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51. Seltzer MJ, Bennett BD, Joshi AD, Gao P, Thomas AG, Ferraris DV, Tsukamoto T, Rojas CJ, Slusher BS, Rabinowitz JD, Dang CV, Riggins GJ: Inhibition of glutaminase preferentially slows growth of glioma cells with mutant IDH1. Cancer Res; 2010 Nov 15;70(22):8981-7
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  • Therefore, we inhibited glutaminase with siRNA or the small molecule inhibitor bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide (BPTES) and found slowed growth of glioblastoma cells expressing mutant IDH1 compared with those expressing wild-type IDH1.

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  • [Copyright] Copyright © 2010 AACR.
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  • (PMID = 21045145.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA057341-20; United States / NINDS NIH HHS / NS / R01 NS052507-04; United States / NINDS NIH HHS / NS / NS052507-04; United States / NCI NIH HHS / CA / R01 CA057341; United States / NCI NIH HHS / CA / R01CA57341; United States / NCI NIH HHS / CA / CA051497-17; United States / NINDS NIH HHS / NS / R01 NS052507; United States / NCI NIH HHS / CA / R01 CA051497; United States / NCI NIH HHS / CA / R37 CA051497-17; United States / NCI NIH HHS / CA / CA057341-20; United States / NINDS NIH HHS / NS / R01NS052507; United States / NCI NIH HHS / CA / R37 CA051497; United States / NCI NIH HHS / CA / R01CA051497
  • [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 / Glutarates; 0 / Ketoglutaric Acids; 0 / Sulfides; 0 / Thiadiazoles; 0 / bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide; 2889-31-8 / alpha-hydroxyglutarate; 328-50-7 / alpha-ketoglutaric acid; 3KX376GY7L / Glutamic Acid; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 3.5.1.2 / Glutaminase
  • [Other-IDs] NLM/ NIHMS240941; NLM/ PMC3058858
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52. Facoetti A, Pasi F, Nano R: Some considerations for the study of TGFbeta in medium of irradiated T98G cells: activation, release and consumption. Anticancer Res; 2010 Sep;30(9):3341-4
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  • AIM: To assess the influence that the presence of latent TGFβ in the medium may have on the modulation of TGFβ1 release and on its receptor (TGFβR2) expression after irradiation of glioblastoma cells or after treatment with medium collected from γ-irradiated cells.
  • [MeSH-major] Bystander Effect / radiation effects. Culture Media, Conditioned / radiation effects. Glioblastoma / metabolism. Transforming Growth Factor beta / metabolism
  • [MeSH-minor] Cell Line, Tumor. Enzyme-Linked Immunosorbent Assay. Gamma Rays. Humans. Immunohistochemistry

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  • (PMID = 20944106.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Transforming Growth Factor beta
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53. Ji H, Wang J, Nika H, Hawke D, Keezer S, Ge Q, Fang B, Fang X, Fang D, Litchfield DW, Aldape K, Lu Z: EGF-induced ERK activation promotes CK2-mediated disassociation of alpha-Catenin from beta-Catenin and transactivation of beta-Catenin. Mol Cell; 2009 Nov 25;36(4):547-59
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  • In addition, levels of alpha-catenin S641 phosphorylation correlate with levels of ERK1/2 activity in human glioblastoma specimens and with grades of glioma malignancy.
  • This EGFR-ERK-CK2-mediated phosphorylation of alpha-catenin promotes beta-catenin transactivation and tumor cell invasion.
  • These findings highlight the importance of the crosstalk between EGFR and Wnt pathways in tumor development.


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4. Tikhmyanova N, Little JL, Golemis EA: CAS proteins in normal and pathological cell growth control. Cell Mol Life Sci; 2010 Apr;67(7):1025-48
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  • Reflecting these complex functions, over-expression of CAS proteins has now been strongly linked to poor prognosis and increased metastasis in cancer, as well as resistance to first-line chemotherapeutics in multiple tumor types including breast and lung cancers, glioblastoma, and melanoma.
  • Further, CAS proteins have also been linked to additional pathological conditions including inflammatory disorders, Alzheimer's and Parkinson's disease, as well as developmental defects.

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  • (PMID = 19937461.001).
  • [ISSN] 1420-9071
  • [Journal-full-title] Cellular and molecular life sciences : CMLS
  • [ISO-abbreviation] Cell. Mol. Life Sci.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA06927; United States / NCI NIH HHS / CA / NIH R01 CA63366; United States / NCI NIH HHS / CA / T32 CA009035-34; United States / NCI NIH HHS / CA / CA063366-15; United States / NCI NIH HHS / CA / R01 CA113342-03; United States / NCI NIH HHS / CA / R01 CA063366; United States / NCI NIH HHS / CA / R01 CA113342; United States / NCI NIH HHS / CA / CA009035-34; United States / NCI NIH HHS / CA / R01 CA063366-15; United States / NCI NIH HHS / CA / P30 CA006927-38; United States / NCI NIH HHS / CA / CA113342-03; United States / NCI NIH HHS / CA / NIH T32 CA009035; United States / NCI NIH HHS / CA / P30 CA006927; United States / NCI NIH HHS / CA / CA006927-38; United States / NCI NIH HHS / CA / T32 CA009035
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / BCAR1 protein, human; 0 / Crk-Associated Substrate Protein; 0 / NEDD9 protein, human; 0 / Phosphoproteins
  • [Number-of-references] 248
  • [Other-IDs] NLM/ NIHMS164651; NLM/ PMC2836406
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55. Wiesner SM, Decker SA, Larson JD, Ericson K, Forster C, Gallardo JL, Long C, Demorest ZL, Zamora EA, Low WC, SantaCruz K, Largaespada DA, Ohlfest JR: De novo induction of genetically engineered brain tumors in mice using plasmid DNA. Cancer Res; 2009 Jan 15;69(2):431-9
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  • [Title] De novo induction of genetically engineered brain tumors in mice using plasmid DNA.
  • Spontaneous mouse models of cancer show promise to more accurately recapitulate human disease and predict clinical efficacy.
  • Transgenic mice or viral vectors have been required to generate spontaneous models of glioma, a lethal brain tumor, because nonviral gene transfer is typically transient.
  • The phenotype of tumors was influenced by the combination of oncogenes delivered, resembling human astrocytoma or glioblastoma in the majority of cases.
  • At least five different genes can be cotransfected simultaneously including reporters, allowing measurement of tumor viability by in vivo imaging.
  • This model can accelerate brain tumor research in a variety of ways such as generation of "humanized" models for high throughput drug screening and candidate gene validation with exceptional speed and flexibility.

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  • (PMID = 19147555.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R21 NS055738; United States / NINDS NIH HHS / NS / NS055738-01A2; United States / NCI NIH HHS / CA / R01CA113636-01A1; United States / NIDA NIH HHS / DA / T32 DA022616; United States / NINDS NIH HHS / NS / 1R21-NS055738-01A2; United States / NIDA NIH HHS / DA / T32DA022616; United States / NCI NIH HHS / CA / R01 CA160782; United States / NINDS NIH HHS / NS / R21 NS055738-01A2; United States / NCI NIH HHS / CA / R01 CA113636
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-98-6 / Polyethyleneimine; 9007-49-2 / DNA
  • [Other-IDs] NLM/ NIHMS79445; NLM/ PMC2701484
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56. Stupp R, Pica A, Mirimanoff RO, Michielin O: [A practical guide for the management of gliomas]. Bull Cancer; 2007 Sep;94(9):817-22
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  • Important progress has been made during the last years with the introduction of a combined treatment associating standard radiotherapy with concomitant chemotherapy using temozolomide, a novel alkylating agent.
  • In this "Practical Guide", we describe the daily practice and aim at answering some common questions in the management of patients suffering from glioblastoma, astrocytoma, oligodendroglioma and low grade glioma.
  • [MeSH-major] Central Nervous System Neoplasms / therapy. Disease Management. Glioma / therapy

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  • (PMID = 17878102.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 51
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57. Chen JH, Bian XW, Yao XH, Yang SX, Xu CR, Zhou XD, Ping YF: [Effect of nordy on FPR function of malignant human glioma cell line U87]. Yao Xue Xue Bao; 2007 Mar;42(3):257-62
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  • To investigate the effects of nordy (25 - 100 micromol x L(-1)) on the function of formylpeptide receptor (FPR) of malignant human glioma cells, human glioblastoma cell line U87 was used to detect its proliferation, migration, calcium mobilization, vascular endothelial growth factor (VEGF) mRNA and protein levels after activation of FPR by its agonist N-formyl-methionyl-leucyl-phenylalanine (fMLF).
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Calcium / metabolism. Cell Line, Tumor. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Glioblastoma / genetics. Glioblastoma / metabolism. Glioblastoma / pathology. Humans. N-Formylmethionine Leucyl-Phenylalanine / pharmacology. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Spectrophotometry / methods. Vascular Endothelial Growth Factor A / biosynthesis. Vascular Endothelial Growth Factor A / genetics

