebrich M, Guo LH, Schluesener HJ, Schwab JM, Dietz K, Will BE, Meyermann R: Expression of interleukin-16 by tumor-associated macrophages/activated microglia in high-grade astrocytic brain tumors. Arch Immunol Ther Exp (Warsz); 2007 Jan-Feb;55(1):41-7
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  • [Title] Expression of interleukin-16 by tumor-associated macrophages/activated microglia in high-grade astrocytic brain tumors.
  • MATERIALS AND METHODS: Expression of IL-16 was analyzed by immunohistochemistry in human astrocytic brain tumors and the rat C6 glioblastoma tumor model.
  • IL-16 was detected in both human astrocytic brain tumors and rat C6 glioma.
  • RESULTS: Compared with human control brains, a significant increase in the percentages of parenchymal IL-16+ macrophages/microglia was observed already in grade II astrocytomas, indicating that IL-16+ immunostaining could be a descriptor of a macrophage/microglia subset in astrocytic brain tumors.
  • This increase in IL-16 immunoreactivity correlated with WHO grades of human astrocytic brain tumors.
  • [MeSH-major] Astrocytoma / immunology. Brain Neoplasms / immunology. Glioblastoma / immunology. Interleukin-16 / biosynthesis. Macrophages / immunology. Microglia / immunology
  • [MeSH-minor] Adult. Aged. Animals. Cell Line, Tumor. Female. Humans. Inflammation Mediators / metabolism. Male. Middle Aged. Rats. Rats, Sprague-Dawley

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  • (PMID = 17221335.001).
  • [ISSN] 0004-069X
  • [Journal-full-title] Archivum immunologiae et therapiae experimentalis
  • [ISO-abbreviation] Arch. Immunol. Ther. Exp. (Warsz.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Inflammation Mediators; 0 / Interleukin-16
  • [Other-IDs] NLM/ PMC3234149
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32. Rushing EJ, Sandberg GD, Horkayne-Szakaly I: High-grade astrocytomas show increased Nestin and Wilms's tumor gene (WT1) protein expression. Int J Surg Pathol; 2010 Aug;18(4):255-9
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  • [Title] High-grade astrocytomas show increased Nestin and Wilms's tumor gene (WT1) protein expression.
  • Wilms's tumor gene (WT1) is overexpressed in a variety of hematologic malignancies and solid tumors.
  • Recently, WT1 protein has been considered as a molecular target of cancer immunotherapy for several solid tumors and as a tool for monitoring minimal residual disease in leukemia patients.
  • There are only few investigations on WT1 expression in central nervous system neoplasms, which suggest that the WT1 gene may play an important role in tumorigenesis of primary astrocytic tumors and that high-grade tumors express high levels of WT1 proteins.
  • WT1 and nestin shared overlapping expression in all gliomas and were increased in high-grade examples, highlighting their potential use as diagnostic and prognostic tumor markers.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Intermediate Filament Proteins / metabolism. Nerve Tissue Proteins / metabolism. WT1 Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor / metabolism. Child. Child, Preschool. Female. Humans. Immunohistochemistry. Infant. Male. Middle Aged. Nestin. Tissue Array Analysis. Young Adult


33. Sharma S, Free A, Mei Y, Peiper SC, Wang Z, Cowell JK: Distinct molecular signatures in pediatric infratentorial glioblastomas defined by aCGH. Exp Mol Pathol; 2010 Oct;89(2):169-74
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  • Glioblastomas (GBM) are rare in children, but reportedly have more varied outcome which suggests differences in tumor etiology compared to typical GBM of adults.
  • Two of these tumors occurred in the brainstem and one in the spinal cord.
  • While histologically typical, one brainstem tumor showed mainly pleomorphic astrocytic cells, whereas the other brainstem and spinal tumors showed a GFAP positive small cell component.
  • Segmental loss involving chromosome 8 was seen in all three tumors (Chr8;133039446-136869494, Chr8;pter-3581577, and Chr8;pter-30480019 respectively), whereas loss involving chromosome 16 was seen in only 2 cases with small cell components (Chr16;31827239-qter and Chr16;pter-29754532).
  • None of the frequent losses, gains and amplifications known to occur in adult GBM were identified, suggesting that pediatric infratentorial glioblastomas show a molecular karyotype that was more characteristic of pediatric embryonal tumors than adult GBM.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20621092.001).
  • [ISSN] 1096-0945
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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34. Keating AK, Kim GK, Jones AE, Donson AM, Ware K, Mulcahy JM, Salzberg DB, Foreman NK, Liang X, Thorburn A, Graham DK: Inhibition of Mer and Axl receptor tyrosine kinases in astrocytoma cells leads to increased apoptosis and improved chemosensitivity. Mol Cancer Ther; 2010 May;9(5):1298-307
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  • Astrocytomas account for the majority of malignant brain tumors diagnosed in both adult and pediatric patients.
  • In this study, we found that Mer and Axl mRNA transcript and protein expression were elevated in astrocytic patient samples and cell lines. shRNA-mediated knockdown of Mer and Axl RTK expression led to an increase in apoptosis in astrocytoma cells.

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  • (PMID = 20423999.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA082086-10; United States / NCI NIH HHS / CA / T32 CA082086; United States / NCI NIH HHS / CA / T32 CA082086-10
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; EC 2.7.10.1 / MERTK protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / axl receptor tyrosine kinase
  • [Other-IDs] NLM/ NIHMS304681; NLM/ PMC3138539
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35. Kotoula V, Cheva A, Barbanis S, Papadimitriou CS, Karkavelas G: hTERT immunopositivity patterns in the normal brain and in astrocytic tumors. Acta Neuropathol; 2006 Jun;111(6):569-78
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  • [Title] hTERT immunopositivity patterns in the normal brain and in astrocytic tumors.
  • Accumulating data about the impact of hTERT in astrocytic tumor carcinogenesis and recent evidence about its association with disease outcome prompt the evaluation of this molecule with methods applicable in routine pathology practice.
  • In this study, we investigated hTERT protein expression with immunohistochemistry (IHC) and the NCL-hTERT antibody in 49 astrocytic tumors.
  • Low- and high-grade astrocytic tumors were found positive for hTERT in 74 and 85% of cases, respectively.
  • Heterogeneity in the distribution of hTERT-positive cells was observed in all tumors.
  • Positive endothelial cells were found in astrocytic tumors of all grades, even when tumor cells showed no hTERT immunoreactivity.
  • A subset of mature normal neurons was positive for hTERT (pattern As), suggesting a role for this molecule in neuronal maintenance in the adult brain.
  • The nuclear hTERT IPs described here may reflect the functional status of non-neoplastic brain and neoplastic astrocytic cells and support the model of a continuum in the development of glioblastomas from diffuse fibrillary astrocytomas.
  • [MeSH-major] Astrocytes / metabolism. Astrocytoma / metabolism. Brain Chemistry / physiology. Brain Neoplasms / metabolism. Telomerase / genetics. Telomerase / metabolism
  • [MeSH-minor] Adult. Aged. Child. Endothelial Cells / pathology. Female. Fixatives. Formaldehyde. Humans. Immunohistochemistry. In Situ Hybridization. Male. Middle Aged. Paraffin Embedding. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16614861.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Fixatives; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 1HG84L3525 / Formaldehyde; EC 2.7.7.49 / Telomerase
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36. Huang X, Bai HM, Chen L, Li B, Lu YC: Reduced expression of LC3B-II and Beclin 1 in glioblastoma multiforme indicates a down-regulated autophagic capacity that relates to the progression of astrocytic tumors. J Clin Neurosci; 2010 Dec;17(12):1515-9
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  • [Title] Reduced expression of LC3B-II and Beclin 1 in glioblastoma multiforme indicates a down-regulated autophagic capacity that relates to the progression of astrocytic tumors.
  • The aim of this study was to investigate the expression of microtubule-associated protein 1 light chain 3B (LC3B) and the autophagy-related gene Beclin 1 in astrocytic tumors and to analyze their expression profiles with respect to the development of astrocytic tumors.
  • The expression patterns of LC3B and Beclin 1 were analyzed by immunohistochemistry and/or western blotting in tumor samples from 62 patients with different grades of astrocytic tumor.
  • Western blot analysis indicated that the average optical densitometry (OD) ratio of Beclin 1 in high-grade astrocytic tumors (World Health Organization [WHO] grade III/IV) was lower than in low-grade astrocytic tumors (WHO grade I/II, p = 0.036).
  • The expression of LC3B-I exhibited no significant difference among the various grades of astrocytic tumor.
  • However, the average OD ratio of LC3B-II was lower in glioblastoma multiforme (GBM) than in other grades of astrocytic tumor (p = 0.030).
  • The progression of astrocytic tumors was related to a decrease in autophagic capacity represented by the loss of LC3B-II and Beclin 1 expression.
  • [MeSH-major] Apoptosis Regulatory Proteins / biosynthesis. Brain Neoplasms / pathology. Gene Expression Regulation, Neoplastic. Glioblastoma / pathology. Membrane Proteins / biosynthesis. Microtubule-Associated Proteins / biosynthesis
  • [MeSH-minor] Adult. Astrocytoma / metabolism. Astrocytoma / pathology. Autophagy. Blotting, Western. Disease Progression. Down-Regulation. Female. Humans. Immunohistochemistry. Male. Middle Aged

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20863706.001).
  • [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 / Apoptosis Regulatory Proteins; 0 / BECN1 protein, human; 0 / Membrane Proteins; 0 / Microtubule-Associated Proteins; 0 / light chain 3, human
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37. Gunal A, Onguru O, Safali M, Beyzadeoglu M: Fascin expression [corrected] in glial tumors and its prognostic significance in glioblastomas. Neuropathology; 2008 Aug;28(4):382-6
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  • [Title] Fascin expression [corrected] in glial tumors and its prognostic significance in glioblastomas.
  • In this study, we evaluated fascin expression in glial tumors and its relation with histologic grade.
  • Seventy-six glial tumors including 44 glioblastomas with known survival time, 18 anaplastic astrocytomas (AAs), six diffuse astrocytomas (DAs), and eight pilocytic astrocytomas (PAs) were examined immunohistochemically for fascin expression.
  • Fascin was observed in the neurons of normal brain tissue and endothelium of vascular spaces in the glial tumors.
  • In conclusion, fascin expression levels are correlated with histologic grade and fascin overexpression may play an important role in the biologic behavior of glial astrocytic tumors and in the prognosis of GBs.
  • [MeSH-major] Brain Neoplasms / metabolism. Carrier Proteins / biosynthesis. Glioblastoma / metabolism. Microfilament Proteins / biosynthesis
  • [MeSH-minor] Adult. Aged. Astrocytoma / metabolism. Astrocytoma / mortality. Astrocytoma / pathology. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Middle Aged. Prognosis

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  • (PMID = 18298442.001).
  • [ISSN] 0919-6544
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Microfilament Proteins; 146808-54-0 / fascin
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38. Crespo-Rodríguez AM, Smirniotopoulos JG, Rushing EJ: MR and CT imaging of 24 pleomorphic xanthoastrocytomas (PXA) and a review of the literature. Neuroradiology; 2007 Apr;49(4):307-15
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  • INTRODUCTION: The aim of our study was to review the imaging appearance of PXA, a rare and usually low-grade, astrocytic tumor that typically occurs in young adults.
  • On CT without contrast enhancement, PXA was an iso- or hypoattenuating mass, and calcification was seen in six tumors and inner table remodeling was seen in three patients younger than 12 years.
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Male. Middle Aged. Retrospective Studies. Statistics, Nonparametric

