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1. Tang J, Shao W, Dorak MT, Li Y, Miike R, Lobashevsky E, Wiencke JK, Wrensch M, Kaslow RA, Cobbs CS: Positive and negative associations of human leukocyte antigen variants with the onset and prognosis of adult glioblastoma multiforme. Cancer Epidemiol Biomarkers Prev; 2005 Aug;14(8):2040-4
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  • [Title] Positive and negative associations of human leukocyte antigen variants with the onset and prognosis of adult glioblastoma multiforme.
  • We examined the relationships of human leukocyte antigen (HLA) and related polymorphisms to glioblastoma multiforme in adult Caucasians (non-Hispanic Whites) from the San Francisco Bay area.
  • For 155 glioblastoma multiforme patients and 157 control subjects closely matched by ethnicity, age, and gender, PCR-based techniques resolved alleles at HLA-A, -B, -C, and -DRB1 loci along with short tandem repeat polymorphisms of MICA exon 5 and TNFb.
  • By multivariable logistic regression, B*13 and the B*07-Cw*07 haplotype were positively associated with glioblastoma multiforme (P=0.01 and <0.001, respectively), whereas Cw*01 was the only variant showing a negative association (P=0.05).
  • Among glioblastoma multiforme patients, progression to death after diagnosis was slower in those with A*32 (relative hazard, 0.45; P<0.01) and faster in those with B*55 (relative hazard, 2.27; P<0.01).
  • Thus, both the occurrence and the prognosis of glioblastoma multiforme could be associated with specific but different HLA genotypes.
  • B*07 and the B*07-Cw*07 haplotype are much more common in Caucasians than other ethnic groups in the U.S., which may partially explain the higher incidence of glioblastoma multiforme in Caucasians.
  • [MeSH-major] Biomarkers, Tumor / genetics. Glioblastoma / genetics. HLA Antigens / genetics
  • [MeSH-minor] Adult. Case-Control Studies. Female. Genetic Variation. Genotype. Humans. Male. Microsatellite Repeats. Polymerase Chain Reaction. Polymorphism, Genetic. Prognosis. San Francisco

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  • (PMID = 16103458.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA097247; United States / NCI NIH HHS / CA / CA097257; United States / NCI NIH HHS / CA / CA52689
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HLA Antigens
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2. Veselska R, Kuglik P, Cejpek P, Svachova H, Neradil J, Loja T, Relichova J: Nestin expression in the cell lines derived from glioblastoma multiforme. BMC Cancer; 2006;6:32
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  • [Title] Nestin expression in the cell lines derived from glioblastoma multiforme.
  • BACKGROUND: Nestin is a protein belonging to class VI of intermediate filaments that is produced in stem/progenitor cells in the mammalian CNS during development and is consecutively replaced by other intermediate filament proteins (neurofilaments, GFAP).
  • Down-regulated nestin may be re-expressed in the adult organism under certain pathological conditions (brain injury, ischemia, inflammation, neoplastic transformation).
  • Our work focused on a detailed study of the nestin cytoskeleton in cell lines derived from glioblastoma multiforme, because re-expression of nestin together with down-regulation of GFAP has been previously reported in this type of brain tumor.
  • METHODS: Two cell lines were derived from the tumor tissue of patients treated for glioblastoma multiforme.
  • RESULTS: Using epifluorescence and confocal microscopy, we described the morphology of nestin-positive intermediate filaments in glioblastoma cells of both primary cultures and the derived cell lines, as well as the reorganization of nestin during mitosis.
  • CONCLUSION: Detailed information concerning the pattern of the nestin cytoskeleton in glioblastoma cell lines and especially the demonstration of nestin in the nucleus represent an important background for further studies of nestin re-expression in relationship to tumor malignancy and invasive potential.
  • [MeSH-major] Glioblastoma / chemistry. Intermediate Filament Proteins / analysis. Nerve Tissue Proteins / analysis
  • [MeSH-minor] Cell Line, Tumor. Cytoskeleton / chemistry. Cytoskeleton / ultrastructure. Fluorescent Antibody Technique, Indirect. Glial Fibrillary Acidic Protein / analysis. Humans. Nestin. Vimentin / analysis

