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1. Fourtassi M, Psimaras D, Ducray F, Sanson M: [Systemic metastases of malignant gliomas]. Bull Cancer; 2008 May;95(5):522-5
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  • [Title] [Systemic metastases of malignant gliomas].
  • Despite malignant gliomas are highly invasive tumors, extracranial metastatases are extremely rare.
  • We report herein four cases (two glioblastomas, a gliosarcoma and an anaplastic oligodendroglioma) with systemic dissemination occurring 3 to 13 months after surgery.
  • Metastases from the anaplastic oligodendroglioma which displayed 1p and 19q chromosome codeletion, responded to chemotherapy and the patient survived 8 months.
  • [MeSH-major] Brain Neoplasms / pathology. Glioma / secondary

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  • (PMID = 18541516.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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2. Jin M, Komohara Y, Shichijo S, Yamanaka R, Nikawa J, Itoh K, Yamada A: Erythropoietin-producing hepatocyte B6 variant-derived peptides with the ability to induce glioma-reactive cytotoxic T lymphocytes in human leukocyte antigen-A2+ glioma patients. Cancer Sci; 2008 Aug;99(8):1656-62
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  • [Title] Erythropoietin-producing hepatocyte B6 variant-derived peptides with the ability to induce glioma-reactive cytotoxic T lymphocytes in human leukocyte antigen-A2+ glioma patients.
  • In the present study, we examined the expression of the EphB6 variant (EphB6v) in a panel of brain tumor cell lines and glioblastoma tissues and we found that EphB6v was preferentially expressed in malignant brain tumors, such as glioblastomas and anaplastic astrocytomas.
  • The two EphB6v-derived peptides exhibited the ability to bind to human leukocyte antigen (HLA)-A0201 molecules, and each of them was able to induce cytotoxic T lymphocytes in vitro in the peripheral blood mononuclear cells of HLA-A2(+) glioma patients.
  • [MeSH-minor] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Case-Control Studies. Cell Line, Tumor. Gene Expression. Glioblastoma / metabolism. HLA-A Antigens. HLA-A2 Antigen. Hepatocytes. Humans

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  • (PMID = 18754880.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; EC 2.7.1.- / EPHB6 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
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3. 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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  • 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 found 165 IDH1 (72.7%) and 2 IDH2 mutations (0.9%) in 227 diffuse astrocytomas WHO grade II, 146 IDH1 (64.0%) and 2 IDH2 mutations (0.9%) in 228 anaplastic astrocytomas WHO grade III, 105 IDH1 (82.0%) and 6 IDH2 mutations (4.7%) in 128 oligodendrogliomas WHO grade II, 121 IDH1 (69.5%) and 9 IDH2 mutations (5.2%) in 174 anaplastic oligodendrogliomas WHO grade III, 62 IDH1 (81.6%) and 1 IDH2 mutations (1.3%) in 76 oligoastrocytomas WHO grade II and 117 IDH1 (66.1%) and 11 IDH2 mutations (6.2%) in 177 anaplastic oligoastrocytomas WHO grade III.
  • 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.
  • In addition, patients with anaplastic glioma harboring IDH1 mutations were on average 6 years younger than those without these alterations.
  • [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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4. de Vries NA, Beijnen JH, van Tellingen O: High-grade glioma mouse models and their applicability for preclinical testing. Cancer Treat Rev; 2009 Dec;35(8):714-23
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  • [Title] High-grade glioma mouse models and their applicability for preclinical testing.
  • High-grade gliomas (WHO grade III anaplastic astrocytoma and grade IV glioblastoma multiforme) are the most common primary tumors in the central nervous system in adults.
  • Unfortunately, despite great efforts in finding better therapies, high-grade glioma remains among the most devastating and deadliest of all human cancers.
  • This review will discuss the advantages and shortcomings of the established high-grade glioma mouse models with emphasis on their potential applicability for preclinical testing of novel drugs and treatment regimens.
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Biomarkers, Tumor / metabolism. Blood-Brain Barrier. Dacarbazine / analogs & derivatives. Dacarbazine / pharmacology. Disease Models, Animal. Mice. Phosphorylcholine / analogs & derivatives. Phosphorylcholine / pharmacology. Prognosis. Transplantation, Heterologous

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  • (PMID = 19767151.001).
  • [ISSN] 1532-1967
  • [Journal-full-title] Cancer treatment reviews
  • [ISO-abbreviation] Cancer Treat. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 107-73-3 / Phosphorylcholine; 2GWV496552 / perifosine; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
  • [Number-of-references] 86
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5. Burzynski SR, Janicki TJ, Weaver RA, Burzynski B: Targeted therapy with antineoplastons A10 and AS2-1 of high-grade, recurrent, and progressive brainstem glioma. Integr Cancer Ther; 2006 Mar;5(1):40-7
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  • [Title] Targeted therapy with antineoplastons A10 and AS2-1 of high-grade, recurrent, and progressive brainstem glioma.
  • BACKGROUND: Brainstem glioma carries the worst prognosis of all malignancies of the brain.
  • Most patients with brainstem glioma fail standard radiation therapy and chemotherapy and do not survive longer than 2 years.
  • Treatment is even more challenging when an inoperable tumor is of high-grade pathology (HBSG).
  • PATIENTS: The following group of 18 patients was evaluable: 4 patients with glioblastomas and 14 patients with anaplastic HBSG.
  • RESULTS: The overall survival at 2 and 5 years was 39% and 22%, respectively, and maximum survival was more than 17 years for a patient with anaplastic astrocytoma and more than 5 years for a patient with glioblastoma.
  • CONCLUSION: Antineoplastons contributed to more than a 5-year survival in recurrent diffuse intrinsic glioblastomas and anaplastic astrocytomas of the brainstem in a small group of patients.
  • [MeSH-major] Benzeneacetamides / administration & dosage. Brain Stem Neoplasms / drug therapy. Glioma / drug therapy. Glutamine / analogs & derivatives. Neoplasm Recurrence, Local / drug therapy. Phenylacetates / administration & dosage. Piperidones / administration & dosage

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  • (PMID = 16484713.001).
  • [ISSN] 1534-7354
  • [Journal-full-title] Integrative cancer therapies
  • [ISO-abbreviation] Integr Cancer Ther
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzeneacetamides; 0 / Drug Combinations; 0 / Phenylacetates; 0 / Piperidones; 0RH81L854J / Glutamine; 104624-98-8 / antineoplaston AS 2-1; 91531-30-5 / antineoplaston A10
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6. Ichimura K, Vogazianou AP, Liu L, Pearson DM, Bäcklund LM, Plant K, Baird K, Langford CF, Gregory SG, Collins VP: 1p36 is a preferential target of chromosome 1 deletions in astrocytic tumours and homozygously deleted in a subset of glioblastomas. Oncogene; 2008 Mar 27;27(14):2097-108
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  • Total 1p deletions were rare (2%), however partial deletions involving 1p36 were frequently identified in anaplastic astrocytomas (22%) and glioblastomas (34%).
  • However, the CpG island of TNFRSF9 was hypermethylated in 19% of astrocytic tumours and 87% of glioma cell lines.
  • TNFRSF9 expression was upregulated after demethylation of glioma cell lines.
  • Our results indicate that 1p deletions are common anaplastic astrocytomas and glioblastomas but are distinct from the 1p abnormalities in oligodendrogliomas.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Chromosome Deletion. Chromosomes, Human, Pair 1 / genetics. Glioblastoma / genetics

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  • (PMID = 17934521.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6618; United Kingdom / Cancer Research UK / / ; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2650419; NLM/ UKMS4022
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7. Green RM, Cloughesy TF, Stupp R, DeAngelis LM, Woyshner EA, Ney DE, Lassman AB: Bevacizumab for recurrent ependymoma. Neurology; 2009 Nov 17;73(20):1677-80
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  • BACKGROUND: Ependymoma is a rare type of glioma, representing 5% of all CNS malignancies.
  • METHODS: In this Institutional Review Board-approved study, we retrospectively analyzed the records of 8 adult patients treated for recurrent ependymoma and anaplastic ependymoma with bevacizumab containing chemotherapy regimens.

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  • (PMID = 19917990.001).
  • [ISSN] 1526-632X
  • [Journal-full-title] Neurology
  • [ISO-abbreviation] Neurology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / UO1 CA-105663-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab
  • [Other-IDs] NLM/ PMC2788805
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8. Kilburn L, Okcu MF, Wang T, Cao Y, Renfro-Spelman A, Aldape KD, Gilbert MR, Bondy M: Glutathione S-transferase polymorphisms are associated with survival in anaplastic glioma patients. Cancer; 2010 May 1;116(9):2242-9
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  • [Title] Glutathione S-transferase polymorphisms are associated with survival in anaplastic glioma patients.
  • The authors of this report hypothesized that patients with anaplastic glioma (AG) who have GST genotypes that encode for lower activity enzymes will have longer survival than similar patients who have higher activity genotypes.
  • In the patients who had anaplastic astrocytoma (n = 113), the patients with all GSTP1 genotypes except GSTP1 *B/*B had a 3.8 times increased risk of death (95% CI, 0.5-29.6) compared with patients who had the GSTP1 *B/*B genotype.
  • CONCLUSIONS: In patients with anaplastic oligodendroglial tumors, the GSTT1 null genotype may be associated with poor survival, possibly because of modifications in therapy secondary to increased toxicity.
  • In patients with anaplastic astrocytoma, the GSTP1 *B/*B genotype may confer a survival advantage.

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  • [Copyright] (c) 2010 American Cancer Society.
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  • (PMID = 20187096.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA094746-02; United States / NCI NIH HHS / CA / R03 CA094746; United States / NCI NIH HHS / CA / 1R03CA094746; United States / NCI NIH HHS / CA / R03 CA094746-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.5.1.18 / Glutathione Transferase
  • [Other-IDs] NLM/ NIHMS189687; NLM/ PMC2861043
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9. Yokota T, Kouno J, Adachi K, Takahashi H, Teramoto A, Matsumoto K, Sugisaki Y, Onda M, Tsunoda T: Identification of histological markers for malignant glioma by genome-wide expression analysis: dynein, alpha-PIX and sorcin. Acta Neuropathol; 2006 Jan;111(1):29-38
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  • [Title] Identification of histological markers for malignant glioma by genome-wide expression analysis: dynein, alpha-PIX and sorcin.
  • Glioblastoma multiforme (GBM), the most malignant class of glial neoplasm (grade IV in WHO criteria), carries the worst clinical prognosis among primary brain tumors in adults.
  • By comparing the profiles with those of normal brain tissue, we identified a number of differentially expressed genes: 54 with increased expression and 45 with reduced expression in GBMs.
  • To establish criteria for this diagnostic approach, we scored glial tumor tissues of different histological grades according to the staining results; the scores were significantly higher in anaplastic astrocytomas and GBMs than in diffuse astrocytomas or normal brain tissues.
  • These findings indicated that levels of these three proteins might serve as histological markers for malignant glioma classification.
  • [MeSH-major] Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Calcium-Binding Proteins / genetics. Cell Cycle Proteins / genetics. Dyneins / genetics. Glioblastoma / genetics. Guanine Nucleotide Exchange Factors / genetics

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  • (PMID = 16320026.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / ARHGEF6 protein, human; 0 / Biomarkers, Tumor; 0 / Calcium-Binding Proteins; 0 / Cell Cycle Proteins; 0 / DNA, Neoplasm; 0 / Guanine Nucleotide Exchange Factors; 0 / Rho Guanine Nucleotide Exchange Factors; 0 / SRI protein, human; EC 3.6.4.2 / Dyneins
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10. Stockhammer F, Plotkin M, Amthauer H, van Landeghem FK, Woiciechowsky C: Correlation of F-18-fluoro-ethyl-tyrosin uptake with vascular and cell density in non-contrast-enhancing gliomas. J Neurooncol; 2008 Jun;88(2):205-10
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  • These tumors are heterogeneous regarding anaplastic and non-anaplastic areas.
  • We investigated histological correlates of tumor grading in biopsies obtained from regions with maximum amino acid uptake revealed by F-18-fluoro-ethyl-tyrosin positron emission tomography (FET-PET).
  • In 13 patients neuronavigated biopsies were obtained during tumor resection.
  • RESULTS: 12 of the 22 non-contrast enhancing gliomas corresponded to anaplastic astrocytomas WHO grade III.
  • Thus, no correlation was found between FET uptake and tumor grade.
  • Although tumor grade cannot be predicted, clinical use of FET PET as an indicator for neovascularization should be addressed in future studies.
  • [MeSH-major] Brain Neoplasms / diagnostic imaging. Fluorodeoxyglucose F18. Glioma / diagnostic imaging. Positron-Emission Tomography. Radiopharmaceuticals. Tyrosine / metabolism

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  • (PMID = 18317691.001).
  • [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 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 42HK56048U / Tyrosine
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11. Brandsma D, van den Bent MJ: Molecular targeted therapies and chemotherapy in malignant gliomas. Curr Opin Oncol; 2007 Nov;19(6):598-605
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  • [Title] Molecular targeted therapies and chemotherapy in malignant gliomas.
  • PURPOSE OF REVIEW: To review current developments in the field of chemotherapy and targeted treatment of high-grade glioma.
  • RECENT FINDINGS: Two independent large phase III trials on adjuvant procarbazine, lomustine and vincristine chemotherapy in anaplastic oligodendroglial tumors have shown this improves progression-free survival, but not overall survival, regardless of 1p/19q status.
  • If given sequentially, the timing of procarbazine, lomustine and vincristine chemotherapy has no clear effect on the survival of anaplastic oligodendroglioma.
  • The role of combined chemo-irradiation for non-glioblastoma multiforme high-grade glioma remains to be identified.
  • [MeSH-major] Brain Neoplasms / drug therapy. Brain Neoplasms / genetics. Glioma / drug therapy. Glioma / genetics

