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1. Lefranc F, Sadeghi N, Camby I, Metens T, Dewitte O, Kiss R: Present and potential future issues in glioblastoma treatment. Expert Rev Anticancer Ther; 2006 May;6(5):719-32
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  • [Title] Present and potential future issues in glioblastoma treatment.
  • The treatment of glioblastomas requires a multidisciplinary approach that takes the presently incurable nature of the disease into consideration.
  • Current recommendations are that patients with glioblastomas should undergo maximum surgical resection, followed by concurrent radiation and chemotherapy with the novel alkylating drug temozolomide.
  • This is then to be followed by additional adjuvant temozolomide for a period of up to 6 months.
  • Major advances in surgical and imaging technologies used to treat glioblastoma patients are described.
  • However, glioblastomas almost invariably recur near their initial sites.
  • Disease progression usually occurs within 6 months and leads rapidly to death.
  • [MeSH-major] Brain Neoplasms / therapy. Glioblastoma / therapy

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  • (PMID = 16759163.001).
  • [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
  • [Number-of-references] 86
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2. Papi A, Tatenhorst L, Terwel D, Hermes M, Kummer MP, Orlandi M, Heneka MT: PPARgamma and RXRgamma ligands act synergistically as potent antineoplastic agents in vitro and in vivo glioma models. J Neurochem; 2009 Jun;109(6):1779-90
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  • Glioblastoma represent the most common primary brain tumor in adults and are currently considered incurable.
  • We investigated antiproliferative and anti-invasive mechanisms of 6-OH-11-O-hydroxyfenantrene (IIF), a retinoid X receptor ligand, and pioglitazone (PGZ), a peroxisome proliferator-activated receptor gamma activator, in three different glioblastoma cell lines.
  • A dose-dependent reduction of tumor invasion and strong decrease of matrix metalloproteinases 2 and 9 expression was observed, especially when a combination therapy of IIF and PGZ was administered.
  • These in vitro findings were further substantiated in a murine glioma model in vivo, where oral administration of PGZ and IIF resulted in significantly reduced tumor volume and proliferation.
  • Collectively, our results demonstrate the effectiveness of a combined treatment of ligands of proliferator-activated receptor and retinoid X receptor against glioblastoma.
  • [MeSH-minor] Analysis of Variance. Animals. Annexin A5 / metabolism. Bromodeoxyuridine / metabolism. Caspase 3 / metabolism. Cell Line, Tumor. Cell Proliferation. Cytochromes c / metabolism. Disease Models, Animal. Dose-Response Relationship, Drug. Drug Synergism. Humans. Ligands. Matrix Metalloproteinases / metabolism. Mice. Mice, Inbred C57BL. Neoplasm Invasiveness / physiopathology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Rats. Retinoid X Receptor gamma / metabolism. Tetrazolium Salts. Thiazoles. Thiazolidinediones / therapeutic use. Transfection / methods. Tumor Stem Cell Assay / methods. bcl-2-Associated X Protein / metabolism

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  • (PMID = 19457135.001).
  • [ISSN] 1471-4159
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Antineoplastic Agents; 0 / BAX protein, human; 0 / IIF compound; 0 / Ligands; 0 / PPAR gamma; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Retinoid X Receptor gamma; 0 / Tetrazolium Salts; 0 / Thiazoles; 0 / Thiazolidinediones; 0 / bcl-2-Associated X Protein; 298-93-1 / thiazolyl blue; 5688UTC01R / Tretinoin; 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspase 3; EC 3.4.24.- / Matrix Metalloproteinases; G34N38R2N1 / Bromodeoxyuridine; X4OV71U42S / pioglitazone
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3. Bertrand J, Begaud-Grimaud G, Bessette B, Verdier M, Battu S, Jauberteau MO: Cancer stem cells from human glioma cell line are resistant to Fas-induced apoptosis. Int J Oncol; 2009 Mar;34(3):717-27
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  • Glioblastoma is the most common primary brain tumor, characterized by its resistance to treatments.
  • To define efficient therapy, the origin of tumor-forming cells needs to be elucidated in order to search for new therapeutic pathways.
  • The objective of this study was to determine the different cell populations constituting a human glioblastoma cell line, U-87 MG and their sensitivity to apoptosis induced through the activation of Fas, a membranous death receptor.
  • Interestingly, while these tumor stem cells, expressing CD133, were resistant to Fas-induced apoptosis, monomeric form of Fas protein was detected predominantly in these cells.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antigens, CD95 / agonists. Apoptosis / physiology. Brain Neoplasms / pathology. Glioblastoma / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Antigens, CD / biosynthesis. Cell Line, Tumor. Cell Survival / drug effects. Flow Cytometry. Glycoproteins / biosynthesis. Humans. Peptides

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  • (PMID = 19212677.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, CD95; 0 / Glycoproteins; 0 / Peptides
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4. He J, Liu Y, Xie X, Zhu T, Soules M, DiMeco F, Vescovi AL, Fan X, Lubman DM: Identification of cell surface glycoprotein markers for glioblastoma-derived stem-like cells using a lectin microarray and LC-MS/MS approach. J Proteome Res; 2010 May 7;9(5):2565-72
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  • [Title] Identification of cell surface glycoprotein markers for glioblastoma-derived stem-like cells using a lectin microarray and LC-MS/MS approach.
  • Despite progress in the treatment of glioblastoma, more than 95% of patients suffering from this disease still die within 2 years.
  • Recent findings support the belief that cancer stem-like cells are responsible for tumor formation and ongoing growth.
  • Here a method combining lectin microarray and LC-MS/MS was used to discover the cell surface glycoprotein markers of a glioblastoma-derived stem-like cell line.
  • Lectin microarray analysis of cell surface glycans showed that two galactose-specific lectins Trichosanthes kirilowii agglutinin (TKA) and Peanut agglutinin (PNA) could distinguish the stem-like glioblastoma neurosphere culture from a traditional adherent glioblastoma cell line.
  • An improved understanding of these proteins may be important for earlier diagnosis and better therapeutic targeting of glioblastoma.

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  • (PMID = 20235609.001).
  • [ISSN] 1535-3907
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM049500-13; United States / NIGMS NIH HHS / GM / GM049500-13; United States / PHS HHS / / R01 49500; United States / NIGMS NIH HHS / GM / R01 GM049500; United States / NCI NIH HHS / CA / R21 CA134623-02; United States / NCI NIH HHS / CA / R21 CA134623
  • [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 / Biomarkers, Tumor; 0 / Membrane Glycoproteins; 0 / Plant Lectins
  • [Other-IDs] NLM/ NIHMS190963; NLM/ PMC2866009
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5. Omar AI, Mason WP: Temozolomide: The evidence for its therapeutic efficacy in malignant astrocytomas. Core Evid; 2010 Jun 15;4:93-111
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  • [Title] Temozolomide: The evidence for its therapeutic efficacy in malignant astrocytomas.
  • Temozolomide (TMZ) is a new second generation DNA alkylating agent that has become part of malignant astrocytoma management paradigms because of its proven efficacy, ease of administration, and favorable toxicity profile.
  • AIMS: To review the role of TMZ in the management of malignant astrocytomas (World Health Organization grades III and IV) including newly diagnosed (n) and recurrent (r) anaplastic astrocytomas (AA) and glioblastomas.
  • EVIDENCE REVIEW: A series of pivotal clinical trials have established a role for TMZ in the treatment of malignant astrocytomas.
  • Evidence for a role of TMZ in nAA is currently limited but research is ongoing in this area.
  • The role of TMZ in the management of glioblastoma at the time of recurrence (rGBM) is less impressive but evidence for its activity was demonstrated in two large phase II trials that led to the approval of TMZ for this indication in Europe and Canada but not in the US.
  • PLACE IN THERAPY: THERE IS EVIDENCE TO SUPPORT THE USE OF TMZ FOR THE FOLLOWING DISEASES IN THE ORDER OF MOST TO LEAST CONVINCING: nGBM, rAA, rGBM, and nAA.

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  • (PMID = 20694068.001).
  • [ISSN] 1555-175X
  • [Journal-full-title] Core evidence
  • [ISO-abbreviation] Core Evid
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2899776
  • [Keywords] NOTNLM ; anaplastic astrocytoma / evidence / glioblastoma / glioma / malignant astrocytoma / temozolomide
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6. Haberer S, Assouline A, Mazeron JJ: [Malignant gliomas]. Cancer Radiother; 2010 Nov;14 Suppl 1:S14-22
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  • Glial tumors represent 2000 to 3000 new cases per year in France and 75% of them are of high grade.
  • Knowledge and precise evaluation of potential late effects of our treatments is necessary due to actual improvement of survival with chemoradiotherapy in glioblastoma.

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  • [Copyright] Copyright © 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 21129657.001).
  • [ISSN] 1769-6658
  • [Journal-full-title] Cancer radiothérapie : journal de la Société française de radiothérapie oncologique
  • [ISO-abbreviation] Cancer Radiother
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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7. Kawabata S, Miyatake S, Nonoguchi N, Hiramatsu R, Iida K, Miyata S, Yokoyama K, Doi A, Kuroda Y, Kuroiwa T, Michiue H, Kumada H, Kirihata M, Imahori Y, Maruhashi A, Sakurai Y, Suzuki M, Masunaga S, Ono K: Survival benefit from boron neutron capture therapy for the newly diagnosed glioblastoma patients. Appl Radiat Isot; 2009 Jul;67(7-8 Suppl):S15-8
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  • [Title] Survival benefit from boron neutron capture therapy for the newly diagnosed glioblastoma patients.
  • In this time, we focused on the survival benefit from BNCT for the newly diagnosed glioblastoma patients.
  • METHODS: BNCT group including 21 newly histological confirmed glioblastoma patients treated with surgical removal followed by BNCT in Osaka Medical College during 2002-2006 period.
  • No chemotherapy was administered until tumor progression was observed.
  • All the patients in classes IV and VI died.
  • Median survival time for the BNCT group compared to the RTOG database was as follows: 20.6 months vs. 17.9 months for class III; 16.9 months vs. 11.1 months for class IV; 13.2 months vs. 8.9 months for class V.
  • [MeSH-major] Boron Neutron Capture Therapy / methods. Brain Neoplasms / radiotherapy. Glioblastoma / radiotherapy

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  • (PMID = 19398348.001).
  • [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] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Borohydrides; 0 / Boron Compounds; 0 / Radiation-Sensitizing Agents; 0 / Sulfhydryl Compounds; 12294-22-3 / mercaptoundecahydrododecaborate; 47E5O17Y3R / Phenylalanine; UID84303EL / 4-boronophenylalanine
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8. Quinn JA, Jiang SX, Reardon DA, Desjardins A, Vredenburgh JJ, Friedman AH, Sampson JH, McLendon RE, Herndon JE 2nd, Friedman HS: Phase II trial of temozolomide (TMZ) plus irinotecan (CPT-11) in adults with newly diagnosed glioblastoma multiforme before radiotherapy. J Neurooncol; 2009 Dec;95(3):393-400
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  • [Title] Phase II trial of temozolomide (TMZ) plus irinotecan (CPT-11) in adults with newly diagnosed glioblastoma multiforme before radiotherapy.
  • This phase II trial evaluated efficacy and safety of temozolomide (TMZ) in combination with irinotecan (CPT-11) before radiotherapy in patients with newly diagnosed glioblastoma multiforme (GBM).
  • Secondary end points included progression-free survival (PFS), overall survival (OS), safety, and tumor O(6)-methylguanine-DNA methyltransferase (MGMT) expression.
  • Grade 3 or 4 AEs were documented in 36% of patients, most of which were hematologic (29%).
  • Twenty-four percent of patients had grade 3 or 4 non-hematologic AEs, with gastrointestinal AEs being the most common (12%) Two patients died, one of intracranial hemorrhage and one of treatment-related renal failure.
  • [MeSH-major] Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Camptothecin / analogs & derivatives. Dacarbazine / analogs & derivatives. Glioblastoma / drug therapy. Glioblastoma / radiotherapy
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Agents, Phytogenic / adverse effects. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Combined Modality Therapy. Disease-Free Survival. Female. Follow-Up Studies. Humans. Male. Middle Aged. Survival Rate. Treatment Outcome

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  • (PMID = 19533023.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA108786; United States / NCI NIH HHS / CA / P50 CA108786-050002; United States / NINDS NIH HHS / NS / P50 NS020023; United States / NINDS NIH HHS / NS / P50 NS020023-17S10018; United States / NCI NIH HHS / CA / R37 CA 011898-38; United States / NINDS NIH HHS / NS / P50 NS020023-200018; United States / NINDS NIH HHS / NS / P50 NS020023-210018; United States / NINDS NIH HHS / NS / 5P50 NS20023-25; United States / NINDS NIH HHS / NS / P50 NS020023-150010; United States / NINDS NIH HHS / NS / P50 NS020023-140018; United States / NINDS NIH HHS / NS / P50 NS020023-250018; United States / NINDS NIH HHS / NS / P50 NS020023-18S10018; United States / NINDS NIH HHS / NS / P50 NS020023-150018; United States / NCI NIH HHS / CA / P50 CA108786-020002; United States / NCI NIH HHS / CA / P50 CA108786-05S10002; United States / NINDS NIH HHS / NS / P50 NS020023-170018; United States / NCI NIH HHS / CA / 5P50 CA108786-4; United States / NCI NIH HHS / CA / P50 CA108786-030002; United States / NINDS NIH HHS / NS / P50 NS020023-160018; United States / NCI NIH HHS / CA / P50 CA108786-010002; United States / NCI NIH HHS / CA / P50 CA108786-040002; United States / NINDS NIH HHS / NS / P50 NS020023-140010; United States / NINDS NIH HHS / NS / P50 NS020023-220018; United States / NINDS NIH HHS / NS / P50 NS020023-240018; United States / NINDS NIH HHS / NS / P50 NS020023-230018; United States / NCRR NIH HHS / RR / TL1 RR024126; United States / NINDS NIH HHS / NS / P50 NS020023-180018; United States / NCI NIH HHS / CA / R37 CA011898; United States / NINDS NIH HHS / NS / P50 NS020023-190018; United States / NINDS NIH HHS / NS / P50 NS020023-16S10018
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 0H43101T0J / irinotecan; 7GR28W0FJI / Dacarbazine; XT3Z54Z28A / Camptothecin; YF1K15M17Y / temozolomide
  • [Other-IDs] NLM/ NIHMS180488; NLM/ PMC2835159
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9. Gaire RK, Bailey J, Bearfoot J, Campbell IG, Stuckey PJ, Haviv I: MIRAGAA--a methodology for finding coordinated effects of microRNA expression changes and genome aberrations in cancer. Bioinformatics; 2010 Jan 15;26(2):161-7
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  • [Title] MIRAGAA--a methodology for finding coordinated effects of microRNA expression changes and genome aberrations in cancer.
  • Present methodologies for finding aberrations usually analyze single datasets, which cannot identify such pairs of coordinating genes and miRNAs.
  • We have evaluated MIRAGAA on The Cancer Genome Atlas (TCGA) Glioblastoma Multiforme datasets.
  • AVAILABILITY AND IMPLEMENTATION: The source code, implemented in R and java, is available from our project web site at http://www.csse.unimelb.edu.au/~rgaire/MIRAGAA/index.html.
  • [MeSH-minor] Computational Biology / methods. Gene Dosage. Glioblastoma / genetics. Humans

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  • (PMID = 19933823.001).
  • [ISSN] 1367-4811
  • [Journal-full-title] Bioinformatics (Oxford, England)
  • [ISO-abbreviation] Bioinformatics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs
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10. Jakopec S, Karlović D, Dubravcić K, Batinić D, Sorić J, Brozović A, Buljan D, Osmak M: Lithium effect on glutamate induced damage in glioblastoma cells. Coll Antropol; 2008 Jan;32 Suppl 1:87-91
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  • [Title] Lithium effect on glutamate induced damage in glioblastoma cells.
  • Previously we have found that the treatment with lithium increased the levels of p21(WAF/Cip1 and survivin in human glioblastoma A1235 cells.
  • Pretreatment with lithium (2 mM) partially reverted change in survivin expression induced by glutamate, suggesting that lithium may have beneficial effect on glutamate induced cell damage in glioblastoma cells.
  • [MeSH-major] Antimanic Agents / pharmacology. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Excitatory Amino Acid Antagonists / pharmacology. Glutamic Acid / drug effects. Lithium Chloride / pharmacology. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Blotting, Western. Dose-Response Relationship, Drug. Glioblastoma. Humans. Inhibitor of Apoptosis Proteins. Tumor Cells, Cultured

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  • (PMID = 18405064.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Croatia
  • [Chemical-registry-number] 0 / Antimanic Agents; 0 / BIRC5 protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Excitatory Amino Acid Antagonists; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 3KX376GY7L / Glutamic Acid; G4962QA067 / Lithium Chloride
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11. Cui Z, Zhao MH, Segelmark M, Hellmark T: Natural autoantibodies to myeloperoxidase, proteinase 3, and the glomerular basement membrane are present in normal individuals. Kidney Int; 2010 Sep;78(6):590-7
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  • The origin of ANCAs and anti-glomerular basement membrane (GBM) antibodies, however, is unknown.
  • In this study, we determined whether natural autoantibodies against myeloperoxidase (MPO), proteinase 3 (PR3), and GBM were present in each of 10 healthy Chinese and Swedish individuals, negative for all three antigens by routine ELISA.
  • Natural anti-GBM autoantibodies gave a linear staining pattern along the GBM of human renal sections.
  • In competition ELISA, the binding of natural anti-MPO autoantibodies could be inhibited by MPO, but not by PR3 or noncollagenous domains from type IV collagen.
  • The same specificity results were found for natural anti-PR3 and anti-GBM autoantibodies.
  • Hence, our study shows that healthy individuals have masked circulating, noncross-reactive, antigen-specific natural autoantibodies against MPO, PR3, and GBM in their serum and IgG fractions.
  • Further studies are needed to determine their role if any in the etiology of ANCA-associated vasculitis and anti-GBM disease.