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  • (PMID = 17205313.001).
  • [ISSN] 0028-3940
  • [Journal-full-title] Neuroradiology
  • [ISO-abbreviation] Neuroradiology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 44
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39. Yi W, Haapasalo H, Holmlund C, Järvelä S, Raheem O, Bergenheim AT, Hedman H, Henriksson R: Expression of leucine-rich repeats and immunoglobulin-like domains (LRIG) proteins in human ependymoma relates to tumor location, WHO grade, and patient age. Clin Neuropathol; 2009 Jan-Feb;28(1):21-7
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  • [Title] Expression of leucine-rich repeats and immunoglobulin-like domains (LRIG) proteins in human ependymoma relates to tumor location, WHO grade, and patient age.
  • LRIG1 has been shown to be a suppressor of tumor growth by counteracting the signaling of epidermal growth factor receptor (EGFR) family members, including EGFR (ERBB1).
  • Expression of LRIG proteins seems to be of importance in the pathogenesis of astrocytic tumors.
  • The indications that expression and subcellular localization of LRIG proteins could be pathogenetically associated with specific clinicopathological features of ependymoma tumors might be of importance in the carcinogeneses and tumor progression of human ependymomas.
  • [MeSH-major] Brain Neoplasms / pathology. Ependymoma / pathology. Membrane Proteins / biosynthesis. Spinal Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Cell Nucleus / metabolism. Child. Child, Preschool. Cytoplasm / metabolism. Female. Gene Expression. Humans. Immunohistochemistry. Infant. Male. Membrane Glycoproteins / biosynthesis. Middle Aged. Tissue Array Analysis. World Health Organization


40. Huijbers IJ, Iravani M, Popov S, Robertson D, Al-Sarraj S, Jones C, Isacke CM: A role for fibrillar collagen deposition and the collagen internalization receptor endo180 in glioma invasion. PLoS One; 2010;5(3):e9808
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  • BACKGROUND: Glioblastoma multiforme (GBM, WHO grade IV) is the most common and most malignant of astrocytic brain tumors, and is associated with rapid invasion into neighboring tissue.
  • In other tumor types it is well established that such invasion involves a complex interaction between tumor cells and locally produced extracellular matrix.
  • In GBMs, surprisingly little is known about the associated matrix components, in particular the fibrillar proteins such as collagens that are known to play a key role in the invasion of other tumor types.
  • Correlated with this collagen deposition we observed high level expression of the collagen-binding receptor Endo180 (CD280) in the tumor cells.
  • CONCLUSIONS/SIGNIFICANCE: This study demonstrates, for the first time, that fibrillar collagens are extensively deposited in GBMs and that the collagen internalization receptor Endo180 is both highly expressed in these tumors and that it serves to mediate the invasion of tumor cells through collagen-containing matrices.
  • Together these data provide important insights into the mechanism of GBM invasion and identify Endo180 as a potential target to limit matrix turnover by glioma cells and thereby restrict tumor progression.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Signal Transduction. Transforming Growth Factor beta / metabolism

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  • (PMID = 20339555.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Endo180; 0 / Receptors, Mitogen; 0 / Transforming Growth Factor beta; 9007-34-5 / Collagen
  • [Other-IDs] NLM/ PMC2842440
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41. Ardeleanu C, Ceauşu M, Butur G, Grămadă ZF, Dănăilă L, Hălălău F, Arsene D: p53 protein and bcl-2 expression in glioblastomas. Pathological correlations in a comprehensive series. Rom J Morphol Embryol; 2005;46(4):275-8
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  • p53 and bcl-2 are two well-known antiapoptotic factors associated with gliomas, and mostly astrocytic tumors.
  • The correlations between their expression and several tumor-related factors (age, location, recurrence, proliferating potential) were investigated.
  • [MeSH-major] Glioblastoma / chemistry. Glioblastoma / pathology. Proto-Oncogene Proteins c-bcl-2 / analysis. Tumor Suppressor Protein p53 / analysis
  • [MeSH-minor] Adult. Aged. Aging. Female. Humans. Immunohistochemistry. Ki-67 Antigen / analysis. Male. Middle Aged

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  • (PMID = 16688362.001).
  • [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] Journal Article
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53
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42. Seiz M, Tuettenberg J, Meyer J, Essig M, Schmieder K, Mawrin C, von Deimling A, Hartmann C: Detection of IDH1 mutations in gliomatosis cerebri, but only in tumors with additional solid component: evidence for molecular subtypes. Acta Neuropathol; 2010 Aug;120(2):261-7
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  • [Title] Detection of IDH1 mutations in gliomatosis cerebri, but only in tumors with additional solid component: evidence for molecular subtypes.
  • The current WHO classification of brain tumors defines gliomatosis cerebri (GC) as an extensively infiltrating astrocytic glioma involving at least three cerebral lobes.
  • Recent reports showed IDH1 mutations in astrocytic and oligodendroglial tumors WHO grades II and III and in secondary glioblastomas with a frequency of up to 90%, whereas IDH1 mutations occurred in only 5% of primary glioblastomas.
  • We identified IDH1 mutations in 10/24 (42%) cases, which also included a solid tumor portion (type 2 GC), but not in 11 "classical" cases without solid tumor mass (type 1 GC).
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Isocitrate Dehydrogenase / genetics. Mutation / genetics. Neoplasms, Neuroepithelial / genetics. Neoplasms, Neuroepithelial / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Arginine / genetics. Astrocytoma / secondary. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. DNA Mutational Analysis. Female. Histidine / genetics. Humans. In Situ Hybridization, Fluorescence / methods. Magnetic Resonance Imaging / methods. Male. Middle Aged. Oligodendroglioma / secondary. Polymorphism, Single Nucleotide / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism


43. Levidou G, El-Habr E, Saetta AA, Bamias C, Katsouyanni K, Patsouris E, Korkolopoulou P: P53 immunoexpression as a prognostic marker for human astrocytomas: a meta-analysis and review of the literature. J Neurooncol; 2010 Dec;100(3):363-71
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  • During the past few decades, researchers have been looking for parameters with an impact on the prognosis of patients with astrocytic tumors. p53 is one of the most widely investigated molecules in human gliomas.
  • A meta-analysis was performed on the studies that applied Cox models and had adjusted the hazard ratio of p53 expression with tumor grade and patients' age.
  • A second meta-analysis performed only on glioblastomas showed that the overall risk of mortality in these tumors was -0.123 (-0.346 to 0.100) and was not statistically significant.
  • After almost 20 years of research, published evidence does not substantiate the usefulness of p53 immunohistochemical expression as a prognostic marker in patients with astrocytic neoplasms.
  • [MeSH-major] Astrocytoma / diagnosis. Astrocytoma / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adult. Biomarkers / metabolism. Biomarkers, Tumor / metabolism. Female. Humans. Linear Models. Male. Middle Aged. Predictive Value of Tests. Prognosis

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  • [ErratumIn] J Neurooncol. 2010 Dec;100(3):373. Katsougiannis, Klea [corrected to Katsouyanni, Klea]
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  • (PMID = 20461443.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Protein p53
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44. Momota H, Narita Y, Matsushita Y, Miyakita Y, Shibui S: p53 abnormality and tumor invasion in patients with malignant astrocytoma. Brain Tumor Pathol; 2010 Oct;27(2):95-101
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  • [Title] p53 abnormality and tumor invasion in patients with malignant astrocytoma.
  • Malignant astrocytomas are characterized by diffusely infiltrating nature, and the abnormality of p53 is a cytogenetic hallmark of astrocytic tumors.
  • To elucidate the relationship between p53 abnormality and invasiveness of the tumors, we studied mutation and protein expression of p53 in 48 consecutive patients with malignant astrocytoma (14 anaplastic astrocytomas and 34 glioblastoma multiformes).
  • The tumors were classified into three categories according to the features of magnetic resonance imaging, and 5, 7, and 36 tumors were classified into diffuse, multiple, and single type, respectively.
  • We then examined how these tumor types correlate with MIB-1 staining index, TP53 gene mutation, and p53 protein expression.
  • Furthermore, diffuse- and multiple-type tumors were significantly correlated with poor progression-free survival, whereas only multiple-type tumors were significantly correlated with poor overall survival.
  • As diffuse and multiple features on imaging modalities represent invasive characteristics of the tumors, p53 abnormalities may affect the invasive and aggressive nature of malignant astrocytomas.
  • [MeSH-major] Astrocytoma / genetics. Astrocytoma / pathology. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Genes, p53 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. DNA, Neoplasm / genetics. Female. Glial Fibrillary Acidic Protein / genetics. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Mitotic Index. Mutation / genetics. Mutation / physiology. Neoplasm Invasiveness / genetics. Neoplasm Invasiveness / pathology. Survival Analysis. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Vascular Endothelial Growth Factor A / metabolism. Young Adult

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  • (PMID = 21046311.001).
  • [ISSN] 1861-387X
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Glial Fibrillary Acidic Protein; 0 / Tumor Suppressor Protein p53; 0 / Vascular Endothelial Growth Factor A
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45. Torii K, Tsuyuguchi N, Kawabe J, Sunada I, Hara M, Shiomi S: Correlation of amino-acid uptake using methionine PET and histological classifications in various gliomas. Ann Nucl Med; 2005 Dec;19(8):677-83
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  • OBJECTIVE: The uptake of L-methyl-11C-methionine (MET) by gliomas is greater than that by intact tissue, making methionine very useful for evaluation of tumor extent.
  • If the degree of malignancy of brain tumors can be evaluated by MET-PET, the usefulness of MET-PET as a means of diagnosing brain tumors will increase.
  • Tumors included diffuse astrocytoma, anaplastic astrocytoma, glioblastoma, ependymoma, oligodendroglioma, medulloblastoma, dysembryoplastic neuroepithelial tumor, choroid plexus papilloma, central neurocytoma, optic glioma, gliomatosis cerebri, pleomorphic xanthoastrocytoma, and ganglioglioma.
  • Tumor activity and degree of malignancy were evaluated using Ki-67LI (LI: labeling index) and Kaplan-Meier survival curves.
  • The correlations between methionine uptake and tumor proliferation (tumor versus contralateral gray matter ratio (T/N) and Ki-67LI) were determined for the group of all subjects.
  • The existence of significant correlations between T/N and Ki-67LI and between SUV and Ki-67LI was determined for astrocytic tumors.
  • Receiver operating characteristics (ROC) analysis of T/N and standardized uptake value (SUV) was performed for the group of astrocytic tumors.
  • Ki-67LI differed significantly between the high-grade group and low-grade group at T/N levels between 1.5 and 1.8 on analysis using tumor proliferative potential (p = 0.019-0.031).
  • CONCLUSIONS: When analysis was confined to cases of astrocytic tumor, a correlation was noted between methionine accumulation and Ki-67LI.
  • For the astrocytic tumors, T/N ratio seemed to be more useful as a diagnostic indicator than SUV.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / radionuclide imaging. Glioma / pathology. Glioma / radionuclide imaging. Methionine / pharmacokinetics. Positron-Emission Tomography / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Image Interpretation, Computer-Assisted / methods. Male. Middle Aged. ROC Curve. Radiopharmaceuticals / pharmacokinetics. Reproducibility of Results. Sensitivity and Specificity. Statistics as Topic. Tissue Distribution


46. Higano S, Yun X, Kumabe T, Watanabe M, Mugikura S, Umetsu A, Sato A, Yamada T, Takahashi S: Malignant astrocytic tumors: clinical importance of apparent diffusion coefficient in prediction of grade and prognosis. Radiology; 2006 Dec;241(3):839-46
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  • [Title] Malignant astrocytic tumors: clinical importance of apparent diffusion coefficient in prediction of grade and prognosis.
  • PURPOSE: To retrospectively assess the apparent diffusion coefficient (ADC) for prediction of malignancy and prognosis of malignant astrocytic tumors.
  • Findings from 37 consecutive patients (21 men, 16 women; mean age, 43 years) with pathologically proved malignant astrocytic tumors that included 22 glioblastomas (GBMs) and 15 anaplastic astrocytomas (AAs) were retrospectively evaluated.
  • The minimum ADC value of each tumor was preoperatively determined from several regions of interest defined in the tumor, preferably with avoidance of cystic or necrotic components, on ADC maps derived from isotropic diffusion-weighted images.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Diffusion Magnetic Resonance Imaging
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Combined Modality Therapy. Female. Humans. Image Processing, Computer-Assisted. Ki-67 Antigen / analysis. Male. Predictive Value of Tests. Prognosis. ROC Curve. Retrospective Studies. Treatment Outcome