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  • (PMID = 17906459.001).
  • [ISSN] 1040-8746
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
  • [Number-of-references] 74
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12. Yi L, Zhou ZH, Ping YF, Chen JH, Yao XH, Feng H, Lu JY, Wang JM, Bian XW: Isolation and characterization of stem cell-like precursor cells from primary human anaplastic oligoastrocytoma. Mod Pathol; 2007 Oct;20(10):1061-8
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  • [Title] Isolation and characterization of stem cell-like precursor cells from primary human anaplastic oligoastrocytoma.
  • A small population of stem cell-like precursors in solid tumors are linked to histological composition, progression, angiogenesis, metastasis, recurrence and drug resistance of a variety of malignant tumors.
  • Oligoastrocytoma is the most common brain mixed glioma composed of mixed cells of oligodendroglial and astrocytic phenotypes.
  • Identification and characterization of stem cell-like precursors in oligoastrocytoma may shed light on the oncogenesis of this unique type of tumor and assist in the design of novel therapeutic strategy.
  • Here, tumor stem cell-like precursors were identified from primary human anaplastic oligoastrocytomas by labeling of the tumor sections with nestin and CD133.
  • Tumor cells were cultured in vitro in stem cell medium with growth factors and the capacity of the surviving stem cell-like precursors to form tumor spheres was tested.
  • The tumor spheres were further injected subcutaneously into nude mice to observe the contribution of stem cell-like precursors to histological composition and tumor progression.
  • These cells differentiated into tumor cells with both oligodendroglial and astrocytic characteristics and formed tumor spheres in vitro, which upon implantation in nude mice, grew into tumor nodules containing nestin+/CD133+ cells at levels higher than in the primary tumor tissues.
  • This study revealed for the first time that anaplastic human oligoastrocytomas contained stem cell-like precursors, which exhibit neural stem cell properties with tumorigenicity.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Animals. Antigens, CD / analysis. Biomarkers, Tumor / analysis. Brain / pathology. Fluorescent Antibody Technique, Indirect. Glycoproteins / analysis. Humans. Intermediate Filament Proteins / analysis. Magnetic Resonance Imaging. Mice. Mice, Nude. Neoplasm Transplantation. Nerve Tissue Proteins / analysis. Nestin. Peptides / analysis. Spheroids, Cellular / chemistry. Spheroids, Cellular / pathology. Tumor Cells, Cultured

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  • (PMID = 17660801.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / Glycoproteins; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / Peptides
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13. Koul D: PTEN signaling pathways in glioblastoma. Cancer Biol Ther; 2008 Sep;7(9):1321-5
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  • Malignant gliomas are the most common primary brain tumor in adults, but the prognosis for patients with these tumors remains poor despite advances in diagnosis and standard therapies such as surgery, radiation therapy, and chemotherapy.
  • Recent insights into the biology of gliomas include the finding that tyrosine kinase receptors and signal transduction pathways play a role in tumor initiation and maintenance.
  • Deregulation of phosphatidylinositol 3-kinase (PI3K) signaling pathways resulting from genetic alterations in the PTEN tumor suppressor gene on 10q23 at the level of LOH, mutation and methylation have been identified in at least 60% of glioblastoma.
  • Loss of PTEN function by mutation or LOH correlates with poor survival in anaplastic astrocytoma and glioblastoma, suggesting that PTEN plays a role in patient outcome.
  • Interestingly, amplification of Epidermal growth factor receptor (EGFR) in the background of heterozygous PTEN knockout mice develop invasive glioma very similar to human glioblastoma, demonstrating the importance of PTEN in glioma progression and providing a model system to evaluate the efficacy of targeting PTEN in glioblastoma.
  • [MeSH-major] Brain Neoplasms / genetics. Glioblastoma / genetics. PTEN Phosphohydrolase / genetics. Signal Transduction / physiology. Tumor Suppressor Proteins / physiology


14. Sharma S, Sarkar C, Gaikwad S, Suri A, Sharma MC: Primary neurocytoma of the spinal cord: a case report and review of literature. J Neurooncol; 2005 Aug;74(1):47-52
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  • Radiologic and operative impression at both surgeries was that of a glioma, possibly anaplastic.
  • The tumor showed rare mitoses, focal mild vascular proliferation in both specimens, and necrosis in the initial specimen.
  • However, the presence of histologic atypia and increased MIB1 index in SN appear to more closely correlate with tumor recurrence and a worse overall outcome, in part due to their location in the critical region of cervical spinal cord.
  • [MeSH-minor] Adult. Cervical Vertebrae. Diagnosis, Differential. Glioma / pathology. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male

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  • (PMID = 16078107.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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15. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.
  • METHODS: We performed this study on 67 glioma patients between 3 and 69 years of age (36 males and 31 females).
  • 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.
  • RESULTS: For the 67 cases of glioma, the degree of accumulation was variable.
  • 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.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / radionuclide imaging. Glioma / pathology. Glioma / radionuclide imaging. Methionine / pharmacokinetics. Positron-Emission Tomography / methods


16. Ohta K, Kuwahara K, Zhang Z, Makino K, Komohara Y, Nakamura H, Kuratsu J, Sakaguchi N: Decreased expression of germinal center-associated nuclear protein is involved in chromosomal instability in malignant gliomas. Cancer Sci; 2009 Nov;100(11):2069-76
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  • [Title] Decreased expression of germinal center-associated nuclear protein is involved in chromosomal instability in malignant gliomas.
  • Malignant glioma (MG) is highly proliferative and invasive, with the malignant characteristics associated with aneuploidy and chromosomal instability (CIN).
  • Glioblastomas showed a significantly lower level of ganp mRNA than anaplastic astrocytomas, as measured by real-time reverse transcription-PCR, in 101 cases of adult MG.
  • MGs of ganp(Low) expression displayed more malignant characteristics, with loss of heterozygosity on chromosome 10, epidermal growth factor receptor gene amplification, and significantly poorer prognosis than the ganp(High) group.
  • [MeSH-major] Acetyltransferases / physiology. Brain Neoplasms / genetics. Chromosomal Instability. Glioma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Cycle. Cell Line, Tumor. Cell Proliferation. Female. Genes, p53. Humans. Intracellular Signaling Peptides and Proteins. Loss of Heterozygosity. Male. Middle Aged. Mutation. RNA Interference. Receptor, Epidermal Growth Factor / genetics

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  • (PMID = 19686285.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; EC 2.3.1.- / Acetyltransferases; EC 2.3.1.- / MCM3AP protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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17. Naydenov E, Tzekov C, Minkin K, Nachev S, Marinov M: [Malignant progression of an anaplastic ganglioglioma into a glioblastoma multiforme--report on two cases and review of the literature]. Khirurgiia (Sofiia); 2009;(2-3):69-74
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  • [Title] [Malignant progression of an anaplastic ganglioglioma into a glioblastoma multiforme--report on two cases and review of the literature].
  • INTRODUCTION: Ganglioglioma is an uncommon type of primary brain tumors.
  • In most of the cases the tumor demonstrates benign clinical behaviour with long-term patients' survival.
  • We present two cases ofhistologically confirmed anaplastic ganglioglioma in which malignant progression into a glioblastoma multiforme was seen.
  • The tumor was excised partially and the histological result was anaplastic ganglioglioma (World Health Organization - WHO. gr. III).
  • A local tumor recurrence was found and the patient underwent second operative intervention with gross total tumor resection.
  • IV glioma). The patient improved after the procedure.
  • An involvement of the contralateral cerebral hemisphere was found on control CT-scan ten months later.
  • The patient died after one month, 23 months after her initial diagnosis.
  • MRI data for large, heterointense tumor lesion in the left frontal lobe was found.
  • A subtotal tumor removal was made.
  • The histological result was anaplastic ganglioglioma (WHO gr. ILL).
  • Data for additional local tumor growth was found on control CT-scan one month later.
  • 20 months after the initial diagnosis.
  • The tumor behaviour may vary between the patients in spite of the similar histological characteristics which indicates the possible presence of different tumor subtypes.
  • [MeSH-major] Brain Neoplasms / pathology. Ganglioglioma / pathology. Glioblastoma / pathology. Neoplasm Recurrence, Local / pathology


18. Chamberlain MC: Emerging clinical principles on the use of bevacizumab for the treatment of malignant gliomas. Cancer; 2010 Sep 1;116(17):3988-99
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  • [Title] Emerging clinical principles on the use of bevacizumab for the treatment of malignant gliomas.
  • Despite advances in adjuvant therapy, the prognosis for most patients with high-grade glioma (HGG) is poor, and almost all HGGs have a likelihood of disease recurrence.
  • A compelling biologic rationale, a pressing need for improved therapeutics and positive results from studies of bevacizumab in other tumor types, led to the evaluation of bevacizumab in the treatment of HGG.
  • Preliminary data on bevacizumab-based therapy in recurrent anaplastic gliomas, in the frontline treatment of GB, and in additional patient populations are also encouraging.
  • With the goal of addressing unanswered questions regarding the optimal use of bevacizumab, the objective of the current review was to provide a summary of the clinical efficacy and safety data on bevacizumab in patients with HGG, the practical issues surrounding the administration of bevacizumab, and ongoing investigations of bevacizumab in additional brain tumor treatment settings.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Brain Neoplasms / drug therapy. Glioma / drug therapy

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  • [Copyright] Cancer 2010. (c) 2010 American Cancer Society.
  • (PMID = 20564141.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab
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19. Hong X, Nelson KK, deCarvalho AC, Kalkanis SN: Heparanase expression of glioma in human and animal models. J Neurosurg; 2010 Aug;113(2):261-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Heparanase expression of glioma in human and animal models.
  • OBJECT: Mammalian heparanase has been shown to function in tumor progression, invasion, and angiogenesis.
  • To clarify its expression in gliomas, human glioma tissues and glioma animal models were investigated.
  • METHODS: The expression of heparanase mRNA was determined in 33 resected human glioma tissues by semiquantitative real-time polymerase chain reaction.
  • RESULTS: The authors found that heparanase mRNA is greatly increased in gliomas including oligodendroglioma (9 samples), anaplastic astrocytoma (11 samples), and GBM (13 samples) as compared with healthy brain mRNA (3 samples).
  • Note, however, that no significant difference was observed among the 3 tumor groups.
  • Increased heparanase expression was also found in tumor tissues on Western blotting.
  • Heparanase-expressing cells, including GBM tumor cells and neovessel endothelial cells, exhibited decreased expression of CD44, a cell adhesion molecule on the cell membrane that is important for regulating tumor invasion.
  • In addition, heparanase-expressing tumor cells showed an elevated density of the cell proliferation marker Ki 67, as compared with its density in non-heparanase-expressing tumor cells, suggesting that heparanase expression is correlated with enhanced tumor proliferation.
  • Two animal glioma models were tested for heparanase expression.
  • Both murine astrocytoma cells (Ast11.9-2) and cultured primary human GBM neurospheres expressed heparanase when grown in animal brain tissue.
  • CONCLUSIONS: Glioma tissues contain increased levels of heparanase.
  • Multiple cell types contribute to the expression of heparanase, including neovessel endothelial cells, tumor cells, and infiltrated neutrophils.
  • [MeSH-major] Brain Neoplasms / physiopathology. Glioblastoma / physiopathology. Glucuronidase / genetics. Glucuronidase / metabolism
  • [MeSH-minor] Animals. Antigens, CD44 / genetics. Antigens, CD44 / metabolism. Astrocytoma / genetics. Astrocytoma / metabolism. Astrocytoma / physiopathology. Blotting, Western. Disease Models, Animal. Endothelial Cells / physiology. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Mice. Mice, Inbred C57BL. Oligodendroglioma / genetics. Oligodendroglioma / metabolism. Oligodendroglioma / physiopathology. RNA, Messenger / metabolism. Rats. Rats, Nude. Reverse Transcriptase Polymerase Chain Reaction. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 19835469.001).
  • [ISSN] 1933-0693
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / CD44 protein, human; 0 / RNA, Messenger; EC 3.2.1.- / heparanase; EC 3.2.1.31 / Glucuronidase
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20. Amberger-Murphy V: Hypoxia helps glioma to fight therapy. Curr Cancer Drug Targets; 2009 May;9(3):381-90
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  • [Title] Hypoxia helps glioma to fight therapy.
  • Despite major improvements in the surgical management the prognosis for patients bearing malignant gliomas is still dismal.
  • Malignant gliomas are notoriously resistant to treatment and the survival time of patients is between 3-8 years for low-grade and anaplastic gliomas and 6 - 12 month for glioblastoma.
  • Increasing malignancy of gliomas correlates with an increase in cellularity and a poorly organized tumor vasculature leading to insufficient blood supply, hypoxic areas and ultimately to the formation of necrosis, a characteristic of glioblastoma.
  • Hypoxia induces either directly or indirectly (through the activation of transcription factors) changes in the biology of a tumor and its microenvironment leading to increased aggressiveness and tumor resistance to chemotherapy and radiation.
  • This review is focused on hypoxia-induced molecular changes affecting glioma biology and therapy.
  • [MeSH-major] Brain Neoplasms / drug therapy. Glioma / drug therapy

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  • (PMID = 19442057.001).
  • [ISSN] 1873-5576
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; 11062-77-4 / Superoxides; 31C4KY9ESH / Nitric Oxide
  • [Number-of-references] 123
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21. Massimino M, Gandola L, Luksch R, Spreafico F, Riva D, Solero C, Giangaspero F, Locatelli F, Podda M, Bozzi F, Pignoli E, Collini P, Cefalo G, Zecca M, Casanova M, Ferrari A, Terenziani M, Meazza C, Polastri D, Scaramuzza D, Ravagnani F, Fossati-Bellani F: Sequential chemotherapy, high-dose thiotepa, circulating progenitor cell rescue, and radiotherapy for childhood high-grade glioma. Neuro Oncol; 2005 Jan;7(1):41-8
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  • [Title] Sequential chemotherapy, high-dose thiotepa, circulating progenitor cell rescue, and radiotherapy for childhood high-grade glioma.
  • Childhood malignant gliomas are rare, but their clinical behavior is almost as aggressive as in adults, with resistance to therapy, rapid progression, and not uncommonly, dissemination.
  • Histologies were glioblastoma multiforme in 10, anaplastic astrocytoma in nine, and anaplastic oligodendroglioma in two; sites of origin were supratentorial areas in 17, spine in two, and posterior fossa in two.
  • Of the 21 patients, 12 have died (10 after relapse, with a median time to progression for the whole series of 14 months; one with intratumoral bleeding at 40 months after diagnosis; and one affected by Turcot syndrome for duodenal cancer relapse).
  • Four of 12 relapsed children had tumor dissemination.
  • Sequential and high-dose chemotherapy can be afforded in front-line therapy of childhood malignant glioma without excessive morbidity and rather encouraging results.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / therapy. Glioma / therapy. Thiotepa / therapeutic use