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  • (PMID = 16457706.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; 0 / Vimentin
  • [Other-IDs] NLM/ PMC1403792
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3. Mikkelsen T, Lush R, Grossman SA, Carson KA, Fisher JD, Alavi JB, Rosenfeld S: Phase II clinical and pharmacologic study of radiation therapy and carboxyamido-triazole (CAI) in adults with newly diagnosed glioblastoma multiforme. Invest New Drugs; 2007 Jun;25(3):259-63
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  • [Title] Phase II clinical and pharmacologic study of radiation therapy and carboxyamido-triazole (CAI) in adults with newly diagnosed glioblastoma multiforme.
  • INTRODUCTION: Carboxyamido-triazole (CAI) is a synthetic inhibitor of non-voltage-gated calcium channels that reversibly inhibits angiogenesis, tumor cell proliferation, and metastatic potential.
  • This study examined the efficacy, safety and pharmacokinetics of oral CAI in the treatment of patients with newly diagnosed glioblastoma multiforme (GBM) in an open-label, single arm non-randomized phase 2 trial.
  • The primary outcome was survival compared to historical controls within the NABTT CNS Consortium database.
  • Overall survival and grade > or = 3 toxicities were comparable by EIAED status.

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  • (PMID = 17080256.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA062475; United States / NCI NIH HHS / CA / CA062475
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / Antineoplastic Agents; 0 / Calcium Channel Blockers; 0 / Triazoles; 99519-84-3 / carboxyamido-triazole
  • [Other-IDs] NLM/ NIHMS507872; NLM/ PMC3963813
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4. Gallia GL, Rand V, Siu IM, Eberhart CG, James CD, Marie SK, Oba-Shinjo SM, Carlotti CG, Caballero OL, Simpson AJ, Brock MV, Massion PP, Carson BS Sr, Riggins GJ: PIK3CA gene mutations in pediatric and adult glioblastoma multiforme. Mol Cancer Res; 2006 Oct;4(10):709-14
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  • [Title] PIK3CA gene mutations in pediatric and adult glioblastoma multiforme.
  • Recently, a large-scale mutational analysis of eight PI3K and eight PI3K-like genes revealed somatic mutations in PIK3CA, which encodes the p110alpha catalytic subunit of class IA PI3K, in several types of cancer, including glioblastoma multiforme.
  • Given this disparity and to address the relation of patient age to mutation frequency, we examined 10 exons of PIK3CA in 73 glioblastoma samples by PCR amplification followed by direct DNA sequencing.
  • Of the primary tumors, PIK3CA mutations were identified in 21% and 17% of pediatric and adult samples, respectively.
  • [MeSH-major] Genetic Predisposition to Disease. Glioblastoma / genetics. Mutation. Phosphatidylinositol 3-Kinases / genetics

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  • (PMID = 17050665.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human
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5. Carson KA, Grossman SA, Fisher JD, Shaw EG: Prognostic factors for survival in adult patients with recurrent glioma enrolled onto the new approaches to brain tumor therapy CNS consortium phase I and II clinical trials. J Clin Oncol; 2007 Jun 20;25(18):2601-6
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  • [Title] Prognostic factors for survival in adult patients with recurrent glioma enrolled onto the new approaches to brain tumor therapy CNS consortium phase I and II clinical trials.
  • The studies had similar inclusion criteria and were conducted within the New Approaches to Brain Tumor Therapy CNS Consortium.
  • RESULTS: Factors associated with an increased risk of death were increased age, lower Karnofsky performance score (KPS), initial and on-study histologies of glioblastoma multiforme (GBM), corticosteroid use, shorter time from original diagnosis to recurrence, and tumor outside frontal lobe.
  • Median survival time was poorest in non-GBM patients with KPS less than 80 or GBM patients, age 50 years, corticosteroid use (4.4 months; 95% CI, 3.6 to 5.4 months); median survival was best in patients with initial histology other than GBM with KPS 80 and tumor confined to the frontal lobe (25.7 months; 95% CI, 18.7 to 52.5), and was 7.0 months (95% CI, 6.2 to 8.0 months) for all patients.