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  • [Copyright] (c) RSNA, 2006.
  • (PMID = 17032910.001).
  • [ISSN] 0033-8419
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen
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47. Combs SE, Nagy M, Edler L, Rausch R, Bischof M, Welzel T, Debus J, Schulz-Ertner D: Comparative evaluation of radiochemotherapy with temozolomide versus standard-of-care postoperative radiation alone in patients with WHO grade III astrocytic tumors. Radiother Oncol; 2008 Aug;88(2):177-82
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  • [Title] Comparative evaluation of radiochemotherapy with temozolomide versus standard-of-care postoperative radiation alone in patients with WHO grade III astrocytic tumors.
  • Outcome after radiochemotherapy (RCHT) with temozolomide (TMZ) versus radiotherapy (RT) for WHO grade III astrocytic tumors was evaluated.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Astrocytoma / drug therapy. Astrocytoma / radiotherapy. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Dacarbazine / analogs & derivatives
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Combined Modality Therapy. Disease Progression. Female. Humans. Male. Middle Aged. Proportional Hazards Models. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • (PMID = 18395280.001).
  • [ISSN] 0167-8140
  • [Journal-full-title] Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology
  • [ISO-abbreviation] Radiother Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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48. Lehnhardt FG, Bock C, Röhn G, Ernestus RI, Hoehn M: Metabolic differences between primary and recurrent human brain tumors: a 1H NMR spectroscopic investigation. NMR Biomed; 2005 Oct;18(6):371-82
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  • [Title] Metabolic differences between primary and recurrent human brain tumors: a 1H NMR spectroscopic investigation.
  • High-resolution proton magnetic resonance spectroscopy was performed on tissue specimens from 33 patients with astrocytic tumors (22 astrocytomas, 11 glioblastomas) and 13 patients with meningiomas.
  • For all patients, samples of primary tumors and their first recurrences were examined.
  • Spectroscopic features of tumor types, as determined on samples of the primary occurrences, were in good agreement with previous studies.
  • Metabolic changes of an evolving tumor were observed in recurrent astrocytomas: owing to their consecutive assessments, more indicators of malignant degeneration were detected in astrocytoma recurrences (e.g.
  • The present investigation demonstrated a correlation of the tCho-signal with tumor progression.
  • This may be related to an early stage of malignant transformation, not yet detectable morphologically, and emphasizes the high sensitivity of 1H NMR spectroscopy in elucidating characteristics of brain tumor metabolism.
  • [MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Glioblastoma / metabolism. Magnetic Resonance Spectroscopy / methods. Meningioma / metabolism. Neoplasm Recurrence, Local / metabolism
  • [MeSH-minor] Adult. Humans. Middle Aged. Protons

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  • [Copyright] Copyright 2005 John Wiley & Sons, Ltd
  • (PMID = 15959923.001).
  • [ISSN] 0952-3480
  • [Journal-full-title] NMR in biomedicine
  • [ISO-abbreviation] NMR Biomed
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Controlled Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Protons
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49. Heimberger AB, McGary EC, Suki D, Ruiz M, Wang H, Fuller GN, Bar-Eli M: Loss of the AP-2alpha transcription factor is associated with the grade of human gliomas. Clin Cancer Res; 2005 Jan 1;11(1):267-72
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  • PURPOSE: The activator protein (AP)-2alpha transcription factor plays a crucial role in the progression of several human tumors, including malignant melanoma, prostate, and breast cancer.
  • The microarray included normal brain tissue, and AP-2alpha expression was determined by immunohistochemistry.
  • RESULTS: AP-2alpha expression was lost on 99% (P < 0.001) and 98% (P < 0.001) of glioblastomas and anaplastic astrocytomas, respectively, compared with grade 2 astrocytomas and normal brain, all of which (100%) maintained expression of AP-2alpha.
  • However, there was no significant effect of loss of AP-2alpha expression on survival observed after adjustment for patient age, Karnofsky Performance Scale score, tumor grade, and extent of resection (rate ratio, 1.2; 95% confidence interval, 0.6-2.2; P = 0.6).
  • Of all the previously characterized markers of progression, the loss of AP-2alpha would be the most common (96.2%) molecular marker as an astrocytic tumor evolves from grade 2 to 3.
  • [MeSH-major] Brain Neoplasms / metabolism. DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / physiology. Gene Expression Regulation, Neoplastic. Glioma / metabolism. Transcription Factors / biosynthesis. Transcription Factors / physiology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Amino Acid Motifs. Antigens, CD / biosynthesis. Antigens, CD146. Astrocytoma / metabolism. Brain / metabolism. Cell Cycle Proteins / biosynthesis. Cell Line, Tumor. Child. Child, Preschool. Cyclin-Dependent Kinase Inhibitor p21. Disease Progression. Humans. Immunohistochemistry. Matrix Metalloproteinase 2 / biosynthesis. Middle Aged. Neural Cell Adhesion Molecules / biosynthesis. Oligodendroglioma / metabolism. Oligonucleotide Array Sequence Analysis. Prognosis. Proportional Hazards Models. Proto-Oncogene Proteins c-kit / biosynthesis. Time Factors. Transcription Factor AP-2. Treatment Outcome. Vascular Endothelial Growth Factor A / biosynthesis

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  • (PMID = 15671555.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / PHS HHS / / T-32-09666
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD146; 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA-Binding Proteins; 0 / MCAM protein, human; 0 / Neural Cell Adhesion Molecules; 0 / TFAP2A protein, human; 0 / Transcription Factor AP-2; 0 / Transcription Factors; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.4.24.24 / Matrix Metalloproteinase 2
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50. Strojnik T, Kavalar R, Trinkaus M, Lah TT: Cathepsin L in glioma progression: comparison with cathepsin B. Cancer Detect Prev; 2005;29(5):448-55
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  • OBJECTIVE: Lysosomal cysteine cathepsins have been implicated in tumor progression.
  • METHODS: The histological slides of 82 patients with primary astrocytic tumors were reviewed.
  • We evaluated the immunostaining of the cathepsins in tumor and endothelial cells.
  • The total score was significantly higher in malignant than in benign tumors, both for cathepsin B (p<0.001) and for cathepsin L (p<0.01).
  • CONCLUSION: Cathepsin L is preferentially expressed in tumor cells, increasing with glioma progression, but is not significantly associated with new vasculature of glioblastoma.
  • [MeSH-major] Brain Neoplasms / chemistry. Brain Neoplasms / pathology. Cathepsin B / biosynthesis. Cathepsin B / physiology. Cathepsins / biosynthesis. Cathepsins / physiology. Cysteine Endopeptidases / biosynthesis. Cysteine Endopeptidases / physiology. Glioma / chemistry. Glioma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Cathepsin L. Child. Child, Preschool. Disease Progression. Female. Gene Expression Profiling. Humans. Male. Middle Aged. Neovascularization, Pathologic. Prognosis. Retrospective Studies. Survival Analysis

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  • (PMID = 16183211.001).
  • [ISSN] 0361-090X
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.- / Cathepsins; EC 3.4.22.- / Cysteine Endopeptidases; EC 3.4.22.1 / Cathepsin B; EC 3.4.22.15 / CTSL1 protein, human; EC 3.4.22.15 / Cathepsin L
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51. Choi YL, Kim CJ, Matsuo T, Gaetano C, Falconi R, Suh YL, Kim SH, Shin YK, Park SH, Chi JG, Thiele CJ: HUlip, a human homologue of unc-33-like phosphoprotein of Caenorhabditis elegans; Immunohistochemical localization in the developing human brain and patterns of expression in nervous system tumors. J Neurooncol; 2005 May;73(1):19-27
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  • [Title] HUlip, a human homologue of unc-33-like phosphoprotein of Caenorhabditis elegans; Immunohistochemical localization in the developing human brain and patterns of expression in nervous system tumors.
  • HUlip is highly expressed only in the fetal brain and spinal cord, and is undetected in the adult brain.
  • The purpose of this study was to investigate the pattern of hUlip expression in the developing human brain and nervous system tumors.
  • Ten human brains at different developmental stages and 118 cases of nervous system tumor tissues were examined by immunohistochemistry.
  • Twelve related tumor cell lines were also analyzed by northern blotting and immunoblotting.
  • HUlip was expressed in late fetal and early postnatal brains; strongly in the neurons of the brain stem, basal ganglia/thalamus, and dentate gyrus of the hippocampus, and relatively weakly in the cerebral and cerebellar cortex.
  • Among tumors, hUlip expression was easily detected in tumor cells undergoing neuronal differentiation such as ganglioneuroblastomas and ganglioneuromas.
  • Furthermore, hUlip immunoreactivity was also found in various brain tumors showing neuronal differentiation: central neurocytomas (6 of 6 cases were positive), medulloblastomas (5/11), atypical teratoid rhabdoid tumor (1/1) and gangliogliomas (4/7).
  • Some astrocytic tumors also showed weak positivity: astrocytomas (1 of 5 cases), anaplastic astrocytomas (2/5), and glioblastomas (3/11).
  • The results of this study indicate that the expression of hUlip protein is distinctly restricted to the late fetal and early postnatal periods of human nervous system development and to certain subsets of nervous system tumors.
  • The exact function of hUlip needs to be further clarified; yet the results of our study strongly imply that hUlip function is important in human nervous system development and its aberrant expression in various types of nervous system tumors suggests a role of hUlip as an oncofetal neural antigen.
  • [MeSH-major] Brain / metabolism. Brain Neoplasms / metabolism. Gene Expression Regulation, Developmental / physiology. Gene Expression Regulation, Neoplastic / physiology. Muscle Proteins / metabolism
  • [MeSH-minor] Astrocytes / cytology. Astrocytes / metabolism. Cell Differentiation / genetics. Cell Differentiation / physiology. Cell Line, Tumor. Female. Gestational Age. Humans. Immunohistochemistry. Male. Neuroblastoma / genetics. Neuroblastoma / metabolism. Neurons / cytology. Neurons / metabolism

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  • (PMID = 15933812.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DPYSL3 protein, human; 0 / Muscle Proteins
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52. Alaraj A, Chan M, Oh S, Michals E, Valyi-Nagy T, Hersonsky T: Astroblastoma presenting with intracerebral hemorrhage misdiagnosed as dural arteriovenous fistula: review of a rare entity. Surg Neurol; 2007 Mar;67(3):308-13
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  • BACKGROUND: Astroblastoma is one of the most unusual types of tumors whose histogenesis has been recently clarified.
  • Immunohistochemically, the tumor cells show diffuse strong positivity for GFAP, S-100 protein, vimentin, as well as neuron-specific enolase and focal positivity for EMA.
  • Because of its high degree of proliferation, the presence of astroblastic pseudorosettes, prominent perivascular hyalinization, regional hyaline changes, and pushing borders with regard to the adjacent brain, the tumor was considered anaplastic.
  • CONCLUSIONS: Astroblastoma is a rare pure pathologic entity--a distinct form of astrocytic gliomas.
  • The diagnosis of astroblastoma is often difficult because of the astroblastic aspects that can be found in astrocytic tumors, in ependymomas, and in nonneuroepithelial tumors.
  • [MeSH-minor] Adult. Cerebral Angiography. Diagnosis, Differential. Humans. Magnetic Resonance Imaging. Male. Neoplasm Staging