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  • (PMID = 17520823.001).
  • [ISSN] 0513-4870
  • [Journal-full-title] Yao xue xue bao = Acta pharmaceutica Sinica
  • [ISO-abbreviation] Yao Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Messenger; 0 / Receptors, Formyl Peptide; 0 / Vascular Endothelial Growth Factor A; 0 / nordy; 59880-97-6 / N-Formylmethionine Leucyl-Phenylalanine; 7BO8G1BYQU / Masoprocol; SY7Q814VUP / Calcium
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58. Bandyopadhyay S, Huang X, Cho H, Greig NH, Youdim MB, Rogers JT: Metal specificity of an iron-responsive element in Alzheimer's APP mRNA 5'untranslated region, tolerance of SH-SY5Y and H4 neural cells to desferrioxamine, clioquinol, VK-28, and a piperazine chelator. J Neural Transm Suppl; 2006;(71):237-47
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  • Desferrioxamine (high affinity Fe3+ chelator), (ii) clioquinol (low affinity Fe/Cu/Zn chelator), (iii) piperazine-1 (oral Fe chelator), (iv) VK-28 (oral Fe chelator), were tested for their relative modulation of APP 5' UTR directed translation of a luciferase reporter gene.
  • Iron chelation based therapeutic strategies for slowing the progression of Alzheimer's disease (and other neurological disorders that manifest iron imbalance) are discussed with regard to the relative neural toxic action of each chelator in SH-SY5Y cells and in H4 glioblastoma cells.
  • [MeSH-minor] Cell Line, Tumor. Clioquinol / pharmacology. Deferoxamine / pharmacology. Dose-Response Relationship, Drug. Glioblastoma. Humans. Models, Molecular. Neuroblastoma. Transfection / methods

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  • (PMID = 17447434.001).
  • [ISSN] 0303-6995
  • [Journal-full-title] Journal of neural transmission. Supplementum
  • [ISO-abbreviation] J. Neural Transm. Suppl.
  • [Language] eng
  • [Grant] United States / NIMH NIH HHS / MH / 5K01MH002001; United States / NIA NIH HHS / AG / AG18884; United States / NIA NIH HHS / AG / AG21081
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Iron Chelating Agents; 0 / Iron-Regulatory Proteins; 0 / RNA, Messenger; 0 / Untranslated Regions; 7BHQ856EJ5 / Clioquinol; J06Y7MXW4D / Deferoxamine
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59. Enam S, Gan DD, White MK, Del Valle L, Khalili K: Regulation of human neurotropic JCV in colon cancer cells. Anticancer Res; 2006 Mar-Apr;26(2A):833-41
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  • MATERIALS AND METHODS: Regulation of JCV was investigated in a human colon cancer cell line (SW480) and compared to a human glioblastoma cell line (U87-MG) that is permissive for JCV replication.
  • [MeSH-minor] Antigens, Viral, Tumor / genetics. Antigens, Viral, Tumor / metabolism. Antigens, Viral, Tumor / physiology. Cell Line, Tumor. DNA, Viral / genetics. DNA, Viral / metabolism. Glioblastoma / genetics. Glioblastoma / virology. Humans. Promoter Regions, Genetic. Signal Transduction. TCF Transcription Factors / genetics. TCF Transcription Factors / physiology. Transcription, Genetic. Transfection. Virus Replication. Wnt Proteins / genetics. Wnt Proteins / physiology

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  • (PMID = 16619477.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Viral, Tumor; 0 / DNA, Viral; 0 / TCF Transcription Factors; 0 / Wnt Proteins
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60. Yao CJ, Lai GM, Chan CF, Cheng AL, Yang YY, Chuang SE: Dramatic synergistic anticancer effect of clinically achievable doses of lovastatin and troglitazone. Int J Cancer; 2006 Feb 1;118(3):773-9
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  • This synergism was found in far majority of cell lines tested including DBTRG 05 MG (glioblastoma) and CL1-0 (lung).
  • [MeSH-minor] Brain Neoplasms / drug therapy. Brain Neoplasms / metabolism. Chromans / administration & dosage. Cyclin A / metabolism. Cyclin-Dependent Kinase 2 / metabolism. Cyclin-Dependent Kinase Inhibitor p27. Dose-Response Relationship, Drug. E2F1 Transcription Factor / metabolism. Glioblastoma / drug therapy. Glioblastoma / metabolism. HeLa Cells. Humans. Lovastatin / administration & dosage. Lung Neoplasms / drug therapy. Lung Neoplasms / metabolism. Male. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / metabolism. Phosphorylation / drug effects. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / metabolism. Retinoblastoma Protein / metabolism. Thiazolidinediones / administration & dosage. Tumor Cells, Cultured / drug effects

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16094629.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromans; 0 / Cyclin A; 0 / E2F1 Transcription Factor; 0 / E2F1 protein, human; 0 / Retinoblastoma Protein; 0 / Thiazolidinediones; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 9LHU78OQFD / Lovastatin; EC 2.7.11.22 / CDK2 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 2; I66ZZ0ZN0E / troglitazone
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61. Berger Y, Dehmlow H, Blum-Kaelin D, Kitas EA, Löffler BM, Aebi JD, Juillerat-Jeanneret L: Endothelin-converting enzyme-1 inhibition and growth of human glioblastoma cells. J Med Chem; 2005 Jan 27;48(2):483-98
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  • [Title] Endothelin-converting enzyme-1 inhibition and growth of human glioblastoma cells.
  • To evaluate this potential, we synthesized and characterized a series of low nanomolar nonpeptidic thiol-containing ECE-1 inhibitors, and evaluated their effect, as well as the effect of inhibitors for the related metalloproteases neprilysin (NEP; EC 3.4.24.11) and angiotensin-converting enzyme (ACE; EC 3.4.15.1), on human glioblastoma cell growth.
  • Only ECE-1 inhibitors inhibited DNA synthesis by human glioblastoma cells.
  • Exogenous addition of ET-1 or bigET-1 to glioblastoma cells did not counterbalance the growth inhibition elicited by ECE-1 inhibitors, suggesting that ECE-1 inhibitors block the proliferation of human glioblastoma cells most likely via a mechanism not involving extracellular production of ET-1.
  • [MeSH-minor] Carbamates / chemical synthesis. Carbamates / chemistry. Cell Line, Tumor. Cell Proliferation / drug effects. Central Nervous System Neoplasms. Drug Screening Assays, Antitumor. Endothelin-1 / pharmacology. Glioblastoma. Humans. Hydrazines / chemical synthesis. Hydrazines / chemistry. Metalloendopeptidases. Proline / analogs & derivatives. Proline / chemical synthesis. Proline / chemistry. Pyrimidines / chemical synthesis. Pyrimidines / chemistry. Pyrrolidines / chemical synthesis. Pyrrolidines / chemistry. Structure-Activity Relationship

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  • (PMID = 15658862.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbamates; 0 / Endothelin-1; 0 / Hydrazines; 0 / Pyrimidines; 0 / Pyrrolidines; 0 / Sulfhydryl Compounds; 9DLQ4CIU6V / Proline; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.24.- / Metalloendopeptidases; EC 3.4.24.71 / endothelin-converting enzyme
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62. Hegi ME, Liu L, Herman JG, Stupp R, Wick W, Weller M, Mehta MP, Gilbert MR: Correlation of O6-methylguanine methyltransferase (MGMT) promoter methylation with clinical outcomes in glioblastoma and clinical strategies to modulate MGMT activity. J Clin Oncol; 2008 Sep 1;26(25):4189-99
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  • [Title] Correlation of O6-methylguanine methyltransferase (MGMT) promoter methylation with clinical outcomes in glioblastoma and clinical strategies to modulate MGMT activity.
  • The relative expression of MGMT in the tumor may determine response to alkylating agents, and epigenetic silencing of the MGMT gene by promoter methylation plays an important role in regulating MGMT expression in gliomas.
  • Another strategy is to deplete MGMT activity in tumor tissue using a dose-dense temozolomide schedule.
  • These alternative schedules are well tolerated; however, it remains unclear whether they are more effective than the standard dosing regimen or whether they effectively deplete MGMT activity in tumor tissue.
  • Of note, not all patients with glioblastoma having MGMT promoter methylation respond to alkylating agents, and even those who respond will inevitably experience relapse.
  • [MeSH-major] Brain Neoplasms / genetics. DNA Methylation. Glioblastoma / genetics. Glioma / genetics. O(6)-Methylguanine-DNA Methyltransferase / genetics. Promoter Regions, Genetic
  • [MeSH-minor] Antineoplastic Agents, Alkylating / pharmacology. CpG Islands. Gene Silencing. Humans. Maximum Tolerated Dose. Medical Oncology / methods. Models, Chemical. RNA Interference. Treatment Outcome

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  • (PMID = 18757334.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
  • [Number-of-references] 86
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63. Shnaper S, Desbaillets I, Brown DA, Murat A, Migliavacca E, Schluep M, Ostermann S, Hamou MF, Stupp R, Breit SN, de Tribolet N, Hegi ME: Elevated levels of MIC-1/GDF15 in the cerebrospinal fluid of patients are associated with glioblastoma and worse outcome. Int J Cancer; 2009 Dec 1;125(11):2624-30
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  • [Title] Elevated levels of MIC-1/GDF15 in the cerebrospinal fluid of patients are associated with glioblastoma and worse outcome.
  • Determination of MIC-1/GDF15 protein levels by ELISA in the CSF of a cohort of 94 patients with intracranial tumors including gliomas, meningioma and metastasis revealed significantly increased concentrations in glioblastoma patients (median, 229 pg/ml) when compared with control cohort of patients treated for non-neoplastic diseases (median below limit of detection of 156 pg/ml, p < 0.0001, Mann-Whitney test).
  • Most interestingly, patients with glioblastoma and increased CSF MIC-1/GDF15 had a shorter survival (p = 0.007, log-rank test).
  • [MeSH-major] Biomarkers, Tumor / cerebrospinal fluid. Brain Neoplasms / cerebrospinal fluid. Glioblastoma / cerebrospinal fluid. Growth Differentiation Factor 15 / cerebrospinal fluid

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  • (PMID = 19521960.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / GDF15 protein, human; 0 / Growth Differentiation Factor 15; 0 / RNA, Messenger
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64. Courtenay-Quirk C, Pals SL, Colfax G, McKirnan D, Gooden L, Eroğlu D: Factors associated with sexual risk behavior among persons living with HIV: gender and sexual identity group differences. AIDS Behav; 2008 Sep;12(5):685-94
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  • Sexually active participants were categorized as gay or bisexual men (GBM) (n = 545), heterosexual men (HSM, n = 223), or women (n = 214).
  • SDUAV was associated with multiple (2 or more) partners, using poppers, and lower safer sex self-efficacy among GBM.
  • These findings are consistent with prior research and facilitate our ability to target those who may be most at risk for transmitting HIV among HIV-positive GBM.