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  • (PMID = 17577040.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / U01 CA062475; United States / NCI NIH HHS / CA / CA62475
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS507874; NLM/ PMC4118746
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6. Badruddoja MA, Keir ST, King I, Zeidner J, Vredenburgh JJ, Muhlbaier LH, Bigner DD, Friedman HS: Activity of VNP40101M (Cloretazine) in the treatment of CNS tumor xenografts in athymic mice. Neuro Oncol; 2007 Jul;9(3):240-4
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  • [Title] Activity of VNP40101M (Cloretazine) in the treatment of CNS tumor xenografts in athymic mice.
  • The current study was designed to assess the activity of VNP40101M administered at a dose of 18 mg/kg daily for five days against a panel of human adult and pediatric CNS tumors growing subcutaneously or intracranially in athymic nude mice.
  • The results demonstrated statistically significant (p < 0.05) growth delays of 15.0, 8.3, 51.0, 60+, 60+, and 60+ days in subcutaneous xenografts derived from childhood glioblastoma multiforme (D-456 MG), childhood ependymoma (D-528 EP and D-612 EP), childhood medulloblastoma (D-425 MED), and adult malignant glioma (D-245 MG and D-54 MG), respectively, with corresponding tumor regressions in 10 of 10, 4 of 10, 8 of 10, 9 of 10, 9 of 10, and 10 of 10 treated mice, respectively.
  • Additional experiments conducted against subcutaneous D-245 MG xenografts by using reduced doses of 13.5 or 9.0 mg/kg daily for five days demonstrated tumor growth delays of 82.2 and 53.5 days, with corresponding tumor regressions in 8 of 9 and 9 of 10 treated mice, respectively (all values, p < 0.001), with one toxic death.
  • These findings suggest that VNP40101M is active in the treatment of a wide range of human central nervous system tumors and warrants translation to the clinic.

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  • (PMID = 17522334.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / P50 NS020023; United States / NINDS NIH HHS / NS / 5P50-NS20023-23
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hydrazines; 0 / Prodrugs; 0 / Sulfonamides; 14J2G0U3NQ / laromustine
  • [Other-IDs] NLM/ PMC1907418
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7. Vredenburgh JJ, Desjardins A, Herndon JE 2nd, Marcello J, Reardon DA, Quinn JA, Rich JN, Sathornsumetee S, Gururangan S, Sampson J, Wagner M, Bailey L, Bigner DD, Friedman AH, Friedman HS: Bevacizumab plus irinotecan in recurrent glioblastoma multiforme. J Clin Oncol; 2007 Oct 20;25(30):4722-9
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  • [Title] Bevacizumab plus irinotecan in recurrent glioblastoma multiforme.
  • PURPOSE: The prognosis for patients with recurrent glioblastoma multiforme is poor, with a median survival of 3 to 6 months.
  • After this regimen was deemed safe and effective, the irinotecan schedule was changed to an accepted brain tumor regimen of four doses in 6 weeks, in anticipation of a phase III randomized trial of irinotecan versus irinotecan and bevacizumab.
  • One patient developed a CNS hemorrhage, which occurred in his 10th cycle.
  • CONCLUSION: Bevacizumab and irinotecan is an effective treatment for recurrent glioblastoma multiforme and has moderate toxicity.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Glioblastoma / drug therapy. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Bevacizumab. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Female. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Survival Rate

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  • [CommentIn] Nat Clin Pract Oncol. 2008 Apr;5(4):186-7 [18285760.001]
  • [CommentIn] J Clin Oncol. 2007 Oct 20;25(30):4705-6 [17947716.001]
  • [CommentIn] J Clin Oncol. 2008 Nov 10;26(32):5304-5; author reply 5305 [18854564.001]
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  • [CommentIn] J Clin Oncol. 2008 Feb 20;26(6):1012-3; author reply 1013 [18281677.001]
  • (PMID = 17947719.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / 4 R37 CA11898; United States / NCI NIH HHS / CA / 5 P50 CA108786; United States / NINDS NIH HHS / NS / 5 P50 NS20023
  • [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 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
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8. Schuhmann MU, Zucht HD, Nassimi R, Heine G, Schneekloth CG, Stuerenburg HJ, Selle H: Peptide screening of cerebrospinal fluid in patients with glioblastoma multiforme. Eur J Surg Oncol; 2010 Feb;36(2):201-7
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  • [Title] Peptide screening of cerebrospinal fluid in patients with glioblastoma multiforme.
  • AIMS: To apply modern mass spectrometry based technology to identify possible CSF peptide markers of glioblastoma multiforme (GBM).
  • Using both, we analyzed CSF samples of 11 patients harbouring a glioblastoma multiforme in comparison to 13 normal controls.
  • CONCLUSION: The study showed that peptidomics technology is able to identify possible biomarkers of neoplastic CNS disease.
  • [MeSH-major] Biomarkers, Tumor / cerebrospinal fluid. Glioblastoma / cerebrospinal fluid. Peptides / cerebrospinal fluid. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Supratentorial Neoplasms / cerebrospinal fluid
  • [MeSH-minor] Adult. Aged. Albumins / cerebrospinal fluid. Chromatography, High Pressure Liquid. Female. Humans. Male. Middle Aged. Osteopontin / cerebrospinal fluid. Peptide Fragments. Prealbumin / cerebrospinal fluid. Proteomics / methods. alpha 1-Antichymotrypsin / cerebrospinal fluid