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  • (PMID = 15701281.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 905Z5W3GKH / Thiotepa
  • [Other-IDs] NLM/ PMC1871624
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22. Wick W, Weller M: [Anaplastic glioma. Neuropathology, molecular diagnostics and current study concepts]. Nervenarzt; 2010 Aug;81(8):928-30, 932-5
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  • [Title] [Anaplastic glioma. Neuropathology, molecular diagnostics and current study concepts].
  • According to the current WHO classification anaplastic gliomas comprise pure astrocytomas and oligodendrogliomas and mixed tumors.
  • This review summarizes findings, discusses problems and defines new questions from the phase III trials on anaplastic gliomas.
  • Therefore, marker profiles should be included into the next WHO brain tumor classification.
  • The current standard of care for first-line treatment in anaplastic gliomas is radiotherapy or chemotherapy.
  • Furthermore, anaplastic gliomas are an important group of brain tumors for developing future molecular targeted therapies and should therefore be in the main focus of academic and industrial drug development, which aims at improved efficacy and avoiding long-term side-effects.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Oligodendroglioma / pathology
  • [MeSH-minor] Antineoplastic Agents, Alkylating / therapeutic use. Brain / pathology. Chromosome Deletion. Clinical Trials as Topic. Clinical Trials, Phase III as Topic. Combined Modality Therapy. Cranial Irradiation. DNA Modification Methylases / genetics. DNA Mutational Analysis. DNA Repair Enzymes / genetics. Disease-Free Survival. Humans. Isocitrate Dehydrogenase / genetics. Promoter Regions, Genetic / genetics. Survival Rate. Tumor Suppressor Proteins / genetics

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  • (PMID = 20635074.001).
  • [ISSN] 1433-0407
  • [Journal-full-title] Der Nervenarzt
  • [ISO-abbreviation] Nervenarzt
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Tumor Suppressor Proteins; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; 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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23. Bulnes S, Lafuente JV: VEGF immunopositivity related to malignancy degree, proliferative activity and angiogenesis in ENU-induced gliomas. J Mol Neurosci; 2007;33(2):163-72
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  • During tumor development, neoplastic cells switch to an angiogenic phenotype, playing a significant role in the expression of the vascular endothelial growth factor (VEGF).
  • Seventy-two brain gliomas were induced in Sprague Dawley rats by prenatal exposure to ethylnitrosourea (ENU).
  • Histopathology allows us to identify microtumors as classic oligodendrogliomas (CO; mean PI of 6.01 +/- 2.8%) and macrotumors as anaplastic oligodendrogliomas (AO; mean PI of 14.06 +/- 5%).
  • Classic oligodendrogliomas show scarce VEGF165 expression whereas anaplastic ones display VEGF165 protein level 100-fold increased respect to CO.
  • Anaplastic gliomas displaying VEGF-positive intratumor capillaries correspond to the highest PI values.
  • To identify the "angiogenic switch," we propose the glioma stage characterized by VEGF immunopositive neoplastic cells inside the tumor and positive endothelial cells surrounding it.
  • [MeSH-major] Alkylating Agents / toxicity. Cell Proliferation. Ethylnitrosourea / toxicity. Glioma. Neovascularization, Pathologic. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 17917075.001).
  • [ISSN] 0895-8696
  • [Journal-full-title] Journal of molecular neuroscience : MN
  • [ISO-abbreviation] J. Mol. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Vascular Endothelial Growth Factor A; P8M1T4190R / Ethylnitrosourea
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24. Marie Y, Carpentier AF, Omuro AM, Sanson M, Thillet J, Hoang-Xuan K, Delattre JY: EGFR tyrosine kinase domain mutations in human gliomas. Neurology; 2005 Apr 26;64(8):1444-5
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  • In this study, the authors tested the presence of such mutations in 95 gliomas including glioblastomas, anaplastic oligodendrogliomas, and low-grade gliomas.
  • [MeSH-major] Brain Neoplasms / enzymology. Brain Neoplasms / genetics. Glioma / enzymology. Glioma / genetics. Mutation / genetics. Receptor, Epidermal Growth Factor / genetics

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  • (PMID = 15851741.001).
  • [ISSN] 1526-632X
  • [Journal-full-title] Neurology
  • [ISO-abbreviation] Neurology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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25. Weller M, Berger H, Hartmann C, Schramm J, Westphal M, Simon M, Goldbrunner R, Krex D, Steinbach JP, Ostertag CB, Loeffler M, Pietsch T, von Deimling A, German Glioma Network: Combined 1p/19q loss in oligodendroglial tumors: predictive or prognostic biomarker? Clin Cancer Res; 2007 Dec 1;13(23):6933-7
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  • PURPOSE: The combined loss of genetic material on chromosomes 1p and 19q is strongly associated with favorable outcome in patients with WHO grade 3 anaplastic oligodendroglial tumors.
  • EXPERIMENTAL DESIGN: Seventy-six patients with oligodendroglioma (n = 33), oligoastrocytoma (n = 30), anaplastic oligodendroglioma (n = 6), or anaplastic oligoastrocytoma (n = 7) were identified who had not received radiotherapy or chemotherapy after their first operation until the end of follow-up or until the first progression and had tissue for 1p/19q status available.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosome Deletion. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Oligodendroglioma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Astrocytoma / genetics. Astrocytoma / pathology. Biomarkers, Tumor / genetics. Disease-Free Survival. Female. Humans. Male. Middle Aged. Neoplasm Staging. Predictive Value of Tests

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  • (PMID = 18056167.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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26. Jenkinson MD, Smith TS, Haylock B, Husband D, Shenoy A, Vinjamuri S, Walker C, Pietronigro D, Warnke PC: Phase II trial of intratumoral BCNU injection and radiotherapy on untreated adult malignant glioma. J Neurooncol; 2010 Aug;99(1):103-13
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  • [Title] Phase II trial of intratumoral BCNU injection and radiotherapy on untreated adult malignant glioma.
  • A phase II clinical trial of DTI-015 and fractionated external beam radiotherapy on newly diagnosed, malignant gliomas investigated early changes in tumour physiology and metabolism, clinical outcome and safety.
  • Pre- and post DTI-015 injection neuro-imaging included computed tomography (CT) cerebral blood flow and volume, glucose and thallium single photon emission computed tomography (SPECT) and magnetic resonance imaging (MRI).
  • Twelve patients were enrolled; eight glioblastoma multiforme (GBM), four anaplastic astrocytoma (AA).
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Carmustine / therapeutic use. Glioma / drug therapy. Glioma / radiotherapy
  • [MeSH-minor] Aged. Brain Mapping. Cerebrovascular Circulation / drug effects. Disease-Free Survival. Female. Fluorodeoxyglucose F18. Humans. Injections, Intramuscular / methods. Karnofsky Performance Status. Magnetic Resonance Imaging / methods. Male. Middle Aged. Thallium. Tomography Scanners, X-Ray Computed. Tomography, Emission-Computed, Single-Photon / methods. Tomography, X-Ray Computed / methods

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  • (PMID = 20063175.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0Z5B2CJX4D / Fluorodeoxyglucose F18; AD84R52XLF / Thallium; U68WG3173Y / Carmustine
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27. Simon M, Neuloh G, von Lehe M, Meyer B, Schramm J: Insular gliomas: the case for surgical management. J Neurosurg; 2009 Apr;110(4):685-95
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  • RESULTS: A > 90% resection was achieved in 42%, and 70-90% tumor removal was accomplished in 51% of cases.
  • Surprisingly good survival rates were seen after surgery for anaplastic gliomas.
  • The median survival for patients with anaplastic astrocytomas (WHO Grade III) was 5 years, and the 5-year survival rate for those with anaplastic oligodendroglial tumors was 80%.
  • CONCLUSIONS: Insular tumor surgery carries substantial complication rates.
  • In view of the oncological benefits of resective surgery, our data would therefore argue for microsurgery as the primary treatment for most patients with a presumed WHO Grade I-III tumor.
  • [MeSH-major] Brain Neoplasms / surgery. Cerebral Cortex. Glioma / surgery

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  • (PMID = 19099379.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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28. Park CK, Lee SH, Han JH, Kim CY, Kim DW, Paek SH, Kim DG, Heo DS, Kim IH, Jung HW: Recursive partitioning analysis of prognostic factors in WHO grade III glioma patients treated with radiotherapy or radiotherapy plus chemotherapy. BMC Cancer; 2009;9:450
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  • [Title] Recursive partitioning analysis of prognostic factors in WHO grade III glioma patients treated with radiotherapy or radiotherapy plus chemotherapy.
  • BACKGROUND: We evaluated the hierarchical risk groups for the estimated survival of WHO grade III glioma patients using recursive partitioning analysis (RPA).
  • METHODS: A total of 133 patients with anaplastic astrocytoma (AA, n = 56), anaplastic oligodendroglioma (AO, n = 67), or anaplastic oligoastrocytoma (AOA, n = 10) were included in the study.
  • CONCLUSION: The present study shows that RPA grouping with clinical prognostic factors can successfully predict the survival of patients with WHO grade III glioma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / diagnosis. Brain Neoplasms / therapy. Classification / methods. Glioma / diagnosis. Glioma / therapy. Neoplasm Staging / methods. Radiotherapy

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  • (PMID = 20017960.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 8N3DW7272P / Cyclophosphamide; Q20Q21Q62J / Cisplatin; RSA8KO39WH / Vindesine; PCV regimen
  • [Other-IDs] NLM/ PMC2806410
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29. Sadones J, Michotte A, Veld P, Chaskis C, Sciot R, Menten J, Joossens EJ, Strauven T, D'Hondt LA, Sartenaer D, Califice SF, Bierau K, Svensson C, De Grève J, Neyns B: MGMT promoter hypermethylation correlates with a survival benefit from temozolomide in patients with recurrent anaplastic astrocytoma but not glioblastoma. Eur J Cancer; 2009 Jan;45(1):146-53
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  • [Title] MGMT promoter hypermethylation correlates with a survival benefit from temozolomide in patients with recurrent anaplastic astrocytoma but not glioblastoma.
  • AIMS: To investigate the correlation between O(6)-methylguanine-DNA-methyltransferase (MGMT) promoter methylation and benefit from temozolomide in patients with recurrent high-grade glioma.
  • RESULTS: A subgroup of 38 patients who were chemotherapy-naive at recurrence was analysed (22 glioblastoma, 12 anaplastic astrocytoma [AA] and 4 anaplastic oligoastrocytoma [AOA]); none had 1p/19q loss.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. O(6)-Methylguanine-DNA Methyltransferase / genetics. Promoter Regions, Genetic

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  • (PMID = 18945611.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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30. Shirahata M, Iwao-Koizumi K, Saito S, Ueno N, Oda M, Hashimoto N, Takahashi JA, Kato K: Gene expression-based molecular diagnostic system for malignant gliomas is superior to histological diagnosis. Clin Cancer Res; 2007 Dec 15;13(24):7341-56
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  • [Title] Gene expression-based molecular diagnostic system for malignant gliomas is superior to histological diagnosis.
  • PURPOSE: Current morphology-based glioma classification methods do not adequately reflect the complex biology of gliomas, thus limiting their prognostic ability.
  • In this study, we focused on anaplastic oligodendroglioma and glioblastoma, which typically follow distinct clinical courses.
  • EXPERIMENTAL DESIGN: The expression of 3,456 genes in 32 patients, 12 and 20 of whom had prognostically distinct anaplastic oligodendroglioma and glioblastoma, respectively, was measured by PCR array.
  • Next to unsupervised methods, we did supervised analysis using a weighted voting algorithm to construct a diagnostic system discriminating anaplastic oligodendroglioma from glioblastoma.
  • The clinical utility was tested on a microarray-based data set of 50 malignant gliomas from a previous study.
  • RESULTS: Unsupervised analysis showed divergent global gene expression patterns between the two tumor classes.
  • Applied to a gene expression data set from a previous study, our model correlated better with outcome than histologic diagnosis, and also displayed 96.6% (28 of 29) consistency with the molecular classification scheme used for these histologically controversial gliomas in the original article.
  • Furthermore, we observed that histologically diagnosed glioblastoma samples that shared anaplastic oligodendroglioma molecular characteristics tended to be associated with longer survival.
  • CONCLUSIONS: Our molecular diagnostic system showed reproducible clinical utility and prognostic ability superior to traditional histopathologic diagnosis for malignant glioma.
  • [MeSH-major] Brain Neoplasms / diagnosis. Brain Neoplasms / genetics. Gene Expression Profiling / methods. Glioblastoma / diagnosis. Glioblastoma / genetics. Oligodendroglioma / diagnosis

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  • (PMID = 18094416.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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31. Guan X, Lai S, Lackey J, Shi J, Techavipoo U, Moulding HD, Flanders AE, Andrews DW: Revisiting anaplastic astrocytomas II: further characterization of an expansive growth pattern with visually enhanced diffusion tensor imaging. J Magn Reson Imaging; 2008 Dec;28(6):1322-36
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  • [Title] Revisiting anaplastic astrocytomas II: further characterization of an expansive growth pattern with visually enhanced diffusion tensor imaging.
  • PURPOSE: To seek to distinguish and visualize the different magnetic resonance imaging (MRI) growth patterns among malignant gliomas utilizing visually enhanced diffusion tensor imaging (DTI).
  • MATERIALS AND METHODS: Nineteen consecutive patients undergoing image-guided resection of a newly diagnosed malignant glioma underwent add-on acquisition of DTI data based on an Institutional Review Board (IRB)-approved imaging protocol during preoperative MRI scans for routine intraoperative image guidance.
  • Tumor growth patterns were assigned to expansive or mixed/infiltrative classes as described in the companion article (24).
  • DTI-based white matter tractography was conducted and the DTI data were fused with anatomical images using an in-house software package we developed to enhance the visualization of the tumor/fiber interface.
  • RESULTS: Out of the 19 tumor patients studied, 11 had infiltrative tumors and the other 8 had expansive tumors.
  • While less clear with 2D axial diffusion color maps, visually enhanced 3D reconstructions of the tumor/fiber interface successfully corroborated distinctive growth patterns.
  • This was particularly evident when viewed in 3D video loops of each tumor/fiber interface.
  • CONCLUSION: We have successfully developed software that visually enhances the anatomic details of the tumor/fiber interface in patients with anaplastic astrocytomas.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Diffusion Magnetic Resonance Imaging / methods. Image Enhancement / methods. Image Processing, Computer-Assisted