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  • (PMID = 17592764.001).
  • [ISSN] 1573-3254
  • [Journal-full-title] AIDS and behavior
  • [ISO-abbreviation] AIDS Behav
  • [Language] eng
  • [Grant] United States / PHS HHS / / PA 01190
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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65. Le Mercier M, Mathieu V, Haibe-Kains B, Bontempi G, Mijatovic T, Decaestecker C, Kiss R, Lefranc F: Knocking down galectin 1 in human hs683 glioblastoma cells impairs both angiogenesis and endoplasmic reticulum stress responses. J Neuropathol Exp Neurol; 2008 May;67(5):456-69
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  • [Title] Knocking down galectin 1 in human hs683 glioblastoma cells impairs both angiogenesis and endoplasmic reticulum stress responses.
  • Galectin (Gal) 1 is a hypoxia-regulated proangiogenic factor that also directly participates in glioblastoma cell migration.
  • To determine how Gal-1 exerts its proangiogenic effects, we investigated Gal-1 signaling in the human Hs683 glioblastoma cell line.
  • These results suggest that decreasing Gal-1 expression (e.g. through brain delivery of nonviral infusions of anti-Gal-1 siRNA in patients) can represent an additional therapeutic strategy for glioblastoma.
  • [MeSH-major] Brain Neoplasms / genetics. Endoplasmic Reticulum / genetics. Galectin 1 / genetics. Glioblastoma / genetics. Neovascularization, Pathologic / genetics. Oxidative Stress / genetics. RNA Interference / physiology
  • [MeSH-minor] Animals. Antineoplastic Agents, Alkylating / pharmacology. Cell Line, Tumor. Dacarbazine / analogs & derivatives. Dacarbazine / pharmacology. Down-Regulation / drug effects. Down-Regulation / genetics. Endoribonucleases / drug effects. Endoribonucleases / genetics. Endoribonucleases / metabolism. Female. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / genetics. Gene Silencing / physiology. Genetic Therapy / methods. HSP40 Heat-Shock Proteins / drug effects. HSP40 Heat-Shock Proteins / genetics. HSP40 Heat-Shock Proteins / metabolism. HSP70 Heat-Shock Proteins. Humans. Membrane Proteins / drug effects. Membrane Proteins / genetics. Membrane Proteins / metabolism. Mice. Molecular Chaperones / drug effects. Molecular Chaperones / genetics. Molecular Chaperones / metabolism. Protein-Serine-Threonine Kinases / drug effects. Protein-Serine-Threonine Kinases / genetics. Protein-Serine-Threonine Kinases / metabolism. Proteins / drug effects. Proteins / genetics. Proteins / metabolism. RNA, Small Interfering / genetics. RNA, Small Interfering / pharmacology. RNA, Small Interfering / therapeutic use. Signal Transduction / genetics. Transplantation, Heterologous

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  • (PMID = 18431251.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / DNAJB9 protein, human; 0 / Galectin 1; 0 / HSP40 Heat-Shock Proteins; 0 / HSP70 Heat-Shock Proteins; 0 / Membrane Proteins; 0 / Molecular Chaperones; 0 / Proteins; 0 / RNA, Small Interfering; 0 / oxygen-regulated proteins; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.7.1.- / ERN2 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.1.- / Endoribonucleases
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66. Baldwin RM, Garratt-Lalonde M, Parolin DA, Krzyzanowski PM, Andrade MA, Lorimer IA: Protection of glioblastoma cells from cisplatin cytotoxicity via protein kinase Ciota-mediated attenuation of p38 MAP kinase signaling. Oncogene; 2006 May 11;25(20):2909-19
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Protection of glioblastoma cells from cisplatin cytotoxicity via protein kinase Ciota-mediated attenuation of p38 MAP kinase signaling.
  • Glioblastoma multiforme is an aggressive form of brain cancer that responds poorly to chemotherapy and is generally incurable.
  • To assess the role of atypical PKC in glioblastoma cell chemoresistance, RNA interference was used to deplete human glioblastoma cells of PKCiota.
  • To screen for possible mechanisms for PKCiota-mediated chemoresistance, microarray analysis of gene expression was performed on RNA from glioblastoma cells that were either untreated or depleted of PKCiota.
  • These data show that PKCiota can confer partial resistance to cisplatin in glioblastoma cells by suppressing GMFbeta-mediated enhancement of p38 MAP kinase signaling.
  • [MeSH-major] Antineoplastic Agents / toxicity. Cell Proliferation / drug effects. Cisplatin / toxicity. Glioblastoma / drug therapy. Isoenzymes / metabolism. Protein Kinase C / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Cytoprotection. Gene Expression Profiling. Glia Maturation Factor / metabolism. Humans. Microarray Analysis. NF-kappa B / genetics. NF-kappa B / metabolism. Signal Transduction. Transfection. Tumor Cells, Cultured

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  • (PMID = 16331246.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glia Maturation Factor; 0 / Isoenzymes; 0 / NF-kappa B; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.13 / protein kinase C lambda; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; Q20Q21Q62J / Cisplatin
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67. Broholm H, Born PW, Guterbaum D, Dyrbye H, Laursen H: Detecting chromosomal alterations at 1p and 19q by FISH and DNA fragment analysis--a comparative study in human gliomas. Clin Neuropathol; 2008 Nov-Dec;27(6):378-87
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  • Histological classification of gliomas is important for treatment and as a prognostic predictor, but classification by histology alone can be a challenge.
  • The material comprised 41 glial tumors including 10 oligodendrogliomas (WHO Grades II and III, 5 each), 10 mixed oligoastrocytomas (WHO Grades II and III, 5 each), 10 astrocytomas (WHO Grades II and III, 5 each), and 11 glioblastomas (WHO Grade IV).
  • Disparity was found among the glioblastomas, where fragment analysis showed 1p/19q loss in three cases, with no changes detected by FISH.

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  • (PMID = 19130734.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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68. Tuettenberg J, Grobholz R, Seiz M, Brockmann MA, Lohr F, Wenz F, Vajkoczy P: Recurrence pattern in glioblastoma multiforme patients treated with anti-angiogenic chemotherapy. J Cancer Res Clin Oncol; 2009 Sep;135(9):1239-44
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  • [Title] Recurrence pattern in glioblastoma multiforme patients treated with anti-angiogenic chemotherapy.
  • PURPOSE: Glioblastoma multiforme is the prototype of an angiogenic tumour.
  • Here we report on the pattern of tumour recurrence in glioblastoma patients treated with an anti-angiogenic chemotherapy.
  • PATIENTS AND METHODS: A total of 32 patients with glioblastoma multiforme and a residual tumour mass after operation were treated with a continuous low-dose chemotherapy with temozolomide and a COX-II inhibitor, a presumably anti-angiogenic therapy.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Neoplasm Recurrence, Local / drug therapy