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19674866.001).
  • [ISSN] 1532-2157
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Albumins; 0 / Biomarkers, Tumor; 0 / Peptide Fragments; 0 / Peptides; 0 / Prealbumin; 0 / alpha 1-Antichymotrypsin; 106441-73-0 / Osteopontin
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9. Gömöri E, Halbauer JD, Kasza G, Varga D, Horvath Z, Komoly S: Glioblastoma multiforme with an unusual location and clinical course. Clin Neuropathol; 2009 May-Jun;28(3):165-7
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  • [Title] Glioblastoma multiforme with an unusual location and clinical course.
  • We present a unique case of a brain tumor patient with atypical location and progression.
  • Postmortally, formalin-fixed brain demonstrated that the main tumor mass was located in the fornix, infiltrating the ventricular system and disseminating over the cortex, cerebellum and spinal cord.
  • The authors recommend closer scrutiny of psychiatric patients presenting CNS symptomatology, negative MRI, CT and CSF.
  • [MeSH-major] Brain Neoplasms / diagnosis. Diagnostic Errors. Glioblastoma / diagnosis. Magnetic Resonance Imaging
  • [MeSH-minor] Accidents, Traffic. Adult. Anxiety / etiology. Fatal Outcome. Humans. Male. Mood Disorders / etiology. Stress Disorders, Post-Traumatic

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  • (PMID = 19537131.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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10. Horger M, Fenchel M, Nägele T, Moehle R, Claussen CD, Beschorner R, Ernemann U: Water diffusivity: comparison of primary CNS lymphoma and astrocytic tumor infiltrating the corpus callosum. AJR Am J Roentgenol; 2009 Nov;193(5):1384-7
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  • [Title] Water diffusivity: comparison of primary CNS lymphoma and astrocytic tumor infiltrating the corpus callosum.
  • OBJECTIVE: The purpose of this study was to determine whether lymphoma and astrocytic tumor infiltrating the corpus callosum can be reliably differentiated with measurement of water diffusivity.
  • MATERIALS AND METHODS: Echo-planar diffusion-weighted MR images of 27 patients with glioblastoma multiforme, five patients with low-grade astrocytoma, five patients with gliomatosis cerebri, and nine patients with primary lymphoma infiltrating the corpus callosum were reviewed retrospectively.
  • Regions of interest were drawn on apparent diffusion coefficient (ADC) maps inside the callosal tumor.
  • ADCs were normalized by calculation of the ratio between the ADC of the tumor and the ADC of an uninvolved region of corpus callosum.
  • RESULTS: The mean ADC of glioblastoma multiforme was 1.13 +/- 0.31 (SD) x 10(-3) mm(2)/s, and the mean tumor to corpus callosum ADC ratio was 1.51 +/- 0.46; of low-grade astrocytoma, 1.14 +/- 0.23 x 10(-3) mm(2)/s and 1.54 +/- 0.28; gliomatosis cerebri, 1.01 +/- 0.20 x 10(-3) mm(2)/s and 1.31 +/- 0.36; and lymphoma, 0.71 +/- 0.13 x 10(-3) mm(2)/s and 0.93 +/- 0.19.
  • The difference between the mean tumor to corpus callosum ADC ratio of lymphoma and that of all grades of astrocytoma (1.48 +/- 0.43) was statistically significant (p < 0.001).
  • The optimal ADC threshold for discriminating astrocytic tumor and lymphoma was 0.90 x 10(-3) mm(2)/s (sensitivity, 84%; specificity, 89%).
  • The optimal threshold for tumor to corpus callosum ADC ratio was 1.22 (sensitivity, 73%; specificity, 100%).
  • CONCLUSION: The water diffusivity and the ADC ratio of the tumor to normal-appearing corpus callosum of astrocytic tumor differ significantly from those of lymphoma infiltrating the corpus callosum, allowing reliable differentiation of the two types of tumor.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Corpus Callosum / pathology. Diffusion Magnetic Resonance Imaging / methods. Glioblastoma / pathology. Lymphoma / pathology. Water / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Analysis of Variance. Female. Humans. Image Processing, Computer-Assisted. Male. Middle Aged. ROC Curve. Retrospective Studies. Sensitivity and Specificity