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 19025901.001).
  • [ISSN] 1053-1807
  • [Journal-full-title] Journal of magnetic resonance imaging : JMRI
  • [ISO-abbreviation] J Magn Reson Imaging
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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32. Nakagawa Y, Kageji T, Mizobuchi Y, Kumada H, Nakagawa Y: Clinical results of BNCT for malignant brain tumors in children. Appl Radiat Isot; 2009 Jul;67(7-8 Suppl):S27-30
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  • [Title] Clinical results of BNCT for malignant brain tumors in children.
  • It is very difficult to treat the patients with malignant brain tumor in children, especially under 3 years, because the conventional irradiation cannot be applied due to the damage of normal brain tissue.
  • However, boron neutron capture therapy (BNCT) has tumor selectivity such that it can make damage only in tumor cells.
  • We evaluated the clinical results and courses in patients with malignant glioma under 15 years.
  • Among 183 patients with brain tumors treated by our group using BSH-based intra-operative BNCT, 23 patients were under 15 years.
  • There were 3 glioblastomas (GBM), 6 anaplastic astrocytomas(AAS), 7 primitive neuroectodermal tumors (PNET), 6 pontine gliomas and 1 anaplastic ependymoma.
  • All GBM and PNET patients died due to CSF and/or CNS dissemination without local tumor regrowth.
  • All pontine glioma patients died due to regrowth of the tumor.
  • Four of 6 anaplastic astrocytoma and 1 anaplastic ependymoma patients alive without tumor recurrence.
  • BNCT can be applied to malignant brain tumors in children, especially under 3 years instead of conventional radiation.
  • [MeSH-major] Boron Neutron Capture Therapy. Brain Neoplasms / radiotherapy. Glioma / radiotherapy

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  • (PMID = 19406652.001).
  • [ISSN] 1872-9800
  • [Journal-full-title] Applied radiation and isotopes : including data, instrumentation and methods for use in agriculture, industry and medicine
  • [ISO-abbreviation] Appl Radiat Isot
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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33. Weller M, Stupp R, Reifenberger G, Brandes AA, van den Bent MJ, Wick W, Hegi ME: MGMT promoter methylation in malignant gliomas: ready for personalized medicine? Nat Rev Neurol; 2010 Jan;6(1):39-51
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  • [Title] MGMT promoter methylation in malignant gliomas: ready for personalized medicine?
  • In other subtypes of glioma, such as anaplastic gliomas, the relevance of MGMT promoter methylation might extend beyond the prediction of chemosensitivity, and could reflect a distinct molecular profile.
  • We critically discuss the prognostic and predictive value of MGMT silencing, reviewing trials in which patients with different types of glioma were treated with various chemotherapy schedules, either up-front or at recurrence.
  • Moreover, future clinical trials will need to determine, for each subtype of glioma, the degree to which MGMT promoter methylation is predictive or prognostic, and whether testing should become routine clinical practice.
  • [MeSH-major] DNA Methylation / genetics. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Glioma / genetics. Precision Medicine / trends. Promoter Regions, Genetic / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 19997073.001).
  • [ISSN] 1759-4766
  • [Journal-full-title] Nature reviews. Neurology
  • [ISO-abbreviation] Nat Rev Neurol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 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
  • [Number-of-references] 93
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34. Riemenschneider MJ, Hegi ME, Reifenberger G: MGMT promoter methylation in malignant gliomas. Target Oncol; 2010 Sep;5(3):161-5
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  • [Title] MGMT promoter methylation in malignant gliomas.
  • Malignant gliomas often have the MGMT gene inactivated due to aberrant methylation of its promoter region.
  • In anaplastic gliomas, MGMT promoter methylation is a favorable prognostic marker independent of the type of therapy, i.e., radio- or chemotherapy.
  • [MeSH-major] Brain Neoplasms / genetics. DNA Methylation. Glioma / genetics. O(6)-Methylguanine-DNA Methyltransferase / genetics. Promoter Regions, Genetic / genetics

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  • (PMID = 20725792.001).
  • [ISSN] 1776-260X
  • [Journal-full-title] Targeted oncology
  • [ISO-abbreviation] Target Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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35. Hashiba T, Izumoto S, Kagawa N, Suzuki T, Hashimoto N, Maruno M, Yoshimine T: Expression of WT1 protein and correlation with cellular proliferation in glial tumors. Neurol Med Chir (Tokyo); 2007 Apr;47(4):165-70; discussion 170
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  • The expression of Wilms' tumor gene WT1 protein was investigated immunohistochemically in 73 glial tumors, including 60 astrocytic tumors, eight oligodendroglial tumors, and five ependymal tumors.
  • Almost all glioblastomas, anaplastic astrocytomas, anaplastic ependymomas, and anaplastic oligodendrogliomas expressed high levels of WT1 protein.
  • Histological examination found that WT1 protein was strongly expressed in the anaplastic portions and areas with perivascular proliferation and high cellularity, implying that WT1 gene might be important in glial tumor cell proliferation.
  • This study indicates that many malignant glial tumors are good candidates for cancer immunotherapy targeting WT1 protein and that WT1 protein expression could be used as a proliferation marker in glial tumors.
  • [MeSH-major] Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Glioma / metabolism. Glioma / pathology. WT1 Proteins / metabolism

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  • (PMID = 17457020.001).
  • [ISSN] 0470-8105
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / WT1 Proteins
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36. Kobayashi T, Masumoto J, Tada T, Nomiyama T, Hongo K, Nakayama J: Prognostic significance of the immunohistochemical staining of cleaved caspase-3, an activated form of caspase-3, in gliomas. Clin Cancer Res; 2007 Jul 1;13(13):3868-74
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  • Survival analysis between CC3 IRS of glioma patients and survival time was carried out using the Kaplan-Meier method with the log-rank test and the Cox proportional hazards regression model.
  • RESULTS: CC3 IRS was statistically analyzed to designate the best provisional cutoff point, and when detected in >10% of glioma cells, it was considered positive.
  • The Kaplan-Meier method with the log-rank test revealed that patients with CC3 IRS-positive tumors had significantly greater survival than those with CC3 IRS-negative tumors among three grades, 2, 3, and 4 (P = 0.0061), and within grade 3 of anaplastic astrocytoma (P = 0.0458).
  • CONCLUSIONS: CC3 IRS could be useful as a good prognostic indicator for glioma patients.
  • [MeSH-major] Brain Neoplasms / diagnosis. Brain Neoplasms / metabolism. Caspase 3 / metabolism. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Glioma / diagnosis. Glioma / metabolism

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  • (PMID = 17606719.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.22.- / Caspase 3
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37. Cetin N, Dienel G, Gokden M: CD117 expression in glial tumors. J Neurooncol; 2005 Nov;75(2):195-202
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  • Because GISTs that express immunohistochemically-detectable CD117 respond dramatically to treatment with tyrosine kinase inhibitors, identification of central nervous system tumors that express CD117 might open new therapeutic approaches for treatment of brain tumors.
  • The proportion of high grade tumors of all tumor types with detectable CD117 immunoreactivity was statistically significantly greater than low grade tumors, and glioblastoma and anaplastic oligodendroglioma showed the highest staining grade.
  • These findings support further investigation into the possibility that CD117 has an important role in growth of glial tumors and that patients with brain tumors expressing CD117 might benefit from treatment with receptor tyrosine kinase inhibitors.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Glioma / metabolism. Proto-Oncogene Proteins c-kit / metabolism

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  • (PMID = 16132504.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS38230
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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38. Feiden S, Feiden W: [WHO classification of tumours of the CNS: revised edition of 2007 with critical comments on the typing und grading of common-type diffuse gliomas]. Pathologe; 2008 Nov;29(6):411-21
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  • Six new entities were codified: angiocentric glioma (AG); papillary glioneuronal tumour (PGNT); rosette-forming glioneuronal tumour of the fourth ventricle (RGNT); papillary tumour of the pineal region (PTPR); spindle cell oncocytoma of the adenohypophysis (SCO); and pituicytoma.
  • Furthermore, six histological variants of well-known brain tumours have been added, partially because they show different biological behaviour and/or prognosis: pilomyxoid astrocytoma; atypical choroid plexus papilloma; medulloblastoma with extensive nodularity; anaplastic medulloblastoma; extraventricular neurocytoma; non-specific variant of dysembryoplastic neuroepithelial tumour (DNT).
  • Moreover, the typing und grading of common-type diffuse gliomas, as well as the WHO grading system, are critically reviewed, particularly with regard to the prognostically important differential diagnosis of diffuse astrocytomas und oligodendrogliomas.
  • [MeSH-major] Brain Neoplasms / pathology. Central Nervous System Neoplasms / classification. Central Nervous System Neoplasms / pathology. Glioma / classification. Glioma / pathology

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  • (PMID = 18820922.001).
  • [ISSN] 1432-1963
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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39. El-Jawahri A, Patel D, Zhang M, Mladkova N, Chakravarti A: Biomarkers of clinical responsiveness in brain tumor patients : progress and potential. Mol Diagn Ther; 2008;12(4):199-208
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  • [Title] Biomarkers of clinical responsiveness in brain tumor patients : progress and potential.
  • Gliomas are the most common primary brain tumors in adults.
  • Anaplastic astrocytoma and glioblastoma multiforme represent malignant astrocytomas, which are the most common type of malignant gliomas.
  • Despite research efforts in cancer therapy, the prognosis of patients with malignant gliomas remains poor.
  • Research efforts in recent years have focused on investigating the cellular, molecular, and genetic pathways involved in the progression of malignant gliomas.
  • As a result, biomarkers have emerged as diagnostic, predictive, and prognostic tools that have the potential to transform the field of brain tumor diagnostics.
  • An increased understanding of the important molecular pathways that have been implicated in the progression of malignant gliomas has led to the identification of potential diagnostic, prognostic, and predictive biomarkers, some bearing clinical implications for targeted therapy.
  • Other promising biomarkers in glioma research include glial fibrillary acidic protein, galectins, Kir potassium channel proteins, angiogenesis, and apoptosis pathway markers.
  • Research into the clinical relevance and applicability of such biomarkers has the potential to revolutionize our approach to the diagnosis and treatment of patients with malignant gliomas.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / chemistry. Glioma / chemistry

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  • (PMID = 18652516.001).
  • [ISSN] 1177-1062
  • [Journal-full-title] Molecular diagnosis & therapy
  • [ISO-abbreviation] Mol Diagn Ther
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA108633
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 71
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40. Grommes C, Conway DS, Alshekhlee A, Barnholtz-Sloan JS: Inverse association of PPARγ agonists use and high grade glioma development. J Neurooncol; 2010 Nov;100(2):233-9
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  • [Title] Inverse association of PPARγ agonists use and high grade glioma development.
  • In a retrospective chart review, we assessed the influence of PPARγ agonists on the odds of having a high grade glioma.
  • We reviewed patients with a diagnosis of anaplastic astrocytoma and glioblastoma multiforme (GBM) between 1999 and 2008.
  • Multivariable unconditional logistic regression models were used to calculate the odds of diabetic hip fracture patients using a PPARγ agonist at time of diagnosis as compared to diabetic glioma patients.
  • We identified 1602 hip fracture patients and 302 high grade glioma patients, 15 and 16% were diabetics, respectively.
  • PPARγ agonists were used by 20% of diabetic hip fracture patients and by 6% of high grade glioma patients (chi-square P-value = 0.02) with an odds ratio of 4.081 (95% CI: 1.119-14.881).
  • The prevalence of PPARγ agonist use was lower in the diabetic high grade glioma group when compared to diabetic hip fracture patients.
  • These findings suggest that diabetic high grade glioma patients are not given PPARγ agonists as often as diabetic hip fracture patients even though these drugs are considered standard of care and should be equally distributed throughout both groups.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Glioma / drug therapy. PPAR gamma / agonists

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  • (PMID = 20443132.001).
  • [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 / Antineoplastic Agents; 0 / PPAR gamma; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; X4OV71U42S / pioglitazone
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41. Krivoshapkin AL, Kanygin VV, Semin PA, Melidi EG: [Results of radical removal of malignant cerebral gliomas, by using computer-assisted navigation, followed by adjuvant therapy]. Zh Vopr Neirokhir Im N N Burdenko; 2006 Oct-Dec;(4):10-3; discussion 13-4
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  • [Title] [Results of radical removal of malignant cerebral gliomas, by using computer-assisted navigation, followed by adjuvant therapy].
  • A retrospective cohort analysis of the results of treatment of patients with malignant gliomas was made in 2 groups, each comprising 43 patients.
  • The results of different adjuvant therapy regimens were analyzed in patients after radical tumor removal under navigation guidance (Group 1).
  • In its first subgroup, 24 patients with anaplastic astrocytes were postoperatively irradiated (60 Gy), followed by treatment with temodal (200 mg/m2 (mean 6 courses).
  • The computer-assisted technologies substantially improve a postoperative outcome in patients with malignant glionas.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / surgery. Glioma / surgery. Neurosurgical Procedures / methods. Surgery, Computer-Assisted

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  • (PMID = 17195370.001).
  • [ISSN] 0042-8817
  • [Journal-full-title] Zhurnal voprosy neĭrokhirurgii imeni N. N. Burdenko
  • [ISO-abbreviation] Zh Vopr Neirokhir Im N N Burdenko
  • [Language] rus
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Nitrosourea Compounds; 0 / Organophosphorus Compounds; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; GQ7JL9P5I2 / fotemustine
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42. Okada H, Lieberman FS, Walter KA, Lunsford LD, Kondziolka DS, Bejjani GK, Hamilton RL, Torres-Trejo A, Kalinski P, Cai Q, Mabold JL, Edington HD, Butterfield LH, Whiteside TL, Potter DM, Schold SC Jr, Pollack IF: Autologous glioma cell vaccine admixed with interleukin-4 gene transfected fibroblasts in the treatment of patients with malignant gliomas. J Transl Med; 2007;5:67
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  • [Title] Autologous glioma cell vaccine admixed with interleukin-4 gene transfected fibroblasts in the treatment of patients with malignant gliomas.
  • BACKGROUND: The prognosis for malignant gliomas remains dismal.
  • We addressed the safety, feasibility and preliminary clinical activity of the vaccinations using autologous glioma cells and interleukin (IL)-4 gene transfected fibroblasts.
  • METHODS: In University of Pittsburgh Cancer Institute (UPCI) protocol 95-033, adult participants with recurrent glioblastoma multiforme (GBM) or anaplastic astrocytoma (AA) received gross total resection (GTR) of the recurrent tumors, followed by two vaccinations with autologous fibroblasts retrovirally transfected with TFG-IL4-Neo-TK vector admixed with irradiated autologous glioma cells.
  • In UPCI 99-111, adult participants with newly diagnosed GBM or AA, following GTR and radiation therapy, received two intradermal vaccinations with the TFG-IL4-Neo-TK-transfected fibroblasts admixed with type-1 dendritic cells (DC) loaded with autologous tumor lysate.
  • Four other participants were withdrawn from the trial because of tumor progression prior to production of the cellular vaccine.
  • Interferon (IFN)-gamma Enzyme-Linked Immuno-SPOT (ELISPOT) assay in another human leukocyte antigen (HLA)-A2+ participant demonstrated systemic T-cell responses against an HLA-A2-restricted glioma-associated antigen (GAA) epitope EphA2883-891.
  • Moreover, both participants demonstrated clinical and radiological improvement with no evidence of allergic encephalitis, although both participants eventually succumbed with the tumor recurrence.
  • Nevertheless, successful generation of type-1 DCs and preliminary safety in the current study provide a strong rationale for further efforts to develop novel glioma vaccines.
  • [MeSH-major] Brain Neoplasms / therapy. Cancer Vaccines / therapeutic use. Fibroblasts / metabolism. Glioblastoma / therapy. Interleukin-4 / genetics. Transfection