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  • (PMID = 17320647.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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53. Ren ZP, Olofsson T, Qu M, Hesselager G, Soussi T, Kalimo H, Smits A, Nistér M: Molecular genetic analysis of p53 intratumoral heterogeneity in human astrocytic brain tumors. J Neuropathol Exp Neurol; 2007 Oct;66(10):944-54
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  • [Title] Molecular genetic analysis of p53 intratumoral heterogeneity in human astrocytic brain tumors.
  • We investigated genetic heterogeneity of astrocytic gliomas using p53 gene mutations as a marker.
  • Different parts of morphologically heterogeneous astrocytic gliomas were microdissected, and direct DNA sequencing of p53 gene exons 5 through 8 was performed.
  • Thirty-five glioma samples and tumor-adjacent normal-appearing brain tissue from 11 patients were analyzed.
  • We found that some tumors were devoid of p53 gene mutations, whereas other tumors carried 1 or often several (up to 3) different mutations.
  • The mutations were present in grade II, III, and IV astrocytic glioma areas.
  • Both severe functionally dead mutants and mutants with remaining transcriptional activity could be observed in the same tumor.
  • These results support the notion that intratumoral heterogeneity in brain tumors originates from different molecular defects.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Genes, p53 / genetics
  • [MeSH-minor] Adult. Aged. DNA Primers. DNA, Neoplasm / genetics. Female. Gene Frequency. Humans. Immunohistochemistry. Loss of Heterozygosity. Male. Microdissection. Middle Aged. Mutation / genetics. Mutation / physiology. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17917588.001).
  • [ISSN] 0022-3069
  • [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 / DNA Primers; 0 / DNA, Neoplasm
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54. Ren XH, Cui XL, Lin S, Wang ZC: [The correlation between combining 1p/19q LOH and pathology in gliomas]. Zhonghua Yi Xue Za Zhi; 2010 Jul 6;90(25):1781-4
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  • METHODS: Tumor samples from 127 glioma patients were collected.
  • RESULTS: The frequencies of combining 1p/19q LOH in astrocytic, oligoastrocytic and oligodendroglial tumors were 19.30%, 50.00% and 80.77% respectively.
  • The frequencies of combining 1p/19q LOH in oligoastrocytic and oligodendroglial tumors were higher than those in astrocytic tumors (P < 0.01) and the frequencies of combining 1p/19q LOH in oligodendroglial tumors was higher than those in oligoastrocytic tumors (P < 0.05).
  • The frequencies of 1p/19q LOH in astrocytic, oligoastrocytic and oligodendroglial tumors were 12.28%, 11.36 and 0 respectively.
  • [MeSH-minor] Adolescent. Adult. Aged. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Female. Humans. Male. Middle Aged. Oligodendroglia / pathology. Oligodendroglioma / genetics. Oligodendroglioma / pathology. Young Adult

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  • (PMID = 20979900.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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55. Eckert A, Kloor M, Giersch A, Ahmadi R, Herold-Mende C, Hampl JA, Heppner FL, Zoubaa S, Holinski-Feder E, Pietsch T, Wiestler OD, von Knebel Doeberitz M, Roth W, Gebert J: Microsatellite instability in pediatric and adult high-grade gliomas. Brain Pathol; 2007 Apr;17(2):146-50
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  • [Title] Microsatellite instability in pediatric and adult high-grade gliomas.
  • About 15% of sporadic gastrointestinal and endometrial tumors show the microsatellite instability (MSI) phenotype because of loss of DNA mismatch repair (MMR) function.
  • The incidence of MSI in tumors of the central nervous system still remains controversial.
  • Based on these data and the fact that in different tumor entities MMR deficiency defines a subgroup of tumors with distinct pathogenesis and particular clinicopathological features that may have impact on prognosis and therapy, we screened 624 gliomas from 71 young and 553 adult patients for MMR deficiency by MSI analysis using three highly sensitive diagnostic markers.
  • A malignant glioma from an adult patient displayed MSI and concomitant loss of nuclear MSH2 and MSH6 protein expression (0.16%; 1/619).
  • No evidence for MSI or loss of MMR protein expression was observed in 71 gliomas from young patients (0%; 0/71) including 41 high-grade astrocytic tumors.
  • [MeSH-major] Brain Neoplasms / genetics. Glioma / genetics. Microsatellite Instability
  • [MeSH-minor] Adult. Child. DNA-Binding Proteins / metabolism. Humans. Immunohistochemistry. Polymerase Chain Reaction

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  • (PMID = 17388945.001).
  • [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 / DNA-Binding Proteins
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56. Vogazianou AP, Chan R, Bäcklund LM, Pearson DM, Liu L, Langford CF, Gregory SG, Collins VP, Ichimura K: Distinct patterns of 1p and 19q alterations identify subtypes of human gliomas that have different prognoses. Neuro Oncol; 2010 Jul;12(7):664-78
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  • We studied the status of chromosomes 1 and 19 in 363 astrocytic and oligodendroglial tumors.
  • Whereas the predominant pattern of copy number abnormality was a concurrent loss of the entire 1p and 19q regions (total 1p/19q loss) among oligodendroglial tumors and partial deletions of 1p and/or 19q in astrocytic tumors, a subset of apparently astrocytic tumors also had total 1p/19q loss.
  • The presence of total 1p/19q loss was associated with longer survival of patients with all types of adult gliomas independent of age and diagnosis (P = .041).
  • The most commonly deleted region on 19q in astrocytic tumors spans 885 kb in 19q13.33-q13.41, which is telomeric to the previously proposed region.
  • Deletion mapping of the centromeric regions of 1p and 19q in the tumors that had total 1p/19q loss, indicating that the breakpoints lie centromeric to NOTCH2 within the pericentromeric regions of 1p and 19q.
  • [MeSH-major] Brain Neoplasms / diagnosis. Brain Neoplasms / genetics. Chromosome Deletion. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Glioma / diagnosis. Glioma / genetics

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  • (PMID = 20164239.001).
  • [ISSN] 1523-5866
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6618; United Kingdom / Cancer Research UK / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2940668
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57. Li X, Wang Y, Wang Y, Zhen H, Yang H, Fei Z, Zhang J, Liu W, Wang Y, Zhang X: Expression of EphA2 in human astrocytic tumors: correlation with pathologic grade, proliferation and apoptosis. Tumour Biol; 2007;28(3):165-72
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  • [Title] Expression of EphA2 in human astrocytic tumors: correlation with pathologic grade, proliferation and apoptosis.
  • A high expression of EphA2 has been detected in many non-central nervous system tumors; however, the EphA2 expression in brain astrocytic tumors remains unclear.
  • In this study, we investigated the expression of EphA2 mRNA and protein in 90 cases of human astrocytic tumors by reverse transcription polymerase chain reaction and immunohistochemistry, respectively.
  • The proliferative index (PI) of tumor cells was evaluated by Ki-67 immunohistochemistry, and the apoptotic index (AI) was determined by TdT-mediated dUTP nick end labeling assay.
  • The correlation between EphA2 expression, pathologic grade, proliferation and apoptosis of astrocytic tumors was further analyzed.
  • Therefore, EphA2 may be a new biomarker for astrocytic tumors.
  • It may also affect the proliferation and apoptosis of tumor cells and be an attractive therapy target for astrocytic tumors.
  • [MeSH-major] Astrocytoma / genetics. Astrocytoma / pathology. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Receptor, EphA2 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Apoptosis. Cell Division. Child. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. RNA, Messenger / genetics


58. Idbaih A, Marie Y, Pierron G, Brennetot C, Hoang-Xuan K, Kujas M, Mokhtari K, Sanson M, Lejeune J, Aurias A, Delattre O, Delattre JY: Two types of chromosome 1p losses with opposite significance in gliomas. Ann Neurol; 2005 Sep;58(3):483-7
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  • Deletion of the short arm of chromosome 1 (1p) is considered a favorable prognostic factor in glial tumors.
  • Complete hemizygous losses of 1p, which are tightly associated with 19q loss and oligodendroglial phenotype, and partial 1p deletions mainly observed in astrocytic tumors and not associated with 19q loss.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosome Deletion. Chromosomes, Human, Pair 1. Glioma / genetics
  • [MeSH-minor] Adult. Aged. Female. Gene Expression Profiling. Humans. Loss of Heterozygosity. Male. Middle Aged

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  • (PMID = 16130103.001).
  • [ISSN] 0364-5134
  • [Journal-full-title] Annals of neurology
  • [ISO-abbreviation] Ann. Neurol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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59. Sepulveda Sanchez JM, Martinez Montero JC, Diez-Lobato R, Hernandez-Lain A, Cabello A, Ramos A, Gonzalez Leon P, Ricoy Campo JR: Classification of oligodendroglial tumors based on histopathology criteria is a significant predictor of survival--clinical, radiological and pathologic long-term follow-up analysis. Clin Neuropathol; 2009 Jan-Feb;28(1):11-20
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  • [Title] Classification of oligodendroglial tumors based on histopathology criteria is a significant predictor of survival--clinical, radiological and pathologic long-term follow-up analysis.
  • BACKGROUND: The clinical course of oligodendroglial tumors is variable and there is a lack of consensus with regard to precisely diagnose which minimal criteria are required to make a diagnosis of a high-grade oligodendrial tumor.
  • The aims of the present study are to assess pathologic factors with prognostic significance, in addiction to clinical and neuroradiologic variables, in an attempt to identify reproducible histological parameters that are useful for classification of oligodendroglial tumors.
  • METHODS: 80 oligodendroglial tumors diagnosed between 1977 and 2004 were analyzed.
  • To make a diagnosis of anaplastic tumor we used reproducible parameters: endothelial proliferation, high cellularity, increased mitotic activity and necrosis.
  • Oligoastrocytomas (mixed gliomas) were diagnosed when the astrocytic component was clearly identified as part of the neoplastic cell population.
  • CONCLUSIONS: Clear cut histopathological criteria (endothelial proliferation, high cellularity, mitotic activity and necrosis) allow to establish different oligodendroglial tumor entities with distinct survival outcome.
  • [MeSH-major] Brain Neoplasms / classification. Brain Neoplasms / pathology. Oligodendroglioma / classification. Oligodendroglioma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Follow-Up Studies. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Prognosis. Retrospective Studies

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  • [ErratumIn] Clin Neuropathol. 2009 Mar-Apr;28(2):150
  • (PMID = 19216215.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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60. Alameda F, Lloreta J, Ariza A, Salido M, Espinet B, Baro T, Garcia-Fructoso G, Galito E, Munne A, Cruz Sanchez FF, Sole F, Serrano S: Primitive neuroectodermal tumor of the central nervous system with glial differentiation: a FISH study of an adult case. Clin Neuropathol; 2007 Jan-Feb;26(1):12-6
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  • [Title] Primitive neuroectodermal tumor of the central nervous system with glial differentiation: a FISH study of an adult case.
  • Primitive neuroectodermal tumors (PNETs) of the central nervous system (CNS), a rare occurrence in adults, may show glial differentiation and can be misinterpreted as pure astrocytic neoplasms.
  • Few fluorescence in situ hybridization (FISH) studies have been carried out on these tumors; isochromosome 17q was found to be the major chromosomal abnormality.
  • We present the case of an adult in which we performed a FISH study of both the glial and neuronal components.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Chromosomes, Human, Pair 17 / genetics. Neuroectodermal Tumors, Primitive / genetics. Neuroectodermal Tumors, Primitive / pathology. Trisomy / genetics
  • [MeSH-minor] Adult. Humans. In Situ Hybridization, Fluorescence. Male

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  • (PMID = 17290931.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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61. Menda Y, O'Dorisio MS, Kao S, Khanna G, Michael S, Connolly M, Babich J, O'Dorisio T, Bushnell D, Madsen M: Phase I trial of 90Y-DOTATOC therapy in children and young adults with refractory solid tumors that express somatostatin receptors. J Nucl Med; 2010 Oct;51(10):1524-31
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  • [Title] Phase I trial of 90Y-DOTATOC therapy in children and young adults with refractory solid tumors that express somatostatin receptors.
  • The purpose of this study was to conduct a phase I trial of (90)Y-DOTATOC to determine the dose-toxicity profile in children and young adults with somatostatin receptor-positive tumors.
  • RESULTS: Seventeen subjects (age, 2-24 y) received at least 1 dose of (90)Y-DOTATOC; diagnoses included neuroblastoma, embryonal and astrocytic brain tumors, paraganglioma, multiple endocrine neoplasia IIB, and neuroendocrine tumors.
  • CONCLUSION: Peptide receptor radionuclide therapy with (90)Y-DOTATOC is safe in children and young adults and demonstrated a 12% partial response plus 29% minor response rate in patients with somatostatin receptor-positive tumors.