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  • (PMID = 19277712.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
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69. Park DM, Li J, Okamoto H, Akeju O, Kim SH, Lubensky I, Vortmeyer A, Dambrosia J, Weil RJ, Oldfield EH, Park JK, Zhuang Z: N-CoR pathway targeting induces glioblastoma derived cancer stem cell differentiation. Cell Cycle; 2007 Feb 15;6(4):467-70
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  • [Title] N-CoR pathway targeting induces glioblastoma derived cancer stem cell differentiation.
  • Nuclear localization of N-CoR is a feature of undifferentiated neural stem cells and cytoplasmic translocation of N-CoR leads to astrocytic differentiation.
  • Comparative proteomic analysis of microdissected glioblastoma multiforme (GBM) specimens and matched normal glial tissue reveals increased expression of N-CoR in GBM.
  • In GBM primary cell cultures, tumor cells with nuclear localization of N-CoR demonstrate an undifferentiated phenotype, but are subject to astroglial differentiation upon exposure to agents promoting phosphorylation of N-CoR and its subsequent translocation to the cytoplasm.
  • The identification of N-CoR in GBM provides insights into the tumorigenesis process and supports the development of differentiation-based therapeutic strategies.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / pathology. Neoplastic Stem Cells / pathology. Nuclear Proteins / physiology. Repressor Proteins / physiology
  • [MeSH-minor] Biomarkers / analysis. Cell Differentiation / drug effects. Cell Proliferation / drug effects. Drug Synergism. Humans. Nuclear Receptor Co-Repressor 1. Okadaic Acid / administration & dosage. Okadaic Acid / pharmacology. Phosphorylation. Protein Transport. Signal Transduction / drug effects. Tretinoin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 17312396.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / NCOR1 protein, human; 0 / Nuclear Proteins; 0 / Nuclear Receptor Co-Repressor 1; 0 / Repressor Proteins; 1W21G5Q4N2 / Okadaic Acid; 5688UTC01R / Tretinoin
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70. Salunke P, Badhe P, Sharma A: Cerebellar glioblastoma multiforme with non-contiguous grade 2 astrocytoma of the temporal lobe in the same individual. Neurol India; 2010 Jul-Aug;58(4):651-3
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  • [Title] Cerebellar glioblastoma multiforme with non-contiguous grade 2 astrocytoma of the temporal lobe in the same individual.
  • Histopathology revealed grade II astrocytoma in the temporal lobe and glioblastoma multiforme in the cerebellum.
  • [MeSH-major] Astrocytoma / complications. Brain Neoplasms / complications. Glioblastoma / complications. Temporal Lobe / pathology

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  • (PMID = 20739816.001).
  • [ISSN] 0028-3886
  • [Journal-full-title] Neurology India
  • [ISO-abbreviation] Neurol India
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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71. Nakagawa T, Ido K, Sakuma T, Takeuchi H, Sato K, Kubota T: Prognostic significance of the immunohistochemical expression of O6-methylguanine-DNA methyltransferase, P-glycoprotein, and multidrug resistance protein-1 in glioblastomas. Neuropathology; 2009 Aug;29(4):379-88
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  • [Title] Prognostic significance of the immunohistochemical expression of O6-methylguanine-DNA methyltransferase, P-glycoprotein, and multidrug resistance protein-1 in glioblastomas.
  • We studied the expression of O(6)-methylguanine-DNA methyltransferase (O(6)-MGMT), P-glycoprotein (Pgp), and multidrug resistance protein-1 (MRP-1) in 23 glioblastomas using RT-PCR, methylation-specific PCR, and immunohistochemistry, and analyzed their association with overall patient survival.
  • Univariate analysis of collected data demonstrated that the expressions of O(6)-MGMT and MRP-1 detected by immunohistochemistry, in addition to the consistent factors, including preoperative Karnofsky performance scale (KPS), radical surgery, and tumor location and extension, were significant prognostic factors for the overall survival (OS) of patients with glioblastoma, who received nimustine (ACNU)-based chemotherapy in association with surgery and radiotherapy.
  • Among them, following multivariate analysis, preoperative KPS, radical surgery, tumor location, and the expression of O(6)-MGMT remained as significant prognostic factors.
  • These findings suggest that immunohistochemical analysis of O(6)-MGMT in patients with glioblastoma can be a useful method to predict the effects of chemotherapy and identify alternative chemotherapeutic regimens for O(6)-MGMT-positive patients.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Glioblastoma / metabolism. O(6)-Methylguanine-DNA Methyltransferase / biosynthesis. P-Glycoprotein / biosynthesis

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  • (PMID = 19019175.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / P-Glycoprotein; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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72. García-Morales P, Carrasco-García E, Ruiz-Rico P, Martínez-Mira R, Menéndez-Gutiérrez MP, Ferragut JA, Saceda M, Martínez-Lacaci I: Inhibition of Hsp90 function by ansamycins causes downregulation of cdc2 and cdc25c and G(2)/M arrest in glioblastoma cell lines. Oncogene; 2007 Nov 8;26(51):7185-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of Hsp90 function by ansamycins causes downregulation of cdc2 and cdc25c and G(2)/M arrest in glioblastoma cell lines.
  • We wanted to study the effect of geldanamycin (GA) and its derivative 17-allylamino-17-demethoxygeldanamycin (17-AAG) on glioblastoma cell lines.
  • [MeSH-major] Brain Neoplasms / metabolism. Brain Neoplasms / pathology. CDC2-CDC28 Kinases / metabolism. Cell Division. Down-Regulation / drug effects. G2 Phase. Glioblastoma / metabolism. Glioblastoma / pathology. HSP90 Heat-Shock Proteins / physiology. Rifabutin / pharmacology. cdc25 Phosphatases / metabolism
  • [MeSH-minor] Calpain / antagonists & inhibitors. Cell Line, Tumor. Humans

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  • (PMID = 17525741.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HSP90 Heat-Shock Proteins; 1W306TDA6S / Rifabutin; EC 2.7.11.22 / CDC2-CDC28 Kinases; EC 3.1.3.48 / CDC25C protein, human; EC 3.1.3.48 / cdc25 Phosphatases; EC 3.4.22.- / Calpain
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73. Huang J, Chen K, Gong W, Zhou Y, Le Y, Bian X, Wang JM: Receptor "hijacking" by malignant glioma cells: a tactic for tumor progression. Cancer Lett; 2008 Aug 28;267(2):254-61
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  • [Title] Receptor "hijacking" by malignant glioma cells: a tactic for tumor progression.
  • In the course of studying the role of chemoattractant receptors in tumor growth and metastasis, we discovered that highly malignant human glioblastoma and anaplastic astrocytoma specimens were stained positively for the formylpeptide receptor (FPR), which is normally expressed in myeloid cells and accounts for their chemotaxis and activation induced by bacterial peptides.
  • FPR expressed in glioblastoma cell lines mediates cell chemotaxis, proliferation and production of an angiogenic factor, vascular endothelial growth factor (VEGF), in response to agonists released by necrotic tumor cells.
  • Furthermore, FPR in glioblastoma cells activates the receptor for epidermal growth factor (EGFR) by increasing the phosphorylation of a selected tyrosine residue in the intracellular tail of EGFR.
  • Thus, FPR hijacked by human glioblastoma cells exploits the function of EGFR to promote rapid tumor progression.

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  • (PMID = 18433988.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / N01CO12400; United States / Intramural NIH HHS / / Z01 BC010015-12; United States / NCI NIH HHS / CO / N01-CO-12400
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Receptors, Formyl Peptide; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 61
  • [Other-IDs] NLM/ NIHMS69649; NLM/ PMC4191659
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74. Il'yasova D, Marcello JE, McCoy L, Rice T, Wrensch M: Total dietary antioxidant index and survival in patients with glioblastoma multiforme. Cancer Causes Control; 2009 Oct;20(8):1255-60
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  • [Title] Total dietary antioxidant index and survival in patients with glioblastoma multiforme.
  • METHODS: The study population includes 814 glioblastoma multiforme cases that were newly diagnosed, histologically confirmed, aged 20 or older, and residing in the San Francisco Bay Area at diagnosis.
  • CONCLUSIONS: Although it is possible that this is a chance finding, the association between dietary antioxidants and survival in the most recently recruited patients warrants further investigations.

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  • (PMID = 19363672.001).
  • [ISSN] 1573-7225
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA108786; United States / NCI NIH HHS / CA / CA52689; United States / NCI NIH HHS / CA / CA108786-04; United States / NCI NIH HHS / CA / P50 CA097257; United States / NCI NIH HHS / CA / CA097257; United States / NCI NIH HHS / CA / R01 CA052689
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antioxidants
  • [Other-IDs] NLM/ NIHMS465445; NLM/ PMC3660721
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75. Jain N, Mirakhur M, Flynn P, Choudhari KA: Cutaneous metastasis from glioblastoma. Br J Neurosurg; 2005 Feb;19(1):65-8
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  • [Title] Cutaneous metastasis from glioblastoma.
  • A rare case of glioblastoma with isolated cutaneous metastasis adjacent to the scar site is described.
  • [MeSH-major] Brain Neoplasms / pathology. Glioblastoma / secondary. Head and Neck Neoplasms / secondary. Scalp. Skin Neoplasms / secondary


76. Seiz M, Nölte I, Pechlivanis I, Freyschlag CF, Schmieder K, Vajkoczy P, Tuettenberg J: Far-distant metastases along the CSF pathway of glioblastoma multiforme during continuous low-dose chemotherapy with temozolomide and celecoxib. Neurosurg Rev; 2010 Jul;33(3):375-81; discussion 381
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  • [Title] Far-distant metastases along the CSF pathway of glioblastoma multiforme during continuous low-dose chemotherapy with temozolomide and celecoxib.
  • Glioblastoma multiforme is the most common and most malignant primary brain tumour.
  • Here, we describe extreme far-distant metastases along the neural axis of glioblastoma multiforme in four patients receiving metronomic antiangiogenic chemotherapy and review the literature to discuss possible mechanisms.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Agents, Alkylating / therapeutic use. Brain Neoplasms / pathology. Central Nervous System Neoplasms / secondary. Cerebrospinal Fluid. Dacarbazine / analogs & derivatives. Glioblastoma / pathology. Pyrazoles / therapeutic use. Sulfonamides / therapeutic use

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  • (PMID = 20306105.001).
  • [ISSN] 1437-2320
  • [Journal-full-title] Neurosurgical review
  • [ISO-abbreviation] Neurosurg Rev
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Pyrazoles; 0 / Sulfonamides; 7GR28W0FJI / Dacarbazine; JCX84Q7J1L / Celecoxib; YF1K15M17Y / temozolomide
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77. Kondo N, Takahashi A, Mori E, Ohnishi K, McKinnon PJ, Sakaki T, Nakase H, Ohnishi T: DNA ligase IV as a new molecular target for temozolomide. Biochem Biophys Res Commun; 2009 Oct 2;387(4):656-60
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  • [Title] DNA ligase IV as a new molecular target for temozolomide.
  • Temozolomide (TMZ) is a methylating agent used in chemotherapy against glioblastoma.
  • Cultured mouse embryonic fibroblasts were used which were deficient in DSB repair genes such as homologous recombination repair-related genes X-ray repair cross-complementing group 2 (XRCC2)and radiation sensitive mutant54 (Rad54), non-homologous end joining repair-related gene DNAligase IV (Lig4).
  • In addition, it was found that small interference RNAs (siRNA) for Lig4 efficiently enhanced cell lethality induced by TMZ in human glioblastoma A172 cells.