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  • (PMID = 18093335.001).
  • [ISSN] 1479-5876
  • [Journal-full-title] Journal of translational medicine
  • [ISO-abbreviation] J Transl Med
  • [Language] eng
  • [Grant] United States / NCATS NIH HHS / TR / UL1 TR000005
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines; 207137-56-2 / Interleukin-4
  • [Other-IDs] NLM/ PMC2254376
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43. Moore LM, Holmes KM, Smith SM, Wu Y, Tchougounova E, Uhrbom L, Sawaya R, Bruner JM, Fuller GN, Zhang W: IGFBP2 is a candidate biomarker for Ink4a-Arf status and a therapeutic target for high-grade gliomas. Proc Natl Acad Sci U S A; 2009 Sep 29;106(39):16675-9
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  • By using a glial-specific transgenic mouse system (RCAS/Ntv-a), we reported previously that IGFBP2 is an oncogenic factor for glioma progression in combination with platelet-derived growth factor-beta (PDGFB).
  • Because the INK4a-ARF locus is often deleted in high-grade gliomas (anaplastic oligodendroglioma and glioblastoma), we investigated the effect of the Ink4a-Arf-null background on IGFBP2-mediated progression of PDGFB-initiated oligodendroglioma.
  • We demonstrate here that homozygous deletion of Ink4a-Arf bypasses the requirement of exogenously introduced IGFBP2 for glioma progression.
  • Instead, absence of Ink4a-Arf resulted in elevated endogenous tumor cell IGFBP2.
  • An inverse relationship between p16(INK4a) and IGFBP2 expression was also observed in human glioma tissue samples and in 90 different cancer cell lines by using Western blotting and reverse-phase protein lysate arrays.
  • When endogenous IGFBP2 expression was attenuated by an RCAS vector expressing antisense IGFBP2 in our mouse model, a decreased incidence of anaplastic oligodendroglioma as well as prolonged survival was observed.
  • Loss of Ink4a-Arf results in increased IGFBP2, which contributes to glioma progression, thereby implicating IGFBP2 as a marker and potential therapeutic target for Ink4a-Arf-deleted gliomas.
  • [MeSH-major] Brain Neoplasms / drug therapy. Brain Neoplasms / metabolism. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Glioma / drug therapy. Glioma / metabolism. Insulin-Like Growth Factor Binding Protein 2 / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Mice. Mice, Knockout. Mice, Transgenic. Proto-Oncogene Proteins c-sis / metabolism

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  • (PMID = 19805356.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdkn2a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Insulin-Like Growth Factor Binding Protein 2; 0 / Proto-Oncogene Proteins c-sis
  • [Other-IDs] NLM/ PMC2757856
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44. Kronik N, Kogan Y, Vainstein V, Agur Z: Improving alloreactive CTL immunotherapy for malignant gliomas using a simulation model of their interactive dynamics. Cancer Immunol Immunother; 2008 Mar;57(3):425-39
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  • [Title] Improving alloreactive CTL immunotherapy for malignant gliomas using a simulation model of their interactive dynamics.
  • Glioblastoma (GBM), a highly aggressive (WHO grade IV) primary brain tumor, is refractory to traditional treatments, such as surgery, radiation or chemotherapy.
  • We constructed a mathematical model for glioma and the immune system interactions, that may ensue upon direct intra-tumoral administration of ex vivo activated alloreactive cytotoxic-T-lymphocytes (aCTL).
  • Our model encompasses considerations of the interactive dynamics of aCTL, tumor cells, major histocompatibility complex (MHC) class I and MHC class II molecules, as well as cytokines, such as TGF-beta and IFN-gamma, which dampen or increase the pro-inflammatory environment, respectively.
  • The mathematical model successfully retrieved clinical trial results of efficacious aCTL immunotherapy for recurrent anaplastic oligodendroglioma and anaplastic astrocytoma (WHO grade III).
  • Model analysis suggests that GBM may be eradicated by new dose-intensive strategies, e.g., 3 x 10(8) aCTL every 4 days for small tumor burden, or 2 x 10(9) aCTL, infused every 5 days for larger tumor burden.
  • Further analysis pinpoints crucial bio-markers relating to tumor growth rate, tumor size, and tumor sensitivity to the immune system, whose estimation enables regimen personalization.
  • Re-initiation of clinical trials, using calculated individualized regimens for grade III-IV malignant glioma, is suggested.
  • [MeSH-major] Brain Neoplasms / immunology. Computer Simulation. Glioblastoma / immunology. Immunotherapy / methods. Models, Immunological. T-Lymphocytes, Cytotoxic / immunology

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  • [ErratumIn] Cancer Immunol Immunother. 2008 Mar;57(3):441
  • (PMID = 17823798.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cytokines
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45. Söling A, Sackewitz M, Volkmar M, Schaarschmidt D, Jacob R, Holzhausen HJ, Rainov NG: Minichromosome maintenance protein 3 elicits a cancer-restricted immune response in patients with brain malignancies and is a strong independent predictor of survival in patients with anaplastic astrocytoma. Clin Cancer Res; 2005 Jan 1;11(1):249-58
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  • [Title] Minichromosome maintenance protein 3 elicits a cancer-restricted immune response in patients with brain malignancies and is a strong independent predictor of survival in patients with anaplastic astrocytoma.
  • Informative tumor markers may represent prognostic factors for response to therapy and outcome as well as potential targets for novel anticancer therapies.
  • EXPERIMENTAL DESIGN: Tumor-associated antigens were identified by immunoscreening of a human glioma cDNA expression library with allogeneic sera from patients with diffuse astrocytoma (WHO grades 2-4).
  • In addition, 98 serum specimens from patients with primary and secondary brain malignancies and 30 serum specimens from healthy controls were examined by serologic immunoscreening for immunoreactivity with MCM3.
  • RESULTS: MCM3 is overexpressed in human astrocytic tumors and elicits a cancer-restricted humoral immune response in 9.3% (9 of 97) of patients with brain tumors (n = 95) and brain metastases (n = 2) but not in healthy controls.
  • CONCLUSIONS: MCM3 may represent a glioma-associated antigen with significant prognostic role as well as have some potential as a target for cancer-directed therapy.
  • [MeSH-major] Astrocytoma / immunology. Astrocytoma / mortality. Brain Neoplasms / immunology. Brain Neoplasms / mortality. DNA-Binding Proteins / physiology. Gene Expression Regulation, Neoplastic. Nuclear Proteins / physiology. Transcription Factors / physiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Astrocytes / metabolism. Cell Cycle Proteins. DNA, Complementary / metabolism. Disease-Free Survival. Escherichia coli / metabolism. Female. Gene Library. Glioma / metabolism. Humans. Immunohistochemistry. Ki-67 Antigen / biosynthesis. Male. Middle Aged. Minichromosome Maintenance Complex Component 3. Neoplasm Metastasis. Oligonucleotide Array Sequence Analysis. Prognosis. Proportional Hazards Models. Recurrence. Time Factors. Treatment Outcome

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  • (PMID = 15671553.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA, Complementary; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; 0 / MCM3 protein, human; 0 / Nuclear Proteins; 0 / Transcription Factors; EC 3.6.4.12 / Minichromosome Maintenance Complex Component 3
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46. Wick A, Pascher C, Wick W, Jauch T, Weller M, Bogdahn U, Hau P: Rechallenge with temozolomide in patients with recurrent gliomas. J Neurol; 2009 May;256(5):734-41
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  • Temozolomide (TMZ) is the standard of care for patients with newly diagnosed glioblastoma (GBM) as well as those with recurrent anaplastic glioma (AG) and GBM.
  • We have conducted a retrospective review of patients with recurrent glioma rechallenged with TMZ.
  • [MeSH-major] Antineoplastic Agents, Alkylating / administration & dosage. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Glioma / drug therapy. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adult. Aged. Brain / drug effects. Brain / pathology. Brain / physiopathology. Cohort Studies. Disease Progression. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / physiology. Female. Humans. Male. Middle Aged. Retrospective Studies. Treatment Outcome. Young Adult

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  • (PMID = 19240962.001).
  • [ISSN] 1432-1459
  • [Journal-full-title] Journal of neurology
  • [ISO-abbreviation] J. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; YF1K15M17Y / temozolomide
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47. Shuangshoti S, Rushing EJ, Mena H, Olsen C, Sandberg GD: Supratentorial extraventricular ependymal neoplasms: a clinicopathologic study of 32 patients. Cancer; 2005 Jun 15;103(12):2598-605
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  • BACKGROUND: Published research on the clinicopathologic features of extraventricular ependymal neoplasms of the cerebral hemispheres has been scant.
  • RESULTS: Among these 32 cases were 2 subependymomas, 19 ependymomas, and 11 anaplastic ependymomas.
  • The left cerebral hemisphere was 1.5 times more commonly involved.
  • Ki-67 proliferation index paralleled tumor grade.
  • Immunoreactivity for p53 protein was observed in the 2 cases of subependymoma, in 10 of 11 anaplastic ependymomas, and in 6 of 17 ependymomas.
  • Flow cytometry performed in 27 tumors revealed diploidy in 20 cases and aneuploidy in 4 cases (3 anaplastic and 1 classic ependymomas), with S-phase fraction ranging from 0.2-9.7.
  • CONCLUSIONS: The results of the current study suggest that there is no significant relation between histopathology, Ki-67 proliferation index, p53 immunolabeling, tumor ploidy, and biologic behavior.
  • [MeSH-major] Brain Neoplasms / pathology. Cerebral Ventricle Neoplasms / pathology. Ependymoma / pathology. Glioma, Subependymal / pathology. Supratentorial Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Proliferation. Child. Child, Preschool. Female. Flow Cytometry. Humans. Infant. Ki-67 Antigen / metabolism. Male. Middle Aged. Ploidies. Prognosis. S Phase. Tumor Suppressor Protein p53

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  • [Copyright] Published 2005 by the American Cancer Society.
  • (PMID = 15861411.001).
  • [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 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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48. Garcia-Navarrete R, Garcia E, Arrieta O, Sotelo J: Hepatocyte growth factor in cerebrospinal fluid is associated with mortality and recurrence of glioblastoma, and could be of prognostic value. J Neurooncol; 2010 May;97(3):347-51
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  • Malignant gliomas--glioblastoma multiforme and anaplastic astrocytoma--are among the most fatal forms of cancer in humans.
  • It has been suggested that hepatocyte growth factor (HGF) is a reliable predictor of glioma malignancy; amounts of HGF are directly related to cellular proliferation, angiogenesis, low apoptotic rate, and poor prognosis (WHO III and IV).
  • We measured the HGF content of cerebrospinal fluid (CSF) from patients with malignant glioma glioblastoma multiforme (WHO IV; n = 14), anaplastic astrocytoma (WHO III; n = 4), and meningioma (WHO I; n = 9), and from control subjects (n = 25), and found a high concentration of HGF in patients with malignant glioma.
  • However, CSF concentrations from glioblastoma multiforme and anaplastic astrocytoma patients were not statistically significantly different (893 +/- 157 vs. 728 +/- 61, respectively; P > 0.01).
  • Also, the HGF concentration in CSF was a reliable means of explaining the highly variable survival of patients with malignant glioma.
  • CSF concentrations of HGF higher than 500 pg/ml were associated with increased mortality whereas values higher than 850 pg/ml were associated with a brief tumor-free period after surgery (9 +/- 0.6 vs. 6 +/- 0.6 months, respectively, P < 0.001).
  • Our findings support the idea that measurement of HGF in CSF could be a useful tool for monitoring the biological activity of malignant glioma.
  • [MeSH-major] Brain Neoplasms / cerebrospinal fluid. Brain Neoplasms / mortality. Glioblastoma / cerebrospinal fluid. Glioblastoma / mortality. Hepatocyte Growth Factor / cerebrospinal fluid

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  • (PMID = 19856144.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 67256-21-7 / Hepatocyte Growth Factor
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49. Kesari S, Schiff D, Doherty L, Gigas DC, Batchelor TT, Muzikansky A, O'Neill A, Drappatz J, Chen-Plotkin AS, Ramakrishna N, Weiss SE, Levy B, Bradshaw J, Kracher J, Laforme A, Black PM, Folkman J, Kieran M, Wen PY: Phase II study of metronomic chemotherapy for recurrent malignant gliomas in adults. Neuro Oncol; 2007 Jul;9(3):354-63
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  • [Title] Phase II study of metronomic chemotherapy for recurrent malignant gliomas in adults.
  • Preclinical evidence suggests that continuous low-dose daily (metronomic) chemotherapy may inhibit tumor endothelial cell proliferation (angiogenesis) and prevent tumor growth.
  • This phase II study evaluated the feasibility of this antiangiogenic chemotherapy regimen in adults with recurrent malignant gliomas.
  • The regimen consisted of low-dose etoposide (35 mg/m2 [maximum, 100 mg/day] daily for 21 days), alternating every 21 days with cyclophosphamide (2 mg/kg [maximum, 100 mg/day] daily for 21 days), in combination with daily thalidomide and celecoxib, in adult patients with recurrent malignant gliomas.
  • Twenty-eight patients had glioblastoma multiforme (GBMs), and 20 had anaplastic gliomas (AGs).
  • [MeSH-major] Angiogenesis Inhibitors / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Brain Neoplasms / drug therapy. Glioma / drug therapy. Neoplasm Recurrence, Local / drug therapy

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  • (PMID = 17452651.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; 4Z8R6ORS6L / Thalidomide; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; JCX84Q7J1L / Celecoxib
  • [Other-IDs] NLM/ PMC1907419
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50. Salajegheh M, Rudnicki A, Smith TW: Expression of urokinase-type plasminogen activator receptor (uPAR) in primary central nervous system neoplasms. Appl Immunohistochem Mol Morphol; 2005 Jun;13(2):184-9
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  • It is a specific cell surface receptor for its ligand, urokinase-type plasminogen activator, which catalyzes the formation of plasmin from plasminogen to generate the proteolytic cascade and leads to the breakdown of the extracellular matrix. uPAR has been shown to correlate with a propensity to tumor invasion and metastasis in several types of non-central nervous system tumors.
  • In this study, the authors examined the immunohistochemical expression of uPAR in 65 primary brain tumors (5 pilocytic astrocytomas, 5 diffuse astrocytomas, 6 anaplastic astrocytomas, 8 glioblastomas, 5 oligodendrogliomas, 4 oligoastrocytomas, 6 anaplastic oligoastrocytomas, 4 gangliogliomas, 4 ependymomas, 5 medulloblastomas, 6 schwannomas, 5 meningiomas, 2 atypical meningiomas).
  • A significant positive correlation (P = 0.0006) between tumor grade and staining intensity was identified within the astrocytoma/glioblastoma subgroup, suggesting a possible correlation with anaplastic change and propensity to tumor invasion.
  • Expression of uPAR in nonmalignant, noninvasive tumors such as schwannoma and meningioma suggests that uPAR may have other biologic functions in addition to promotion of tumor invasion.