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  • [CommentIn] Kidney Int. 2010 Sep;78(6):533-5 [20805814.001]
  • (PMID = 20592714.001).
  • [ISSN] 1523-1755
  • [Journal-full-title] Kidney international
  • [ISO-abbreviation] Kidney Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antineutrophil Cytoplasmic; 0 / Autoantibodies; 0 / Immunoglobulin G; 0 / antiglomerular basement membrane antibody; EC 1.11.1.7 / Peroxidase; EC 3.4.21.76 / Myeloblastin
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12. Kawabata S, Miyatake S, Kuroiwa T, Yokoyama K, Doi A, Iida K, Miyata S, Nonoguchi N, Michiue H, Takahashi M, Inomata T, Imahori Y, Kirihata M, Sakurai Y, Maruhashi A, Kumada H, Ono K: Boron neutron capture therapy for newly diagnosed glioblastoma. J Radiat Res; 2009 Jan;50(1):51-60
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  • [Title] Boron neutron capture therapy for newly diagnosed glioblastoma.
  • We evaluate the clinical results of a form of tumor selective particle radiation known as boron neutron capture therapy (BNCT) for newly-diagnosed glioblastoma (NDGB) patients, especially in combination with X-ray treatment (XRT).
  • The first 10 were treated with only BNCT (protocol 1), and the last 11 were treated with BNCT followed by XRT of 20 to 30 Gy (protocol 2) to reduce the possibility of local tumor recurrence.
  • No chemotherapy was applied until tumor progression was observed.
  • [MeSH-major] Boron Neutron Capture Therapy / methods. Brain Neoplasms / radiotherapy. Glioblastoma / radiotherapy

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  • (PMID = 18957828.001).
  • [ISSN] 0449-3060
  • [Journal-full-title] Journal of radiation research
  • [ISO-abbreviation] J. Radiat. Res.
  • [Language] eng
  • [Publication-type] Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
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13. Wang CH, Rockhill JK, Mrugala M, Peacock DL, Lai A, Jusenius K, Wardlaw JM, Cloughesy T, Spence AM, Rockne R, Alvord EC Jr, Swanson KR: Prognostic significance of growth kinetics in newly diagnosed glioblastomas revealed by combining serial imaging with a novel biomathematical model. Cancer Res; 2009 Dec 1;69(23):9133-40
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  • [Title] Prognostic significance of growth kinetics in newly diagnosed glioblastomas revealed by combining serial imaging with a novel biomathematical model.
  • Glioblastomas are the most aggressive primary brain tumors, characterized by their rapid proliferation and diffuse infiltration of the brain tissue.
  • Survival patterns in patients with glioblastoma have been associated with a number of clinicopathologic factors including age and neurologic status, yet a significant quantitative link to in vivo growth kinetics of each glioma has remained elusive.
  • Using our biologically based mathematical model for glioma growth and invasion, examination of serial pretreatment MRIs of 32 glioblastoma patients allowed quantification of these rates for each patient's tumor.
  • To our knowledge, this is the first report indicating that dynamic insight from routinely obtained pretreatment imaging may be quantitatively useful in characterizing the survival of individual patients with glioblastoma.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / pathology. Models, Biological
  • [MeSH-minor] Cell Growth Processes / physiology. Humans. Magnetic Resonance Imaging. Neoplasm Invasiveness. Proportional Hazards Models. Survival Analysis

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  • (PMID = 19934335.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS060752
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS394496; NLM/ PMC3467150
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14. Opel D, Westhoff MA, Bender A, Braun V, Debatin KM, Fulda S: Phosphatidylinositol 3-kinase inhibition broadly sensitizes glioblastoma cells to death receptor- and drug-induced apoptosis. Cancer Res; 2008 Aug 1;68(15):6271-80
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  • [Title] Phosphatidylinositol 3-kinase inhibition broadly sensitizes glioblastoma cells to death receptor- and drug-induced apoptosis.
  • The aberrant activity of the phosphatidylinositol 3-kinase (PI3K) pathway has been reported to correlate with adverse clinical outcome in human glioblastoma in vivo.
  • However, the question of how this survival network can be successfully targeted to restore the sensitivity of glioblastoma to apoptosis induction has not yet been answered.
  • Here, we report that inhibition of PI3K by LY294002 broadly sensitizes wild-type and mutant PTEN glioblastoma cells to both death receptor- and chemotherapy-induced apoptosis, whereas mammalian target of rapamycin (mTOR) inhibition is not sufficient to restore apoptosis sensitivity.
  • LY294002 significantly enhances apoptosis triggered by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), agonistic anti-CD95 antibodies, or several anticancer drugs (i.e., doxorubicin, etoposide, and vincristine) in a highly synergistic manner.
  • Similarly, genetic knockdown of PI3K subunits p110alpha and/or p110beta by RNA interference (RNAi) primes glioblastoma cells for TRAIL- or doxorubicin-mediated apoptosis.
  • Most importantly, PI3K inhibition by LY294002 sensitizes primary cultured glioblastoma cells obtained from surgical specimens to TRAIL- or chemotherapy-induced cell death.
  • By showing that PI3K inhibition broadly primes glioblastoma cells for apoptosis, our findings provide the rationale for using PI3K inhibitors in combination regimens to enhance TRAIL- or chemotherapy-induced apoptosis in glioblastoma.
  • [MeSH-major] Apoptosis / physiology. Brain Neoplasms / pathology. Glioblastoma / pathology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Receptors, Death Domain / physiology

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  • (PMID = 18676851.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Death Domain; 80168379AG / Doxorubicin; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases
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15. Shawky H, Abo Hamar AH, Galal S, Zakaria F, El-Shorbagy D: The outcomes of concomitant radiation plus temozolomide followed by adjuvant temozolomide for newly diagnosed high grade gliomas: the preliminary results of single center prospective study. J Egypt Natl Canc Inst; 2009 Jun;21(2):107-19
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  • [Title] The outcomes of concomitant radiation plus temozolomide followed by adjuvant temozolomide for newly diagnosed high grade gliomas: the preliminary results of single center prospective study.
  • PURPOSE: Temozolomide (TMZ) is an oral alkylating agent with demonstrated efficacy as second-line therapy for patients with recurrent anaplastic astrocytoma and glioblastoma multiforme (GBM).
  • We reported the preliminary results of the treatment with concomitant radiation therapy (RT) plus TMZ followed by adjuvant TMZ therapy in patients with newly diagnosed high grade gliomas (HGG) to determine the safety, tolerability, and efficacy.
  • PATIENTS AND METHODS: Between January, 2006 and December, 2007, a total of 27 patients over the age of 18 years with newly diagnosed, histologically confirmed HGG were assigned to receive oral TMZ (75 mg/m2/d x 7 d/wk for 6 weeks, from the first to the last day of RT) with fractionated RT (60 Gy total dose: 2 Gy x 5 d/wk for 6 weeks) followed by TMZ monotherapy (150 to 200 mg/m2/d x 5 days, every 28 days for six cycles) at Clinical Oncology Department, Faculty of Medicine, Tanta University Hospital.
  • Patients with GBM were analyzed separately from HGG, and the median overall survival (OS) was 17 months, and the one-year OS rate was 83.3%.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Astrocytoma / drug therapy. Astrocytoma / radiotherapy. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Cranial Irradiation. Dacarbazine / analogs & derivatives

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  • (PMID = 21057562.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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16. Postovsky S, Vlodavsky E, Eran A, Guilburd J, Ben Arush MW: Secondary glioblastoma multiforme after treatment for primary choroid plexus carcinoma in childhood. J Pediatr Hematol Oncol; 2007 Apr;29(4):248-52
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  • [Title] Secondary glioblastoma multiforme after treatment for primary choroid plexus carcinoma in childhood.
  • After complete macroscopic resection of the tumor, the patient was treated with chemotherapy consisting of vincristine, cisplatin, etoposide, and carboplatin, followed by radiotherapy for a total dose of 34.2 Gy on the whole craniospinal axis plus a boost of 19.8 Gy at the tumor region.
  • The patient remained in complete clinical and radiologic remission over the next 5 years when a secondary malignant tumor, glioblastoma multiforme, a rare complication of the treatment of CPC, was diagnosed.
  • [MeSH-major] Choroid Plexus Neoplasms / pathology. Glioblastoma / pathology. Neoplasms, Second Primary / pathology

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  • (PMID = 17414567.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin; Q20Q21Q62J / Cisplatin
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17. Matsuda M, Yamamoto T, Kumada H, Nakai K, Shirakawa M, Tsurubuchi T, Matsumura A: Dose distribution and clinical response of glioblastoma treated with boron neutron capture therapy. Appl Radiat Isot; 2009 Jul;67(7-8 Suppl):S19-21
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  • [Title] Dose distribution and clinical response of glioblastoma treated with boron neutron capture therapy.
  • BSH (5 g/body) and BPA (250 mg/kg) based BNCT was performed in eight patients with newly diagnosed glioblastoma.
  • The gross tumor volume (GTV) and clinical target volume (CTV)-1 were defined as the residual gadolinium-enhancing volume.
  • Five of the eight patients were alive at analysis for a mean follow-up time of 20.3 months.
  • The minimum tumor dose of GTV, CTV-2, and CTV-3 averaged 29.8+/-9.9, 15.1+/-5.4, and 12.4+/-2.9 Gy, respectively.
  • The minimum tumor non-boron dose of GTV, CTV-2, and CTV-3 averaged 2.0+/-0.5, 1.3+/-0.3, and 1.1+/-0.2 Gy, respectively.
  • The mean minimum dose at the failure site in cases of in-field recurrence (IR) and out-field recurrence (OR) was 26.3+/-16.7 and 14.9 GyEq, respectively.
  • The calculated doses at the failure site were at least equal to the tumor control doses which were previously reported.
  • Further improvement of the microdistribution of boron compounds is expected, and may improve the tumor control by BNCT.
  • [MeSH-major] Boron Neutron Capture Therapy / methods. Brain Neoplasms / radiotherapy. Glioblastoma / radiotherapy
  • [MeSH-minor] Adult. Aged. Borohydrides / therapeutic use. Boron Compounds / therapeutic use. Disease-Free Survival. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / prevention & control. Phenylalanine / analogs & derivatives. Phenylalanine / therapeutic use. Photons / therapeutic use. Radiotherapy Dosage. Retrospective Studies. Sulfhydryl Compounds / therapeutic use. Survival Rate. Treatment Failure

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  • (PMID = 19375933.001).
  • [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] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Borohydrides; 0 / Boron Compounds; 0 / Sulfhydryl Compounds; 12294-22-3 / mercaptoundecahydrododecaborate; 47E5O17Y3R / Phenylalanine; UID84303EL / 4-boronophenylalanine
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18. Andersson U, Osterman P, Sjöström S, Johansen C, Henriksson R, Brännström T, Broholm H, Christensen HC, Ahlbom A, Auvinen A, Feychting M, Lönn S, Kiuru A, Swerdlow A, Schoemaker M, Roos G, Malmer B: MNS16A minisatellite genotypes in relation to risk of glioma and meningioma and to glioblastoma outcome. Int J Cancer; 2009 Aug 15;125(4):968-72
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  • [Title] MNS16A minisatellite genotypes in relation to risk of glioma and meningioma and to glioblastoma outcome.
  • The MNS16A genotype was not associated with risk of occurrence of glioma, glioblastoma (GBM) or meningioma.
  • For GBM there were median survivals of 15.3, 11.0 and 10.7 months for the LL, LS and SS genotypes, respectively; the hazard ratio for having the LS genotype compared with the LL was significantly increased HR 2.44 (1.56-3.82) and having the SS genotype versus the LL was nonsignificantly increased HR 1.46 (0.81-2.61).
  • [MeSH-major] Glioblastoma / genetics. Meningeal Neoplasms / genetics. Meningioma / genetics. Minisatellite Repeats / genetics

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  • (PMID = 19405125.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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19. Germano IM, Uzzaman M, Benveniste RJ, Zaurova M, Keller G: Apoptosis in human glioblastoma cells produced using embryonic stem cell-derived astrocytes expressing tumor necrosis factor-related apoptosis-inducing ligand. J Neurosurg; 2006 Jul;105(1):88-95
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  • [Title] Apoptosis in human glioblastoma cells produced using embryonic stem cell-derived astrocytes expressing tumor necrosis factor-related apoptosis-inducing ligand.
  • The aim of this study was to test the proapoptotic effects of ES cell-derived astrocytes expressing transgenic tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in human malignant glioma cells.
  • [MeSH-major] Apoptosis. Apoptosis Regulatory Proteins / genetics. Astrocytes / physiology. Genes, Transgenic, Suicide / physiology. Glioblastoma / pathology. Membrane Glycoproteins / genetics. Tissue Engineering / methods. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Animals. Cell Culture Techniques. Cell Differentiation. Cell Line, Tumor. Coculture Techniques. Doxycycline. Humans. Mice. Stem Cells / cytology. TNF-Related Apoptosis-Inducing Ligand

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  • (PMID = 16871882.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tnfsf10 protein, mouse; 0 / Tumor Necrosis Factor-alpha; N12000U13O / Doxycycline
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20. Kang X, Xiao X, Harata M, Bai Y, Nakazaki Y, Soda Y, Kurita R, Tanaka T, Komine F, Izawa K, Kunisaki R, Setoyama M, Nishimori H, Natsume A, Sunamura M, Lozonshi L, Saitoh I, Tokino T, Asano S, Nakamura Y, Tani K: Antiangiogenic activity of BAI1 in vivo: implications for gene therapy of human glioblastomas. Cancer Gene Ther; 2006 Apr;13(4):385-92
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  • [Title] Antiangiogenic activity of BAI1 in vivo: implications for gene therapy of human glioblastomas.
  • Glioblastomas are the most common primary brain tumors in adults.
  • These tumors exhibit a high degree of vascularization, and malignant progression from astrocytoma to glioblastoma is often accompanied by increased angiogenesis and the upregulation of vascular endothelial growth factor and its receptors.
  • In this study, we investigated the in vivo antiangiogenic and antitumor effects of brain-specific angiogenesis inhibitor 1 (BAI1) using human glioblastoma cell lines.
  • Glioblastoma cells were transduced with an adenoviral vector encoding BAI1 (AdBAI1), and Northern and Western blot analyses, respectively, demonstrated BAI1 mRNA and protein expression in the transduced tumor cells.
  • Using an in vivo neovascularization assay, we found that angiogenesis surrounding AdBAI1-transduced glioblastoma cells transplanted into transparent skinfold chambers of SCID mice was significantly impaired compared to control treated cells.
  • Additionally, in vivo inoculation with AdBAI1 of established subcutaneous or intracerebral transplanted tumors significantly impaired tumor growth and promoted increased mouse survival.
  • Taken together, these data strongly indicate that BAI1 may be an excellent gene therapy candidate for the treatment of brain tumors, especially human glioblastomas.
  • [MeSH-major] Angiogenic Proteins / biosynthesis. Brain Neoplasms / blood supply. Glioblastoma / blood supply. Neovascularization, Pathologic / therapy
  • [MeSH-minor] Adenoviridae / genetics. Animals. Cell Line, Tumor. Genetic Therapy. Genetic Vectors. Humans. Mice. Mice, SCID. Neoplasm Transplantation. RNA, Messenger / metabolism. Transduction, Genetic


21. Jenny B, Harrison JA, Baetens D, Tille JC, Burkhardt K, Mottaz H, Kiss JZ, Dietrich PY, De Tribolet N, Pizzolato GP, Pepper MS: Expression and localization of VEGF-C and VEGFR-3 in glioblastomas and haemangioblastomas. J Pathol; 2006 May;209(1):34-43
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  • [Title] Expression and localization of VEGF-C and VEGFR-3 in glioblastomas and haemangioblastomas.
  • Surprisingly, however, VEGF-C and VEGF-D, as well as VEGFR-3, were expressed in some tumour types such as haemangioblastomas and glioblastomas, despite their lack of lymphatic vessels.
  • VEGF-C and VEGFR-3 transcripts were localized to the tumour palisade around necrotic areas in glioblastomas and were evenly distributed throughout haemangioblastomas.
  • VEGF-C protein was localized by immunohistochemistry to the palisade layer in glioblastomas.
  • [MeSH-major] Brain Neoplasms / metabolism. Glioblastoma / metabolism. Hemangioblastoma / metabolism. Vascular Endothelial Growth Factor C / metabolism. Vascular Endothelial Growth Factor Receptor-3 / metabolism
  • [MeSH-minor] Biomarkers, Tumor / biosynthesis. Biomarkers, Tumor / genetics. Gene Expression. Glycoproteins / metabolism. Humans. In Situ Hybridization / methods. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Polymerase Chain Reaction / methods. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Retrospective Studies. Vascular Endothelial Growth Factor A / biosynthesis. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor B / biosynthesis. Vascular Endothelial Growth Factor B / genetics. Vascular Endothelial Growth Factor D / biosynthesis. Vascular Endothelial Growth Factor D / genetics. Vascular Endothelial Growth Factor Receptor-1 / biosynthesis. Vascular Endothelial Growth Factor Receptor-1 / genetics. Vascular Endothelial Growth Factor Receptor-2 / biosynthesis. Vascular Endothelial Growth Factor Receptor-2 / genetics. Vesicular Transport Proteins