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  • (PMID = 19615340.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA096832-06A18121; United States / NCI NIH HHS / CA / P01 CA096832; United States / NCI NIH HHS / CA / P01 CA096832-06A18121
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Enzyme Inhibitors; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 6.5.1.- / DNA Ligases; EC 6.5.1.1 / DNA ligase (ATP)
  • [Other-IDs] NLM/ NIHMS173878; NLM/ PMC2831288
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78. Ducray F, Dutertre G, Ricard D, Gontier E, Idbaih A, Massard C: [Advances in adults' gliomas biology, imaging and treatment]. Bull Cancer; 2010 Jan;97(1):17-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] Actualités dans la biologie, l'imagerie et le traitement des gliomes de l'adulte.
  • A better understanding of gliomas biology is now leading to a combined histo-molecular classification of these tumors.
  • In anaplastic gliomas ongoing studies depend on 1p/19q codeletion status and in glioblastomas on MGMT methylation status.
  • Advanced brain tumor imaging elicits a better identification of gliomas evolutive potential of.
  • In low-grade gliomas, the importance of maximal resection and the role of chemotherapy are being increasingly recognized.
  • In glioblastomas concomitant chemoradiotherapy is the standard.
  • [MeSH-minor] Adult. Astrocytoma / diagnosis. Astrocytoma / genetics. Astrocytoma / therapy. Combined Modality Therapy / methods. Diagnostic Imaging / methods. Humans. Oligodendroglioma / diagnosis. Oligodendroglioma / genetics. Oligodendroglioma / therapy. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors

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  • (PMID = 20028650.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 166
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79. Patel M, Siddiqui F, Jin JY, Mikkelsen T, Rosenblum M, Movsas B, Ryu S: Salvage reirradiation for recurrent glioblastoma with radiosurgery: radiographic response and improved survival. J Neurooncol; 2009 Apr;92(2):185-91
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  • [Title] Salvage reirradiation for recurrent glioblastoma with radiosurgery: radiographic response and improved survival.
  • PURPOSE: To determine the radiographic and clinical efficacy of stereotactic single dose radiosurgery (SRS) and fractionated stereotactic radiotherapy (FSRT) as salvage therapy for glioblastoma (GBM) at recurrence.
  • METHODS: Thirty-six patients with pathologically proven recurrent GBM were treated with salvage reirradiation by either SRS or FSRT between March of 2001 and August of 2006.
  • Thirty-one patients had an initial diagnosis of GBM.
  • Of 26 patients treated with SRS, radiographic tumor response or stable disease was observed in eight (35%) patients and tumor progression was seen in 18 (65%) patients.
  • Of 10 patients treated by FSRT, radiographic tumor response or stable disease was observed in four (40%) patients and tumor progression was observed in four (40%) patients (two lost to follow-up).
  • CONCLUSION: Salvage reirradiation with SRS or FSRT for recurrent GBM results in radiographic response in a proportion of patients.
  • Survival was significantly improved among patients who either responded or had stable disease after salvage reirradiation, compared to non-responders.
  • Further study is warranted to investigate the method and time of reirradiation for recurrent GBM.
  • [MeSH-major] Brain Neoplasms / surgery. Glioblastoma / surgery. Neoplasm Recurrence, Local / surgery. Radiosurgery / methods. Salvage Therapy / methods

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  • (PMID = 19066727.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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80. Roth J, Constantini S, Blumenthal DT, Ram Z: The value of ventriculo-peritoneal shunting in patients with glioblastoma multiforme and ventriculomegaly. Acta Neurochir (Wien); 2008 Jan;150(1):41-6; discussion 46-7
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  • [Title] The value of ventriculo-peritoneal shunting in patients with glioblastoma multiforme and ventriculomegaly.
  • BACKGROUND: Patients with an advanced-stage glioblastoma multiforme (GBM) often show general motor, gait, and cognitive deterioration.
  • Distinction between tumour patients who have dilated fluid spaces as a consequence of tissue loss from surgery or treatment, and those who have a symptomatic hydrocephalic process, one who may gain benefit from insertion of a ventriculo-peritoneal shunt, is an important clinical challenge.
  • METHODS: From a series of 530 GBM patients treated by a single surgeon (ZR), we retrospectively reviewed 16 patients with advanced-stage GBM who had presented with non-obstructive ventriculomegaly and clinical deterioration not explained by progressive disease.
  • Each had been treated by insertion of a ventriculo- peritoneal shunt (VPS).
  • CONCLUSIONS: Insertion of a ventriculo-peritoneal shunt can improve cognitive and motor function in a small subset of patients with advanced-stage glioblastoma multiforme and ventriculomegaly.
  • [MeSH-major] Glioblastoma / surgery. Ventriculoperitoneal Shunt / methods

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  • (PMID = 18180865.001).
  • [ISSN] 0942-0940
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Austria
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81. Chen KT, Lin JD, Liou MJ, Weng HF, Chang CA, Chan EC: An aberrant autocrine activation of the platelet-derived growth factor alpha-receptor in follicular and papillary thyroid carcinoma cell lines. Cancer Lett; 2006 Jan 18;231(2):192-205
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  • Platelet-derived growth factor receptor (PDGFR) can bind to its ligand and consequently possess a kinase activity, and which is associated with the carcinogenesis of different cell types, including astrocytomas, oligodendrogliomas, and glioblastoma.
  • [MeSH-minor] Blotting, Western. Cell Proliferation / drug effects. DNA, Complementary. Enzyme Activation. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Phosphorylation. Platelet-Derived Growth Factor / genetics. Platelet-Derived Growth Factor / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Tumor Cells, Cultured. Tyrosine / metabolism. Tyrphostins / pharmacology


82. Struck RF, Waud WR: Thiolo-, thiono- and dithiocarbonate and thiocarbamate derivatives of demethylpenclomedine as novel anticancer agents. Cancer Chemother Pharmacol; 2006 Jan;57(2):180-4
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  • PURPOSE: The purpose of this investigation was to synthesize a series of thiolo-, thiono- and dithiocarbonate and thiocarbamate derivatives of 4-demethylpenclomedine (DM-PEN), the major plasma metabolite of penclomedine (PEN) in patients observed subsequently to be an active antitumor agent and non-neurotoxic in a rat model, in order to compare their antitumor activity with that of DM-PEN.
  • METHODS: Derivatives were prepared from DM-PEN and evaluated in vivo against human MX-1 breast tumor xenografts implanted in the mammary fat pad, several of which were also evaluated against human brain tumor xenografts.
  • RESULTS: Thiolocarbonate and thiocarbamate derivatives were found to be superior to DM-PEN against MX-1 tumor and modestly active against glioblastoma.
  • CONCLUSION: The activity of the thiolocarbonates and thiocarbamates against human tumor xenografts in vivo suggests consideration of these two series of derivatives of DM-PEN for clinical development.

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  • (PMID = 16096790.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA34200
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbamates; 0 / Carbonates; 0 / Picolines; 108030-77-9 / penclomedine
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83. Wolf A, Agnihotri S, Guha A: Targeting metabolic remodeling in glioblastoma multiforme. Oncotarget; 2010 Nov;1(7):552-62
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  • [Title] Targeting metabolic remodeling in glioblastoma multiforme.
  • A key aberrant biological difference between tumor cells and normal differentiated cells is altered metabolism, whereby cancer cells acquire a number of stable genetic and epigenetic alterations to retain proliferation, survive under unfavorable microenvironments and invade into surrounding tissues.
  • This review discusses the role of key metabolic enzymes and their association with aerobic glycolysis in Glioblastoma Multiforme (GBM), an aggressive, highly glycolytic and deadly brain tumor.
  • Targeting key metabolic enzymes involved in modulating the "Warburg Effect" may provide a novel therapeutic approach either singularly or in combination with existing therapies in GBMs.