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  • (PMID = 20847174.001).
  • [ISSN] 1535-5667
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA91578; United States / FDA HHS / FD / R01 FD002595; United States / FDA HHS / FD / R01FD002595; United States / NCI NIH HHS / CA / R01 CA167632; United States / NCI NIH HHS / CA / R21 CA091578
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 90Y-octreotide, DOTA-Tyr(3)-; 0 / Radiopharmaceuticals; 0 / Receptors, Somatostatin; RWM8CCW8GP / Octreotide
  • [Other-IDs] NLM/ NIHMS495708; NLM/ PMC3753801
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62. Mikami S, Hirose Y, Yoshida K, Kawase T, Ohnishi A, Nagashima K, Mukai M, Okada Y, Ikeda E: Predominant expression of OLIG2 over ID2 in oligodendroglial tumors. Virchows Arch; 2007 May;450(5):575-84
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  • [Title] Predominant expression of OLIG2 over ID2 in oligodendroglial tumors.
  • This study aims to examine if the analysis of OLIG2 and ID2 expression in glioma tissues helps the differential diagnosis of chemosensitive oligodendroglial tumors from astrocytic tumors.
  • Expression levels of OLIG2 and ID2 in 11 oligodendroglial and 27 astrocytic tumors were analyzed by reverse transcription-polymerase chain reaction (RT-PCR), real-time quantitative PCR, and immunohistochemistry.
  • The mean expression level of OLIG2 was higher in oligodendroglial tumors than astrocytic tumors, but some astrocytic tumors showed high OLIG2 expression, indicating that OLIG2 cannot be an independent marker of oligodendroglial tumors.
  • No significant difference was observed between ID2 expression in oligodendroglial tumors and astrocytic tumors.
  • It was notable that OLIG2 expression was predominant over ID2 expression in oligodendroglial tumors, while ID2 expression was predominant over OLIG2 expression in astrocytic tumors.
  • These results indicate that the immunohistochemical study on the relative expression level of OLIG2 to ID2 can be a useful screening for oligodendroglial tumors.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / metabolism. Brain Neoplasms / metabolism. Inhibitor of Differentiation Protein 2 / metabolism. Nerve Tissue Proteins / metabolism. Oligodendroglia / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Astrocytoma / metabolism. Astrocytoma / secondary. Astrocytoma / surgery. Biomarkers, Tumor / metabolism. Child. Chromosome Deletion. Chromosomes, Human, Pair 1. Female. Fluorescent Antibody Technique, Direct. Gene Expression. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Staging. Nucleic Acid Hybridization. Oligodendroglioma / metabolism. Oligodendroglioma / secondary. Oligodendroglioma / surgery. RNA, Messenger / metabolism

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  • (PMID = 17431671.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / ID2 protein, human; 0 / Inhibitor of Differentiation Protein 2; 0 / Nerve Tissue Proteins; 0 / OLIG2 protein, human; 0 / RNA, Messenger
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63. Korshunov A, Sycheva R, Gorelyshev S, Golanov A: Clinical utility of fluorescence in situ hybridization (FISH) in nonbrainstem glioblastomas of childhood. Mod Pathol; 2005 Sep;18(9):1258-63
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  • Astrocytic gliomas are the most common pediatric brain tumors; however, nonbrainstem glioblastomas are extremely rare compared with their adult counterparts.
  • The current study was focused on the molecular analysis and clinico-pathological correlations in a set of 44 tumor samples obtained from pediatric patients with nonbrainstem glioblastomas.
  • [MeSH-major] Brain Neoplasms / genetics. Genetic Markers. Glioblastoma / genetics


64. Ido K, Nakagawa T, Sakuma T, Takeuchi H, Sato K, Kubota T: Expression of vascular endothelial growth factor-A and mRNA stability factor HuR in human astrocytic tumors. Neuropathology; 2008 Dec;28(6):604-11
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  • [Title] Expression of vascular endothelial growth factor-A and mRNA stability factor HuR in human astrocytic tumors.
  • High-grade astrocytic tumors, such as glioblastoma, possess rich vascular components, which are necessary for their growth.
  • VEGF-A is considered to be the major mediator of angiogenesis in malignant neoplasms including high-grade astrocytic tumors.
  • The upregulation of VEGF-A expression in tumor cells is induced by two mechanisms: the transcriptional activation and the post-transcriptional stabilization of VEGF-A mRNA.
  • While the former mechanism mediated by hypoxia inducible factor-1 alpha (HIF-1alpha) has been revealed, the latter mediated by mRNA stability factor HuR remains unclear in astrocytic tumors.
  • In the present study, we investigated the expression of VEGF-A and mRNA stability factor HuR in supratentorial astrocytic tumors of 27 adults using RT-PCR, ELISA, and immunohistochemistry.
  • In higher-grade astrocytic tumors, the level of VEGF-A and microvascular density were elevated, cytoplasmic expression of HuR, which potentially means the protection of VEGF-A mRNA from degradation by ribonucleases, appeared, and they were correlated positively.
  • In in vitro experiments, the inhibition of the cytoplasmic translocation of HuR protein by leptomycin B (LMB) reduced the upregulation of VEGF-A expression in malignant astrocytic tumor cells under hypoxic conditions.
  • These findings suggest that the expression of VEGF-A and cytoplasmic translocation of HuR relates to the histological grade, and that HuR is involved in the upregulation of VEGF-A expression, in human astrocytic tumors.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Angiogenesis Inducing Agents. Cytoplasm / metabolism. ELAV Proteins. ELAV-Like Protein 1. Enzyme-Linked Immunosorbent Assay. Fatty Acids, Unsaturated / pharmacology. Female. Glioblastoma / genetics. Glioblastoma / metabolism. Glioblastoma / pathology. Humans. Immunohistochemistry. Male. Middle Aged. RNA Processing, Post-Transcriptional. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured. Up-Regulation. Young Adult

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  • (PMID = 18498284.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Angiogenesis Inducing Agents; 0 / Antigens, Surface; 0 / ELAV Proteins; 0 / ELAV-Like Protein 1; 0 / ELAVL1 protein, human; 0 / Fatty Acids, Unsaturated; 0 / RNA-Binding Proteins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 87081-35-4 / leptomycin B
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65. Motta FJ, Valera ET, Lucio-Eterovic AK, Queiroz RG, Neder L, Scrideli CA, Machado HR, Carlotti-Junior CG, Marie SK, Tone LG: Differential expression of E-cadherin gene in human neuroepithelial tumors. Genet Mol Res; 2008;7(2):295-304
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  • [Title] Differential expression of E-cadherin gene in human neuroepithelial tumors.
  • This study aimed to evaluate the expression of E-cadherin and their correlation with clinical features in microdissected brain tumor samples from 81 patients, divided into 62 astrocytic tumors grades I to IV and 19 medulloblastomas, and from 5 white matter non-neoplasic brain tissue samples.
  • We observed a decrease in expression among pathological grades of neuroepithelial tumors.
  • Non-neoplasic brain tissue showed a higher expression level of CDH1 gene than did neuroepithelial tumors.
  • Expression of E-cadherin gene was higher in astrocytic than embryonal tumors (P = 0.0168).
  • Non-neoplasic brain tissue showed a higher expression level of CDH1 gene than grade I malignancy astrocytomas, considered as benign tumors (P = 0.0473).
  • These results suggest that a decrease in E-cadherin gene expression level in high-grade neuroepithelial tumors may be a hallmark of malignancy in dedifferentiated tumors and that it may be possibly correlated with their progression and dissemination.
  • [MeSH-minor] Adolescent. Adult. Brain / metabolism. Gene Expression Regulation, Neoplastic. Humans. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18551395.001).
  • [ISSN] 1676-5680
  • [Journal-full-title] Genetics and molecular research : GMR
  • [ISO-abbreviation] Genet. Mol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Cadherins; 0 / RNA, Messenger
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66. Beppu T, Inoue T, Shibata Y, Yamada N, Kurose A, Ogasawara K, Ogawa A, Kabasawa H: Fractional anisotropy value by diffusion tensor magnetic resonance imaging as a predictor of cell density and proliferation activity of glioblastomas. Surg Neurol; 2005 Jan;63(1):56-61; discussion 61
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  • The FA value has been suggested as an indicator of the cell density of astrocytic tumors.
  • METHODS: We performed DTI in 19 patients with glioblastoma and measured the FA values of tumor and normal brain regions prior to computed tomography-guided stereotactic biopsy.
  • Differences in mean FA value between normal brain regions and glioblastoma lesion were compared.
  • Cell density and MIB-1 indices were examined using tumor specimens obtained from biopsies.
  • RESULTS: The mean FA value significantly differed between normal brain regions and glioblastoma lesions.
  • [MeSH-major] Brain Neoplasms / diagnosis. Brain Neoplasms / physiopathology. Diffusion Magnetic Resonance Imaging / methods. Glioblastoma / diagnosis. Glioblastoma / physiopathology
  • [MeSH-minor] Adult. Aged. Anisotropy. Body Water / physiology. Brain / pathology. Brain / physiology. Brain / physiopathology. Cell Proliferation. Diffusion. Female. Humans. Male. Middle Aged. Predictive Value of Tests. Prognosis

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  • (PMID = 15639528.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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67. Kato T, Shinoda J, Nakayama N, Miwa K, Okumura A, Yano H, Yoshimura S, Maruyama T, Muragaki Y, Iwama T: Metabolic assessment of gliomas using 11C-methionine, [18F] fluorodeoxyglucose, and 11C-choline positron-emission tomography. AJNR Am J Neuroradiol; 2008 Jun;29(6):1176-82
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  • We measured the tumor/normal brain uptake ratio (T/N ratio) on each PET and investigated the correlations among the tracer uptake, tumor grade, tumor type, and tumor proliferation activity.
  • In addition, we compared the ease of visual evaluation for tumor detection.
  • RESULTS: All 3 of the tracers showed positive correlations with astrocytic tumor (AT) grades (II/IV and III/IV).
  • The MET T/N ratio of oligodendroglial tumors (OTs) was significantly higher than that of ATs of the same grade.
  • Tumor grade and type influenced MET uptake only.
  • All of the tracers showed significantly positive correlations with Mib-1 labeling index in ATs but not in OTs and oligoastrocytic tumors.
  • In terms of visual evaluation of tumor localization, MET PET is superior to FDG and CHO PET in all of the gliomas, due to its straightforward detection of "hot lesions".
  • [MeSH-major] Brain Neoplasms / metabolism. Choline / pharmacokinetics. Fluorodeoxyglucose F18 / pharmacokinetics. Glioma / metabolism. Methionine / pharmacokinetics. Positron-Emission Tomography / methods
  • [MeSH-minor] Adult. Carbon Radioisotopes / pharmacokinetics. Female. Gene Expression Profiling / methods. Humans. Male. Metabolic Clearance Rate. Middle Aged. Radiopharmaceuticals / pharmacokinetics. Tissue Distribution