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  • [Copyright] Copyright 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 16523449.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glycoproteins; 0 / LYVE1 protein, human; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / VEGFA protein, human; 0 / VEGFB protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor B; 0 / Vascular Endothelial Growth Factor C; 0 / Vascular Endothelial Growth Factor D; 0 / Vesicular Transport Proteins; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-3
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22. Zhang R, Banik NL, Ray SK: Combination of all-trans retinoic acid and interferon-gamma suppressed PI3K/Akt survival pathway in glioblastoma T98G cells whereas NF-kappaB survival signaling in glioblastoma U87MG cells for induction of apoptosis. Neurochem Res; 2007 Dec;32(12):2194-202
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  • [Title] Combination of all-trans retinoic acid and interferon-gamma suppressed PI3K/Akt survival pathway in glioblastoma T98G cells whereas NF-kappaB survival signaling in glioblastoma U87MG cells for induction of apoptosis.
  • Phosphatase and tension homolog located on chromosome ten (PTEN) is a tumor suppressor as it negatively regulates activation of Akt.
  • Mutation or deletion of PTEN has been found in as high as 80% of glioblastomas, which harbor aberrant cell signaling passing through the phosphatidylinositol-3-kinase (PI3K) and Akt (PI3K/Akt) survival pathway.
  • Glioblastoma cells without functional PTEN are not easily amenable to apoptosis.
  • We investigated the possibility of modulation of signal transduction pathways for induction of apoptosis in human glioblastoma T98G (PTEN-harboring) and U87MG (PTEN-deficient) cell lines after treatment with the combination of all-trans retinoic acid (ATRA) and interferon-gamma (IFN-gamma).
  • Therefore, the combination of ATRA and IFN-gamma could modulate different survival signal transduction pathways for induction of apoptosis and should be considered as an effective therapeutic strategy for controlling the growth of both PTEN-harboring and PTEN-deficient glioblastomas.
  • [MeSH-major] Apoptosis / drug effects. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Interferon-gamma / pharmacology. NF-kappa B / physiology. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Signal Transduction / drug effects. Tretinoin / pharmacology

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  • (PMID = 17616812.001).
  • [ISSN] 0364-3190
  • [Journal-full-title] Neurochemical research
  • [ISO-abbreviation] Neurochem. Res.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS-57811; United States / NCI NIH HHS / CA / R01 CA-91460
  • [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 / NF-kappa B; 0 / Nerve Tissue Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Recombinant Proteins; 0 / bcl-2-Associated X Protein; 5688UTC01R / Tretinoin; 82115-62-6 / Interferon-gamma; 9007-43-6 / Cytochromes c; EC 1.13.12.- / Luciferases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.67 / PTEN Phosphohydrolase
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23. Yoshida Y, Nakada M, Harada T, Tanaka S, Furuta T, Hayashi Y, Kita D, Uchiyama N, Hayashi Y, Hamada J: The expression level of sphingosine-1-phosphate receptor type 1 is related to MIB-1 labeling index and predicts survival of glioblastoma patients. J Neurooncol; 2010 May;98(1):41-7
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  • [Title] The expression level of sphingosine-1-phosphate receptor type 1 is related to MIB-1 labeling index and predicts survival of glioblastoma patients.
  • Although there are many reports on the clinical use of the MIB-1 labeling index (LI), which is a measure of proliferative activity in astrocytomas; its significance varies between studies.
  • There are no known molecules that are directly linked to the MIB-1 LI in astrocytomas.
  • We evaluated the clinical value of the MIB-1 LI in our human glioblastoma cases and determined the molecules that possibly influenced the MIB-1 LI.
  • An immunohistochemical study of the MIB-1 protein was performed and MIB-1 LIs of 38 glioblastomas were determined.
  • Kaplan-Meier survival curves for 38 patients with glioblastomas showed that a high MIB-1 LI correlated with poor survival (P < 0.05).
  • Among the molecules tested, only the low expression of S1P(1) was significantly correlated with the high MIB-1 LI in glioblastomas (P < 0.05).
  • Our results indicate that the MIB-1 LI is an important prognostic factor in human glioblastomas.
  • Furthermore, downregulation of S1P(1) expression increases proliferative activity, and thus enhances the malignancy of glioblastomas, resulting in a poor survival.
  • [MeSH-major] Antibodies, Antinuclear. Antibodies, Monoclonal. Brain Neoplasms / metabolism. Brain Neoplasms / mortality. Glioblastoma / metabolism. Glioblastoma / mortality. Receptors, Lysosphingolipid / metabolism

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  • (PMID = 19937366.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antinuclear; 0 / Antibodies, Monoclonal; 0 / MIB-1 antibody; 0 / Receptors, Lysosphingolipid; 0 / S1PR1 protein, human
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24. Szentirmai O, Baker CH, Bullain SS, Lin N, Takahashi M, Folkman J, Mulligan RC, Carter BS: Successful inhibition of intracranial human glioblastoma multiforme xenograft growth via systemic adenoviral delivery of soluble endostatin and soluble vascular endothelial growth factor receptor-2: laboratory investigation. J Neurosurg; 2008 May;108(5):979-88
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  • [Title] Successful inhibition of intracranial human glioblastoma multiforme xenograft growth via systemic adenoviral delivery of soluble endostatin and soluble vascular endothelial growth factor receptor-2: laboratory investigation.
  • OBJECT: Glioblastoma multiforme (GBM) is characterized by neovascularization, raising the question of whether angiogenic blockade may be a useful therapeutic strategy for this disease.
  • It has been suggested, however, that, to be useful, angiogenic blockade must be persistent and at levels sufficient to overcome proangiogenic signals from tumor cells.
  • In this report, the authors tested the hypothesis that sustained high concentrations of 2 different antiangiogenic proteins, delivered using a systemic gene therapy strategy, could inhibit the growth of established intracranial U87 human GBM xenografts in nude mice.
  • RESULTS: Three weeks after treatment, magnetic resonance imaging-based determination of tumor volume showed that treatment with Ad-VEGFR2-Fc, Ad-ES, or Ad-VEGFR2-Fc in combination with Ad-ES, produced 69, 59, and 74% growth inhibition, respectively.
  • Bioluminescent monitoring of tumor growth revealed growth inhibition in the same treatment groups to be 62, 74, and 72%, respectively.
  • Staining with proliferating cell nuclear antigen and with terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling showed reduced tumor cell proliferation and increased apoptosis in all antiangiogenic treatment groups.
  • CONCLUSIONS: These results suggest that systemic delivery and sustained production of endostatin and soluble VEGFR2 can slow intracranial glial tumor growth by both reducing cell proliferation and increasing tumor apoptosis.
  • This work adds further support to the concept of using antiangiogenesis therapy for intracranial GBM.
  • [MeSH-major] Brain Neoplasms / pathology. Endostatins / administration & dosage. Glioblastoma / pathology. Vascular Endothelial Growth Factor Receptor-2 / administration & dosage
  • [MeSH-minor] Adenoviridae. Animals. Apoptosis. Genetic Vectors. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Male. Mice. Mice, Nude. Neoplasm Transplantation. Neovascularization, Pathologic / drug therapy. Transplantation, Heterologous

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  • (PMID = 18447716.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K08 CA082773; United States / NCI NIH HHS / CA / K08 CA082773-01A1
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Endostatins; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  • [Other-IDs] NLM/ NIHMS327136; NLM/ PMC4459889
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25. Mii A, Shimizu A, Masuda Y, Ishizaki M, Sato S, Hara K, Kaneko T, Utsumi K, Iino Y, Katayama Y, Fukuda Y: A case of lupus nephritis with diffuse podocytic infolding into the glomerular basement membrane. Clin Exp Nephrol; 2008 Dec;12(6):479-84
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  • In this manuscript, we describe a case of lupus nephritis with diffuse podocytic infolding in the glomerular basement membrane (GBM).
  • A renal biopsy was performed which showed diffuse change in the GBM and focal segmental mesangial hypercellularity under light microscopy.
  • The GBM showed diffuse mild thickening and diffuse irregular stippling (bubble-like appearance) on staining with periodic acid-silver methenamine.
  • Diffuse irregular GBM thickening with dispersed distribution of microspheres and microtubules was observed using electron microscopy.
  • In addition, these structures were chiefly detected on the epithelial side of the GBM.
  • This case shows a unique pathological finding, and may belong to a new glomerular disease entity characterized by podocytic infolding.

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  • (PMID = 18958394.001).
  • [ISSN] 1342-1751
  • [Journal-full-title] Clinical and experimental nephrology
  • [ISO-abbreviation] Clin. Exp. Nephrol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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26. Horton D, Khare A: Inhibitory activity of four demethoxy fluorinated anthracycline analogs against five human-tumor cell lines. Bioorg Med Chem Lett; 2010 Nov 1;20(21):6179-81
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  • [Title] Inhibitory activity of four demethoxy fluorinated anthracycline analogs against five human-tumor cell lines.
  • Four anthracycline analogs synthesized in our laboratory were evaluated in comparison with adriamycin (doxorubicin) for their growth-inhibitory effect against five human-tumor cell lines, including lung carcinoma, colon adenocarcinoma, breast adenocarcinoma, melanoma, and glioblastoma.
  • [MeSH-minor] Cell Line, Tumor. Cell Survival / drug effects. DNA / metabolism. Daunorubicin / analogs & derivatives. Daunorubicin / pharmacology. Doxorubicin / analogs & derivatives. Doxorubicin / pharmacology. Drug Screening Assays, Antitumor. Humans

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20850305.001).
  • [ISSN] 1464-3405
  • [Journal-full-title] Bioorganic & medicinal chemistry letters
  • [ISO-abbreviation] Bioorg. Med. Chem. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antibiotics, Antineoplastic; 80168379AG / Doxorubicin; 9007-49-2 / DNA; ZS7284E0ZP / Daunorubicin
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27. Peipp M, Dechant M, Valerius T: Sensitivity and resistance to EGF-R inhibitors: approaches to enhance the efficacy of EGF-R antibodies. MAbs; 2009 Nov-Dec;1(6):590-9
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  • The epidermal growth factor receptor (EGF-R) constitutes one of the most broadly targeted antigens in tumor therapy since it is commonly expressed on many epithelial cancers, as well as on glioblastomas.
  • [MeSH-minor] Animals. Biomarkers, Pharmacological / metabolism. Disease Progression. Drug Resistance, Neoplasm. Humans

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  • (PMID = 20068398.001).
  • [ISSN] 1942-0870
  • [Journal-full-title] mAbs
  • [ISO-abbreviation] MAbs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Biomarkers, Pharmacological; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 109
  • [Other-IDs] NLM/ PMC2791317
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28. Combs SE, Gutwein S, Thilmann Ch, Huber P, Debus J, Schulz-Ertner D: Stereotactically guided fractionated re-irradiation in recurrent glioblastoma multiforme. J Neurooncol; 2005 Sep;74(2):167-71
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  • [Title] Stereotactically guided fractionated re-irradiation in recurrent glioblastoma multiforme.
  • PURPOSE: To assess the feasibility, efficacy and toxicity of fractionated stereotactic radiotherapy in the treatment of recurrent glioblastoma multiforme.
  • PATIENTS AND METHODS: From January 1995 to July 2003, 53 patients with histologically proven glioblastoma multiforme were treated at recurrence with fractionated stereotactic radiation therapy.
  • CONCLUSION: Stereotactically guided fractionated re-irradiation is a safe and effective treatment modality in selected cases of recurring glioblastoma multiforme.
  • Also, based on recent results of radiochemotherapy in the treatment of primary glioblastoma multiforme, concomitant chemotherapy at relapse might be considered in the future.
  • [MeSH-major] Brain Neoplasms / radiotherapy. Glioblastoma / radiotherapy. Neoplasm Recurrence, Local / radiotherapy

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  • (PMID = 16193388.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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29. Aki K, Shimizu A, Masuda Y, Kuwahara N, Arai T, Ishikawa A, Fujita E, Mii A, Natori Y, Fukunaga Y, Fukuda Y: ANG II receptor blockade enhances anti-inflammatory macrophages in anti-glomerular basement membrane glomerulonephritis. Am J Physiol Renal Physiol; 2010 Apr;298(4):F870-82
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  • We examined the anti-inflammatory effect of ANG II type 1 receptor (AT(1)R) blocker (ARB) on glomerular inflammation in a rat model of anti-glomerular basement membrane (GBM) glomerulonephritis (GN).
  • Wistar-Kyoto rats were treated with high-dose olmesartan (3 mg.kg(-1).day(-1)), low-dose olmesartan (0.3 mg.kg(-1).day(-1)), or vehicle (control) 7 days before induction of anti-GBM GN.
  • Low-dose ARB had no anti-inflammatory effects in anti-GBM GN.
  • [MeSH-major] Angiotensin II Type 1 Receptor Blockers / pharmacology. Angiotensin Receptor Antagonists. Anti-Glomerular Basement Membrane Disease / immunology. Inflammation / pathology. Macrophages / physiology
  • [MeSH-minor] Animals. Blood Pressure / drug effects. CD4-Positive T-Lymphocytes / drug effects. CD4-Positive T-Lymphocytes / physiology. CD8-Positive T-Lymphocytes / drug effects. CD8-Positive T-Lymphocytes / physiology. Cytokines / genetics. Cytokines / metabolism. Disease Models, Animal. Dose-Response Relationship, Drug. Gene Expression Regulation / drug effects. Gene Expression Regulation / physiology. Imidazoles / pharmacology. Kidney Glomerulus / drug effects. Kidney Glomerulus / metabolism. Kidney Glomerulus / pathology. Male. Rats. Rats, Inbred WKY. Tetrazoles / pharmacology

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  • [CommentIn] Am J Physiol Renal Physiol. 2010 Apr;298(4):F868-9 [20130123.001]
  • (PMID = 20071465.001).
  • [ISSN] 1522-1466
  • [Journal-full-title] American journal of physiology. Renal physiology
  • [ISO-abbreviation] Am. J. Physiol. Renal Physiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiotensin II Type 1 Receptor Blockers; 0 / Angiotensin Receptor Antagonists; 0 / Cytokines; 0 / Imidazoles; 0 / Tetrazoles; 8W1IQP3U10 / olmesartan
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30. Nandi S, Ulasov IV, Rolle CE, Han Y, Lesniak MS: A chimeric adenovirus with an Ad 3 fiber knob modification augments glioma virotherapy. J Gene Med; 2009 Nov;11(11):1005-11
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  • Ex vivo analysis of primary glioblastoma multiforme samples infected with CRAd-Survivin-5/3 showed an increase in cytotoxicity of 20-30% compared to adenovirus wild-type (AdWT).
  • In an intracranial xenograft model of glioma, this oncolytic virus increased tumor-free survival and overall lifespan by 50% compared to controls (p < 0.05).

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  • (PMID = 19688792.001).
  • [ISSN] 1521-2254
  • [Journal-full-title] The journal of gene medicine
  • [ISO-abbreviation] J Gene Med
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / K08-NS046430; None / None / / R01 CA122930-02; United States / NINDS NIH HHS / NS / K08 NS046430-05; United States / NINDS NIH HHS / NS / K08 NS046430; United States / NCI NIH HHS / CA / R01 CA122930; None / None / / R21 CA135728-02; United States / NCI NIH HHS / CA / R21 CA135728-02; United States / NCI NIH HHS / CA / R01 CA122930-02; United States / NCI NIH HHS / CA / R21 CA135728; None / None / / K08 NS046430-05; United States / NCI NIH HHS / CA / R01-CA122930
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Microtubule-Associated Proteins
  • [Other-IDs] NLM/ NIHMS162541; NLM/ PMC2793323
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31. Cornut G, Fortin C, Soulières D: Antineoplastic properties of bacteriocins: revisiting potential active agents. Am J Clin Oncol; 2008 Aug;31(4):399-404
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  • Moreover, modified bacteriocins proved to be effective in a glioblastoma xenograft mouse model.