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  • (PMID = 19843757.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 059QF0KO0R / Water
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11. Lasky JL 3rd, Choe M, Nakano I: Cancer stem cells in pediatric brain tumors. Curr Stem Cell Res Ther; 2009 Dec;4(4):298-305
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  • [Title] Cancer stem cells in pediatric brain tumors.
  • Central nervous system (CNS) tumors remain the leading cause of death among pediatric neoplasms.
  • Although standard therapies cure many pediatric CNS tumors, the long-term cognitive and physical consequences of these therapies are devastating.
  • Although recent studies have focused on molecular mechanisms that underlie the initiation and progression of adult glioblastoma multiforme (GBM), these tumors differ phenotypically and at a molecular level from pediatric brain tumors.
  • Recent investigations have identified a stem cell population, termed "brain tumor stem cells" (BTSC) within the heterogeneous cell populations that comprise malignant brain tumors which may be partly responsible for the resistance to current therapies.
  • By exploiting molecular differences present within these heterogeneous populations of brain tumor cells, we may be able to achieve specific eradication of BTSC and long-lasting remissions, while causing less toxicity to normal tissues.
  • In this review, we describe the issues surrounding the identification and characterization of BTSC, the molecular biology of BTSC for different pediatric brain tumors, and suggest future avenues for the development of treatments for this devastating disease.
  • [MeSH-major] Brain Neoplasms / pathology. Ependymoma / pathology. Medulloblastoma / pathology. Neoplastic Stem Cells / pathology. Optic Nerve Glioma / pathology
  • [MeSH-minor] Adult Stem Cells / pathology. Biomarkers / metabolism. Cell Differentiation. Chemotherapy, Adjuvant. Child. Humans. Surgical Procedures, Operative


12. Comincini S, Ferrara V, Arias A, Malovini A, Azzalin A, Ferretti L, Benericetti E, Cardarelli M, Gerosa M, Passarin MG, Turazzi S, Bellazzi R: Diagnostic value of PRND gene expression profiles in astrocytomas: relationship to tumor grades of malignancy. Oncol Rep; 2007 May;17(5):989-96
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  • [Title] Diagnostic value of PRND gene expression profiles in astrocytomas: relationship to tumor grades of malignancy.
  • It is abundant in testis and, unlike PRNP, it is expressed at low levels in the adult central nervous system (CNS).
  • Recently, ectopic expression of doppel was found in two different tumor types, specifically in glial and haematological cancers.
  • In order to address clinical important issues, PRND mRNA expression was investigated in a panel of 111 astrocytoma tissue samples, histologically classified according to the World Health Organization (WHO) criteria (6 grade I pilocytic astrocytomas, 15 grade II low-grade astrocytomas, 26 grade III anaplastic astrocytomas and 64 grade IV glioblastoma multiforme).
  • Real-time PRND gene expression profiling, after normalisation with GAPDH, revealed large differences between low (WHO I and II) and high grade (III and IV) of malignancy (P<0.001).
  • Extensive differences in PRND gene expression were also found within each grade of malignancy, suggesting that PRND mRNA quantitation might be useful to distinguish astrocytoma subtypes, and important in disease stratification and in the assessment of specific treatment strategies.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Prions / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Algorithms. Child. Cluster Analysis. Female. GPI-Linked Proteins. Gene Expression Profiling. Glioblastoma / genetics. Glioblastoma / metabolism. Glioblastoma / pathology. Humans. Male. Middle Aged. Prognosis

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  • (PMID = 17390034.001).
  • [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 / GPI-Linked Proteins; 0 / PRND protein, human; 0 / Prions
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13. Hur H, Jung S, Jung TY, Kim IY: Cerebellar glioblastoma multiforme in an adult. J Korean Neurosurg Soc; 2008 Apr;43(4):194-7

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  • [Title] Cerebellar glioblastoma multiforme in an adult.
  • Primary cerebellar glioblastoma multiforme (GBM) is a rare tumor in adults that accounts for just 1% of all cases of GBM.
  • After operation, glioblastoma was histologically confirmed.