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  • [CommentIn] Nat Clin Pract Neurol. 2008 Sep;4(9):470-1 [18628750.001]
  • [CommentIn] AJNR Am J Neuroradiol. 2008 Nov;29(10):e96 [19008320.001]
  • (PMID = 18388218.001).
  • [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
  • [Chemical-registry-number] 0 / Carbon Radioisotopes; 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18; AE28F7PNPL / Methionine; N91BDP6H0X / Choline
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68. Erdamar S, Bagci P, Oz B, Dirican A: Correlation of endothelial nitric oxide synthase and vascular endothelial growth factor expression with malignancy in patients with astrocytic tumors. J BUON; 2006 Apr-Jun;11(2):213-6
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  • [Title] Correlation of endothelial nitric oxide synthase and vascular endothelial growth factor expression with malignancy in patients with astrocytic tumors.
  • PURPOSE: Many characteristics of malignant brain tumors (increased vascular permeability, vasodilatation, neovascularisation and free radical injury to the tumor and adjacent normal tissues) are believed to be mediated by nitric oxide (NO) synthetized by endothelial NO synthase (eNOS).
  • Overexpression of vascular endothelial growth factor (VEGF) is associated with several central nervous system (CNS) diseases and tumors.
  • Our aim was to study immunohistochemically the coexpression of eNOS and VEGF in astrocytic tumors and to analyse their possible correlation with tumor grade, angiogenesis and proliferation index.
  • MATERIALS AND METHODS: Sections from 120 randomly selected patients with supratentorial astrocytic tumors [38 glioblastomas (GB), 22 anaplastic astrocytomas (AA) and 20 low-grade astrocytomas (LA)], also including oligodendrogliomas (n=20) and mixed oligoastrocytomas (n=20), were immunostained with monoclonal antibodies for eNOS and VEGF using the avidin-biotin method.
  • The proliferative potential was assessed as the MIB-1 staining index for tumor cells.
  • CONCLUSION: Overexpressions of eNOS and VEGF in astrocytic tumors were significantly correlated with histological grade, proliferative potential and malignant transformation.
  • The expression of VEGF in a necrotic and ischemic tumor such as GB is more intense and diffuse than low-grade astrocytomas.
  • These findings suggest that eNOS overexpression in tumor vasculature would be precipitated by transformation into an angiogenic phenotype in the process of neovascularisation in astrocytic tumors.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Nitric Oxide Synthase Type III / biosynthesis. Vascular Endothelial Growth Factor A / biosynthesis
  • [MeSH-minor] Adult. Aged. Humans. Immunohistochemistry. Middle Aged. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / pathology

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  • (PMID = 17318973.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; EC 1.14.13.39 / Nitric Oxide Synthase Type III
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69. Chen Y, Tachibana O, Hasegawa M, Xu R, Hamada J, Yamashita J, Hashimoto N, Takahashi JA: Absence of tight junctions between microvascular endothelial cells in human cerebellar hemangioblastomas. Neurosurgery; 2006 Sep;59(3):660-70; discussion 660-70
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  • OBJECTIVE: Endothelial tight junctions form the main barrier of the blood-brain barrier (BBB).
  • Tight junctions in the microvessels of hemangioblastomas and the control brain were examined by electron microscopy.
  • Immunohistochemistry and double immunofluorescent microscopy were used to analyze the expression of CLN5 and its relationship with astrocytic endfeet in the control brain and hemangioblastomas.
  • RESULTS: In the control brain, the paracellular cleft between adjacent endothelial cells is sealed by continuous strands of tight junctions.
  • Compared with the control brain, expression of CLN5 was decreased in cystic hemangioblastomas (P < 0.05).
  • Phosphorylated CLN5 was detected in most hemangioblastomas, but not in the control brain.
  • Microvessels in hemangioblastomas showed a significant absence of astrocytic endfeet.
  • Significant absence of astrocytic endfeet and tight junctions can be found in microvessels of hemangioblastomas, which may lead to the breakdown of the BBB in these tumors.
  • [MeSH-major] Blood-Brain Barrier / ultrastructure. Cerebellar Neoplasms / pathology. Endothelial Cells / ultrastructure. Hemangioblastoma / pathology. Tight Junctions / ultrastructure
  • [MeSH-minor] Adult. Female. Humans. Male. Middle Aged. Retrospective Studies

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  • (PMID = 16955048.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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70. Plotkin M, Amthauer H, Eisenacher J, Wurm R, Michel R, Wust P, Stockhammer F, Röttgen R, Gutberlet M, Ruf J, Felix R: Value of 123I-IMT SPECT for diagnosis of recurrent non-astrocytic intracranial tumours. Neuroradiology; 2005 Jan;47(1):18-26
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  • [Title] Value of 123I-IMT SPECT for diagnosis of recurrent non-astrocytic intracranial tumours.
  • In the current study we investigated whether IMT-SPECT could also be useful in the follow-up of brain metastases and other intracranial tumours of non-astrocytic origin.
  • The study included 22 patients with suspected recurrent intracranial tumours of non-astrocytic origin (12 brain metastases, one supratentorial primitive neuroendocrine tumour (PNET), one rhabdoid tumour, two clivus chordomas, three ependymomas, two pituitary tumours, one anaplastic meningioma) who had previously been treated by surgery and/or radio/chemotherapy.
  • We concluded that the IMT-SPECT is a promising complementary imaging tool for the detection of recurrences of non-astrocytic intracranial tumours and their distinguishing from treatment-induced changes.
  • [MeSH-major] Brain Neoplasms / diagnostic imaging. Iodine Radioisotopes. Methyltyrosines. Neoplasm Recurrence, Local / diagnostic imaging. Radiopharmaceuticals. Tomography, Emission-Computed, Single-Photon / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Chordoma / diagnostic imaging. Ependymoma / diagnostic imaging. False Negative Reactions. False Positive Reactions. Female. Follow-Up Studies. Glioma / diagnostic imaging. Humans. Magnetic Resonance Imaging. Male. Meningioma / diagnostic imaging. Middle Aged. Neuroendocrine Tumors / diagnostic imaging. Pituitary Neoplasms / diagnostic imaging. Retrospective Studies. Rhabdoid Tumor / diagnostic imaging. Sensitivity and Specificity. Supratentorial Neoplasms / diagnostic imaging

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  • (PMID = 15630586.001).
  • [ISSN] 0028-3940
  • [Journal-full-title] Neuroradiology
  • [ISO-abbreviation] Neuroradiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 0 / Methyltyrosines; 0 / Radiopharmaceuticals; A77N8J5H5T / 3-iodo-alpha-methyltyrosine
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71. Juhász C, Chugani DC, Muzik O, Wu D, Sloan AE, Barger G, Watson C, Shah AK, Sood S, Ergun EL, Mangner TJ, Chakraborty PK, Kupsky WJ, Chugani HT: In vivo uptake and metabolism of alpha-[11C]methyl-L-tryptophan in human brain tumors. J Cereb Blood Flow Metab; 2006 Mar;26(3):345-57
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  • [Title] In vivo uptake and metabolism of alpha-[11C]methyl-L-tryptophan in human brain tumors.
  • Abnormal metabolism of tryptophan has been implicated in modulation of tumor cell proliferation and immunoresistance. alpha-[(11)C]Methyl-L-tryptophan (AMT) is a PET tracer to measure cerebral tryptophan metabolism in vivo.
  • In the present study, we have measured tumor tryptophan uptake in 40 patients with primary brain tumors using AMT PET and standard uptake values (SUV).
  • All grade II to IV gliomas and glioneuronal tumors showed increased AMT SUV, including all recurrent/residual tumors.
  • Gadolinium enhancement on MRI was associated with high VD' values, suggesting impaired blood-brain barrier, while k(3)' values were not related to contrast enhancement.
  • Low-grade astrocytic gliomas showed increased tryptophan metabolism, as measured by k(3)'.
  • In astrocytic tumors, low grade was associated with high k(3)' and lower VD', while high-grade tumors showed the reverse pattern.
  • The findings show high AMT uptake in primary and residual/recurrent gliomas and glioneuronal tumors.
  • Increased AMT uptake can be due to increased metabolism of tryptophan and/or high volume of distribution, depending on tumor type and grade.
  • High tryptophan metabolic rates in low-grade tumors may indicate activation of the kynurenine pathway, a mechanism regulating tumor cell growth.
  • AMT PET might be a useful molecular imaging method to guide therapeutic approaches aimed at controlling tumor cell proliferation by acting on tryptophan metabolism.
  • [MeSH-major] Brain Neoplasms / metabolism. Cerebral Cortex / metabolism. Tryptophan / analogs & derivatives
  • [MeSH-minor] Adolescent. Adult. Aged. Carbon Radioisotopes. Child. Child, Preschool. Electroencephalography / methods. Electroencephalography / standards. Female. Gadolinium. Glucose / metabolism. Humans. Infant. Magnetic Resonance Imaging / methods. Magnetic Resonance Imaging / standards. Male. Middle Aged. Neoplasm Staging. Positron-Emission Tomography / methods. Positron-Emission Tomography / standards. Seizures / metabolism. Sensitivity and Specificity

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  • (PMID = 16079785.001).
  • [ISSN] 0271-678X
  • [Journal-full-title] Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • [ISO-abbreviation] J. Cereb. Blood Flow Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carbon Radioisotopes; 13510-08-2 / alpha-methyltryptophan; 8DUH1N11BX / Tryptophan; AU0V1LM3JT / Gadolinium; IY9XDZ35W2 / Glucose
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72. 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
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  • [Title] Expression of hypoxia-related tissue factors in astrocytic gliomas. A multivariate survival study with emphasis upon carbonic anhydrase IX.
  • It has been recently postulated that the hypoxia-inducible factor (HIF-1) pathway up-regulated by hypoxia accounts for CAIX overexpression in most human tumors.
  • 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.
  • 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
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cohort Studies. Female. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Immunohistochemistry. Ki-67 Antigen / biosynthesis. Male. Middle Aged. Survival Analysis. Vascular Endothelial Growth Factor A / 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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73. Fernandez A, Karavitaki N, Ansorge O, Fazal-Sanderson V, Wass JA: Acromegaly and anaplastic astrocytoma: coincidence or pathophysiological relation? Pituitary; 2008;11(3):325-30
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  • In astrocytic-cell tumors, the role of autocrine and paracrine IGF-I expression in enhancing tumoral progression is well established.
  • However, the influence of systemic IGF-I levels on the clinical behavior of astrocytic neoplasms remains an open subject of research.
  • The coexistence of systemic IGF-I hypersecretion with a quick progression in the histopathological grade of the astrocytoma raises the compelling question of whether the clinical behavior of the astrocytic tumor was influenced by the acromegalic status.
  • The role of IGF-I signaling in the pathogenesis of astrocytic-cell tumors and the experience with therapeutic strategies addressing this pathway in astrocytomas are also discussed.
  • [MeSH-major] Acromegaly / complications. Astrocytoma / complications. Brain Neoplasms / complications
  • [MeSH-minor] Adult. Cranial Irradiation. Craniotomy. Disease Progression. Ergolines / therapeutic use. Humans. Insulin-Like Growth Factor I / metabolism. Magnetic Resonance Imaging. Male. Neoplasm Staging. Peptides, Cyclic / therapeutic use. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use. Treatment Outcome. Up-Regulation

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  • (PMID = 18000757.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ergolines; 0 / Peptides, Cyclic; 0G3DE8943Y / lanreotide; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I; LL60K9J05T / cabergoline
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74. Cui XL, Zhao ZG, Ren XH, Sui DL, Chu JS, Tang K, Zeng C, Lin S: [Characteristics of combining loss of heterozygosity of 1p/19q in glioma]. Zhonghua Wai Ke Za Zhi; 2010 Jun 1;48(11):852-5
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  • METHODS: The status of 1p and 19q of 138 glioma specimen from January 2009 to December 2009 was evaluated by Fluorescence in situ hybridization (FISH) method, and the frequencies of combining LOH of 1p/19q were compared between different pathologies, brain sub-regions, genders and ages.
  • RESULTS: The frequencies of combined LOH of 1p and 19q of oligodendroglial (81.3%) and oligo astrocytic tumors (55.8%) were significantly higher than that of astrocytic tumor (22.2%) (P < 0.01), and the frequency of oligodendroglial tumor was significantly higher than that of oligo astrocytic tumor (P < 0.05).
  • CONCLUSION: Combining LOH of 1p and 19q has significant correlation with the pathologies and brain sub-regions.
  • [MeSH-major] Brain Neoplasms / genetics. Glioma / genetics. Loss of Heterozygosity
  • [MeSH-minor] Adolescent. Adult. Aged. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Female. Humans. Male. Middle Aged. Young Adult