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  • (PMID = 18846002.001).
  • [ISSN] 1537-453X
  • [Journal-full-title] American journal of clinical oncology
  • [ISO-abbreviation] Am. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antineoplastic Agents; 0 / Bacteriocins
  • [Number-of-references] 68
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32. Mentrikoski M, Johnson MD, Korones DN, Scott GA: Glioblastoma multiforme in skin: a report of 2 cases and review of the literature. Am J Dermatopathol; 2008 Aug;30(4):381-4
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  • [Title] Glioblastoma multiforme in skin: a report of 2 cases and review of the literature.
  • Despite an aggressive clinical course, glioblastoma multiforme (GBM) rarely develops extracranial metastasis, with only 6 cases of skin involvement reported in the literature.
  • We report 2 cases of GBM that spread to the scalp.
  • Both patients presented with a firm nodule adjacent to their original craniotomy site.
  • Histologic examination revealed highly anaplastic tumor cells invading the subcutaneous tissues.
  • Although it is possible that these cases represent true metastatic GBM, the close proximity of the nodules to suture lines suggests extension of GBM to the skin through surgical sites or seeding of tumor cells.
  • It is important to have an accurate clinical history when evaluating scalp nodules in patients with GBM, so that a diagnosis of GBM is not overlooked.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / pathology. Neoplasm Recurrence, Local / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Craniotomy. Female. Humans. Immunohistochemistry. Male. Middle Aged. Scalp / pathology

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  • (PMID = 18645311.001).
  • [ISSN] 1533-0311
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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33. Carson HJ, Eilers SG: Death from undiagnosed glioblastoma multiforme and toxic self-medication presenting with concurrent dysfunctional behavior. J Forensic Leg Med; 2008 Aug;15(6):395-7
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  • [Title] Death from undiagnosed glioblastoma multiforme and toxic self-medication presenting with concurrent dysfunctional behavior.
  • We encountered a decedent with an unexpected glioblastoma multiforme.
  • At autopsy, the brain showed a glioblastoma multiforme.
  • The presence of a brain tumor likely caused a severe headache.
  • The present case is interesting in that it had evidence of behavioral dysfunction that could be related to the brain tumor, and death arising from the glioblastoma multiforme (cerebral hemorrhage and edema) with concurrent multiple drug intoxication.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / pathology. Headache Disorders, Secondary / drug therapy. Mental Disorders / etiology. Self Medication / adverse effects

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  • (PMID = 18586212.001).
  • [ISSN] 1752-928X
  • [Journal-full-title] Journal of forensic and legal medicine
  • [ISO-abbreviation] J Forensic Leg Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Analgesics, Non-Narcotic; 0 / Analgesics, Opioid; 0 / Serotonin Uptake Inhibitors; 362O9ITL9D / Acetaminophen; 41VRH5220H / Paroxetine; 6YKS4Y3WQ7 / Hydrocodone; C812VVS96K / norpropoxyphene; S2F83W92TK / Dextropropoxyphene
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34. Wan Y, Kim YT, Li N, Cho SK, Bachoo R, Ellington AD, Iqbal SM: Surface-immobilized aptamers for cancer cell isolation and microscopic cytology. Cancer Res; 2010 Nov 15;70(22):9371-80
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  • Exposing rare but highly malignant tumor cells that migrate from the primary tumor mass into adjacent tissue(s) or circulate in the bloodstream is critical for early detection and effective intervention(s).
  • Here, we report on an aptamer-based strategy directed against epidermal growth factor receptor (EGFR), the most common oncogene in glioblastoma (GBM), to detect these deadly tumor cells.
  • GBMs are characterized by diffuse infiltration into normal brain regions, and the inability to detect GBM cells renders the disease surgically incurable with a median survival of just 14.2 months.
  • Cells tested included primary human GBM cells expressing high levels of the wild-type EGFR, as well as genetically engineered murine glioma cells overexpressing the most common EGFR mutant (EGFRvIII lacking exons 2-7) in Ink4a/Arf-deficient astrocytes.
  • We found that surfaces functionalized with anti-EGFR aptamers could capture both the human and murine GBM cells with high sensitivity and specificity.
  • Our findings show how novel aptamer substrates could be used to determine whether surgical resection margins are free of tumor cells, or more widely for detecting tumor cells circulating in peripheral blood to improve early detection and/or monitoring residual disease after treatment.
  • [MeSH-minor] Animals. Antibodies / immunology. Antibodies / metabolism. Astrocytes / metabolism. Base Sequence. Binding, Competitive. Brain Neoplasms / genetics. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Cell Separation / methods. Cells, Cultured. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Fibroblasts / cytology. Fibroblasts / metabolism. Glioblastoma / genetics. Glioblastoma / metabolism. Glioblastoma / pathology. Humans. Mice. Mice, Knockout. Microscopy, Fluorescence / methods. Molecular Sequence Data. Mutation. Neurons / metabolism. Rats. Stem Cells / metabolism. Surface Properties. Tumor Cells, Cultured

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  • [Copyright] Copyright © 2010 AACR.
  • [ErratumIn] Cancer Res. 2011 Jan 15;71(2):626
  • [ErratumIn] Cancer Res. 2011 Mar 15;71(6):2408
  • (PMID = 21062984.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5R01CA119388-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Aptamers, Nucleotide; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RNA, Antisense; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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35. Higashi M, Ishikawa C, Yu J, Toyoda A, Kawana H, Kurokawa K, Matsuda M, Kitagawa M, Harigaya K: Human Mena associates with Rac1 small GTPase in glioblastoma cell lines. PLoS One; 2009;4(3):e4765
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  • [Title] Human Mena associates with Rac1 small GTPase in glioblastoma cell lines.
  • Here we report that human Mena (hMena) colocalizes with Rac1 in lamellipodia, and using an unmixing assisted acceptor depletion fluorescence resonance energy transfer (u-adFRET) analysis that hMena associates with Rac1 in vivo in the glioblastoma cell line U251MG.
  • This cellular phenotype is canceled by introduction of a dominant negative form of Rac1.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / pathology. Microfilament Proteins / physiology. Neoplasm Proteins / physiology. Pseudopodia / chemistry. rac1 GTP-Binding Protein / physiology
  • [MeSH-minor] Cell Line, Tumor / chemistry. Cell Line, Tumor / ultrastructure. Cell Movement. Cell Shape. Fluorescence Resonance Energy Transfer. HeLa Cells / chemistry. HeLa Cells / ultrastructure. Humans. Protein Interaction Mapping. RNA Interference. RNA, Small Interfering / pharmacology. Recombinant Fusion Proteins / chemistry. Recombinant Fusion Proteins / physiology. Signal Transduction


36. Corso JJ, Sharon E, Dube S, El-Saden S, Sinha U, Yuille A: Efficient multilevel brain tumor segmentation with integrated bayesian model classification. IEEE Trans Med Imaging; 2008 May;27(5):629-40
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  • [Title] Efficient multilevel brain tumor segmentation with integrated bayesian model classification.
  • We integrate the resulting model-aware affinities into the multilevel segmentation by weighted aggregation algorithm, and apply the technique to the task of detecting and segmenting brain tumor and edema in multichannel magnetic resonance (MR) volumes.
  • Our quantitative results indicate the benefit of incorporating model-aware affinities into the segmentation process for the difficult case of glioblastoma multiforme brain tumor.

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  • (PMID = 18450536.001).
  • [ISSN] 1558-254X
  • [Journal-full-title] IEEE transactions on medical imaging
  • [ISO-abbreviation] IEEE Trans Med Imaging
  • [Language] eng
  • [Grant] United States / NLM NIH HHS / LM / LM07356
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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37. Jinguji Y, Nukui I, Wakasugi M, Yamashita H: Two cases of systemic lupus erythematosus complicated by hydronephrosis and unique small structures observed in the glomerular basement membrane. Clin Exp Nephrol; 2008 Dec;12(6):467-74
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  • We report two cases having a similar clinical profile of systemic lupus erythematosus (SLE) complicated by hydronephrosis that developed concurrently with a similar pathological recognition of numerous unique microspherical and microtubular structures in the glomerular basement membrane (GBM).
  • The pathological findings of the kidney revealed "bubbling" of the GBM, microspherical and microtubular structures in the GBM, and a suspicion of podocytic infolding into the GBM.
  • The renal disorder of the two cases exhibited pathological abnormality atypical of lupus nephritis.
  • Histopathological abnormality similar to that detected in the two cases has rarely been reported until recently.
  • The pathogenesis of the GBM lesions of the two cases has not yet been elucidated, but we believe that there is a possibility the persistent mild autoimmune disorder and the concurrence of an obstructive state of the urinary tract may facilitate the occurrence of the pathological abnormality, because the clinical feature of the two cases are conspicuously similar to each other.

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  • (PMID = 18956137.001).
  • [ISSN] 1342-1751
  • [Journal-full-title] Clinical and experimental nephrology
  • [ISO-abbreviation] Clin. Exp. Nephrol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
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38. Debinski W: Drug cocktails for effective treatment of glioblastoma multiforme. Expert Rev Neurother; 2008 Apr;8(4):515-7
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  • [Title] Drug cocktails for effective treatment of glioblastoma multiforme.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Brain Neoplasms / drug therapy. Brain Neoplasms / metabolism. Drug Delivery Systems / methods. Glioblastoma / drug therapy. Glioblastoma / metabolism

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  • (PMID = 18416653.001).
  • [ISSN] 1744-8360
  • [Journal-full-title] Expert review of neurotherapeutics
  • [ISO-abbreviation] Expert Rev Neurother
  • [Language] eng
  • [Publication-type] Editorial; Review
  • [Publication-country] England
  • [Number-of-references] 20
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39. Panet-Raymond V, Souhami L, Roberge D, Kavan P, Shakibnia L, Muanza T, Lambert C, Leblanc R, Del Maestro R, Guiot MC, Shenouda G: Accelerated hypofractionated intensity-modulated radiotherapy with concurrent and adjuvant temozolomide for patients with glioblastoma multiforme: a safety and efficacy analysis. Int J Radiat Oncol Biol Phys; 2009 Feb 1;73(2):473-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Accelerated hypofractionated intensity-modulated radiotherapy with concurrent and adjuvant temozolomide for patients with glioblastoma multiforme: a safety and efficacy analysis.
  • PURPOSE: Despite multimodality treatments, the outcome of patients with glioblastoma multiforme remains poor.
  • METHODS AND MATERIALS: Between March 2004 and June 2006, 35 unselected patients with glioblastoma multiforme were treated with hypo-IMRT.
  • During a 4-week period, using a concomitant boost technique, a dose of 60 Gy and 40 Gy were delivered in 20 fractions prescribed to the periphery of the gross tumor volume and planning target volume, respectively.
  • The median overall survival was 14.4 months, and the median disease-free survival was 7.7 months.
  • The pattern of failure was predominantly central, within 2 cm of the initial gross tumor volume.
  • Grade 3-4 toxicity was limited to 1 patient with nausea and emesis during adjuvant TMZ administration.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Brain Neoplasms. Dacarbazine / analogs & derivatives. Glioblastoma. Radiotherapy, Intensity-Modulated / methods
  • [MeSH-minor] Adult. Aged. Analysis of Variance. Chemotherapy, Adjuvant / adverse effects. Disease-Free Survival. Dose Fractionation. Drug Administration Schedule. Female. Humans. Male. Methylation. Middle Aged. O(6)-Methylguanine-DNA Methyltransferase / metabolism. Retrospective Studies. Treatment Outcome. Tumor Burden

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  • (PMID = 18554821.001).
  • [ISSN] 1879-355X
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [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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40. Ma YH, Mentlein R, Knerlich F, Kruse ML, Mehdorn HM, Held-Feindt J: Expression of stem cell markers in human astrocytomas of different WHO grades. J Neurooncol; 2008 Jan;86(1):31-45
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  • [Title] Expression of stem cell markers in human astrocytomas of different WHO grades.
  • According to new hypotheses astrocytomas/gliomas either arise from or attract neural stem cells.
  • Because these studies have been performed with single experimental samples mostly from gliomas, we investigated the expression of the stem cell markers CD133/Prominin, Nestin, Sox-2, Musashi-1, CXCR4, Flt-4/VEGFR-3 and CD105/Endoglin in 72 astrocytomas of different WHO-grades and compared it to normal adult human brain.
  • However, their mean expression was significantly increased in astrocytomas, but this depended on the WHO grade only for CD133, Nestin, Sox-2 and Musashi-1.
  • Our results show that most astrocytomas contain considerable portions of cells expressing stem cell markers.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Gene Expression / physiology. Nerve Tissue Proteins / metabolism. Stem Cells / metabolism

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  • (PMID = 17611714.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Nerve Tissue Proteins
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41. Esther Gil-Alegre M, González-Alvarez I, Gutiérrez-Paúls L, Torres-Suárez AI: Three weeks release BCNU loaded hydrophilic-PLGA microspheres for interstitial chemotherapy: Development and activity against human glioblastoma cells. J Microencapsul; 2008 Dec;25(8):561-8
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  • [Title] Three weeks release BCNU loaded hydrophilic-PLGA microspheres for interstitial chemotherapy: Development and activity against human glioblastoma cells.
  • The cytotoxic effects of these microspheres on human glioblastoma cells were demonstrated all through 21 days and the value of percentage of viable cells was less than 40%.
  • [MeSH-major] Carmustine / administration & dosage. Drug Carriers / chemistry. Glioblastoma / drug therapy. Lactic Acid. Microspheres. Polyglycolic Acid
  • [MeSH-minor] Antineoplastic Agents, Alkylating / administration & dosage. Brain Neoplasms / drug therapy. Cell Survival / drug effects. Humans. Time Factors. Tumor Cells, Cultured

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  • (PMID = 18608792.001).
  • [ISSN] 1464-5246
  • [Journal-full-title] Journal of microencapsulation
  • [ISO-abbreviation] J Microencapsul
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Drug Carriers; 0 / polylactic acid-polyglycolic acid copolymer; 26009-03-0 / Polyglycolic Acid; 33X04XA5AT / Lactic Acid; U68WG3173Y / Carmustine
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42. Milano V, Piao Y, LaFortune T, de Groot J: Dasatinib-induced autophagy is enhanced in combination with temozolomide in glioma. Mol Cancer Ther; 2009 Feb;8(2):394-406
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  • Glioblastoma is defined by its aggressive invasion, microvascular proliferation, and central necrosis.
  • In studying the action of dasatinib in human glioblastoma, we found that levels of phospho-SRC, AKT, and ribosomal protein S6 were decreased in cell lines treated with low nanomolar concentrations of dasatinib at baseline and following stimulation with epidermal growth factor.
  • These results strongly support the clinical use of dasatinib in the treatment of glioblastoma and provide a rationale for combination therapy with dasatinib and temozolomide.
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Cell Movement / drug effects. Cell Proliferation / drug effects. Dasatinib. Drug Screening Assays, Antitumor. Drug Synergism. G1 Phase / drug effects. Humans. PTEN Phosphohydrolase / metabolism


43. Delion M, Moraru C, Almayrac F, Von Langsdorff D, Paquis P, Menei P: [Glioblastoma incident studies from May 2006 to May 2007 in Angers and Nice, France]. Neurochirurgie; 2010 Dec;56(6):499-502
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  • [Title] [Glioblastoma incident studies from May 2006 to May 2007 in Angers and Nice, France].
  • [Transliterated title] Études des glioblastomes incidents de mai 2006 à mai 2007, Angers-Nice.
  • The present work is a retrospective study on glioblastomas treated in the Angers and Nice Hospital Departments of Neurosurgery between 2006 and 2007.
  • This study was conducted 2 years after the audit on incident glioblastoma in France in 2004.
  • New events that may modify the care or survival of glioblastoma have occurred since 2004, justifying the present study.
  • The results show that the Karnowsky Index is more often included in the clinical files and that the rate of complete resection has increased, indicating that neurosurgeons are becoming aware of neuro-oncology.
  • [MeSH-major] Brain Neoplasms / therapy. Glioblastoma / therapy

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  • [Copyright] Copyright © 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20870254.001).
  • [ISSN] 1773-0619
  • [Journal-full-title] Neuro-Chirurgie
  • [ISO-abbreviation] Neurochirurgie
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Multicenter Study
  • [Publication-country] France
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44. Vladimirova V, Waha A, Lückerath K, Pesheva P, Probstmeier R: Runx2 is expressed in human glioma cells and mediates the expression of galectin-3. J Neurosci Res; 2008 Aug 15;86(11):2450-61
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  • A similar correlation in the expression pattern of galectin-3 and Runx2 transcripts was detected in distinct types of 70 primary neural tumors, such as glioblastoma multiforme, but not in others, such as gangliocytomas.
  • Knockdown of Runx2 was thus accompanied by a reduction of both galectin-3 mRNA and protein levels by at least 50%, dependent on the glial tumor cell line tested.
  • Reverse transcriptase-polymerase chain reaction analyses, aimed at finding other potential target genes of Runx2 in glial tumor cells, revealed the presence of bone sialoprotein, osteocalcin, osteopontin, and osteoprotegerin.
  • These data suggest a functional contribution of Runx-2-regulated galectin-3 expression to glial tumor malignancy.
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Gene Expression. Humans. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18438928.001).
  • [ISSN] 1097-4547
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 1 Subunit; 0 / Galectin 3; 0 / RNA, Messenger; 0 / RUNX2 protein, human
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45. Sciaccaluga M, Gianfranceschi GL, Rocco S, Germano G, Roti G, Gorello P, La Starza R, Castigli E: Constitutive phosphorylation of Janus kinase 2 in the GL15 glioblastoma derived human cell line. Oncol Rep; 2007 Jan;17(1):17-23
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  • [Title] Constitutive phosphorylation of Janus kinase 2 in the GL15 glioblastoma derived human cell line.
  • We show that the GL15 glioblastoma derived human cell line displays a high expression of nestin which, combined with the previously demonstrated high expression of vimentin, constitutes a characteristic of astrocyte restricted precursors.
  • The constitutive activation of JAK2 does not result from chromosomal aberrations involving the JAK2 gene, but most probably from abnormally activated transduction systems operative in glioblastoma cells.
  • The abnormally activated JAK2 could then potentially represent a target for a selective pharmacological approach in glioblastoma cells in which a combination of glial precursor characteristics and genetic alterations occurs.
  • [MeSH-major] Glioblastoma / enzymology. Janus Kinase 2 / metabolism
  • [MeSH-minor] Cell Cycle / drug effects. Cell Differentiation / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. Glial Fibrillary Acidic Protein / biosynthesis. Humans. Immunohistochemistry. Intermediate Filament Proteins / biosynthesis. Nerve Tissue Proteins / biosynthesis. Nestin. Phosphorylation / drug effects. Tyrphostins / pharmacology. Vimentin / biosynthesis