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  • (PMID = 15894933.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / PLAUR protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Urokinase Plasminogen Activator
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51. Oshiro S, Tsugu H, Komatsu F, Abe H, Onishi H, Ohmura T, Iwaasa M, Sakamoto S, Fukushima T: Quantitative assessment of gliomas by proton magnetic resonance spectroscopy. Anticancer Res; 2007 Nov-Dec;27(6A):3757-63
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  • PATIENTS AND METHODS: Eight patients with histologically verified gliomas, comprising 2 cases with glioblastoma multiforme (GBM, grade 4), 5 cases with anaplastic oligodendroglioma (AO, grade 3; high-grade glioma), and 1 case with fibrillary astrocytoma (FA, grade 2; low-grade glioma) were evaluated using the 1H-MRS protocol following conventional MR imaging, diffusion-weighted imaging (DWI), and perfusion-weighted imaging (PWI) preoperatively.
  • RESULTS: High-grade gliomas tended to demonstrate signal hyperintensity by DWI and higher relative cerebral blood volume (rCBV) by PWI.
  • Increased ratios of choline (Cho) to N-acetylaspartate (NAA) (Cho/NAA) and Cho to creatine (Cr) (Cho/Cr) correlated highly with tumor malignancy.
  • The presence of lactate and lipid was predominately detected in patients with high-grade glioma.
  • CONCLUSION: The combination of multiple MR parameters, based on DWI, PWI and 1H-MRS, appears valuable for preoperatively predicting the degree of malignancy in glioma.
  • [MeSH-major] Brain Neoplasms / diagnosis. Glioma / diagnosis. Magnetic Resonance Spectroscopy

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  • (PMID = 17970039.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Protons
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52. Ziobro M, Rolski J, Grela-Wojewoda A, Zygulska A, Niemiec M: Effects of palliative treatment with temozolomide in patients with high-grade gliomas. Neurol Neurochir Pol; 2008 May-Jun;42(3):210-5
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  • Glioblastoma multiforme was histologically diagnosed in 24 (47%) patients; anaplastic astrocytomas and other grade III gliomas (according to WHO classification) were diagnosed in 27 (53%) patients.
  • Forty-five patients were eligible for efficacy assessment because 6 patients received only one chemotherapy cycle (due to rapid progression of the glioma).
  • RESULTS: According to the radiological assessment, 6 patients (13%) had an objective response and a further 16 patients (36%) had stabilization of the glioma.
  • The median survival in the whole group was 41 weeks (40 weeks in patients with glioblastoma multiforme and 54 weeks in patients with anaplastic gliomas).
  • CONCLUSIONS: Objective benefit from the temozolomide treatment (stabilization or objective remission) was observed in 49% of patients irrespective of histological diagnosis.
  • [MeSH-major] Antineoplastic Agents, Alkylating / administration & dosage. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Glioma / drug therapy. Palliative Care / methods

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  • (PMID = 18651326.001).
  • [ISSN] 0028-3843
  • [Journal-full-title] Neurologia i neurochirurgia polska
  • [ISO-abbreviation] Neurol. Neurochir. Pol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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53. Erreni M, Solinas G, Brescia P, Osti D, Zunino F, Colombo P, Destro A, Roncalli M, Mantovani A, Draghi R, Levi D, Rodriguez Y Baena R, Gaetani P, Pelicci G, Allavena P: Human glioblastoma tumours and neural cancer stem cells express the chemokine CX3CL1 and its receptor CX3CR1. Eur J Cancer; 2010 Dec;46(18):3383-92
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  • Human gliomas represent an unmet clinical challenge as nearly two-thirds of them are highly malignant lesions with fast progression, resistance to treatment and poor prognosis.
  • The most severe form, the glioblastoma multiforme, is characterised by a marked and diffuse infiltration through the normal brain parenchyma.
  • Given the multiple effects of chemokines on tumour progression, aim of this study was to analyse the expression of the chemokine CX3CL1 and of its specific receptor CX3CR1 in 36 human surgical glioma samples, with different degrees of histological malignancy and in glioblastoma-derived neurospheres.
  • While receptor expression was similarly detected in low or high grade tumours, the uppermost scores of CX3CL1 were found in grades III-IV tumours: oligodendrogliomas, anaplastic astrocytomas and glioblastomas.
  • The high expression of CXC3L1 in the most severe forms of gliomas suggests the involvement of this chemokine and its receptor in the malignant behaviour of these tumours.
  • [MeSH-major] Brain Neoplasms / metabolism. Chemokine CX3CL1 / metabolism. Glioblastoma / metabolism. Neoplasm Proteins / metabolism. Neoplastic Stem Cells / metabolism. Receptors, Interleukin-8A / metabolism
  • [MeSH-minor] Adult. Aged. Female. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Tumor Cells, Cultured

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20728344.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chemokine CX3CL1; 0 / Neoplasm Proteins; 0 / Receptors, Interleukin-8A
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54. Vitaz TW, Warnke PC, Tabar V, Gutin PH: Brachytherapy for brain tumors. J Neurooncol; 2005 May;73(1):71-86
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  • [Title] Brachytherapy for brain tumors.
  • Over the past several decades neurooncologists have attempted to find an adjuvant treatment that prolongs survival for patients with malignant brain tumors.
  • Brachytherapy, radiotherapy delivered by placing radioactive sources directly into the tumor, was initially thought to be the solution to this problem.
  • Despite this, brachytherapy continues to be used in a number of centers throughout the world for the treatment of various types of brain tumors including low-grade gliomas, anaplastic astrocytomas, glioblastomas, meningiomas and metastases.
  • This article reviews brachytherapy's rationale, radiobiology, complications, indications, and results from numerous studies that have focused on its application for brain tumors with emphasis on its application for glial tumors.
  • [MeSH-major] Brachytherapy / methods. Brain Neoplasms / radiotherapy. Glioma / radiotherapy

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  • (PMID = 15933821.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 171
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55. Poulsen HS: [Gliomas in adults: primary non-surgical treatment]. Ugeskr Laeger; 2006 Nov 20;168(47):4082-5
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  • 900 to 1000 new cases of primary brain tumour occur each year in Denmark, and half of them are gliomas.
  • Anaplastic astrocytomas should be treated with postoperative radiation therapy with or without adjuvant chemotherapy.
  • Anaplastic oligodendroglioma should be treated with radiation therapy only.
  • [MeSH-major] Brain Neoplasms / therapy. Glioma / therapy

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  • (PMID = 17134603.001).
  • [ISSN] 1603-6824
  • [Journal-full-title] Ugeskrift for laeger
  • [ISO-abbreviation] Ugeskr. Laeg.
  • [Language] dan
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 10
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56. Idoate MA, Echeveste J: [Update on the molecular biology of gliomas: towards a pathomolecular classification of gliomas]. Rev Neurol; 2007 Feb 16-28;44(4):217-24
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  • The relationship between the oligodendroglial phenotype and the loss of chromosomes 1p and 19q is a useful data in the histopathologic differential diagnosis.
  • For treatment purposes, the combined deletion 1p/19q identifies the anaplastic type of oligodendrogliomas that are more responsive to chemotherapy.
  • [MeSH-major] Brain Neoplasms. Glioma
  • [MeSH-minor] Biomarkers, Tumor. Chromosomes, Human, Pair 10. Humans. Treatment Outcome


57. Oshiro S, Tsugu H, Komatsu F, Ohmura T, Ohta M, Sakamoto S, Fukushima T, Inoue T: Efficacy of temozolomide treatment in patients with high-grade glioma. Anticancer Res; 2009 Mar;29(3):911-7
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  • [Title] Efficacy of temozolomide treatment in patients with high-grade glioma.
  • BACKGROUND: Numerous studies have reported the clinical efficacy of temozolomide (TMZ) treatment for high-grade glioma, but information on Japanese populations has been limited.
  • PATIENTS AND METHODS: The subjects comprised ten patients with high-grade glioma [glioblastoma multiforme (GBM), n=3, gliosarcoma (GS), n=1, anaplastic oligodendroglioma (AO), n=3, anaplastic mixed oligoastrocytoma (AOA), n=1, and anaplastic ependymoma (AE), n=2].
  • As second- or third-line chemotherapy, patients received TMZ for recurrence or tumor progression.
  • As combination therapy, the local administration of tumor necrosis factor-alpha and the addition of carboplatin and etoposide were included for three patients during the course of oral TMZ treatment.
  • One of the patients receiving combination therapy has continued to show shrinkage of the relapsed tumor.
  • CONCLUSION: TMZ chemotherapy is effective for the treatment of high-grade glioma in some patients without serious toxicity.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Gliosarcoma / drug therapy. Oligodendroglioma / drug therapy
  • [MeSH-minor] Adult. Aged. Carboplatin / administration & dosage. Chemotherapy, Adjuvant. Combined Modality Therapy. Dacarbazine / administration & dosage. Dacarbazine / analogs & derivatives. Etoposide / administration & dosage. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Prognosis. Treatment Outcome. Tumor Necrosis Factor-alpha / therapeutic use

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  • Hazardous Substances Data Bank. ETOPOSIDE .
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  • (PMID = 19414327.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 6PLQ3CP4P3 / Etoposide; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; BG3F62OND5 / Carboplatin
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58. Zhou YH, Hess KR, Liu L, Linskey ME, Yung WK: Modeling prognosis for patients with malignant astrocytic gliomas: quantifying the expression of multiple genetic markers and clinical variables. Neuro Oncol; 2005 Oct;7(4):485-94
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  • [Title] Modeling prognosis for patients with malignant astrocytic gliomas: quantifying the expression of multiple genetic markers and clinical variables.
  • The disparate lengths of survival among patients with malignant astrocytic gliomas (anaplastic astrocytomas [AAs] and glioblastoma multiforme [GBM]) cannot be adequately accounted for by clinical variables (patient age, histology, and recurrent status).
  • Using real-time quantitative reverse transcription-polymerase chain reaction, we quantified the expression of four genes that were putative prognostic markers (CDK4, IGFBP2, MMP2, and RPS9) in a set of 43 AAs, 41 GBMs, and seven adjacent normal brain tissues.
  • We previously explicated the expression and prognostic value of PAX6, PTEN, VEGF, and EGFR in these glioma tissues and established a comprehensive prognostic model (Zhou et al., 2003).
  • This study attempts to improve that model by including four additional genetic markers, which exhibited a differential expression (P < 0.001) among tumor grades and between tumor and normal tissues.
  • [MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / analysis. Brain Neoplasms / genetics. Models, Statistical


59. Temel SG, Kahveci Z: Cyclooxygenase-2 expression in astrocytes and microglia in human oligodendroglioma and astrocytoma. J Mol Histol; 2009 Oct;40(5-6):369-77
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  • Cox-2 is cytokine-inducible in inflammatory cells and enhanced cox-2 expression has been attributed a key role in the development of edema and immunomodulation in pathologically altered brain tissues.
  • In normal cerebral cortex cox-2 is present only in neurons, but not in the glial or vascular endothelial cells.
  • The function of microglia in glioma biology is unclear.
  • The results showed that cox-2 immunoreactivity is up-regulated in the neurons according to the tumor grade.
  • Most of the cox-2 immunoreactive glia were GFAP-positive in anaplastic oligodendrogliomas and at lesser extend in glioblastomas.
  • It may be speculated that the induction of cox-2 in microglia may contribute to the deleterious effects of prostanoids in cerebral edema formation during the progression of oligodendrogliomas.
  • The detection of cox-2 in astrocytes surrounding the necrotic areas might be important to develop new strategies, such as the usage of cox-2 inhibitors combine with chemotherapy and radiotherapy in the treatment of glioma patients.