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  • (PMID = 21163056.001).
  • [ISSN] 0529-5815
  • [Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]
  • [ISO-abbreviation] Zhonghua Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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75. Choi KC, Kwak SE, Kim JE, Sheen SH, Kang TC: Enhanced glial fibrillary acidic protein-delta expression in human astrocytic tumor. Neurosci Lett; 2009 Oct 9;463(3):182-7
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  • [Title] Enhanced glial fibrillary acidic protein-delta expression in human astrocytic tumor.
  • Astrocytic tumor is one of the most common primary tumors of the adult brain.
  • Although there are several biochemical markers for the categorization of astrocytic tumor, few markers are used for histopathological diagnosis.
  • In tissue samples from patients with low-grade astrocytic tumor (grades I and II), GFAP-delta(+) cells appeared stellate, polygonal or round shape.
  • In tissue samples from patients with high-grade astrocytic tumor (grades III and IV), GFAP-delta(+) cells showed round or spindle shape.
  • GFAP-delta immunoreactivities in grades III and IV astrocytic tumor cells were increased by 1.4- and 1.7-fold in comparison to grade I astrocytic tumor cells.
  • GFAP-delta immunoreactivity was also observed in cell bodies along the margins of astrocytic tumor showing normal histological findings, even though astroglia had normal morphology (showing strong GFAP and glutamine synthase immunoreactivities and a stellate shape with well-developed processes).
  • Furthermore, the malignancy of astrocytic tumor was directly correlated with the degree of GFAP-delta immunoreactivity.
  • These findings suggest that GFAP-delta may be a useful diagnostic marker for the evaluation of functional cataplasia or proliferation of astrocytic tumor.
  • [MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor / biosynthesis. Brain Neoplasms / metabolism. Glial Fibrillary Acidic Protein / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Alternative Splicing. Child. Female. Glutamate-Ammonia Ligase / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Young Adult

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  • (PMID = 19647039.001).
  • [ISSN] 1872-7972
  • [Journal-full-title] Neuroscience letters
  • [ISO-abbreviation] Neurosci. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glial Fibrillary Acidic Protein; EC 6.3.1.2 / Glutamate-Ammonia Ligase
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76. Jeuken JW, van der Maazen RW, Wesseling P: Molecular diagnostics as a tool to personalize treatment in adult glioma patients. Technol Cancer Res Treat; 2006 Jun;5(3):215-29
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  • [Title] Molecular diagnostics as a tool to personalize treatment in adult glioma patients.
  • Gliomas, the most frequent primary brain tumors in humans, form a heterogeneous group, encompassing many different histological types and malignancy grades.
  • The major representatives in this subgroup are the diffuse astrocytic, oligodendroglial, and mixed oligo-astrocytic tumors.
  • After summarizing the most relevant genetic aberrations and pathways in these tumors detected up till now, this review will discuss the clinical relevance of this information.
  • [MeSH-major] Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Glioma / genetics. Molecular Diagnostic Techniques
  • [MeSH-minor] Cell Cycle Proteins / genetics. DNA Methylation. DNA Repair. Gene Dosage. Humans. Neovascularization, Pathologic. Receptor Protein-Tyrosine Kinases / genetics. Retinoblastoma Protein / genetics. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 16700618.001).
  • [ISSN] 1533-0346
  • [Journal-full-title] Technology in cancer research & treatment
  • [ISO-abbreviation] Technol. Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  • [Number-of-references] 94
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77. Vajtai I, Arnold M, Kappeler A, Jeless O, Lukes A, Mariani L, Paulus W: Rosette-forming glioneuronal tumor of the fourth ventricle: report of two cases with a differential diagnostic overview. Pathol Res Pract; 2007;203(8):613-9
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  • [Title] Rosette-forming glioneuronal tumor of the fourth ventricle: report of two cases with a differential diagnostic overview.
  • We report on clinicopathological findings in two cases of rosette-forming glioneuronal tumor of the fourth ventricle (RGNT) occurring in females aged 16 years (Case 1) and 30 years (Case 2).
  • Magnetic resonance imaging (MRI) indicated a cerebellar-based tumor of 1.8 cm (Case 1) and 5 cm (Case 2) diameter each, bulging into the fourth ventricle.
  • On microscopy, both tumors comprised an admixture of low-grade astrocytoma interspersed with circular aggregates of synaptophysin-expressing round cells harboring oligodendrocyte-like nuclei.
  • The astrocytic moiety in Case 1 was nondescript, and overtly pilocytic in Case 2.
  • Despite sharing some overlapping histologic traits with dysembryoplastic neuroepithelial tumor (DNT), the presentation of RGNT with respect to both patient age and location is consistent enough for this lesion to be singled out as an autonomous entity.
  • [MeSH-minor] Adolescent. Adult. Diagnosis, Differential. Female. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Neurosurgical Procedures. Synaptophysin / metabolism

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  • (PMID = 17651910.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Synaptophysin
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78. Chen Z, Ma L, Lou X, Zhou Z: Diagnostic value of minimum apparent diffusion coefficient values in prediction of neuroepithelial tumor grading. J Magn Reson Imaging; 2010 Jun;31(6):1331-8
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  • [Title] Diagnostic value of minimum apparent diffusion coefficient values in prediction of neuroepithelial tumor grading.
  • PURPOSE: To retrospectively evaluate the diagnostic accuracy of diffusion weighted image (DWI) in the prediction of neuroepithelial tumors grading, and to appraise the apparent diffusion coefficient (ADC) value of neuroepithelial tumors with histologic findings as a reference standard.
  • MATERIALS AND METHODS: ADC values in 110 patients with pathologically proved neuroepithelial tumors, including 77 astrocytic tumors, 16 oligodendroglial tumors, 11 oligoastrocytic tumors, and 6 ependymal tumors, were investigated retrospectively.
  • The minimum ADC (MinADC) value of tumors was measured postoperatively on ADC maps, avoiding cystic, necrotic, or hemorrhagic components.
  • The area under the ROC curve (AUC) was 0.809, and the cutoff MinADC value of 0.900 x 10(-3) mm(2)/s for the differentiation between high and low grade neuroepithelial tumors provided the best combination of sensitivity (85.4%) and specificity (71.0%).
  • CONCLUSION: MinADC value may be a simple and effective optional tool for the prediction of neuroepithelial tumor grading.
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Diffusion. Female. Humans. Ki-67 Antigen / biosynthesis. Male. Middle Aged. ROC Curve. Reproducibility of Results. Retrospective Studies. Sensitivity and Specificity

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  • [CommentIn] J Magn Reson Imaging. 2011 Mar;33(3):755; author reply 756 [21563262.001]
  • (PMID = 20512884.001).
  • [ISSN] 1522-2586
  • [Journal-full-title] Journal of magnetic resonance imaging : JMRI
  • [ISO-abbreviation] J Magn Reson Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen
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79. Lavon I, Zrihan D, Zelikovitch B, Fellig Y, Fuchs D, Soffer D, Siegal T: Longitudinal assessment of genetic and epigenetic markers in oligodendrogliomas. Clin Cancer Res; 2007 Mar 1;13(5):1429-37
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  • PURPOSE: Because little is known about the evolution of genetic and epigenetic changes that occur during tumor progression in oligodendrogliomas, we evaluated these changes in paired early and progressive oligodendrogliomas.
  • RESULTS: In early tumors, 60.8% were of low grade compared with only 17% low-grade tumors at recurrence.
  • Of 17 early tumors described as pure oligodendrogliomas, 76.5% remained in this lineage, regardless of their grade, whereas others changed to astrocytic tumors.
  • Oligoastrocytic tumors had a significantly higher tendency to transform to astrocytic tumors.
  • All pure oligodendrogliomas with 1p/19q codeletions remained phenotypically unchanged, unlike mixed tumors with codeletions, of which 83% changed their cell lineage.
  • Of tumors with early 1p deletion, 80% remained oligodendroglial at progression, whereas 75% of tumors with an intact 1p changed to astrocytic phenotype.
  • 10q loss was uncommon in both early and progressive tumors.
  • The proportional gain in methylation at progression was 31% for tumors with early 1p deletion, unlike tumors with an intact 1p, which had an 87.5% gain of methylation at progression.
  • CONCLUSIONS: Pure oligodendrogliomas with 1p/19q deletion tend to retain their cell phenotype and genetic profile unlike tumors with no deletions or mixed histology.
  • MGMT promoter methylation is more pronounced at tumor progression, particularly in tumors with an intact 1p.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. DNA Methylation. Epigenesis, Genetic. Oligodendroglioma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Female. Humans. Immunohistochemistry. Male. Microsatellite Repeats. Middle Aged. Phenotype. Polymerase Chain Reaction. Promoter Regions, Genetic. Tumor Suppressor Proteins / genetics

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  • (PMID = 17332285.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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80. Benedetti E, Galzio R, D'Angelo B, Cerù MP, Cimini A: PPARs in Human Neuroepithelial Tumors: PPAR Ligands as Anticancer Therapies for the Most Common Human Neuroepithelial Tumors. PPAR Res; 2010;2010:427401
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  • [Title] PPARs in Human Neuroepithelial Tumors: PPAR Ligands as Anticancer Therapies for the Most Common Human Neuroepithelial Tumors.
  • Neuroepithelial tumors represent a heterogeneous class of human tumors including benignant and malignant tumors.
  • Among malignant neuroepithelial tumors, with regard to PPAR ligands, the most extensively studied were tumors of astrocytic origin and neuroblastoma.
  • PPARs are expressed in developing and adult neuroepithelial cells, even if with different localization and relative abundance.
  • The majority of malignant neuroepithelial tumors have poor prognosis and do not respond to conventional therapeutic protocols, therefore, new therapeutic approaches are needed.

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  • (PMID = 20339586.001).
  • [ISSN] 1687-4765
  • [Journal-full-title] PPAR research
  • [ISO-abbreviation] PPAR Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2841252
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81. Robe PA, Martin D, Albert A, Deprez M, Chariot A, Bours V: A phase 1-2, prospective, double blind, randomized study of the safety and efficacy of Sulfasalazine for the treatment of progressing malignant gliomas: study protocol of [ISRCTN45828668]. BMC Cancer; 2006;6:29
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  • BACKGROUND: The prognosis of patients suffering from WHO grade 3 and 4 astrocytic glioma remains poor despite surgery, radiation therapy and the use of current chemotherapy regimen.
  • Recent evidence suggests that the transcription factor NF-kappaB is constitutively expressed in malignant gliomas and that its inhibition by drugs like Sulfasalazine may block the growth of astrocytic tumors in vitro and in experimental models of malignant gliomas.
  • Primary endpoints are drug safety in the setting of malignant gliomas and tumor response as measured according to MacDonald's criteria.
  • [MeSH-minor] Administration, Oral. Adult. Aged. Brain Neoplasms. Disease Progression. Double-Blind Method. Female. Glioma. Humans. Male. Middle Aged. Prognosis. Prospective Studies. Survival Analysis. Treatment Outcome

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  • (PMID = 16448552.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Databank-accession-numbers] ISRCTN/ ISRCTN45828668
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 3XC8GUZ6CB / Sulfasalazine
  • [Other-IDs] NLM/ PMC1368982
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82. Wrensch M, Fisher JL, Schwartzbaum JA, Bondy M, Berger M, Aldape KD: The molecular epidemiology of gliomas in adults. Neurosurg Focus; 2005 Nov;19(5):E5
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  • Several biomarkers do predict prognosis, but only evaluation of loss of 1p and 19q in oligodendroglial tumors are incorporated in clinical practice.
  • Ongoing research focuses on classifying homogeneous groups of tumors on the basis of molecular markers and identifying inherited polymorphisms that may influence survival or risk.
  • Improving survival rates for patients harboring astrocytic tumors will probably require many randomized clinical trials of novel treatment strategies.
  • [MeSH-minor] Adult. Brain Neoplasms / epidemiology. Brain Neoplasms / genetics. Genetic Markers / genetics. Humans. Molecular Epidemiology. Polymorphism, Genetic / genetics. Risk Factors

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  • (PMID = 16398469.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50CA097257; United States / NCI NIH HHS / CA / R01CA52689; United States / NCI NIH HHS / CA / R03CA103379
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers
  • [Number-of-references] 191
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83. 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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  • [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.
  • These tumors are characterized by unrelenting growth that is often resistant to chemotherapy and radiation therapy.
  • Tumor expansion into the healthy surrounding brain tissue produces severe and often fatal consequences.