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  • (PMID = 17143473.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; 0 / Tyrphostins; 0 / Vimentin; 0 / alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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46. Turner CD, Chi S, Marcus KJ, MacDonald T, Packer RJ, Poussaint TY, Vajapeyam S, Ullrich N, Goumnerova LC, Scott RM, Briody C, Chordas C, Zimmerman MA, Kieran MW: Phase II study of thalidomide and radiation in children with newly diagnosed brain stem gliomas and glioblastoma multiforme. J Neurooncol; 2007 Mar;82(1):95-101
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  • [Title] Phase II study of thalidomide and radiation in children with newly diagnosed brain stem gliomas and glioblastoma multiforme.
  • A phase II study was conducted to assess the efficacy of administering daily thalidomide concomitantly with radiation and continuing for up to 1 year following radiation in children with brain stem gliomas (BSG) or glioblastoma multiforme (GBM).
  • Thirteen patients (2-14 years old) with newly diagnosed BSG (12 patients) or GBM (one patient) were enrolled between July 1999 and June 2000.
  • No patients completed the planned 12 months of thalidomide therapy and all have since died of disease progression.
  • Nine patients came off study for progressive disease (PD), three patients due to toxicity and one patient withdrew consent.
  • However, advanced imaging with techniques such as MR spectroscopy, MR perfusion and 18-fluorodeoxyglucose positron emission tomography (FDG-PET) were helpful in distinguishing growing tumor from treatment effect and necrosis in some patients.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Brain Stem Neoplasms / drug therapy. Glioblastoma / drug therapy. Glioma / drug therapy. Thalidomide / therapeutic use
  • [MeSH-minor] Adolescent. Child. Combined Modality Therapy. Disease-Free Survival. Dose-Response Relationship, Drug. Feasibility Studies. Female. Humans. Male. Treatment Failure

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  • (PMID = 17031553.001).
  • [ISSN] 0167-594X
  • [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 / Angiogenesis Inhibitors; 4Z8R6ORS6L / Thalidomide
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47. Hasegawa Y, Kinoh H, Iwadate Y, Onimaru M, Ueda Y, Harada Y, Saito S, Furuya A, Saegusa T, Morodomi Y, Hasegawa M, Saito S, Aoki I, Saeki N, Yonemitsu Y: Urokinase-targeted fusion by oncolytic Sendai virus eradicates orthotopic glioblastomas by pronounced synergy with interferon-β gene. Mol Ther; 2010 Oct;18(10):1778-86
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  • [Title] Urokinase-targeted fusion by oncolytic Sendai virus eradicates orthotopic glioblastomas by pronounced synergy with interferon-β gene.
  • Glioblastoma multiforme (GM), the most frequent primary malignant brain tumor, is highly invasive due to the expression of proteases, including urokinase-type plasminogen activator (uPA).
  • [MeSH-major] Glioblastoma / therapy. Interferon-beta / metabolism. Oncolytic Viruses / physiology. Sendai virus / physiology. Urokinase-Type Plasminogen Activator / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Cell Line. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / genetics. Enzyme-Linked Immunosorbent Assay. Female. Humans. Magnetic Resonance Imaging. Mice. Mice, Nude. Plasminogen Activator Inhibitor 1 / pharmacology. Rats. Rats, Inbred F344. Receptors, Urokinase Plasminogen Activator / genetics. Receptors, Urokinase Plasminogen Activator / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20606645.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Plasminogen Activator Inhibitor 1; 0 / Receptors, Urokinase Plasminogen Activator; 77238-31-4 / Interferon-beta; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator
  • [Other-IDs] NLM/ PMC2951556
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48. Braganhol E, Huppes D, Bernardi A, Wink MR, Lenz G, Battastini AM: A comparative study of ectonucleotidase and P2 receptor mRNA profiles in C6 cell line cultures and C6 ex vivo glioma model. Cell Tissue Res; 2009 Feb;335(2):331-40
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  • Glioblastoma multiforme is the most common type of primary brain tumour and has the worst clinical outcome.
  • [MeSH-minor] Adenosine Triphosphate / metabolism. Adenosine Triphosphate / pharmacology. Animals. Biomarkers / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Male. Neoplasm Transplantation. Neovascularization, Pathologic / metabolism. RNA, Messenger / metabolism. Rats. Rats, Wistar

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  • (PMID = 19023597.001).
  • [ISSN] 1432-0878
  • [Journal-full-title] Cell and tissue research
  • [ISO-abbreviation] Cell Tissue Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers; 0 / RNA, Messenger; 0 / Receptors, Purinergic P2; 8L70Q75FXE / Adenosine Triphosphate; EC 3.1.3.5 / 5'-Nucleotidase
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49. Pan JJ, Chang WJ, Barone TA, Plunkett RJ, Ostrow PT, Greenberg SJ: Increased expression of TGF-beta1 reduces tumor growth of human U-87 Glioblastoma Cells in vivo. Cancer Immunol Immunother; 2006 Aug;55(8):918-27
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  • [Title] Increased expression of TGF-beta1 reduces tumor growth of human U-87 Glioblastoma Cells in vivo.
  • To further understand the potential growth-regulatory effects of TGF-beta1,we constructed an animal astroglial tumor model by injecting either wild-type or virally transduced human U-87 glioblastoma cells into nude rat brains.
  • In contrast, U-87 cells transduced to express high levels of TGF-beta1 showed reduced tumor size in vivo, in a dose-dependent manner.
  • This reduction in tumor size was not due to either decreased vascularity or increased apoptosis.
  • To test whether TGF-beta1 overproduction inhibited tumor growth through an autocrine mechanism, the highest TGF-beta1 producing cells were then double transduced with a vector expressing the kinase-truncated type II TGF-beta receptor.
  • The data suggest that the degree of tumorigenicity of the U-87 high-grade glioblastoma cell line may be associated with correspondingly low level of production of TGF-beta1.
  • These results also would tend to support the possibility that TGF-beta1 may be useful in treating some high-grade gliomas.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Cell Proliferation. Glioblastoma / metabolism. Transforming Growth Factor beta1 / biosynthesis
  • [MeSH-minor] Animals. Blotting, Northern. Blotting, Western. Cell Line, Tumor. DNA Fragmentation. Disease Models, Animal. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Rats. Rats, Nude. Receptors, Transforming Growth Factor beta / biosynthesis. Transduction, Genetic

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  • (PMID = 16187082.001).
  • [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 / Biomarkers, Tumor; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1
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50. Huttner AJ, Kieran MW, Yao X, Cruz L, Ladner J, Quayle K, Goumnerova LC, Irons MB, Ullrich NJ: Clinicopathologic study of glioblastoma in children with neurofibromatosis type 1. Pediatr Blood Cancer; 2010 Jul 1;54(7):890-6
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  • [Title] Clinicopathologic study of glioblastoma in children with neurofibromatosis type 1.
  • BACKGROUND: Neurofibromatosis type 1 (NF1) is characterized by low-grade tumors of the central and peripheral nervous system.
  • Glioblastoma is an uncommon, malignant tumor of children that is even less frequently observed in children with NF1.
  • PROCEDURE: We performed a retrospective review of patients with NF1 and glioblastoma to determine specific clinical and pathologic indicators of overall prognosis.
  • In the same time period, there were 56 patients without NF1 diagnosed with glioblastoma who were treated at our institution.
  • CONCLUSIONS: This study provides preliminary evidence that children with NF1 may be at risk for glioblastoma, but that these patients have an increased survival compared to children without NF1.
  • Additional molecular studies will be required to determine if the pathogenesis of these tumors differs from glioblastoma in children without NF1.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / pathology. Neurofibromatosis 1 / complications
  • [MeSH-minor] Child. Child, Preschool. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Gene Dosage. Humans. Immunohistochemistry. In Situ Hybridization. Infant. Kaplan-Meier Estimate. Male. PTEN Phosphohydrolase / genetics. Receptor, Epidermal Growth Factor / genetics. Retrospective Studies. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Proteins / genetics


51. Hattermann K, Held-Feindt J, Lucius R, Müerköster SS, Penfold ME, Schall TJ, Mentlein R: The chemokine receptor CXCR7 is highly expressed in human glioma cells and mediates antiapoptotic effects. Cancer Res; 2010 Apr 15;70(8):3299-308
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  • The chemokine CXCL12/stromal cell-derived factor-1 and its receptor CXCR4 play a major role in tumor invasion, proliferation, and metastasis.
  • Because both chemokines are expressed abundantly in human astrocytomas and glioblastomas, we investigated the occurrence and function of both receptors in astroglial tumors.
  • In situ, CXCR7 is highly expressed on tumor endothelial, microglial, and glioma cells whereas CXCR4 has a much more restricted localization; CXCL12 is often colocalized with CXCR7.
  • CXCR7 transcription in tumor homogenates increased with malignancy.
  • In contrast, a tumor stem-like cell line preferentially expressed CXCR4 which diminished upon differentiation, whereas CXCR7 increased drastically.
  • Thus, CXCR7 is a functional receptor for CXCL12 in astrocytomas/glioblastomas and mediates resistance to drug-induced apoptosis.


52. de la Iglesia N, Konopka G, Lim KL, Nutt CL, Bromberg JF, Frank DA, Mischel PS, Louis DN, Bonni A: Deregulation of a STAT3-interleukin 8 signaling pathway promotes human glioblastoma cell proliferation and invasiveness. J Neurosci; 2008 Jun 4;28(23):5870-8
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  • [Title] Deregulation of a STAT3-interleukin 8 signaling pathway promotes human glioblastoma cell proliferation and invasiveness.
  • Inactivation of the tumor suppressor phosphatase and tensin homolog (mutated in multiple advanced cancers 1) (PTEN) is recognized as a major event in the pathogenesis of the brain tumor glioblastoma.
  • However, the mechanisms by which PTEN loss specifically impacts the malignant behavior of glioblastoma cells, including their proliferation and propensity for invasiveness, remain poorly understood.
  • Genetic studies suggest that the transcription factor signal transducers and activators of transcription 3 (STAT3) harbors a PTEN-regulated tumor suppressive function in mouse astrocytes.
  • Here, we report that STAT3 plays a critical tumor suppressive role in PTEN-deficient human glioblastoma cells.
  • Endogenous STAT3 signaling is specifically inhibited in PTEN-deficient glioblastoma cells.
  • Strikingly, reactivation of STAT3 in PTEN-deficient glioblastoma cells inhibits their proliferation, invasiveness, and ability to spread on myelin.
  • We also identify the chemokine interleukin 8 (IL8) as a novel target gene of STAT3 in human glioblastoma cells.
  • Consistent with these results, IL8 is upregulated in PTEN-deficient human glioblastoma tumors.
  • Importantly, IL8 repression mediates STAT3 inhibition of glioblastoma cell proliferation, invasiveness, and spreading on myelin.
  • Collectively, our findings uncover a novel link between STAT3 and IL8, the deregulation of which plays a key role in the malignant behavior of PTEN-deficient glioblastoma cells.

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  • (PMID = 18524891.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS041021-08; United States / NINDS NIH HHS / NS / R01 NS047188-02; United States / NINDS NIH HHS / NS / NS051255; United States / NINDS NIH HHS / NS / R01 NS051255-04; United States / NINDS NIH HHS / NS / R01 NS047188; United States / NCI NIH HHS / CA / R01 CA57683; United States / NINDS NIH HHS / NS / NS41021; United States / NINDS NIH HHS / NS / NS047188; None / None / / R01 NS051255-04; None / None / / R01 NS047188-02; None / None / / R01 NS041021-08; United States / NINDS NIH HHS / NS / R01 NS041021; United States / NINDS NIH HHS / NS / R01 NS051255
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Growth Inhibitors; 0 / Interleukin-8; 0 / STAT3 Transcription Factor; 0 / Tumor Suppressor Proteins; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ NIHMS67743; NLM/ PMC2700037
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53. Hede SM, Hansson I, Afink GB, Eriksson A, Nazarenko I, Andrae J, Genove G, Westermark B, Nistér M: GFAP promoter driven transgenic expression of PDGFB in the mouse brain leads to glioblastoma in a Trp53 null background. Glia; 2009 Aug 15;57(11):1143-53
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  • [Title] GFAP promoter driven transgenic expression of PDGFB in the mouse brain leads to glioblastoma in a Trp53 null background.
  • Glioblastomas are the most common and malignant astrocytic brain tumors in human adults.
  • The tumor suppressor gene TP53 is commonly mutated and/or lost in astrocytic brain tumors and the TP53 alterations are often found in combination with excessive growth factor signaling via PDGF/PDGFRalpha.
  • This occurred at 2-6 months of age and tumors displayed human glioblastoma-like features with integrated development of Pdgfralpha+ tumor cells and Pdgfrbeta+/Nestin+ vasculature.
  • The transgene was expressed in subependymal astrocytic cells, in glia limitans, and in astrocytes throughout the brain substance, and subsequently, microscopic tumor lesions were initiated equally in all these areas.
  • With tumor size, there was an increase in Nestin positivity and variability in lineage markers.
  • These results indicate an unexpected plasticity of all astrocytic cells in the adult brain, not only of SVZ cells.
  • [MeSH-major] Brain / metabolism. Brain Neoplasms / genetics. Genes, p53. Glial Fibrillary Acidic Protein / genetics. Glioblastoma / genetics. Promoter Regions, Genetic. Proto-Oncogene Proteins c-sis / metabolism
  • [MeSH-minor] Animals. Astrocytes / metabolism. Disease Models, Animal. Gene Expression. Humans. Intermediate Filament Proteins / metabolism. Mice. Mice, Transgenic. Nerve Tissue Proteins / metabolism. Nestin. Neuroglia / metabolism. Receptor, Platelet-Derived Growth Factor alpha / metabolism

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  • (PMID = 19115382.001).
  • [ISSN] 1098-1136
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / Proto-Oncogene Proteins c-sis; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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54. Riemenschneider MJ, Mueller W, Betensky RA, Mohapatra G, Louis DN: In situ analysis of integrin and growth factor receptor signaling pathways in human glioblastomas suggests overlapping relationships with focal adhesion kinase activation. Am J Pathol; 2005 Nov;167(5):1379-87
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  • [Title] In situ analysis of integrin and growth factor receptor signaling pathways in human glioblastomas suggests overlapping relationships with focal adhesion kinase activation.
  • Deregulated integrin signaling is common in cancers, including glioblastoma.
  • Most studies of this pathway have used in vitro systems or tumor lysate-based approaches.
  • We examined these pathways primarily in situ using a panel of 30 glioblastomas and gene expression arrays, immunohistochemistry, and fluorescence in situ hybridization, emphasizing the histological distribution of molecular changes.
  • Thus, FAK may act in glioblastoma as a downstream target of growth factor signaling, with integrins enhancing the impact of such signaling in the tumor microenvironment.

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  • (PMID = 16251422.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA057683; United States / NCI NIH HHS / CA / CA57683
  • [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 / Integrin beta Chains; 0 / Integrins; 0 / Paxillin; 0 / RNA, Messenger; 0 / Receptors, Growth Factor; 0 / integrin beta8; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
  • [Other-IDs] NLM/ PMC1603783
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55. Dong H, Luo L, Hong S, Siu H, Xiao Y, Jin L, Chen R, Xiong M: Integrated analysis of mutations, miRNA and mRNA expression in glioblastoma. BMC Syst Biol; 2010 Nov 29;4:163
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  • [Title] Integrated analysis of mutations, miRNA and mRNA expression in glioblastoma.
  • BACKGROUND: Glioblastoma arises from complex interactions between a variety of genetic alterations and environmental perturbations.
  • Little attention has been paid to understanding how genetic variations, altered gene expression and microRNA (miRNA) expression are integrated into networks which act together to alter regulation and finally lead to the emergence of complex phenotypes and glioblastoma.
  • RESULTS: We identified association of somatic mutations in 14 genes with glioblastoma, of which 8 genes are newly identified, and association of loss of heterozygosity (LOH) is identified in 11 genes with glioblastoma, of which 9 genes are newly discovered.
  • We also constructed miRNA coexpression networks and found 19 important miRNAs of which 3 were significantly related to glioblastoma patients' survival.
  • Finally, we developed new methods to decipher the pathway connecting mutations, expression information and glioblastoma.
  • CONCLUSIONS: Our results demonstrate that integrated analysis of multi-dimensional data has the potential to unravel the mechanism of tumor initiation and progression.