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  • (PMID = 20052522.001).
  • [ISSN] 1567-2387
  • [Journal-full-title] Journal of molecular histology
  • [ISO-abbreviation] J. Mol. Histol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 3.1.3.48 / Antigens, CD45
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60. Callovini GM: Is it appropriate to redefine the indication for stereotactic brain biopsy in the MRI Era? Correlation with final histological diagnosis in supratentorial gliomas. Minim Invasive Neurosurg; 2008 Apr;51(2):109-13
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  • [Title] Is it appropriate to redefine the indication for stereotactic brain biopsy in the MRI Era? Correlation with final histological diagnosis in supratentorial gliomas.
  • BACKGROUND: The aim of this study was to evaluate the advisability of modifying the indications for stereotactic brain biopsy (SBB) in high- and low-grade supratentorial glial tumors in correlation with the diagnostic accuracy of magnetic resonance imaging (MRI).
  • Only one preoperative diagnosis was allowed.
  • RESULTS: A final histological diagnosis was achieved in 95% of the 174 cases.
  • In 11 cases (10%) the histological analysis changed the presumptive diagnosis and the consequent management.
  • In the group of low-grade gliomas (LGG) there was diagnostic coincidence in 63% (42 cases), whereas there was discordance in 30%: 10 cases were upgraded to anaplastic astrocytoma, and in 10 cases no tumors were observed at all.
  • CONCLUSIONS: In the future, the histological diagnosis of glial tumors will include molecular genetic definition, thus making it crucial for management using the new therapeutic options.
  • Today, the indications for biopsy in lesions mimicking high-grade gliomas are mainly linked to the site of the tumor, coexisting differential diagnoses or more than one treatment option.
  • [MeSH-major] Astrocytoma / pathology. Brain / pathology. Glioma / pathology. Magnetic Resonance Imaging / standards. Neoplasm Recurrence, Local / pathology. Stereotaxic Techniques / standards. Supratentorial Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Corpus Callosum / pathology. Corpus Callosum / radiography. Diagnosis, Differential. Diagnostic Errors / prevention & control. Female. Humans. Male. Middle Aged. Necrosis. Observer Variation. Predictive Value of Tests. Radiation Injuries / pathology. Radiation Injuries / radiography. Retrospective Studies. Tomography, X-Ray Computed

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  • (PMID = 18401825.001).
  • [ISSN] 0946-7211
  • [Journal-full-title] Minimally invasive neurosurgery : MIN
  • [ISO-abbreviation] Minim Invasive Neurosurg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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61. Xiong J, Liu Y, Li C, Zhu JJ, Ye ZR, Mao Y, Wang Y: [Loss of heterozygosity of chromosome 1p/19q and p53 protein expression in oligodendroglioma]. Zhonghua Bing Li Xue Za Zhi; 2009 Jul;38(7):445-50
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  • METHODS: One hundred and ninety-one cases of glioma of different histologic types and grades, including 116 cases of low-grade of oligodendroglioma (86 paraffin-embedded and 30 fresh tissues), 45 cases of anaplastic oligodendroglioma (all paraffin-embedded tissues) and 30 cases of astrocytoma of various grades (all paraffin-embedded tissues), were enrolled into the study.
  • RESULTS: The rates of 1p loss, 19q loss and 1p/19q loss were 69.8%, 64%, and 57.0% respectively in the 86 paraffin-embedded low-grade oligodendroglioma samples, as compared to 71.1%, 60.0% and 55.6% respectively in the 45 paraffin-embedded anaplastic oligodendroglioma samples.
  • There was no difference of LOH of 1p/19q between low-grade oligodendroglioma and anaplastic oligodendroglioma (P>0.05).
  • The expression of p53 protein was significantly lower in low-grade oligodendroglioma (8.1%) than in anaplastic oligodendroglioma (31.1%, P=0.007).
  • Furthermore, p53 protein expression negatively correlated with 1p/19q loss in anaplastic oligodendroglioma (P<0.05).
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Loss of Heterozygosity. Oligodendroglioma / genetics. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 19781190.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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62. Sonoda Y, Kumabe T, Nakamura T, Saito R, Kanamori M, Yamashita Y, Suzuki H, Tominaga T: Analysis of IDH1 and IDH2 mutations in Japanese glioma patients. Cancer Sci; 2009 Oct;100(10):1996-8
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  • [Title] Analysis of IDH1 and IDH2 mutations in Japanese glioma patients.
  • In the present study, R172 mutation of the IDH2 gene was detected in one anaplastic astrocytoma.
  • IDH1 or IDH2 mutations were frequently in oligodendrogliomas (67%), anaplastic astrocytomas (62%), anaplastic oligoastrocytomas (75%), anaplastic oligodendrogliomas (50%), secondary glioblastomas (67%), gangliogliomas (38%), and anaplastic gangliogliomas (60%).
  • Mutations of the IDH1 or IDH2 genes were significantly associated with improved outcome in patients with anaplastic astrocytomas.
  • Our data suggest that IDH1 or IDH2 mutation plays a role in early tumor progression of several types of glioma and might arise from a common glial precursor.
  • [MeSH-major] Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Glioma / genetics. Isocitrate Dehydrogenase / genetics

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  • (PMID = 19765000.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human
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63. Dehais C, Laigle-Donadey F, Marie Y, Kujas M, Lejeune J, Benouaich-Amiel A, Pedretti M, Polivka M, Xuan KH, Thillet J, Delattre JY, Sanson M: Prognostic stratification of patients with anaplastic gliomas according to genetic profile. Cancer; 2006 Oct 15;107(8):1891-7
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  • [Title] Prognostic stratification of patients with anaplastic gliomas according to genetic profile.
  • BACKGROUND: There is a need to improve the current, controversial, and poorly reproducible classification of anaplastic gliomas, which represent a highly heterogeneous entity in terms of survival.
  • METHODS: The impact of the most common genetic alterations on survival was investigated based on 156 anaplastic gliomas: Among the patients who were included, the gender ratio was 1.32, the median age was 45.5 years (range, 20-83 years), and the median Karnofsky performance status was 70 (range, 40-100).
  • [MeSH-major] Brain Neoplasms / genetics. Glioma / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 9. Disease-Free Survival. Female. Humans. Loss of Heterozygosity. Male. Middle Aged. Molecular Diagnostic Techniques. Prognosis. Receptor, Epidermal Growth Factor / genetics. Survival Analysis. Tumor Suppressor Protein p53 / metabolism


64. Higgins RJ, Dickinson PJ, LeCouteur RA, Bollen AW, Wang H, Wang H, Corely LJ, Moore LM, Zang W, Fuller GN: Spontaneous canine gliomas: overexpression of EGFR, PDGFRalpha and IGFBP2 demonstrated by tissue microarray immunophenotyping. J Neurooncol; 2010 May;98(1):49-55
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  • Thirty-eight oligodendrogliomas were classified as either grade III (anaplastic) n = 35 or low grade II n = 3.
  • Tissue microarray (TMA) immunohistochemistry was used to evaluate tumor expression of EGFR, PDGFRa and IGFBP2, three key molecules of known pathophysiological importance in human gliomas.
  • Findings were correlated with tumor classification and grade.
  • IGFBP2 expression occurred in 48% of anaplastic and in 33% of low grade oligodendrogliomas.
  • These findings support a role for the spontaneous canine glioma model in directed pathway-targeting therapeutic studies.
  • [MeSH-major] Brain Neoplasms / metabolism. Brain Neoplasms / veterinary. Glioma / metabolism. Glioma / veterinary. Immunophenotyping / methods. Insulin-Like Growth Factor Binding Protein 2 / metabolism. Receptor, Epidermal Growth Factor / metabolism. Receptor, Platelet-Derived Growth Factor alpha / metabolism

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  • (PMID = 19967449.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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65. Kreisl TN, Kotliarova S, Butman JA, Albert PS, Kim L, Musib L, Thornton D, Fine HA: A phase I/II trial of enzastaurin in patients with recurrent high-grade gliomas. Neuro Oncol; 2010 Feb;12(2):181-9
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  • Enzastaurin, a potent inhibitor of protein kinase C-beta, inhibits angiogenesis and has direct cytotoxic activity against glioma cells in preclinical studies.
  • The 6-month PFS was 7% for patients with glioblastoma and 16% for patients with anaplastic glioma.
  • Enzastaurin has anti-glioma activity in patients with recurrent high-grade glioma, but does not appear to have enough single-agent activity to be useful as monotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Glioma / drug therapy. Indoles / therapeutic use

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  • (PMID = 20150385.001).
  • [ISSN] 1523-5866
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / Antineoplastic Agents; 0 / Indoles; UC96G28EQF / enzastaurin
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66. Capper D, Weissert S, Balss J, Habel A, Meyer J, Jäger D, Ackermann U, Tessmer C, Korshunov A, Zentgraf H, Hartmann C, von Deimling A: Characterization of R132H mutation-specific IDH1 antibody binding in brain tumors. Brain Pathol; 2010 Jan;20(1):245-54
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  • [Title] Characterization of R132H mutation-specific IDH1 antibody binding in brain tumors.
  • Immunohistochemistry of 345 primary brain tumors demonstrated a strong cytoplasmic and weaker nuclear staining in 122 cases.
  • Intriguing is the ability of mIDH1R132H to detect single infiltrating tumor cells.
  • The very high frequency and the distribution of this mutation among specific brain tumor entities allow the highly sensitive and specific discrimination of various tumors by immunohistochemistry, such as anaplastic astrocytoma from primary glioblastoma or diffuse astrocytoma World Health Organization (WHO) grade II from pilocytic astrocytoma or ependymoma.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / enzymology. Brain Neoplasms / genetics. Ependymoma / genetics. Glioma / enzymology. Glioma / genetics. Isocitrate Dehydrogenase / genetics. Isocitrate Dehydrogenase / immunology

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  • (PMID = 19903171.001).
  • [ISSN] 1750-3639
  • [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, Neoplasm; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human
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67. de Groot JF, Piao Y, Lu L, Fuller GN, Yung WK: Knockdown of GluR1 expression by RNA interference inhibits glioma proliferation. J Neurooncol; 2008 Jun;88(2):121-33
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  • [Title] Knockdown of GluR1 expression by RNA interference inhibits glioma proliferation.
  • High-grade gliomas release excitotoxic concentrations of glutamate which contributes to their malignant phenotype.
  • To improve our understanding of the mechanisms by which glutamate enhances tumor growth and invasion, we examined alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-mediated signaling in glioma cell lines. shRNA was used to stably knockdown GluR1, the most abundant AMPA receptor subunit in glioma, to evaluate its role in tumor signaling, proliferation and tumorigenicity.
  • In a tissue array, there was a statistically significant increase in GluR1 expression in glioblastoma samples compared to anaplastic astrocytoma and low-grade tumors.
  • Retroviral delivery of GluR1 shRNA in U251 and U87 glioma cells reduced GluR1 protein expression, inhibited AMPA-mediated increases in MAPK phosphorylation, and decreased glioma proliferation in vitro.
  • These results suggest that AMPA receptors are abundantly expressed in high-grade gliomas and gene silencing of the GluR1 AMPA receptor subunit results in abrogation of AMPA-mediated signaling and tumor growth.
  • [MeSH-major] Brain Neoplasms / metabolism. Gene Expression Regulation / drug effects. Glioma / prevention & control. RNA Interference / physiology. RNA, Small Interfering / therapeutic use. Receptors, AMPA / metabolism
  • [MeSH-minor] Animals. Carcinogenicity Tests. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Down-Regulation / drug effects. Down-Regulation / genetics. Humans. Ki-67 Antigen / metabolism. Mice. Mice, Nude. Microarray Analysis / methods. RNA, Double-Stranded / pharmacology. Signal Transduction / drug effects

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  • (PMID = 18317690.001).
  • [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 / Ki-67 Antigen; 0 / RNA, Double-Stranded; 0 / RNA, Small Interfering; 0 / Receptors, AMPA; 0 / glutamate receptor ionotropic, AMPA 1
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68. Sugo N, Yokota K, Kondo K, Harada N, Aoki Y, Miyazaki C, Nemoto M, Kano T, Ohishi H, Seiki Y: Early dynamic 201Tl SPECT in the evaluation of brain tumours. Nucl Med Commun; 2006 Feb;27(2):143-9
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  • [Title] Early dynamic 201Tl SPECT in the evaluation of brain tumours.
  • OBJECTIVE: To estimate the usefulness of early dynamic 201Tl single photon emission computed tomography (SPECT) studies in distinguishing the histological malignancy of brain tumours.
  • METHODS: Dynamic 201Tl SPECT was performed for 3 min per scan for 15 min immediately after the administration of 201TlCl in 110 patients with brain tumours (111 lesions).
  • For static SPECT, the static thallium index (STI) was calculated as the ratio of 201Tl uptake in the tumour to that of the contralateral normal brain.
  • RESULTS: In static SPECT, there was no significant difference between the STI of malignant tumours (glioblastoma and anaplastic astrocytoma) and that of benign tumours (low-grade glioma, meningioma, pituitary adenoma, neurinoma and haemangioblastoma) (3.7+/-1.5, 5.0+/-3.5, respectively).
  • On dynamic SPECT, DTI increased markedly over 15 min for malignant tumours.
  • The slope of the linear functions calculated from the DTRs was much higher in the malignant tumour group than in the benign tumour group (P<0.001).
  • CONCLUSIONS: We suggest that the performance of 201Tl dynamic SPECT for 15 min is useful for distinguishing malignant brain tumours from benign brain tumours and reduces the examination stress of patients.
  • [MeSH-major] Brain Neoplasms / classification. Brain Neoplasms / radionuclide imaging. Image Enhancement / methods. Image Interpretation, Computer-Assisted / methods. Severity of Illness Index. Thallium. Tomography, Emission-Computed, Single-Photon / methods

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  • (PMID = 16404227.001).
  • [ISSN] 0143-3636
  • [Journal-full-title] Nuclear medicine communications
  • [ISO-abbreviation] Nucl Med Commun
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 7791-12-0 / thallium chloride; AD84R52XLF / Thallium
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69. Nomiya T, Nemoto K, Kumabe T, Takai Y, Yamada S: Prospective single-arm study of 72 Gy hyperfractionated radiation therapy and combination chemotherapy for anaplastic astrocytomas. BMC Cancer; 2008;8:11
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  • [Title] Prospective single-arm study of 72 Gy hyperfractionated radiation therapy and combination chemotherapy for anaplastic astrocytomas.
  • BACKGROUND: Despite intensive multimodal treatment, outcome of patients with malignant glioma remains poor, and a standard dose of radiotherapy for anaplastic astrocytoma has not been defined.
  • In the past RTOG study (83-02), the arm of 72 Gy hyperfractionated radiotherapy (HFRT) for malignant gliomas showed better outcome than the arms of higher doses (76.8 - 81.6 Gy) and the arms of lower doses (48 - 54.4 Gy).
  • METHODS: From July 1995, 44 consecutive eligible patients with histologically proven anaplastic astrocytoma were enrolled in this study (HFRT group).
  • One (2%) of the patients clinically diagnosed as brain necrosis due to radiation therapy.
  • CONCLUSION: The results of this study suggested that 72 Gy HFRT seemed to show favorable outcome for patients with anaplastic astrocytoma with tolerable toxicity.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Astrocytoma / radiotherapy. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Nimustine / therapeutic use

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  • (PMID = 18199339.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0S726V972K / Nimustine
  • [Other-IDs] NLM/ PMC2254433
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70. 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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  • [Title] 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].
  • 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.
  • Indeed, the median survival of glioblastoma multiforme (WHO grade 4) patients is at best 14.6 month with only 26.5 percent of the patients still alive after 2 years and the median survival of anaplastic astrocytomas (WHO grade 3) is 19.2 month.
  • 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.
  • A total of twenty patients with progressive malignant glioma despite surgery, radiation therapy and a first line of chemotherapy will be recruited and assigned to four dosage regimen of Sulfasalazine.
  • Primary endpoints are drug safety in the setting of malignant gliomas and tumor response as measured according to MacDonald's criteria.
  • DISCUSSION: The aim of this study is to evaluate the safety and efficacy of Sulfasalazine as a treatment for recurring malignant gliomas.
  • [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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71. Su YW, Chang MC, Chiang MF, Hsieh RK: Treatment-related myelodysplastic syndrome after temozolomide for recurrent high-grade glioma. J Neurooncol; 2005 Feb;71(3):315-8
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  • [Title] Treatment-related myelodysplastic syndrome after temozolomide for recurrent high-grade glioma.
  • In patients with recurrent malignant glioma, treatment-related myelodysplastic syndrome (t-MDS) and acute leukemia are rare adverse effects because the median survival after relapse is limited.
  • We report a 44-year-old woman with t-MDS (refractory anemia with excess blasts) following treatment of recurrent anaplastic astrocytoma with temozolomide (TMZ).
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Dacarbazine / adverse effects. Dacarbazine / analogs & derivatives. Leukemia / chemically induced. Myelodysplastic Syndromes / chemically induced. Neoplasm Recurrence, Local / drug therapy