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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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84. Hiremath GK, Bingaman WE, Prayson RA, Nair D: Oligoastrocytoma presenting with intractable epilepsy. Epileptic Disord; 2007 Sep;9(3):315-22
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  • OBJECTIVE: Oligoastrocytomas (OA) are mixed gliomas with distinct oligodendroglial and astrocytic neoplastic components.
  • Tumors arose from the left side in all patients and from the temporal lobe in five patients.
  • There were no surgical complications, clinical or radiographic tumor recurrence at a mean follow up period of 3.2 years (range 2-8).
  • CONCLUSION: As a result of our small sample size, general conclusions may be imprecise, but this review suggests that OA behave similar to other tumors related to intractable epilepsy: they usually have a preoperative seizure course of many years, an excellent rate of seizure-freedom following surgery, and are in general, low-grade tumors with an indolent course for which serial imaging is sufficient follow-up.
  • [MeSH-major] Astrocytoma / complications. Brain Neoplasms / complications. Epilepsy / drug therapy. Epilepsy / etiology
  • [MeSH-minor] Adolescent. Adult. Anticonvulsants / therapeutic use. Craniotomy. Drug Resistance. Epilepsy, Complex Partial / etiology. Epilepsy, Complex Partial / surgery. Female. Humans. Magnetic Resonance Imaging. Male. Memory / physiology. Neoplasm Recurrence, Local. Neurosurgical Procedures. Temporal Lobe / pathology. Temporal Lobe / surgery

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  • (PMID = 17884756.001).
  • [ISSN] 1294-9361
  • [Journal-full-title] Epileptic disorders : international epilepsy journal with videotape
  • [ISO-abbreviation] Epileptic Disord
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anticonvulsants
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85. Sharma S, Sharma MC, Gupta DK, Sarkar C: Angiogenic patterns and their quantitation in high grade astrocytic tumors. J Neurooncol; 2006 Aug;79(1):19-30
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  • [Title] Angiogenic patterns and their quantitation in high grade astrocytic tumors.
  • BACKGROUND: The objectives of this study on high grade astrocytic tumors were (i) to establish differences, if any, between grades III & IV tumors among angiogenic parameters, both qualitative and quantitative, and (ii) to correlate angiogenic parameters with proliferation indices, namely T2a and MIB1 labeling indices.
  • DESIGN: Twenty nine consecutive cases of WHO grades III (11) and IV (18) astrocytic tumors diagnosed in the year-2004 were studied, using H&E and CD34, MIB1 and T2a immunostaining by streptavidin biotin technique.
  • Limited follow up data showed all recurrent grade IV tumors to be of glomeruloid type.
  • CONCLUSION: Increased angiogenesis in grade IV, as compared to grade III, astrocytic tumors is characterized by an increased number/density of vessels: an increase in vessels characterized by disproportionate lengthening and likely associated with the infiltrative properties of the tumors; and an increase in pliable, irregularly shaped or structured vessels.
  • Further studies are needed to determine the usefulness of the angiogenic parameters in the improved diagnosis (grading) and prognosis of astrocytic tumors.
  • [MeSH-major] Astrocytoma / blood supply. Astrocytoma / pathology. Brain Neoplasms / blood supply. Brain Neoplasms / pathology. Neovascularization, Pathologic
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Proliferation. Female. Humans. Image Processing, Computer-Assisted. Immunohistochemistry. Male. Middle Aged. Retrospective Studies

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  • (PMID = 16807783.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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86. Comincini S, Paolillo M, Barbieri G, Palumbo S, Sbalchiero E, Azzalin A, Russo MA, Schinelli S: Gene expression analysis of an EGFR indirectly related pathway identified PTEN and MMP9 as reliable diagnostic markers for human glial tumor specimens. J Biomed Biotechnol; 2009;2009:924565
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  • [Title] Gene expression analysis of an EGFR indirectly related pathway identified PTEN and MMP9 as reliable diagnostic markers for human glial tumor specimens.
  • In this study the mRNA levels of five EGFR indirectly related genes, EGFR, HB-EGF, ADAM17, PTEN, and MMP9, have been assessed by Real-time PCR in a panel of 37 glioblastoma multiforme specimens and in 5 normal brain samples; as a result, in glioblastoma, ADAM17 and PTEN expression was significantly lower than in normal brain samples, and, in particular, a statistically significant inverse correlation was found between PTEN and MMP9 mRNA levels.
  • To verify if this correlation was conserved in gliomas, PTEN and MMP9 expression was further investigated in an additional panel of 16 anaplastic astrocytoma specimens and, in parallel, in different human normal and astrocytic tumor cell lines.
  • In conclusion, this gene expression survey highlighted that the combined measurement of PTEN and MMP9 transcripts might represent a novel reliable tool for the differential diagnosis of high-grade gliomas, and it also suggested a functional link involving these genes in glial tumors.
  • [MeSH-major] Biomarkers, Tumor / genetics. Gene Expression Regulation, Neoplastic. Glioma / diagnosis. Glioma / enzymology. Matrix Metalloproteinase 9 / metabolism. PTEN Phosphohydrolase / metabolism. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Gene Expression Profiling. Humans. Male. Middle Aged. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Young Adult

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  • (PMID = 19657395.001).
  • [ISSN] 1110-7251
  • [Journal-full-title] Journal of biomedicine & biotechnology
  • [ISO-abbreviation] J. Biomed. Biotechnol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / RNA, Messenger; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ PMC2718324
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87. McCarthy BJ, Propp JM, Davis FG, Burger PC: Time trends in oligodendroglial and astrocytic tumor incidence. Neuroepidemiology; 2008;30(1):34-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Time trends in oligodendroglial and astrocytic tumor incidence.
  • BACKGROUND: We hypothesized that the incidences of oligodendrogliomas, anaplastic oligodendrogliomas, and mixed gliomas have significantly increased from the early 1990 s forward, while the incidences of anaplastic and grade II astrocytic tumors have significantly decreased.
  • METHODS: Data for the years 1973-2004 from the Surveillance, Epidemiology and End Results (SEER) public-use data and for 1985-2004 from six collaborating registries of the Central Brain Tumor Registry of the US (CBTRUS) were obtained.
  • CONCLUSIONS: This study has demonstrated that increases in oligodendroglial tumor incidence correspond to decreases in astrocytic tumor incidence over the same time period.
  • Minimizing misclassification of glial tumors will be essential for accurately assessing incidence, survival, and mortality rates, as well as for identifying homogeneous subgroups for epidemiologic and treatment studies.
  • [MeSH-major] Astrocytoma / epidemiology. Brain Neoplasms / epidemiology. Glioma / epidemiology. Oligodendroglioma / epidemiology
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Child. Child, Preschool. Humans. Incidence. Infant. Infant, Newborn. Middle Aged. Registries / statistics & numerical data. Time. United States / epidemiology

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  • [Copyright] (c) 2008 S. Karger AG, Basel.
  • (PMID = 18259099.001).
  • [ISSN] 1423-0208
  • [Journal-full-title] Neuroepidemiology
  • [ISO-abbreviation] Neuroepidemiology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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88. Kirsch M, Mörz M, Pinzer T, Schackert HK, Schackert G: Frequent loss of the CDKN2C (p18INK4c) gene product in pituitary adenomas. Genes Chromosomes Cancer; 2009 Feb;48(2):143-54
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  • Genomic alterations of cyclin-dependent kinase inhibitors have been demonstrated in a variety of tumor types including brain tumors.
  • Among them, the cyclin-dependent kinase inhibitor 2A (CDKN2A or p16(INK4a)) gene has been shown to be frequently deleted or inactivated in astrocytic tumors.
  • This is the first report to describe that the tumor suppressor gene CDKN2C is frequently targeted by genomic alterations in pituitary adenoma.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chi-Square Distribution. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. DNA Methylation / genetics. Female. Humans. Immunohistochemistry. Infant. Loss of Heterozygosity. Male. Middle Aged. Pituitary Gland / metabolism. Promoter Regions, Genetic. Retinoblastoma Protein / genetics. Retinoblastoma Protein / metabolism. Sequence Analysis, DNA. Tumor Suppressor Protein p14ARF / genetics. Tumor Suppressor Protein p14ARF / metabolism


89. De Tommasi A, De Tommasi C, Occhiogrosso G, Cimmino A, Parisi M, Sanguedolce F, Ciappetta P: Primary intramedullary primitive neuroectodermal tumor (PNET)--case report and review of the literature. Eur J Neurol; 2006 Mar;13(3):240-3
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  • [Title] Primary intramedullary primitive neuroectodermal tumor (PNET)--case report and review of the literature.
  • Spinal primitive neuroectodermal tumors (PNET) are very rare tumors, and intramedullary localization is even less common.
  • Following the WHO 2000 classification, PNETs have been considered embryonal tumors composed of undifferentiated neuroepithelial cells with a capacity of differentiation into different cellular lines, such as astrocytic, ependymal, melanotic and muscular.
  • The optimal treatment for these malignant tumors is not yet clear, although, over the years, radiotherapy has been considered the best treatment for spinal PNETs.
  • The patient, 18 months after the onset of his symptomatology, died without cerebral tumor involvement.
  • [MeSH-major] Brain Neoplasms. Laminectomy / methods. Neuroectodermal Tumors, Primitive
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Male. Middle Aged

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  • (PMID = 16618339.001).
  • [ISSN] 1351-5101
  • [Journal-full-title] European journal of neurology
  • [ISO-abbreviation] Eur. J. Neurol.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 25
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90. Hartmann C, Meyer J, Balss J, Capper D, Mueller W, Christians A, Felsberg J, Wolter M, Mawrin C, Wick W, Weller M, Herold-Mende C, Unterberg A, Jeuken JW, Wesseling P, Reifenberger G, von Deimling A: Type and frequency of IDH1 and IDH2 mutations are related to astrocytic and oligodendroglial differentiation and age: a study of 1,010 diffuse gliomas. Acta Neuropathol; 2009 Oct;118(4):469-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Type and frequency of IDH1 and IDH2 mutations are related to astrocytic and oligodendroglial differentiation and age: a study of 1,010 diffuse gliomas.
  • IDH2 encoding mitochondrial NADP+-dependent isocitrate dehydrogenase is also mutated in these tumors, albeit at much lower frequencies.
  • Preliminary data suggest an importance of IDH1 mutation for prognosis showing that patients with anaplastic astrocytomas, oligodendrogliomas and oligoastrocytomas harboring IDH1 mutations seem to fare much better than patients without this mutation in their tumors.
  • We report on an inverse association of IDH1 and IDH2 mutations in these gliomas and a non-random distribution of the mutation types within the tumor entities.
  • IDH1 mutations of the R132C type are strongly associated with astrocytoma, while IDH2 mutations predominantly occur in oligodendroglial tumors.
  • [MeSH-major] Brain Neoplasms / genetics. Glioma / genetics. Isocitrate Dehydrogenase / genetics
  • [MeSH-minor] Adult. Age Factors. Brain / pathology. Cell Differentiation. DNA Mutational Analysis. Female. Humans. Male. Middle Aged. Mutation. Prognosis. Tumor Cells, Cultured

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  • (PMID = 19554337.001).
  • [ISSN] 1432-0533
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 1.1.1.41 / Isocitrate Dehydrogenase
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91. Anan M, Inoue R, Ishii K, Abe T, Fujiki M, Kobayashi H, Goya T, Nakazato Y: A rosette-forming glioneuronal tumor of the spinal cord: the first case of a rosette-forming glioneuronal tumor originating from the spinal cord. Hum Pathol; 2009 Jun;40(6):898-901