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  • (PMID = 21114830.001).
  • [ISSN] 1752-0509
  • [Journal-full-title] BMC systems biology
  • [ISO-abbreviation] BMC Syst Biol
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / P01 AR052915-01A1; United States / NIAMS NIH HHS / AR / P50 AR054144-01; United States / NIAMS NIH HHS / AR / R01AR057120-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC3002314
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56. Linkous AG, Yazlovitskaya EM, Hallahan DE: Cytosolic phospholipase A2 and lysophospholipids in tumor angiogenesis. J Natl Cancer Inst; 2010 Sep 22;102(18):1398-412
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  • [Title] Cytosolic phospholipase A2 and lysophospholipids in tumor angiogenesis.
  • BACKGROUND: Lung cancer and glioblastoma multiforme are highly angiogenic and, despite advances in treatment, remain resistant to therapy.
  • METHODS: Glioblastoma (GL261) and Lewis lung carcinoma (LLC) heterotopic tumor models were used to study the effects of cPLA(2) expression on tumor growth and vascularity in C57/BL6 mice wild type for (cPLA(2)α(+/+)) or deficient in (cPLA(2)α(-/-)) cPLA(2)α, the predominant isoform in endothelium (n = 6-7 mice per group).
  • The effect of inhibiting cPLA(2) activity on GL261 and LLC tumor growth was studied in mice treated with the chemical cPLA(2) inhibitor 4-[2-[5-chloro-1-(diphenylmethyl)-2-methyl-1H-indol-3-yl]-ethoxy]benzoic acid (CDIBA).
  • RESULTS: GL261 tumor progression proceeded normally in cPLA(2)α(+/+) mice, whereas no GL261 tumors formed in cPLA(2)α(-/-) mice.
  • In the LLC tumor model, spontaneous tumor regression was observed in 50% of cPLA(2)α(-/-) mice.
  • Inhibition of cPLA(2) activity by CDIBA resulted in a delay in tumor growth (eg, LLC model: average number of days to reach tumor volume of 700 mm(3), CDIBA vs vehicle: 16.8 vs 11.8, difference = 5, 95% confidence interval = 3.6 to 6.4, P = .04) and a decrease in tumor size (eg, GL261 model: mean volume on day 21, CDIBA vs vehicle: 40.1 vs 247.4 mm(3), difference = 207.3 mm(3), 95% confidence interval = 20.9 to 293.7 mm(3), P = .021).
  • CONCLUSIONS: In these mouse models of brain and lung cancer, cPLA(2) and lysophospholipids have key regulatory roles in tumor angiogenesis. cPLA(2) inhibition may be a novel effective antiangiogenic therapy.

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  • (PMID = 20729478.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / PHS HHS / / R01-140220; United States / NCI NIH HHS / CA / R01-CA112385; United States / NCI NIH HHS / CA / R01-CA88076
  • [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 / Drug Combinations; 0 / Laminin; 0 / Lysophospholipids; 0 / Proteoglycans; 119978-18-6 / matrigel; 9007-34-5 / Collagen; EC 3.1.1.4 / Group IV Phospholipases A2
  • [Other-IDs] NLM/ PMC2943523
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57. Ali K, Lu Y, Das U, Sharma RK, Wiebe S, Meguro K, Sadanand V, Fourney DR, Vitali A, Kelly M, May T, Gomez J, Pellerin E: Biomolecular diagnosis of human glioblastoma multiforme using Synchrotron mid-infrared spectromicroscopy. Int J Mol Med; 2010 Jul;26(1):11-6
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  • [Title] Biomolecular diagnosis of human glioblastoma multiforme using Synchrotron mid-infrared spectromicroscopy.
  • Glioblastoma multiforme (GBM) is one of the most malignant human tumors, with a uniformly poor outcome.
  • One obstacle in curing malignant brain tumors is the limitation of conventional light microscopy in detecting microscopic residual tumor in biopsy samples from the perimeter of the surgically resected tumor.
  • We further refined the identification of GBM tumor tissue at the sub-cellular level, utilising the technique of Synchrotron, sourced mid-infrared (mid-IR) spectromicroscopy.
  • Paired, thin (5 microm) cryosections of snap-frozen human GBM tumor samples removed at elective surgery were mounted on glass slides (hematoxylin and eosin-stained tissue section) and calcium fluoride (CaF2) windows (unstained tissue section for transmission spectromicroscopy), respectively.
  • Concordance of tumor bearing areas identified in the stained section with the unstained IR tissue section was confirmed by the pathologist of the study.
  • Compared with molecular signatures obtained from normal control brain tissue, unique spectroscopic patterns were detected in GBM tumor samples from 6 patients.
  • The identifying features of GBM were: i) high protein-to-lipid ratios (amide I+II/CH2 symmetric stretch; amide I+II/CH2+CH3 symmetric and asymmetric stretch), and ii) considerable enhancement of the intensities of characteristic peaks at 2,957 and 2,871 cm(-1) representing CH3 asymmetric and symmetric stretch, respectively.
  • False color images of 5 clusters obtained by HCA identified dominant clusters corresponding to tumor tissue.
  • Corroboration of these findings in a larger number of GBM may allow for more precise identification of these and other types of brain tumors.
  • [MeSH-major] Brain Neoplasms / diagnosis. Glioblastoma / diagnosis. Spectrophotometry, Infrared / methods. Synchrotrons

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  • (PMID = 20514416.001).
  • [ISSN] 1791-244X
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Lipids; 0 / Proteins; O3B55K4YKI / Calcium Fluoride
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58. Hadjipanayis CG, DeLuca NA: Inhibition of DNA repair by a herpes simplex virus vector enhances the radiosensitivity of human glioblastoma cells. Cancer Res; 2005 Jun 15;65(12):5310-6
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  • [Title] Inhibition of DNA repair by a herpes simplex virus vector enhances the radiosensitivity of human glioblastoma cells.
  • Expression of the herpes simplex virus (HSV) protein, ICP0, from the viral genome, rendered two radioresistant human glioblastoma multiforme cell lines more sensitive to the effects of ionizing radiation.
  • Our results suggest that expression of ICP0 in human glioblastoma multiforme cells inhibits the repair of DNA double-strand breaks after ionizing radiation treatment, decreasing the survival of these cells in part by induction of apoptosis.
  • [MeSH-major] Central Nervous System Neoplasms / radiotherapy. DNA Repair. Glioblastoma / radiotherapy. Herpesvirus 1, Human / physiology. Immediate-Early Proteins / physiology. Radiation Tolerance / physiology
  • [MeSH-minor] Apoptosis / physiology. Apoptosis / radiation effects. Cell Growth Processes / physiology. Cell Survival / physiology. Cell Survival / radiation effects. DNA, Neoplasm / genetics. DNA, Neoplasm / radiation effects. DNA-Activated Protein Kinase. DNA-Binding Proteins / metabolism. Humans. Nuclear Proteins. Protein-Serine-Threonine Kinases / metabolism. Ubiquitin-Protein Ligases

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  • (PMID = 15958578.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / Immediate-Early Proteins; 0 / Nuclear Proteins; EC 2.7.11.1 / DNA-Activated Protein Kinase; EC 2.7.11.1 / PRKDC protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / Vmw110 protein, Human herpesvirus 1
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59. Marchan EM, Sekula RF Jr, Jannetta PJ, Quigley MR: Long-term survival enhanced by cordectomy in a patient with a spinal glioblastoma multiforme and paraplegia. Case report. J Neurosurg Spine; 2007 Dec;7(6):656-9
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  • [Title] Long-term survival enhanced by cordectomy in a patient with a spinal glioblastoma multiforme and paraplegia. Case report.
  • Spinal glioblastomas multiforme (GBMs) are rare lesions of the central nervous system with a prognosis as poor as that of their intracranial counterpart.
  • The authors present a case of a 50-year-old man with a GBM of the spinal cord treated with surgical removal of the mass and cordectomy after the onset of paraplegia.
  • Six months after the start of interferon therapy, magnetic resonance imaging revealed a right cerebellar mass pathologically consistent with a GBM.
  • Although intracranial dissemination of spinal GBMs has been reported, this case illustrates the longest reported interval between the occurrence of a spinal GBM and its intracranial dissemination.
  • Thus, cordectomy should be considered as a reasonable alternative in patients with complete loss of neurological function at and below the level where they harbor a malignant spinal cord astrocytoma.
  • [MeSH-major] Glioblastoma / complications. Glioblastoma / surgery. Neurosurgical Procedures. Paraplegia / etiology. Spinal Cord Neoplasms / complications. Spinal Cord Neoplasms / surgery

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  • (PMID = 18074692.001).
  • [ISSN] 1547-5654
  • [Journal-full-title] Journal of neurosurgery. Spine
  • [ISO-abbreviation] J Neurosurg Spine
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon-alpha; 0 / Recombinant Proteins; 0 / peginterferon alfa-2b; 30IQX730WE / Polyethylene Glycols; 99210-65-8 / interferon alfa-2b
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60. Mishima K, Kato Y, Kaneko MK, Nishikawa R, Hirose T, Matsutani M: Increased expression of podoplanin in malignant astrocytic tumors as a novel molecular marker of malignant progression. Acta Neuropathol; 2006 May;111(5):483-8
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  • [Title] Increased expression of podoplanin in malignant astrocytic tumors as a novel molecular marker of malignant progression.
  • However, little information exists about its role in CNS astrocytic tumors.
  • In this study, 188 astrocytic tumors (30 diffuse astrocytomas, 43 anaplastic astrocytomas, and 115 glioblastomas) were investigated using immunohistochemistry with an anti-podoplanin antibody, YM-1.
  • In 11 of 43 anaplastic astrocytomas (25.6%) and in 54 of 115 glioblastomas (47.0%), podoplanin was expressed on the surface of anaplastic astrocytoma cells and glioblastoma cells, especially around necrotic areas and proliferating endothelial cells.
  • On the other hand, podoplanin expression was not observed in diffuse astrocytoma (0/30: 0%).
  • Furthermore, we investigated the expression of podoplanin using quantitative real-time PCR and Western blot analysis in 54 frozen astrocytic tumors (6 diffuse astrocytomas, 14 anaplastic astrocytomas, and 34 glioblastomas).
  • Podoplanin mRNA and protein expression were markedly higher in glioblastomas than in anaplastic astrocytomas.
  • These data suggest that podoplanin expression might be associated with malignancy of astrocytic tumors.
  • [MeSH-major] Astrocytoma / metabolism. Central Nervous System Neoplasms / metabolism. Glioblastoma / metabolism. Membrane Glycoproteins / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Blotting, Western. Disease Progression. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. RNA, Messenger / genetics. RNA, Messenger / metabolism

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  • (PMID = 16596424.001).
  • [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 / Biomarkers, Tumor; 0 / Membrane Glycoproteins; 0 / PDPN protein, human; 0 / RNA, Messenger
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61. King GD, Kroeger KM, Bresee CJ, Candolfi M, Liu C, Manalo CM, Muhammad AK, Pechnick RN, Lowenstein PR, Castro MG: Flt3L in combination with HSV1-TK-mediated gene therapy reverses brain tumor-induced behavioral deficits. Mol Ther; 2008 Apr;16(4):682-90
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  • [Title] Flt3L in combination with HSV1-TK-mediated gene therapy reverses brain tumor-induced behavioral deficits.
  • Glioblastoma multiforme (GBM) is an invasive and aggressive primary brain tumor which is associated with a dismal prognosis.
  • We have earlier developed a macroscopic, intracranial, syngeneic GBM model, in which treatment with adenoviral vectors (Ads) expressing herpes simplex virus type 1 thymidine kinase (HSV1-TK) plus ganciclovir (GCV) resulted in survival of approximately 20% of the animals.
  • We hypothesized that the growth of a large intracranial tumor mass would cause behavioral abnormalities that can be reversed by the combined gene therapy.
  • We assessed the behavior and neuropathology of tumor-bearing animals treated with the combined gene therapy, 3 days after treatment, in long-term survivors, and in a recurrent model of glioma.
  • We demonstrate that the intracranial GBM induces behavioral deficits that are resolved after treatment with Ad-Flt3L/Ad-TK (+GCV).
  • The lack of long-term behavioral deficits and limited neuropathological abnormalities demonstrate the efficacy and safety of the combined Ad-Flt3L/Ad-TK gene therapy for GBM.
  • These findings can serve to underpin further developments of this therapeutic modality, leading toward implementation of a Phase I clinical trial.
  • [MeSH-major] Brain Neoplasms / therapy. Glioblastoma / therapy. Herpesvirus 1, Human / enzymology. Membrane Proteins / genetics. Thymidine Kinase / genetics
  • [MeSH-minor] Adenoviridae / metabolism. Animals. Cell Line, Tumor. Genetic Therapy. Genetic Vectors. Male. Motor Activity. Neoplasm Transplantation. Rats. Rats, Inbred Lew. Stereotyped Behavior

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  • (PMID = 18283279.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / U54 NS045309-010005; United States / NINDS NIH HHS / NS / U54 NS045309-01; United States / NINDS NIH HHS / NS / R01 NS054193; United States / NINDS NIH HHS / NS / R01 NS042893-01A1; United States / NINDS NIH HHS / NS / U01 NS052465-01A2; United States / NINDS NIH HHS / NS / R21 NS054143-01A2; United States / NINDS NIH HHS / NS / R21 NS047298; United States / NINDS NIH HHS / NS / R01 NS044556; United States / NINDS NIH HHS / NS / 1R01 NS44556.01; United States / NINDS NIH HHS / NS / NS445561.01; United States / NINDS NIH HHS / NS / U01 NS052465; United States / PHS HHS / / 1R21-NSO54143.01; United States / NINDS NIH HHS / NS / R01 NS054193-01A1; United States / NINDS NIH HHS / NS / U54 NS045309; United States / NINDS NIH HHS / NS / 1UO1 NS052465.01; United States / NINDS NIH HHS / NS / 1 R01 NS 054193.01; United States / NINDS NIH HHS / NS / R01 NS044556-01; United States / PHS HHS / / 1F32 N50503034-01; United States / FIC NIH HHS / TW / 1 R03 TW006273-01; United States / NINDS NIH HHS / NS / F32 NS058156; United States / NINDS NIH HHS / NS / R01 NS 42893.01; United States / NINDS NIH HHS / NS / R01 NS042893; United States / FIC NIH HHS / TW / R03 TW006273-01A1; United States / NINDS NIH HHS / NS / 1R21 NS047298-01; United States / FIC NIH HHS / TW / R03 TW006273; United States / NINDS NIH HHS / NS / R21 NS047298-01; United States / NINDS NIH HHS / NS / R21 NS054143; United States / NINDS NIH HHS / NS / 1F32 NS058156.01
  • [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 / Membrane Proteins; 0 / flt3 ligand protein; EC 2.7.1.21 / Thymidine Kinase
  • [Other-IDs] NLM/ NIHMS49676; NLM/ PMC2593113
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62. Aghi M, Chiocca EA: Gene therapy for glioblastoma. Neurosurg Focus; 2006;20(4):E18
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  • [Title] Gene therapy for glioblastoma.
  • Established treatments such as surgery, radiation, and chemotherapy have only minimally altered the median survival time of patients with glioblastoma multiforme, the most common malignant brain tumor.
  • These failures reflect the highly invasive nature of the disease, as well as the fact that few cells are actively dividing at any given time.
  • As a result, therapies need to act in areas of the brain that are spatially separated from the site of tumor origin and over extended periods of time temporally separated from their introduction.
  • [MeSH-major] Brain Neoplasms / therapy. Genetic Therapy / trends. Glioblastoma / therapy. Transfection / trends


63. Wibom C, Pettersson F, Sjöström M, Henriksson R, Johansson M, Bergenheim AT: Protein expression in experimental malignant glioma varies over time and is altered by radiotherapy treatment. Br J Cancer; 2006 Jun 19;94(12):1853-63
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  • Radiotherapy is one of the mainstays of glioblastoma (GBM) treatment.
  • In a further perspective these findings may prove to be useful in the development of new GBM treatment approaches.
  • [MeSH-minor] Animals. Neoplasm Transplantation. Principal Component Analysis. Rats. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Time Factors

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  • (PMID = 16736004.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proteins
  • [Other-IDs] NLM/ PMC2361353
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64. Leimgruber A, Ostermann S, Yeon EJ, Buff E, Maeder PP, Stupp R, Meuli RA: Perfusion and diffusion MRI of glioblastoma progression in a four-year prospective temozolomide clinical trial. Int J Radiat Oncol Biol Phys; 2006 Mar 1;64(3):869-75
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  • [Title] Perfusion and diffusion MRI of glioblastoma progression in a four-year prospective temozolomide clinical trial.
  • PURPOSE: This study was performed to determine the impact of perfusion and diffusion magnetic resonance imaging (MRI) sequences on patients during treatment of newly diagnosed glioblastoma.
  • Special emphasis has been given to these imaging technologies as tools to potentially anticipate disease progression, as progression-free survival is frequently used as a surrogate endpoint.
  • Classical criteria on tumor size variation and clinical parameters were used to set disease progression date.
  • At disease progression (32 patients), a multivariate Cox regression determined 2 significant survival parameters: T1 largest diameter (p < 0.02) and T2 size variation (p < 0.05), whereas perfusion and diffusion were not significant.
  • CONCLUSION: Perfusion and diffusion techniques cannot be used to anticipate tumor progression.
  • Decision making at disease progression is critical, and classical T1 and T2 imaging remain the gold standard.
  • [MeSH-major] Brain Neoplasms / pathology. Disease Progression. Glioblastoma / pathology. Magnetic Resonance Imaging / methods

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  • (PMID = 16226399.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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65. 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.
  • For example, in neurologically intact patients < or = 40 years of age with WHO Grade I-III tumors, good outcomes (Karnofsky Performance Scale Score 80-100) were seen in 91% of cases.
  • Predictors of an unfavorable functional outcome included histological features of glioblastoma, advanced age, and a low preoperative Karnofsky Performance Scale score.
  • 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%.
  • Independent predictors of survival included younger age, favorable histological features (WHO Grade I and oligodendroglial tumors), Yaşargil Type 5A/B tumors with frontal extensions, and more extensive resections.
  • 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.
  • Patients with glioblastomas and/or age > 60 years require a more cautious approach.
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Astrocytoma / surgery. Child. Female. Humans. Male. Middle Aged. Postoperative Complications. Survival Rate. Treatment Outcome