72. Kostron H, Rössler K: [Surgical intervention in patients with malignant glioma]. Wien Med Wochenschr; 2006 Jun;156(11-12):338-41
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  • [Title] [Surgical intervention in patients with malignant glioma].
  • Glial tumors occur at an incidence from 2 to 10/ 100.000 (Japan vs. Sweden) and building up to 50 % of all patients suffering from brain tumors.
  • 50 % of those are again malignant gliomas Grade III and Grade IV.
  • Despite all therapeutic approaches the median survival for glioblastomas is 15 months and for anaplastic gliomas Grade III 30 months.
  • After diagnosis, preferably by MRI, a neurosurgical procedure is performed under microsurgical guidelines mostly by means of neuronavigation and intraoperative guidance.
  • Depending on the preoperative diagnosis and localisation of the pathologic lesion an open craniotomy or a stereotactic biopsy is performed.
  • Tumor removal in eloquent areas such as speech area is performed under local anesthesia as an awake operation.
  • New developments in the treatment of patients harboring malignant brain tumors allow an individual neurooncological treatment concept to be established to enhance overall survival and quality of life.
  • [MeSH-major] Brain Neoplasms / surgery. Glioma / surgery
  • [MeSH-minor] Brain / pathology. Brain / surgery. Craniotomy / instrumentation. Humans. Image Processing, Computer-Assisted / instrumentation. Magnetic Resonance Imaging / instrumentation. Microsurgery / instrumentation. Neoplasm Invasiveness / pathology. Neuronavigation / instrumentation. Positron-Emission Tomography / instrumentation. Prognosis. Survival Rate

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  • (PMID = 16944364.001).
  • [ISSN] 0043-5341
  • [Journal-full-title] Wiener medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Wien Med Wochenschr
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Austria
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73. Hirose Y, Yoshida K: Chromosomal abnormalities subdivide neuroepithelial tumors into clinically relevant groups. Keio J Med; 2006 Jun;55(2):52-8
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  • Gliomas are the most common primary brain tumor, and are histopathologically classified according to their cell type and the degree of malignancy.
  • However, sometimes diagnosis can be controversial,and tumors of the same entity possibly have a wide range of survival.
  • Previous studies using comparative genomic hybridization (CGH) demonstrated that copy number aberrations(CNAs) were frequently recognized in these tumors, and revealed that a gain on chromosomal arm 7q was the most common CNA in diffuse astrocytomas, whereas a small population of the tumor showed losses on 1p/19q which characterizes oligodendrogliomas with good responsiveness to chemotherapeutic regime using procarbazine, nitrosourea and vincristine.
  • High grade (malignant) gliomas(i.e. anaplastic astrocytomas, anaplastic oligodendrogliomas and glioblastomas) have been reported to have a gain on 7p and losses on 9p and 10q.
  • [MeSH-minor] Glioma / genetics. Glioma / pathology. Humans. Neoplasm Staging. Nucleic Acid Hybridization

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  • (PMID = 16823260.001).
  • [ISSN] 0022-9717
  • [Journal-full-title] The Keio journal of medicine
  • [ISO-abbreviation] Keio J Med
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 51
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74. Sanders RP, Kocak M, Burger PC, Merchant TE, Gajjar A, Broniscer A: High-grade astrocytoma in very young children. Pediatr Blood Cancer; 2007 Dec;49(7):888-93
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  • Histology included anaplastic astrocytoma (n = 9), glioblastoma multiforme (n = 5), and malignant glioma (n = 2).
  • Age at diagnosis was a significant predictor of the hazard of death in a Cox model (HR 2.871, 95%CI 1.015-8.123).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / therapy. Brain Neoplasms / therapy

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  • [Copyright] 2007 Wiley-Liss, Inc
  • [CommentIn] Pediatr Blood Cancer. 2007 Dec;49(7):879-80 [17941062.001]
  • (PMID = 17554787.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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75. Franceschi E, Omuro AM, Lassman AB, Demopoulos A, Nolan C, Abrey LE: Salvage temozolomide for prior temozolomide responders. Cancer; 2005 Dec 1;104(11):2473-6
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  • BACKGROUND: Temozolomide (TMZ) often is used as adjuvant or first-line therapy for patients with glioma.
  • METHODS: A retrospective review of patients with recurrent/progressive glioma who had a history of response to TMZ and were treated with the same agent at the time of disease recurrence was conducted.
  • The median age of the patients was 56 years (range, 25-67 yrs) at the time of diagnosis; 9 patients had glioblastoma, 3 had anaplastic astrocytoma, and 2 patients had low-grade oligodendroglioma.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Glioblastoma / drug therapy. Oligodendroglioma / drug therapy. Salvage Therapy / methods

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  • (PMID = 16270316.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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76. Wolff JE, Berrak S, Koontz Webb SE, Zhang M: Nitrosourea efficacy in high-grade glioma: a survival gain analysis summarizing 504 cohorts with 24193 patients. J Neurooncol; 2008 May;88(1):57-63
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  • [Title] Nitrosourea efficacy in high-grade glioma: a survival gain analysis summarizing 504 cohorts with 24193 patients.
  • Even though past studies have suggested efficacy of nitrosourea drugs in patients with high-grade glioma and temozolomide has recently been shown significantly to be beneficial, no conclusive comparisons between these agents have been published.
  • We performed a survival gain analysis of 364 studies describing 24,193 patients with high-grade glioma treated in 504 cohorts, and compared the effects of drugs.
  • The most frequent diagnoses were glioblastoma multiforme (GBM) (72%) and anaplastic astrocytoma (22%).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Glioma / drug therapy. Nitrosourea Compounds / therapeutic use

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  • (PMID = 18253699.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 16672
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Nitrosourea Compounds; 0S726V972K / Nimustine; 7BRF0Z81KG / Lomustine; U68WG3173Y / Carmustine
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77. Hau P, Jachimczak P, Bogdahn U: Treatment of malignant gliomas with TGF-beta2 antisense oligonucleotides. Expert Rev Anticancer Ther; 2009 Nov;9(11):1663-74
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  • [Title] Treatment of malignant gliomas with TGF-beta2 antisense oligonucleotides.
  • A randomized, controlled international Phase III study was initiated in March 2009 and will compare trabedersen 10 microM versus conventional alkylating chemotherapy in patients with recurrent or refractory anaplastic astrocytoma after standard radio- and chemotherapy.
  • [MeSH-major] Glioma / drug therapy. Oligodeoxyribonucleotides / therapeutic use. Oligonucleotides, Antisense / therapeutic use. Thionucleotides / therapeutic use. Transforming Growth Factor beta2 / genetics
  • [MeSH-minor] Animals. Brain Neoplasms / drug therapy. Brain Neoplasms / metabolism. Clinical Trials as Topic. Humans. Injections, Intralesional

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  • (PMID = 19895249.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oligodeoxyribonucleotides; 0 / Oligonucleotides, Antisense; 0 / Thionucleotides; 0 / Trabedersen; 0 / Transforming Growth Factor beta2
  • [Number-of-references] 87
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78. Bodey B, Siegel SE, Kaiser HE: Cyclooxygenase-2 (COX-2) overexpression in childhood brain tumors. In Vivo; 2006 Jul-Aug;20(4):519-25
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  • [Title] Cyclooxygenase-2 (COX-2) overexpression in childhood brain tumors.
  • The overexpression of COX enzymes has been demonstrated in human neoplasms at various sites, including the colon, gastrointestinal tract, lung, skin and recently in brain tumors.
  • In this study, COX-2 receptor overexpression in primary childhood brain tumors was determined and the distribution pattern of COX-2 receptors was examined.
  • A sensitive, 4-step, alkaline phosphatase conjugated antigen detection technique was used and a specific monoclonal antibody for medulloblastomas/ primitive neuroectodermal tumors (MEDs/PNETs), anaplastic, high-grade astrocytomas (ASTRs) and in glioblastoma multiformes (GMs) was employed.
  • However, significant differences were found when comparing low grade pilocytic ASTRs to high grade anaplastic ASTRs and glioblastomas.
  • In two low grade pilocytic ASTRs, the expression level never exceeded 20%, while in high grade glial tumors (6 anaplastic ASTRs and 6 GMs) 30 to 50% of the tumor cells overexpressed COX-2 receptors, documenting an increase in COX-2 receptor overexpression with the increasing grade of the astrocytic tumor.
  • In view of these findings, it would appear likely that COX-2 inhibitors may represent a chemo-preventive tool in treating childhood brain tumors, which are the leading cause of solid tumor cancer death in children under the age of 20.
  • [MeSH-major] Brain Neoplasms / enzymology. Brain Neoplasms / metabolism. Cyclooxygenase 2 / metabolism. Glioma / enzymology. Glioma / metabolism

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  • (PMID = 16900783.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] EC 1.14.99.1 / Cyclooxygenase 2
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79. Roessler K, Gatterbauer B, Becherer A, Paul M, Kletter K, Prayer D, Hoeftberger R, Hainfellner J, Asenbaum S, Knosp E: Surgical target selection in cerebral glioma surgery: linking methionine (MET) PET image fusion and neuronavigation. Minim Invasive Neurosurg; 2007 Oct;50(5):273-80
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  • [Title] Surgical target selection in cerebral glioma surgery: linking methionine (MET) PET image fusion and neuronavigation.
  • OBJECTIVE: The objective of this study was to investigate the histological correlate of (11)C-methionine (MET) PET uptake of brain gliomas by image fusion for navigated surgery.
  • RESULTS: MET PET tumor uptake was detected in 26 of 27 patients (96.3%).
  • The quantitative MET tumor standardized uptake value (SUV) ratio was significantly higher in malignant gliomas and oligodendrogliomas than in low-grade gliomas (2.76/2.62 vs. 1.67, p=0.03).
  • Focal uptake corresponded to malignant glioma histology in 66.7%, and uniform global uptake to oligodendroglial histology in 72.7%.
  • In oligodendrogliomas, global MET uptake constituted 81.5% (range 53.8-135%) of the MRI T(1) tumor volume on average and was limited to the MRI FLAIR tumor volume in 86% (7/8) of patients.
  • Tissue samples of focal MET uptake areas correlated with histological anaplasia in 66.6% (8/12 glioma patients), although 62.5% (5/8 patients) lacked MRI contrast enhancement.
  • CONCLUSION: MET PET image fusion may facilitate the targeting of anaplastic foci in homogeneous MRI non-enhancing gliomas for biopsy, may identify oligodendroglial histology preoperatively as well as characterize biologically active tumor volumes within MRI T(1)/FLAIR tumor areas of candidate patients for resection.
  • [MeSH-major] Brain Neoplasms / radionuclide imaging. Brain Neoplasms / surgery. Glioma / radionuclide imaging. Glioma / surgery. Neuronavigation / methods. Positron-Emission Tomography / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Carbon Radioisotopes. Child. Diagnosis, Differential. Female. Humans. Image Processing, Computer-Assisted / instrumentation. Image Processing, Computer-Assisted / methods. Male. Methionine / metabolism. Middle Aged. Oligodendroglioma / pathology. Oligodendroglioma / radionuclide imaging. Oligodendroglioma / surgery. Predictive Value of Tests. Preoperative Care / instrumentation. Preoperative Care / methods. Sensitivity and Specificity


80. Hau P, Kunz-Schughart L, Bogdahn U, Baumgart U, Hirschmann B, Weimann E, Muhleisen H, Ruemmele P, Steinbrecher A, Reichle A: Low-dose chemotherapy in combination with COX-2 inhibitors and PPAR-gamma agonists in recurrent high-grade gliomas - a phase II study. Oncology; 2007;73(1-2):21-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: Combined treatment approaches targeting tumor as well as other cells contributing to tumor progression may control chemorefractory malignancies.
  • METHODS: A phase II trial was initiated to analyze the activity of continuously administered pioglitazone and rofecoxib combined with low-dose chemotherapy (capecitabine or temozolomide) in patients with high-grade gliomas (glioblastoma or anaplastic glioma).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Brain Neoplasms / pathology. Cyclooxygenase 2 Inhibitors / therapeutic use. Glioma / drug therapy. Glioma / pathology. Neoplasm Recurrence, Local / drug therapy. PPAR gamma / agonists

  • MedlinePlus Health Information. consumer health - Brain Tumors.
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  • Hazardous Substances Data Bank. PIOGLITAZONE .
  • Hazardous Substances Data Bank. CAPECITABINE .
  • Hazardous Substances Data Bank. DACARBAZINE .
  • Hazardous Substances Data Bank. FLUOROURACIL .
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  • [Copyright] (c) 2008 S. Karger AG, Basel
  • (PMID = 18332649.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Lactones; 0 / PPAR gamma; 0 / Sulfones; 0 / Thiazolidinediones; 0QTW8Z7MCR / rofecoxib; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; U3P01618RT / Fluorouracil; X4OV71U42S / pioglitazone
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81. Kunitz A, Wolter M, van den Boom J, Felsberg J, Tews B, Hahn M, Benner A, Sabel M, Lichter P, Reifenberger G, von Deimling A, Hartmann C: DNA hypermethylation and aberrant expression of the EMP3 gene at 19q13.3 in Human Gliomas. Brain Pathol; 2007 Oct;17(4):363-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, the tumor suppressor genes (TSG) on 19q are still elusive.
  • EMP3 hypermethylation was detected in more than 80% of diffuse, anaplastic astrocytomas and secondary glioblastomas.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 19 / genetics. DNA Methylation. Gene Expression Regulation, Neoplastic / genetics. Glioma / genetics. Membrane Glycoproteins / genetics

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  • (PMID = 17610521.001).
  • [ISSN] 1015-6305
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / EMP3 protein, human; 0 / Membrane Glycoproteins
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82. Arko L, Katsyv I, Park GE, Luan WP, Park JK: Experimental approaches for the treatment of malignant gliomas. Pharmacol Ther; 2010 Oct;128(1):1-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Experimental approaches for the treatment of malignant gliomas.
  • Malignant gliomas, which include glioblastomas and anaplastic astrocytomas, are the most common primary tumors of the brain.
  • There has, however, been recent substantial progress in our mechanistic understanding of tumor development and growth.
  • [MeSH-major] Glioma / therapy