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  • (PMID = 21317451.001).
  • [ISSN] 1949-2553
  • [Journal-full-title] Oncotarget
  • [ISO-abbreviation] Oncotarget
  • [Language] ENG
  • [Grant] None / None / / 83392; Canada / Canadian Institutes of Health Research / / 84294; Canada / Canadian Institutes of Health Research / / 83392; None / None / / 84294; Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Enzymes
  • [Keywords] NOTNLM ; cancer / drug discovery / oncotarget / stem cells / wnt
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84. Pellettieri L, H-Stenstam B, Rezaei A, Giusti V, Sköld K: An investigation of boron neutron capture therapy for recurrent glioblastoma multiforme. Acta Neurol Scand; 2008 Mar;117(3):191-7
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  • [Title] An investigation of boron neutron capture therapy for recurrent glioblastoma multiforme.
  • Objectives - To explore the use of boron neutron capture therapy (BNCT) for patients with glioblastoma multiforme (GBM), recurring after surgery and conventional radiotherapy (photon radiotherapy).
  • Materials and Methods - Boron uptake in recurrent GBM was measured for four patients.
  • BNCT was well tolerated and quality of life remained stable until tumor progression for all 12 patients.
  • No correlation was found between survival times and minimum tumor dose and number of radiation fields.
  • Conclusions - Boron neutron capture therapy, with the prolonged procedure for infusion, is at least as effective as other radiation therapies for recurrent GBM and is delivered in one treatment session, with low radiation dose to the healthy brain.
  • [MeSH-major] Boron Neutron Capture Therapy / methods. Brain Neoplasms / radiotherapy. Glioblastoma / radiotherapy. Neoplasm Recurrence, Local / radiotherapy
  • [MeSH-minor] Adult. Aged. Body Weight. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Radiotherapy Dosage. Tomography, X-Ray Computed

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  • (PMID = 18297764.001).
  • [ISSN] 1600-0404
  • [Journal-full-title] Acta neurologica Scandinavica
  • [ISO-abbreviation] Acta Neurol. Scand.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
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85. Harris DA, Pellikka R, Gasser O, Blaeuenstein P, Waibel R, Schubiger PA, King SW, Parseghian MH: In-line radiolabeling: a novel continuous-flow system for commercial-scale protein labeling. J Nucl Med; 2009 Jul;50(7):1178-86
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  • CONCLUSION: Simple to construct, our system is already used to manufacture a radiolabeled antibody, both in the United States and in India, as part of clinical trials to treat glioblastoma multiforme.

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  • (PMID = 19525454.001).
  • [ISSN] 0161-5505
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Radioisotopes; 0 / Radiopharmaceuticals
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86. Gil-Salú JL, Bosco-López J, Domi Nguez-Villar M, Domínguez-Pascual I, Pérez-Requena J, Palomo MJ, López-Escobar M: [Chemosensitivity test on brain tumors]. Neurocirugia (Astur); 2008 Feb;19(1):5-11
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  • [Transliterated title] Ensayos de quimiosensibilidad en cultivos primarios de tumores cerebrales.
  • In vitro chemosensitivity is an attractive method for knowing about responses of a tumor to ChT treatment and assess the best dose in the patient with cancer.
  • METHODS: Five different drugs (carmustin, camptotecin, taxol, hydroxyurea and tamoxifen) were tested on short-term cultures from 7 patients with Glioblastoma multiforme, 15 patients with meningiomas and one patient with meduloblastoma.
  • For each drug we used from 10-2 M to 10-12 M gap, and IC50 result was representative of tumor sensitivity to the drug.
  • [MeSH-minor] Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Formazans / metabolism. Humans. Tetrazolium Salts / metabolism. Tumor Cells, Cultured

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  • (PMID = 18335150.001).
  • [ISSN] 1130-1473
  • [Journal-full-title] Neurocirugía (Asturias, Spain)
  • [ISO-abbreviation] Neurocirugia (Astur)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Formazans; 0 / Tetrazolium Salts; 23305-68-2 / MTT formazan
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87. Cancer Genome Atlas Research Network: Comprehensive genomic characterization defines human glioblastoma genes and core pathways. Nature; 2008 Oct 23;455(7216):1061-8
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  • [Title] Comprehensive genomic characterization defines human glioblastoma genes and core pathways.
  • Here we report the interim integrative analysis of DNA copy number, gene expression and DNA methylation aberrations in 206 glioblastomas--the most common type of adult brain cancer--and nucleotide sequence aberrations in 91 of the 206 glioblastomas.
  • This analysis provides new insights into the roles of ERBB2, NF1 and TP53, uncovers frequent mutations of the phosphatidylinositol-3-OH kinase regulatory subunit gene PIK3R1, and provides a network view of the pathways altered in the development of glioblastoma.
  • Furthermore, integration of mutation, DNA methylation and clinical treatment data reveals a link between MGMT promoter methylation and a hypermutator phenotype consequent to mismatch repair deficiency in treated glioblastomas, an observation with potential clinical implications.

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  • (PMID = 18772890.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U24 CA126544-01; United States / NCI NIH HHS / CA / R01 CA099041-05; United States / NCI NIH HHS / CA / U24CA126561; United States / NCI NIH HHS / CA / CA126551-01; United States / NHGRI NIH HHS / HG / U54 HG003067; United States / NHGRI NIH HHS / HG / U54HG003273; United States / NCI NIH HHS / CA / U24CA126551; United States / NCI NIH HHS / CA / U24CA126543; United States / NCI NIH HHS / CA / U24 CA126561-01; United States / NCI NIH HHS / CA / U24CA126554; United States / NCI NIH HHS / CA / R01 CA099041; United States / NCI NIH HHS / CA / CA126554-01; United States / NCI NIH HHS / CA / U24 CA126546-01; United States / NHGRI NIH HHS / HG / HG003273-01; United States / NCI NIH HHS / CA / U24CA126544; United States / NHGRI NIH HHS / HG / HG003079-05; United States / NCI NIH HHS / CA / U24 CA126551; United States / NCI NIH HHS / CA / CA126544-01; United States / NHGRI NIH HHS / HG / U54HG003067; United States / NHGRI NIH HHS / HG / U54 HG003067-01; None / None / / R01 CA099041-05; United States / NIGMS NIH HHS / GM / T32 GM007753; United States / NCI NIH HHS / CA / U24 CA126543-01; United States / NHGRI NIH HHS / HG / U54 HG003273; United States / NCI NIH HHS / CA / CA126563-01; United States / NCI NIH HHS / CA / U24 CA126563-01; United States / NHGRI NIH HHS / HG / U54HG003079; United States / NCI NIH HHS / CA / U24 CA126554; United States / NHGRI NIH HHS / HG / U54 HG003273-01; United States / NCI NIH HHS / CA / U24 CA126561; United States / NCI NIH HHS / CA / U24 CA126551-01; United States / NCI NIH HHS / CA / U24 CA126543; United States / NCI NIH HHS / CA / U24CA126563; United States / NCI NIH HHS / CA / U24CA126546; United States / NHGRI NIH HHS / HG / U54 HG003079; United States / NCI NIH HHS / CA / CA126546-01; United States / NCI NIH HHS / CA / CA126561-01; United States / NHGRI NIH HHS / HG / U54 HG003079-05; United States / NCI NIH HHS / CA / U24 CA126554-01; United States / NCI NIH HHS / CA / CA126543-01; United States / NCI NIH HHS / CA / U24 CA126546; United States / NCI NIH HHS / CA / U24 CA126563; United States / NCI NIH HHS / CA / U24 CA126544; United States / NHGRI NIH HHS / HG / HG003067-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neurofibromin 1; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 6.5.1.- / DNA Repair Enzymes
  • [Other-IDs] NLM/ NIHMS68048; NLM/ PMC2671642
  • [Investigator] McLendon R; Friedman A; Bigner D; Van Meir EG; Brat DJ; Mastrogianakis GM; Olson JJ; Mikkelsen T; Lehman N; Aldape K; Yung WK; Bogler O; Weinstein JN; VandenBerg S; Berger M; Prados M; Muzny D; Morgan M; Scherer S; Sabo A; Nazareth L; Lewis L; Hall O; Zhu Y; Ren Y; Alvi O; Yao J; Hawes A; Jhangiani S; Fowler G; San Lucas A; Kovar C; Cree A; Dinh H; Santibanez J; Joshi V; Gonzalez-Garay ML; Miller CA; Milosavljevic A; Donehower L; Wheeler DA; Gibbs RA; Cibulskis K; Sougnez C; Fennell T; Mahan S; Wilkinson J; Ziaugra L; Onofrio R; Bloom T; Nicol R; Ardlie K; Baldwin J; Gabriel S; Lander ES; Ding L; Fulton RS; McLellan MD; Wallis J; Larson DE; Shi X; Abbott R; Fulton L; Chen K; Koboldt DC; Wendl MC; Meyer R; Tang Y; Lin L; Osborne JR; Dunford-Shore BH; Miner TL; Delehaunty K; Markovic C; Swift G; Courtney W; Pohl C; Abbott S; Hawkins A; Leong S; Haipek C; Schmidt H; Wiechert M; Vickery T; Scott S; Dooling DJ; Chinwalla A; Weinstock GM; Mardis ER; Wilson RK; Getz G; Winckler W; Verhaak RG; Lawrence MS; O'Kelly M; Robinson J; Alexe G; Beroukhim R; Carter S; Chiang D; Gould J; Gupta S; Korn J; Mermel C; Mesirov J; Monti S; Nguyen H; Parkin M; Reich M; Stransky N; Weir BA; Garraway L; Golub T; Meyerson M; Chin L; Protopopov A; Zhang J; Perna I; Aronson S; Sathiamoorthy N; Ren G; Yao J; Wiedemeyer WR; Kim H; Kong SW; Xiao Y; Kohane IS; Seidman J; Park PJ; Kucherlapati R; Laird PW; Cope L; Herman JG; Weisenberger DJ; Pan F; Van den Berg D; Van Neste L; Yi JM; Schuebel KE; Baylin SB; Absher DM; Li JZ; Southwick A; Brady S; Aggarwal A; Chung T; Sherlock G; Brooks JD; Myers RM; Spellman PT; Purdom E; Jakkula LR; Lapuk AV; Marr H; Dorton S; Choi YG; Han J; Ray A; Wang V; Durinck S; Robinson M; Wang NJ; Vranizan K; Peng V; Van Name E; Fontenay GV; Ngai J; Conboy JG; Parvin B; Feiler HS; Speed TP; Gray JW; Brennan C; Socci ND; Olshen A; Taylor BS; Lash A; Schultz N; Reva B; Antipin Y; Stukalov A; Gross B; Cerami E; Wang WQ; Qin LX; Seshan VE; Villafania L; Cavatore M; Borsu L; Viale A; Gerald W; Sander C; Ladanyi M; Perou CM; Hayes DN; Topal MD; Hoadley KA; Qi Y; Balu S; Shi Y; Wu J; Penny R; Bittner M; Shelton T; Lenkiewicz E; Morris S; Beasley D; Sanders S; Kahn A; Sfeir R; Chen J; Nassau D; Feng L; Hickey E; Barker A; Gerhard DS; Vockley J; Compton C; Vaught J; Fielding P; Ferguson ML; Schaefer C; Zhang J; Madhavan S; Buetow KH; Collins F; Good P; Guyer M; Ozenberger B; Peterson J; Thomson E
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88. Voelzke WR, Petty WJ, Lesser GJ: Targeting the epidermal growth factor receptor in high-grade astrocytomas. Curr Treat Options Oncol; 2008 Feb;9(1):23-31
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  • [Title] Targeting the epidermal growth factor receptor in high-grade astrocytomas.
  • OPINION STATEMENT: High-grade astrocytomas, including glioblastoma multiforme (GBM) and anaplastic astrocytoma (AA), are the most common and aggressive primary malignant brain tumors in adults.
  • EGFR-targeted therapy is a rational approach since EGFR overexpression and mutant EGFRvIII expression occur in approximately 50% of patients with GBM.
  • Retrospective analyses have highlighted co-expression of EGFRvIII and wild-type PTEN (phosphatase and tensin homologue deleted in chromosome 10) as a significant predictor of EGFR TKI response in patients with GBM.
  • [MeSH-major] Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use. Receptor, Epidermal Growth Factor / antagonists & inhibitors