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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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66. Calli C, Kitis O, Yunten N, Yurtseven T, Islekel S, Akalin T: Perfusion and diffusion MR imaging in enhancing malignant cerebral tumors. Eur J Radiol; 2006 Jun;58(3):394-403
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  • OBJECTIVE: Common contrast-enhancing malignant tumors of the brain are glioblastoma multiforme (GBMs), anaplastic astrocytomas (AAs), metastases, and lymphomas, all of which have sometimes similar conventional MRI findings.
  • MATERIALS AND METHODS: Forty-eight patients with contrast-enhancing and histologically proven brain tumors, 14 AAs, 17 GBMs, nine metastases, and eight lymphomas, were included in the study.
  • Minimum ADC values (ADC(min)) of each tumor was later calculated from ADC map images.
  • PWI was applied using dynamic susceptibility contrast technique and maximum relative cerebral blood volume (rCBV(max)) was calculated from each tumor, given in ratio with contralateral normal white matter.
  • RESULTS: The ADC(min) values (mean+/-S.D.) in GBMs, AAs, lymphomas, and metastases were 0.79+/-0.21 (x10(-3)mm(2)/s), 0.75+/-0.21 (x10(-3)mm(2)/s), 0.51+/-0.09 (x10(-3)mm(2)/s), and 0.68+/-0.11 (x10(-3)mm(2)/s), respectively.
  • The difference in ADC(min) values were statistically significant between lymphomas and GBMs (P<0.05).
  • However, there were no differences between lymphomas and metastasis, and between GBMs, AAs, and metastasis.
  • The rCBV(max) ratio (mean+/-S.D.) in GBMs were 6.33+/-2.03, whereas it was 3.66+/-1.79 in AAs, 2.33+/-0.68 in lymphomas, and 4.45+/-1.87 in metastases.
  • These values were statistically different between GBMs and AAs (P<0.001), GBMs and lymphoma (P<0.0001).
  • Although there seemed to be difference between GBMs and metastases, it was not statistically significant (P<0.083).
  • [MeSH-major] Astrocytoma / diagnosis. Brain Neoplasms / diagnosis. Diffusion Magnetic Resonance Imaging / methods. Glioblastoma / diagnosis. Image Enhancement / methods. Lymphoma / diagnosis. Magnetic Resonance Angiography / methods

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  • (PMID = 16527438.001).
  • [ISSN] 0720-048X
  • [Journal-full-title] European journal of radiology
  • [ISO-abbreviation] Eur J Radiol
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Contrast Media
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67. Shirahata M, Oba S, Iwao-Koizumi K, Saito S, Ueno N, Oda M, Hashimoto N, Ishii S, Takahashi JA, Kato K: Using gene expression profiling to identify a prognostic molecular spectrum in gliomas. Cancer Sci; 2009 Jan;100(1):165-72
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  • Histopathological classification of gliomas is often clinically inadequate due to the diversity of tumors that fall within the same class.
  • The expression levels of these genes in 152 gliomas (100 glioblastomas, 21 anaplastic astrocytomas, 19 diffuse astrocytomas, and 12 anaplastic oligodendrogliomas) were measured using adapter-tagged competitive polymerase chain reaction, a high-throughput reverse transcription-polymerase chain reaction technique.
  • The gene expression data matrix was significantly correlated with the histological grades, oligo-astro histology, and prognosis.
  • Using 110 gliomas, we constructed a prediction model based on the expression profile of 58 genes, resulting in a scheme that reliably classified the glioblastomas into two distinct prognostic subgroups.
  • Multivariate Cox analysis of the glioblastoma patients using other clinical prognostic factors, including age and the extent of surgical resection, indicated that the gene expression profile was a strong and independent prognostic parameter.
  • The gene expression profiling identified clinically informative prognostic molecular features in astrocytic and oligodendroglial tumors that were more reliable than the traditional histological classification scheme.

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  • (PMID = 19038000.001).
  • [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
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68. Ren Y, Kang CS, Yuan XB, Zhou X, Xu P, Han L, Wang GX, Jia Z, Zhong Y, Yu S, Sheng J, Pu PY: Co-delivery of as-miR-21 and 5-FU by poly(amidoamine) dendrimer attenuates human glioma cell growth in vitro. J Biomater Sci Polym Ed; 2010;21(3):303-14
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  • Down-regulation of miR-21 in glioblastoma cells leads to repression of cell growth, increased cellular apoptosis and cell-cycle arrest, which can theoretically enhance the chemotherapeutic effect in cancer therapy.
  • In this study, the poly(amidoamine) (PAMAM) dendrimer was employed as a carrier to co-deliver antisense-miR-21 oligonucleotide (as-miR-21) and 5-fluorouracil (5-FU) to achieve delivery of as-miR-21 to human glioblastoma cells and enhance the cytotoxicity of 5-FU antisense therapy.
  • Both the chemotherapeutant and as-miR-21 could be efficiently introduced into tumor cells.
  • The co-delivery of as-miR-21 significantly improved the cytotoxicity of 5-FU and dramatically increased the apoptosis of U251 cells, while the migration ability of the tumor cells was decreased.
  • These results suggest that our co-delivery system may have important clinical applications in the treatment of miR-21-overexpressing glioblastoma.
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Cell Movement / drug effects. Gene Expression Regulation, Neoplastic. Humans. Transfection

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  • (PMID = 20178687.001).
  • [ISSN] 1568-5624
  • [Journal-full-title] Journal of biomaterials science. Polymer edition
  • [ISO-abbreviation] J Biomater Sci Polym Ed
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Dendrimers; 0 / MIRN21 microRNA, human; 0 / MicroRNAs; 0 / PAMAM Starburst; U3P01618RT / Fluorouracil
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69. Kawamoto K, Li Q, Azuma K, Ryu T, Sakurai Y: [Brain glioblastoma and astrocytoma]. Nihon Rinsho; 2005 Sep;63 Suppl 9:105-9
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  • [Title] [Brain glioblastoma and astrocytoma].
  • [MeSH-minor] Biomarkers, Tumor / analysis. Cyclins. Genes, Tumor Suppressor. Humans. Immunohistochemistry. Intraoperative Period. Ki-67 Antigen / analysis. Laser Scanning Cytometry. Neoplasm Staging. Retinoblastoma-Like Protein p130 / analysis. Tumor Suppressor Protein p53

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  • (PMID = 16201508.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cyclins; 0 / Ki-67 Antigen; 0 / Retinoblastoma-Like Protein p130; 0 / Tumor Suppressor Protein p53
  • [Number-of-references] 14
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70. Sanli AM, Turkoglu E, Dolgun H, Sekerci Z: Unusual manifestations of primary Glioblastoma Multiforme: A report of three cases. Surg Neurol Int; 2010;1:87
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  • [Title] Unusual manifestations of primary Glioblastoma Multiforme: A report of three cases.
  • BACKGROUND: Brain tumors, especially high-grade gliomas, can present with focal or generalized signs due to mass effect, parenchymal infiltration and destruction.
  • Microscopic total tumor excision was done and histopathological analysis revealed that these tumors were glioblastoma multiforme.

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  • [Language] eng
  • [Publication-type] Journal Article
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  • [Other-IDs] NLM/ PMC3011111
  • [Keywords] NOTNLM ; Astrocytoma / brain tumor / glioblastoma multiforme / presentation / symptom
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71. Port RE, Bernstein LJ, Barboriak DP, Xu L, Roberts TP, van Bruggen N: Noncompartmental kinetic analysis of DCE-MRI data from malignant tumors: Application to glioblastoma treated with bevacizumab. Magn Reson Med; 2010 Aug;64(2):408-17
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  • [Title] Noncompartmental kinetic analysis of DCE-MRI data from malignant tumors: Application to glioblastoma treated with bevacizumab.
  • Dynamic contrast enhanced MRI contrast agent kinetics in malignant tumors are typically complex, requiring multicompartment tumor models for adequate description.
  • For consistent comparisons among tumors or among successive studies of the same tumor, we propose to estimate the total contrast agent-accessible volume fraction of tumor, including blood plasma, v(pe), and an average transfer rate constant across all tumor compartments, K(trans.av), by fitting a three-compartment tumor model and then calculating the area under the tumor impulse-response function (= v(pe)) and the ratio area under the tumor impulse response function over mean residence time in tumor (= K(trans.av)).
  • If the duration of dynamic contrast enhanced MRI was too short to extrapolate the tumor impulse-response function to infinity with any confidence, then conditional parameters v(pe)(*) and K(trans.av*) should be calculated from the available incomplete impulse response function.
  • Median decreases of 33% were found for both v(pe)(*) and K(trans.av*) in glioblastoma patients (n = 16) 24 hours after the administration of bevacizumab (P < 0.001).
  • Median total contrast-enhancing tumor volume was reduced by 18% (P < 0.0001).
  • The combined changes of tumor volume, v(pe)(*), and K(trans.av*) suggest a reduction of true v(pe), possibly accompanied by a reduction of true K(trans.av).
  • The proposed method provides estimates of a scale and a shape parameter to describe contrast agent kinetics of varying complexity in a uniform way.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Brain Neoplasms / metabolism. Diffusion Magnetic Resonance Imaging / methods. Gadolinium DTPA / pharmacokinetics. Glioblastoma / drug therapy. Glioblastoma / metabolism

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  • (PMID = 20665785.001).
  • [ISSN] 1522-2594
  • [Journal-full-title] Magnetic resonance in medicine
  • [ISO-abbreviation] Magn Reson Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Contrast Media; 2S9ZZM9Q9V / Bevacizumab; K2I13DR72L / Gadolinium DTPA
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72. Lefranc F, Facchini V, Kiss R: Proautophagic drugs: a novel means to combat apoptosis-resistant cancers, with a special emphasis on glioblastomas. Oncologist; 2007 Dec;12(12):1395-403
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  • [Title] Proautophagic drugs: a novel means to combat apoptosis-resistant cancers, with a special emphasis on glioblastomas.
  • The therapeutic goal of cancer treatment has been to trigger tumor-selective cell death.
  • Although cell death can be achieved not only by apoptosis (type I programmed cell death) but also by necrosis, mitotic catastrophe, and autophagy, drugs inducing apoptosis remain the main chemotherapeutic agents in medical oncology.
  • The most striking evidence for proautophagic chemotherapy to overcome apoptosis resistance in cancer cells comes from the use of temozolomide, a proautophagic cytotoxic drug, which has demonstrated real therapeutic benefits in glioblastoma patients and is in clinical trials for several types of apoptosis-resistant cancers.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Autophagy. Glioblastoma / drug therapy. Neoplasms / drug therapy
  • [MeSH-minor] Apoptosis / drug effects. Dacarbazine / analogs & derivatives. Dacarbazine / pharmacology. Dacarbazine / therapeutic use. Drug Delivery Systems. Drug Resistance, Neoplasm / drug effects. Humans


73. Koyama A, Yamagata K, Makino H, Arimura Y, Wada T, Nitta K, Nihei H, Muso E, Taguma Y, Shigematsu H, Sakai H, Tomino Y, Matsuo S, Japan RPGN Registry Group: A nationwide survey of rapidly progressive glomerulonephritis in Japan: etiology, prognosis and treatment diversity. Clin Exp Nephrol; 2009 Dec;13(6):633-50
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  • RESULT: The most frequent primary disease was renal-limited vasculitis (RLV) (42.1%); the second was microscopic polyangiitis (MPA) (19.4%); the third was anti-GBM-associated RPGN (6.1%).
  • The proportion of primary renal diseases of RPGN was constant during those periods.

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  • [Cites] Nephron Clin Pract. 2004;97(4):c142-6 [15331937.001]
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  • (PMID = 19533266.001).
  • [ISSN] 1437-7799
  • [Journal-full-title] Clinical and experimental nephrology
  • [ISO-abbreviation] Clin. Exp. Nephrol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 9PHQ9Y1OLM / Prednisolone; AYI8EX34EU / Creatinine
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74. Rueger MA, Winkeler A, Miletic H, Kaestle C, Richter R, Schneider G, Hilker R, Heneka MT, Ernestus RI, Hampl JA, Fraefel C, Jacobs AH: Variability in infectivity of primary cell cultures of human brain tumors with HSV-1 amplicon vectors. Gene Ther; 2005 Apr;12(7):588-96
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  • We investigated the variability in infectivity of cells in primary brain tumor samples from different patients using an HSV-1 amplicon vector.
  • We studied the infectivity of HSV-1 amplicon vectors in tumor samples derived from neurosurgical resections of 20 patients.
  • Transduction efficiency in primary tumor cell cultures was compared to an established human glioma line.
  • Moreover, duration of transgene expression was monitored in different tumor cell types.
  • Transduction efficiency was significantly greater in anaplastic gliomas and meningiomas (26.7+/-17.4%) compared to more malignant tumor types (glioblastomas, metastases; 11.2+/-8.5%; P=0.05).
  • The tumor cells expressed the exogenous gene for 7 to 61 days with significant shorter expression in glioblastomas (18+/-13 d) compared to anaplastic gliomas (42+/-24 d; P<0.05).
  • Interindividual variability of infectivity by HSV-1 virions might explain, at least in part, why some patients enrolled in gene therapy for glioblastoma in the past exhibited a sustained response to HSV-1-based gene- and virus therapy.
  • Infectivity of primary tumor samples from respective patients should be tested to enable the development of efficient and safe herpes vector-based gene and virus therapy for clinical application.
  • [MeSH-minor] Cell Adhesion Molecules / metabolism. Cell Proliferation. Gene Expression. Humans. Neoplasm Proteins / metabolism. Receptors, Virus / metabolism. Time Factors. Transduction, Genetic. Tumor Cells, Cultured

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  • (PMID = 15674397.001).
  • [ISSN] 0969-7128
  • [Journal-full-title] Gene therapy
  • [ISO-abbreviation] Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Neoplasm Proteins; 0 / Receptors, Virus; 0 / nectins
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75. Henze AT, Riedel J, Diem T, Wenner J, Flamme I, Pouyseggur J, Plate KH, Acker T: Prolyl hydroxylases 2 and 3 act in gliomas as protective negative feedback regulators of hypoxia-inducible factors. Cancer Res; 2010 Jan 1;70(1):357-66
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  • In glioblastomas, PHD2 and PHD3 are hypoxia-inducible in vitro and expressed in hypoxic areas of tumors in vivo.
  • This negative feedback loop protected tumor cells against hypoxia-induced cell death, functionally implicating this pathway in the control of the tumor-suppressive components of the HIF system in glioblastoma.
  • Moreover, PHD inhibition facilitated cell death induction by staurosporine or tumor necrosis factor-related apoptosis-inducing ligand, hinting at a more general protective role of PHD in the regulation of cell viability.
  • In summary, our findings recognize the PHD/HIF regulatory axis as a novel therapeutic target to disable a tumor's ability to adjust to hypoxic conditions and control cell survival, helping to potentially overcome therapeutic cell death resistance in glioblastomas.
  • [MeSH-minor] Blotting, Western. Cell Hypoxia / physiology. Cell Line, Tumor. Feedback, Physiological / physiology. Gene Expression. Gene Expression Regulation, Neoplastic. Humans. Hypoxia-Inducible Factor-Proline Dioxygenases. Immunohistochemistry. In Situ Hybridization, Fluorescence. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 20028863.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / endothelial PAS domain-containing protein 1; EC 1.13.11.- / Dioxygenases; EC 1.14.11.2 / EGLN1 protein, human; EC 1.14.11.2 / Procollagen-Proline Dioxygenase; EC 1.14.11.29 / EGLN3 protein, human; EC 1.14.11.29 / Hypoxia-Inducible Factor-Proline Dioxygenases
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76. Bhat KP, Pelloski CE, Zhang Y, Kim SH, deLaCruz C, Rehli M, Aldape KD: Selective repression of YKL-40 by NF-kappaB in glioma cell lines involves recruitment of histone deacetylase-1 and -2. FEBS Lett; 2008 Sep 22;582(21-22):3193-200
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  • Here we show that in contrast to other cancer types, tumor necrosis factor (TNF)-alpha suppresses YKL-40 expression in glioma cell lines in a nuclear factor kappaB (NF-kappaB) dependent manner.
  • Importantly, using chromatin immunoprecipitation assays in frozen glioblastoma multiforme tissues, we show that YKL-40 levels decrease consistent with HDAC1 recruitment despite high levels of nuclear p-p65.
  • [MeSH-minor] Acetylation. Adipokines. Cell Line, Tumor. Chromatin Immunoprecipitation. Down-Regulation. Histone Deacetylase 1. Histone Deacetylase 2. Histones / metabolism. Humans. Lectins. NF-kappa B p50 Subunit / metabolism. Promoter Regions, Genetic. Transcription Factor RelA / metabolism. Tumor Necrosis Factor-alpha / pharmacology. Tumor Necrosis Factor-alpha / physiology

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  • (PMID = 18708058.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adipokines; 0 / CHI3L1 protein, human; 0 / Glycoproteins; 0 / Histones; 0 / Lectins; 0 / NF-kappa B; 0 / NF-kappa B p50 Subunit; 0 / Repressor Proteins; 0 / Transcription Factor RelA; 0 / Tumor Necrosis Factor-alpha; EC 3.5.1.98 / HDAC1 protein, human; EC 3.5.1.98 / Histone Deacetylase 1; EC 3.5.1.98 / Histone Deacetylase 2; EC 3.5.1.98 / Histone Deacetylases
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77. Zhang PL, Yahya TM, Prichard JW, Shaw JH 4th, Hartle JE, Lin F, Schwartzman MS: Case report: IgM type of membranous glomerulopathy in a diabetic patient. Ann Clin Lab Sci; 2005;35(2):184-8
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  • We report the case of a 46-yr-old man with a 16-yr history of type I diabetes mellitus who developed rapid onset of nephrotic syndrome.
  • Renal biopsy revealed diabetic nephropathy, characterized by thickened glomerular basement membranes (GBM), mild nodular glomerulosclerosis, and focal arteriolar hyalinization.