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  • (PMID = 18247132.001).
  • [ISSN] 1534-6277
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 54
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89. Hoang-Xuan K, Idbaih A, Mokhtari K, Sanson M: [Towards a molecular classification of gliomas]. Bull Cancer; 2005 Apr;92(4):310-6
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  • [Title] [Towards a molecular classification of gliomas].
  • [Transliterated title] Vers une classification moléculaire des gliomes.
  • Molecular profiles have been associated with specific histologic and prognostic tumor subgroups, contributing to improve the classification of gliomas.
  • At least two alternative molecular pathways have been suggested in the astrocytoma progression involving TP53 inactivation (secondary glioblastomas) and EGFR amplification (de novo glioblastomas) respectively.
  • Oligodendroglial tumors have demonstrated recurrent combined loss of chromosome 1p/19q, which represent a favorable prognosis marker and probably a predictor of a good chemosensitivity of the tumor.
  • [MeSH-minor] Astrocytoma / genetics. Astrocytoma / pathology. Chromosome Deletion. Chromosomes, Human, Pair 1. Genes, erbB-1 / genetics. Genes, p53 / genetics. Humans. Oligodendroglioma / genetics. Oligodendroglioma / pathology. Prognosis


90. Inoue Y, Kanda Y, Kinoshita C, Kanda C, Joh K: Intramembranous microspherical structures in focal segmental glomerulosclerosis. Clin Exp Nephrol; 2008 Dec;12(6):504-8
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  • A 45-year-old male had proteinuria for 3 years.
  • A few cytoplasmic processes of the podocytes showed infolding to the GBM.
  • The patient exhibited no symptoms and no physical and serological findings suggesting autoimmune disease, such as systemic lupus erythematosus or Sjögren's syndrome.
  • Therefore, the present case is important, because the peculiar microstructure in the GBM was noted in focal segmental glomerulosclerosis, which has never been reported in the literature.

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  • (PMID = 19002748.001).
  • [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
  • [Chemical-registry-number] 0 / Immunoglobulin G
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91. Karaczyn A, Bani-Yaghoub M, Tremblay R, Kubu C, Cowling R, Adams TL, Prudovsky I, Spicer D, Friesel R, Vary C, Verdi JM: Two novel human NUMB isoforms provide a potential link between development and cancer. Neural Dev; 2010 Dec 01;5:31
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  • These novel isoforms, NUMB5 and NUMB6, lack exon 10 and are expressed in cells known for polarity and migratory behavior, such as human amniotic fluid cells, glioblastoma and metastatic tumor cells.


92. Eder-Czembirek C, Erovic BM, Czembirek C, Brunner M, Selzer E, Pötter R, Thurnher D: Betulinic acid a radiosensitizer in head and neck squamous cell carcinoma cell lines. Strahlenther Onkol; 2010 Mar;186(3):143-8
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  • BACKGROUND AND PURPOSE: Betulinic acid, a pentacyclic triterpene, is a new cytotoxic compound active on melanoma, neuroblastoma, glioblastoma and head and neck squamous cell carcinoma (HNSCC) cells.
  • MATERIAL AND METHODS: Two HNSCC cell lines, SCC9 and SCC25, were treated with increasing doses of betulinic acid and sequentially irradiated with a single boost of 4 Gy from a conventional radiation source.

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  • (PMID = 20339825.001).
  • [ISSN] 1439-099X
  • [Journal-full-title] Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al]
  • [ISO-abbreviation] Strahlenther Onkol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Radiation-Sensitizing Agents; 0 / Triterpenes; 4G6A18707N / betulinic acid
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93. Guinipero T, Finn OJ: Cancer vaccines: emphasis on pediatric cancers. Curr Pharm Des; 2010 Jan;16(3):292-9
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  • The success that vaccines have had in the fight with infectious diseases has not been mirrored in their use in the fight against cancer.
  • Cancer is considered to be primarily a disease of the older age and yet many children suffer from or succumb to cancers such as leukemias, glioblastomas, neuroblastomas and sarcomas.
  • Due to the greater capacity of a young immune system to recover after cancer treatment, therapeutic vaccines are expected to have a better chance to elicit protective immunity and prevent cancer recurrence in children.
  • In this review, we discuss the current efforts at designing and testing cancer vaccines in children with the focus on specific tumor antigens expressed by pediatric cancers.
  • [MeSH-major] Antigens, Neoplasm / immunology. Cancer Vaccines / immunology. Neoplasms / therapy
  • [MeSH-minor] Age Factors. Animals. Child. Drug Design. Humans. Immunosuppression / methods. Immunotherapy / methods. Neoplasm Recurrence, Local / immunology. Neoplasm Recurrence, Local / prevention & control

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  • (PMID = 20109138.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA090440
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines
  • [Number-of-references] 62
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94. Tate MC, Aghi MK: Biology of angiogenesis and invasion in glioma. Neurotherapeutics; 2009 Jul;6(3):447-57
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  • Treatment of adult brain tumors, in particular glioblastoma, remains a significant clinical challenge, despite modest advances in surgical technique, radiation, and chemotherapeutics.
  • The formation of abnormal, dysfunctional tumor vasculature and glioma cell invasion along white matter tracts are believed to be major components of the inability to treat these tumors effectively.
  • Recent insight into the fundamental processes governing glioma angiogenesis and invasion provide a renewed hope for development of novel strategies aimed at reducing the morbidity of this uniformly fatal disease.
  • In this review, we discuss background biology of the blood brain barrier and its pertinence to blood vessel formation and tumor invasion.

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  • (PMID = 19560735.001).
  • [ISSN] 1933-7213
  • [Journal-full-title] Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
  • [ISO-abbreviation] Neurotherapeutics
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 135
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95. Vanderzalm PJ, Pandey A, Hurwitz ME, Bloom L, Horvitz HR, Garriga G: C. elegans CARMIL negatively regulates UNC-73/Trio function during neuronal development. Development; 2009 Apr;136(7):1201-10
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  • Although mammalian CARMIL acts to promote the migration of glioblastoma cells, we found that CRML-1 acts as a negative regulator of neuronal cell and axon growth cone migrations.

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  • (PMID = 19244282.001).
  • [ISSN] 0950-1991
  • [Journal-full-title] Development (Cambridge, England)
  • [ISO-abbreviation] Development
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS32057; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / K08 CA-104890; United States / NINDS NIH HHS / NS / R01 NS032057; United States / NIGMS NIH HHS / GM / GM24663
  • [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] England
  • [Chemical-registry-number] 0 / Caenorhabditis elegans Proteins; 0 / DNA Primers; 0 / Nerve Tissue Proteins; 0 / Receptors, Immunologic; 0 / UNC-73 protein, C elegans; 0 / crml-1 protein, C elegans; 0 / roundabout protein; EC 3.6.5.2 / rac GTP-Binding Proteins
  • [Other-IDs] NLM/ PMC2685937
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96. Farray D, Ahluwalia MS, Snyder J, Barnett GH, Cohen BH, Suh JH, Peereboom DM: Pre-irradiation 9-amino [20s] camptothecin (9-AC) in patients with newly diagnosed glioblastoma multiforme. Invest New Drugs; 2006 May;24(3):177-80
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  • [Title] Pre-irradiation 9-amino [20s] camptothecin (9-AC) in patients with newly diagnosed glioblastoma multiforme.
  • PURPOSE: To evaluate the efficacy of 9-amino [20s] camptothecin (9-AC) given before radiation therapy to patients with newly diagnosed glioblastoma multiforme (GBM).
  • METHODS: Eligible patients had newly diagnosed GBM who had residual measurable contrast-enhancing tumor.
  • The trial was a phase 2 trial of 9-AC at 1100 microg/m2 /24 h infused over 72 h every two weeks for up to six cycles in patients with newly diagnosed GBM before radiation therapy.
  • All of the patients had progressive disease by imaging criteria after at least two cycles of 9-AC (1 month).
  • The most common adverse event was transient lymphopenia (grade 3-4).
  • One patient developed grade 4 neutropenic fever that resolved after three days of diagnosis.
  • CONCLUSIONS: 9-AC lacks activity against glioblastoma multiforme (GBM).
  • Further studies looking at the efficacy of 9-AC in GBM may be futile.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Camptothecin / analogs & derivatives. Glioblastoma / drug therapy

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  • (PMID = 16086097.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5MB77ICE2Q / 9-aminocamptothecin; XT3Z54Z28A / Camptothecin
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97. von Lehe M, Schramm J: Gliomas of the cingulate gyrus: surgical management and functional outcome. Neurosurg Focus; 2009 Aug;27(2):E9
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  • RESULTS: In 7 cases (18%) the tumor was located in the posterior (parietal) part of the cingulate gyrus, and in 31 (82%) the tumor was in the anterior (frontal) part.
  • In 10 cases (26%) the glioma was solely located in the cingulate gyrus, and in 28 cases (74%) the tumor extended to the supracingular frontal/parietal cortex.
  • The authors chose an interhemispheric approach for tumor resection in 11 (29%) and a transcortical approach in 27 (71%) cases; intraoperative electrophysiological monitoring was applied in 23 (61%) and neuronavigation in 15 (39%) cases.
  • Tumors were classified as low-grade gliomas in 11 cases (29%).
  • A glioblastoma multiforme (WHO Grade IV, 10 cases [26%]) and oligoastrocytoma (WHO Grade III, 9 cases [24%]) were the most frequent histopathological results.
  • In case of resection of gliomas arising from the anterior cingulate gyrus a supplementary motor area syndrome has to be considered, particularly when the tumor extends to the supracingular cortex.

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  • (PMID = 19645564.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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98. Lai PH, Weng HH, Chen CY, Hsu SS, Ding S, Ko CW, Fu JH, Liang HL, Chen KH: In vivo differentiation of aerobic brain abscesses and necrotic glioblastomas multiforme using proton MR spectroscopic imaging. AJNR Am J Neuroradiol; 2008 Sep;29(8):1511-8
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  • [Title] In vivo differentiation of aerobic brain abscesses and necrotic glioblastomas multiforme using proton MR spectroscopic imaging.
  • BACKGROUND AND PURPOSE: Abscesses caused by aerobic bacteria (aerobic abscesses) can simulate intracranial glioblastomas multiforme (GBMs) in MR imaging appearance and single voxel (SV) proton MR spectroscopy of the central cavity.
  • The purpose of our study was to determine whether MR spectroscopic imaging (SI) can be used to differentiate aerobic abscesses from GBMs.
  • Our hypothesis was that metabolite levels of choline (Cho) are decreased in the ring-enhancing portion of abscesses compared with GBMs.
  • Proton MR spectra of 15 GBMs with similar conventional MR imaging appearances were used for comparison.
  • Maximum Cho/Cr, Cho/NAA, LL/Cr-n, and Cho/Cho-n and minimum Cr/Cr-n and NAA/NAA-n ratios in abscesses and GBMs were compared using the Wilcoxon rank sum test.
  • Means and SDs of maximum Cho/Cr, Cho/NAA, LL/Cr-n, and Cho/Cho-n and minimum Cr/Cr-n and NAA/NAA-n ratios were 3.38 +/- 1.09, 3.88 +/- 2.13, 2.72 +/- 1.45, 1.98 +/- 0.53, 0.53 +/- 0.16, and 0.44 +/- 0.09, respectively, in the GBMs, and 1.77 +/- 0.49, 1.48 +/- 0.51, 2.11 +/- 0.67, 0.81 +/- 0.21, 0.48 +/- 0.2, and 0.5 +/- 0.15, respectively, in the abscesses.
  • Significant differences were found in the maximum Cho/Cr (P = .001), Cho/NAA (P = .006), and Cho/Cho-n ratios (P < .001) between abscesses and GBMs.
  • CONCLUSION: Metabolite ratios and maximum Cho/Cho-n, Cho/Cr, and Cho/NAA ratios of the contrast-enhancing rim were significantly different and useful in differentiating aerobic abscesses from GBMs by MRSI.
  • [MeSH-major] Brain Abscess / diagnosis. Glioblastoma / diagnosis. Gram-Positive Bacterial Infections / diagnosis. Magnetic Resonance Imaging / methods. Magnetic Resonance Spectroscopy / methods

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  • (PMID = 18499784.001).
  • [ISSN] 1936-959X
  • [Journal-full-title] AJNR. American journal of neuroradiology
  • [ISO-abbreviation] AJNR Am J Neuroradiol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protons
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99. Lytle RA, Jiang Z, Zheng X, Higashikubo R, Rich KM: Retinamide-induced apoptosis in glioblastomas is associated with down-regulation of Bcl-xL and Bcl-2 proteins. J Neurooncol; 2005 Sep;74(3):225-32
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  • [Title] Retinamide-induced apoptosis in glioblastomas is associated with down-regulation of Bcl-xL and Bcl-2 proteins.
  • Glioblastomas are among the most difficult neoplasms to treat with continued poor prognosis for long-term survival.
  • Glioblastomas have developed effective mechanisms to resist chemotherapy including levels anti-apoptotic proteins, Bcl-xL and Bcl-2.
  • Chemotherapy agents that promote down-regulation of Bcl-xL and Bcl-2 may enhance sensitivity to chemotherapy in glioblastomas.
  • The ability of the synthetic retinoid N-(4-hydroxyphenyl) retinamide to modulate these anti-apoptotic proteins and to enhance apoptosis and chemotherapy was examined in glioblastoma cells.
  • Expression of Bcl-2 family member proteins Bcl-xL and Bcl-2 were assessed in glioblastomas from three cell lines including U87, U251, and U138.
  • Based on Western blots the levels of Bcl-2 and Bcl-xL were decreased in glioblastoma cells after treatment with retinamide.
  • BCNU chemotherapy combined with retinamide markedly down-regulated levels of both Bcl-xL and Bcl-2 proteins in glioblastoma and enhanced the incidence of apoptosis in U87 cells.
  • These studies demonstrate that modulation of levels of the anti-apoptotic proteins, Bcl-xL and Bcl-2, may enhance the sensitivity of glioblastoma toward chemotherapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Proto-Oncogene Proteins c-bcl-2 / drug effects. Tretinoin / analogs & derivatives
  • [MeSH-minor] Antineoplastic Agents, Alkylating / pharmacology. Antineoplastic Combined Chemotherapy Protocols. Blotting, Western. Carmustine / pharmacology. Caspases. Down-Regulation. Flow Cytometry. Humans. Tumor Cells, Cultured

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  • (PMID = 16187019.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Proto-Oncogene Proteins c-bcl-2; 5688UTC01R / Tretinoin; BQC43T81DZ / retinamide; EC 3.4.22.- / Caspases; U68WG3173Y / Carmustine
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100. Suzuki K, Momota H, Tonooka A, Noguchi H, Yamamoto K, Wanibuchi M, Minamida Y, Hasegawa T, Houkin K: Glioblastoma simultaneously present with adjacent meningioma: case report and review of the literature. J Neurooncol; 2010 Aug;99(1):147-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glioblastoma simultaneously present with adjacent meningioma: case report and review of the literature.
  • However, most of these tumors arise after cranial radiotherapy or in association with familial tumor syndromes.
  • Postoperative histological examination revealed the presence of two distinct tumors, meningioma and glioblastoma multiforme.
  • To elucidate the mechanism of synchronous tumor formation, we performed immunohistochemical analysis of the proteins involved in the receptor tyrosine kinase, Wnt, and Notch signaling pathways.
  • The PDGF-mediated paracrine system may induce one tumor from another.
  • [MeSH-major] Brain Neoplasms / complications. Glioblastoma / complications. Meningeal Neoplasms / complications. Meningioma / complications

  • Genetic Alliance. consumer health - Glioblastoma.
  • Genetic Alliance. consumer health - Meningioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
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  • (PMID = 20063176.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
  • [Number-of-references] 29
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