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  • (PMID = 15943183.001).
  • [ISSN] 0091-7370
  • [Journal-full-title] Annals of clinical and laboratory science
  • [ISO-abbreviation] Ann. Clin. Lab. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin M
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78. Galloway M: CD34 expression in glioblastoma and giant cell glioblastoma. Clin Neuropathol; 2010 Mar-Apr;29(2):89-93
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  • [Title] CD34 expression in glioblastoma and giant cell glioblastoma.
  • OBJECTIVE: This study aimed to determine whether CD34 is expressed in glioblastomas and giant cell glioblastomas, as this information may be of value when attempting to differentiate between giant cell glioblastomas and other relevant differential diagnoses such as pleomorphic xanthoastrocytomas with anaplastic features and anaplastic gangliogliomas.
  • MATERIAL: 11 giant cell glioblastomas and 16 non-giant cell glioblastomas were assessed with immunocytochemical staining for CD34.
  • RESULTS: 73% of giant cell glioblastomas showed some degree of staining for CD34, and 55% showed strong widespread staining.
  • 56% of non-giant cell glioblastomas showed some degree of CD34 staining, and 25% showed strong widespread staining.
  • CONCLUSIONS: Both giant cell and non-giant cell glioblastomas frequently show CD34 expression by neoplastic cells, which may in some cases be strong and diffuse.
  • Strong widespread staining of neoplastic cells for CD34 was more frequent in giant cell than non-giant cell glioblastomas, however this difference was not statistically significant.
  • CD34 staining in isolation is unlikely to be of assistance in differentiating between giant cell glioblastoma and pleomorphic xanthoastrocytomas with anaplastic features or anaplastic gangliogliomas.
  • [MeSH-major] Antigens, CD34 / biosynthesis. Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Brain Neoplasms / pathology
  • [MeSH-minor] Astrocytoma / pathology. Diagnosis, Differential. Ganglioglioma / pathology. Glioblastoma / metabolism. Glioblastoma / pathology. Humans

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  • (PMID = 20175958.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Biomarkers, Tumor
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79. Taphoorn MJ, Stupp R, Coens C, Osoba D, Kortmann R, van den Bent MJ, Mason W, Mirimanoff RO, Baumert BG, Eisenhauer E, Forsyth P, Bottomley A, European Organisation for Research and Treatment of Cancer Brain Tumour Group, EORTC Radiotherapy Group, National Cancer Institute of Canada Clinical Trials Group: Health-related quality of life in patients with glioblastoma: a randomised controlled trial. Lancet Oncol; 2005 Dec;6(12):937-44
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  • [Title] Health-related quality of life in patients with glioblastoma: a randomised controlled trial.
  • BACKGROUND: A randomised controlled trial of radiotherapy alone versus radiotherapy with concomitant and adjuvant temozolomide for patients with glioblastoma showed that survival was higher for patients assigned combination treatment compared with those assigned standard radiotherapy alone.
  • METHODS: 573 patients with newly diagnosed glioblastoma were randomly allocated either radiotherapy alone or radiotherapy and temozolomide.
  • INTERPRETATION: Addition of temozolomide during and after radiotherapy for patients with newly diagnosed glioblastoma significantly improved survival without a negative effect on HRQOL.


80. Arvanitis DL, Arvanitis LD, Panourias IG, Kitsoulis P, Kanavaros P: The expression of the epitope H recognized by the monoclonal antibody H is higher in astrocytomas compared to anaplastic astrocytomas and glioblastomas. Histol Histopathol; 2005 10;20(4):1057-63
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  • [Title] The expression of the epitope H recognized by the monoclonal antibody H is higher in astrocytomas compared to anaplastic astrocytomas and glioblastomas.
  • In the present study we used the mAbH to investigate the immunohistochemical expression of the epitope H in 41 cases of astrocytic tumors including 19 cases of astrocytomas, 8 cases of anaplastic astrocytomas and 14 cases of glioblastomas.
  • Seven out of 19 cases (37%) of astrocytomas showed weak staining, 10 cases (53%) moderate staining and 2 cases (10%) intense staining.
  • Two out of 8 cases (25%) of anaplastic astrocytomas appeared negative, 3 cases (37.5%) showed weak staining and 3 cases (37.5%) moderate staining.
  • Four out of 14 cases (28.5) of glioblastomas appeared negative, 7 cases (50%) showed weak staining, 2 cases (14%) showed moderate staining and only one case (7.5%) showed intense staining.
  • There was a statistically significant elevation of the expression of the epitope H in astrocytomas compared to anaplastic astrocytomas and glioblastomas (p=0.047).
  • These results indicate that the expression of the epitope H decreases in parallel with the increase of the grade of astrocytic tumors from low to higher grade neoplasms.
  • This could be of interest for predicting the progression of an astrocytic tumor since it is documented that astrocytomas progress to tumors of higher grade of malignancy.
  • Further investigation of the antigens bearing the epitope H might help to gain further insight into the mechanisms which regulate the progression of astrocytic tumors and to examine the relevance of the mAbH staining with respect to the prognosis of these neoplasms.
  • [MeSH-major] Antibodies, Monoclonal / metabolism. Astrocytoma / immunology. Epitopes / biosynthesis. Glioblastoma / immunology

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  • (PMID = 16136487.001).
  • [ISSN] 0213-3911
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Epitopes; 0 / Glial Fibrillary Acidic Protein
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81. Reardon DA, Desjardins A, Vredenburgh JJ, Gururangan S, Friedman AH, Herndon JE 2nd, Marcello J, Norfleet JA, McLendon RE, Sampson JH, Friedman HS: Phase 2 trial of erlotinib plus sirolimus in adults with recurrent glioblastoma. J Neurooncol; 2010 Jan;96(2):219-30
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  • [Title] Phase 2 trial of erlotinib plus sirolimus in adults with recurrent glioblastoma.
  • We evaluated the anti-tumor activity and safety of erlotinib, a receptor tyrosine kinase inhibitor of the epidermal growth factor receptor, plus sirolimus, an inhibitor of the mammalian target of rapamycin, among patients with recurrent glioblastoma (GBM) in a phase 2, open-label, single-arm trial.
  • Archival tumor samples were assessed for EGFR, EGFRvIII, PTEN, pAKT and pS6.
  • The most common grade > or = 2 adverse events were rash (59%), mucositis (34%) and diarrhea (31%).
  • Grade 3 or higher events were rare.
  • Best radiographic response included stable disease in 15 patients (47%); no patients achieved either a CR or PR.
  • Tumor markers failed to show an association with PFS except for increased pAKT expression which achieved borderline significance (P = 0.045).
  • Erlotinib plus sirolimus was well tolerated but had negligible activity among unselected recurrent GBM patients. (ClinicalTrials.gov number: NCT0062243).

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  • (PMID = 19562254.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] ENG
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00672243
  • [Grant] United States / NINDS NIH HHS / NS / NS20023; United States / NINDS NIH HHS / NS / P50 NS020023; United States / NINDS NIH HHS / NS / NS020023-268626; United States / NINDS NIH HHS / NS / NS020023-240020; United States / NINDS NIH HHS / NS / NS020023-220020; United States / NINDS NIH HHS / NS / NS020023-250020; United States / NINDS NIH HHS / NS / P50 NS020023-210020; United States / NINDS NIH HHS / NS / P50 NS020023-230020; United States / NCI NIH HHS / CA / CA11898; United States / NINDS NIH HHS / NS / P50 NS020023-240020; United States / NCI NIH HHS / CA / P20 CA096890; United States / NINDS NIH HHS / NS / P50 NS020023-268626; United States / NCI NIH HHS / CA / CA096890-019003; United States / NINDS NIH HHS / NS / P50 NS020023-220020; United States / NCRR NIH HHS / RR / MO1 RR 30; United States / NINDS NIH HHS / NS / P50 NS020023-250020; United States / NCI NIH HHS / CA / P20 CA096890-019003; United States / NCI NIH HHS / CA / R37 CA011898; United States / NINDS NIH HHS / NS / NS020023-210020; United States / NINDS NIH HHS / NS / NS020023-230020; United States / NCI NIH HHS / CA / 1 P20 CA096890
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Biomarkers, Tumor; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ NIHMS180484; NLM/ PMC2844073
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82. Moyal EC, Laprie A, Delannes M, Poublanc M, Catalaa I, Dalenc F, Berchery D, Sabatier J, Bousquet P, De Porre P, Alaux B, Toulas C: Phase I trial of tipifarnib (R115777) concurrent with radiotherapy in patients with glioblastoma multiforme. Int J Radiat Oncol Biol Phys; 2007 Aug 1;68(5):1396-401
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial of tipifarnib (R115777) concurrent with radiotherapy in patients with glioblastoma multiforme.
  • PURPOSE: To conduct a Phase I trial to determine the maximally tolerated dose (MTD) of tipifarnib in combination with conventional three-dimensional conformal radiotherapy (RT) for patients with glioblastoma multiforme.
  • Of the 9 evaluable patients, 1 had partial response, 4 had stable disease, and 3 had rapid progression; the patient with gross total resection was relapse-free after 21 months.
  • CONCLUSION: Tipifarnib (200 mg/day) concurrent with standard radiotherapy is well tolerated in patients with glioblastoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Quinolones / therapeutic use. Radiotherapy, Conformal

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  • (PMID = 17570606.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinolones; 192185-72-1 / tipifarnib
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83. Chiba Y, Hashimoto N, Tsuboi A, Rabo C, Oka Y, Kinoshita M, Kagawa N, Oji Y, Sugiyama H, Yoshimine T: Prognostic value of WT1 protein expression level and MIB-1 staining index as predictor of response to WT1 immunotherapy in glioblastoma patients. Brain Tumor Pathol; 2010 Apr;27(1):29-34
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  • [Title] Prognostic value of WT1 protein expression level and MIB-1 staining index as predictor of response to WT1 immunotherapy in glioblastoma patients.
  • The use of Wilms' tumor 1 (WT1) immunotherapy is considered to be an innovative approach for the treatment of malignant gliomas.
  • In this article, we investigated the role of WT1 protein expression level (score 1-4) and MIB-1 staining index in predicting survival outcome after therapy in patients with recurrent or progressive glioblastoma multiforme.
  • Tumor samples from 37 patients enrolled in a phase II clinical trial on WT1 immunotherapy were immunohistochemically analyzed for WT1 levels and MIB-1 index.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / diagnosis. Brain Neoplasms / therapy. Glioblastoma / diagnosis. Glioblastoma / therapy. Immunotherapy. Ki-67 Antigen / analysis. Staining and Labeling. WT1 Proteins / administration & dosage. WT1 Proteins / analysis

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  • (PMID = 20425045.001).
  • [ISSN] 1861-387X
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / WT1 Proteins
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84. Gopalakrishna-Pillai S, Iverson LE: Astrocytes derived from trisomic human embryonic stem cells express markers of astrocytic cancer cells and premalignant stem-like progenitors. BMC Med Genomics; 2010 Apr 27;3:12
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  • [Title] Astrocytes derived from trisomic human embryonic stem cells express markers of astrocytic cancer cells and premalignant stem-like progenitors.
  • METHODS: Diploid and trisomic hESCs were differentiated into astrocytic progenitors cells (APCs), RNA extracted and hybridized to human exon-specific microarrays.
  • Global gene expression profiles of diploid and trisomic APCs were compared to that of an astrocytoma cell line and glioblastoma samples, analyzed by others, using the same microarray platform.
  • RESULTS: Bioinformatic analysis of microarray data indicates that differentiated trisomic APCs exhibit global expression profiles with similarities to the malignant astrocytoma cell line.
  • An analogous trend is observed in comparison to glioblastoma samples indicating that trisomic APCs express markers of astrocytic cancer cells.
  • The analysis also allowed identification of transcripts predicted to be differentially expressed in brain tumor stem cells.
  • These data indicate that in vitro differentiation of trisomic hESCs along astrocytic pathways give rise to cells exhibiting properties of premalignant astrocytic stem/progenitor cells.

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  • (PMID = 20423517.001).
  • [ISSN] 1755-8794
  • [Journal-full-title] BMC medical genomics
  • [ISO-abbreviation] BMC Med Genomics
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 5P30CA033572
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Other-IDs] NLM/ PMC2873256
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85. Carson-Walter EB, Hampton J, Shue E, Geynisman DM, Pillai PK, Sathanoori R, Madden SL, Hamilton RL, Walter KA: Plasmalemmal vesicle associated protein-1 is a novel marker implicated in brain tumor angiogenesis. Clin Cancer Res; 2005 Nov 1;11(21):7643-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Plasmalemmal vesicle associated protein-1 is a novel marker implicated in brain tumor angiogenesis.
  • PURPOSE: Plasmalemmal vesicle associated protein-1 (PV-1) is up-regulated in the endothelium of human glioblastoma.
  • We sought to further characterize the expression pattern of PV-1 in human brain tumors and interrogate its role in brain tumor angiogenesis.
  • RESULTS: PV-1 is selectively up-regulated in a variety of high-grade human brain tumors, including glioblastoma and metastatic carcinoma, as well as other cerebral disorders associated with blood-brain barrier disruption, such as acute ischemia.
  • Expression levels were reduced in low-grade neoplasia; however, tumors associated with the ependyma and choroid plexus, known sites of PV-1 expression, also exhibited robust expression.
  • PV-1 expression was induced in HMVEC cells in vitro by exposure to medium conditioned by U87MG and U251MG human brain tumor cell lines and by medium supplemented with exogenous vascular endothelial growth factor or scatter factor/hepatocyte growth factor.
  • CONCLUSIONS: Our results confirm that PV-1 is preferentially induced in the endothelium of high-grade human brain tumors.
  • PV-1 represents a novel marker of brain tumor angiogenesis and integrity of the blood-brain barrier and is a potential therapeutic target.
  • [MeSH-major] Biomarkers, Tumor. Brain Neoplasms / pathology. Carrier Proteins / biosynthesis. Gene Expression Regulation, Neoplastic. Membrane Proteins / biosynthesis. Neovascularization, Pathologic
  • [MeSH-minor] Blood-Brain Barrier. Blotting, Western. Cell Line, Tumor. Cell Movement. Cells, Cultured. Collagen / chemistry. Culture Media, Conditioned / pharmacology. Drug Combinations. Endothelium, Vascular / cytology. Endothelium, Vascular / pathology. Humans. In Situ Hybridization. Ischemia. Laminin / chemistry. Microcirculation. Neoplasm Metastasis. Proteoglycans / chemistry. RNA / metabolism. RNA Interference. RNA, Messenger / metabolism. RNA, Small Interfering / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic. Up-Regulation. Vascular Endothelial Growth Factor A / metabolism

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  • [CommentIn] Clin Cancer Res. 2006 Apr 15;12(8):2649; 2649-50 [16638883.001]
  • (PMID = 16278383.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / K08 NS046461
  • [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 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / Culture Media, Conditioned; 0 / Drug Combinations; 0 / Laminin; 0 / Membrane Proteins; 0 / PLVAP protein, human; 0 / Proteoglycans; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Vascular Endothelial Growth Factor A; 119978-18-6 / matrigel; 63231-63-0 / RNA; 9007-34-5 / Collagen
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86. Kitaura K, Asano K: [A case of anti-GBM-antibody positive rapidly progressive glomerulonephritis who was weaned from hemodialysis after combination therapy with steroid and plasmapheresis]. Nihon Jinzo Gakkai Shi; 2005;47(8):887-92
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  • [Title] [A case of anti-GBM-antibody positive rapidly progressive glomerulonephritis who was weaned from hemodialysis after combination therapy with steroid and plasmapheresis].
  • We report an anti-GBM antibody-positive crescentic glomerulonephritis patient who benefitted from maintenance hemodialysis 4 months after the initial treatment, which included steroid pulse therapy and plasma exchange.
  • No abnormal finding was observed in the lung and the nasopharyngeal region.
  • Although P-ANCA and C-ANCA were negative, anti-GBM antibody was proven to be positive thereafter (169 U) and six sessions of plasmapheresis were additionally performed to remove the antibody.
  • In conclusion, residual renal function might improve even after 4 months of hemodialysis in cases of intensively treated anti-GBM-positive crescentic glomerulonephritis, though consecutive renoprotective therapy is required.
  • [MeSH-major] Anti-Glomerular Basement Membrane Disease / therapy. Anti-Inflammatory Agents / administration & dosage. Plasmapheresis. Prednisolone / administration & dosage. Renal Dialysis