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  • (PMID = 19096643.001).
  • [ISSN] 2005-3711
  • [Journal-full-title] Journal of Korean Neurosurgical Society
  • [ISO-abbreviation] J Korean Neurosurg Soc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2588262
  • [Keywords] NOTNLM ; Cerebellum / Differential diagnosis / Glioblastoma multiforme / Pathogenesis
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14. Selkirk SM, Morrow J, Barone TA, Hoffer A, Lock J, DeChant A, Mangla S, Plunkett RJ, Miller RH: Elevation of osteopontin levels in brain tumor cells reduces burden and promotes survival through the inhibition of cell dispersal. J Neurooncol; 2008 Feb;86(3):285-96
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  • [Title] Elevation of osteopontin levels in brain tumor cells reduces burden and promotes survival through the inhibition of cell dispersal.
  • Osteopontin (OPN) is a pleotrophic molecule that has been associated with multiple disorders of the central nervous system (CNS).
  • Its roles in CNS malignancy are unclear but suggest that higher levels of OPN expression correlate with increased tumor grade and increased migratory capacity of tumor cells.
  • In this study OPN cDNA was cloned into a retroviral vector and used to infect F98 Fischer rat-derived glioma cells and U87 human-derived glioblastoma multiforme (GBM) cells in vitro.
  • Implantation of tumor cells expressing high levels of OPN into adult Fischer rats and nude rats resulted in morphologically distinct tumors and prolonged host survival relative to controls.
  • We propose that local produced, high level OPN expression limits the malignant character of glioma cells and that the downstream mechanisms involved represent pathways that may have therapeutic value in the treatment of human CNS malignancy.

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  • (PMID = 17928956.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA10373602; United States / NINDS NIH HHS / NS / R01 NS036674; United States / NINDS NIH HHS / NS / NS030800-14; United States / NINDS NIH HHS / NS / R01 NS030800; United States / NINDS NIH HHS / NS / NS-3080011; United States / NINDS NIH HHS / NS / R37 NS036674; United States / NINDS NIH HHS / NS / R01 NS030800-14; United States / NINDS NIH HHS / NS / NS-36674-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD31; 106441-73-0 / Osteopontin; 147336-22-9 / Green Fluorescent Proteins; G34N38R2N1 / Bromodeoxyuridine
  • [Other-IDs] NLM/ NIHMS196650; NLM/ PMC2911624
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15. Perry SL, Bohlin C, Reardon DA, Desjardins A, Friedman AH, Friedman HS, Vredenburgh JJ: Tinzaparin prophylaxis against venous thromboembolic complications in brain tumor patients. J Neurooncol; 2009 Oct;95(1):129-134
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  • [Title] Tinzaparin prophylaxis against venous thromboembolic complications in brain tumor patients.
  • The purpose of this study was to determine the safety of tinzaparin for deep vein thrombosis prophylaxis in newly diagnosed grade III-IV malignant glioma patients.
  • Forty patients were enrolled into the study, 35 with glioblastoma multiforme and 5 with anaplastic astrocytoma.
  • Possible attributable toxicity was limited to two patients who developed CNS hemorrhages (one grade 1 and one grade 2) and one patient with an increase in liver enzymes (grade 3).
  • There were no patients with a grade 4 or 5 CNS hemorrhages or systemic hemorrhages >or=grade 2.
  • Tinzaparin at a fixed prophylactic dose is safe and may decrease the incidence of thromboembolic complications in brain tumor patients.
  • [MeSH-major] Brain Neoplasms / complications. Fibrinolytic Agents / therapeutic use. Glioma / complications. Heparin, Low-Molecular-Weight / therapeutic use. Venous Thromboembolism / etiology. Venous Thromboembolism / prevention & control
  • [MeSH-minor] Adult. Aged. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Male. Middle Aged. Pulmonary Embolism / etiology. Pulmonary Embolism / prevention & control. Tomography, X-Ray Computed

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  • (PMID = 19415455.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / K23 HL084233-02; United States / NHLBI NIH HHS / HL / K23 HL084233-03; United States / NHLBI NIH HHS / HL / K23 HL084233; United States / NHLBI NIH HHS / HL / K23 HL084233-01A1; United States / NHLBI NIH HHS / HL / K23-HL084233-02
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fibrinolytic Agents; 0 / Heparin, Low-Molecular-Weight; 7UQ7X4Y489 / tinzaparin
  • [Other-IDs] NLM/ NIHMS180651; NLM/ PMC2837514
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16. Mattos JP, Marenco HA, Campos JM, Faria AV, Queiroz LS, Borges G, Oliveira Ed: Cerebellar glioblastoma multiforme in an adult. Arq Neuropsiquiatr; 2006 Mar;64(1):132-5
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  • [Title] Cerebellar glioblastoma multiforme in an adult.
  • Cerebellar glioblastoma multiforme (GBM) is a rare tumor.
  • In conjunction, we present a literature review including particular issues, clinical data, advances in imaging studies, pathological characteristics, treatment options and the behavior of such malignant tumor.
  • [MeSH-major] Cerebellar Neoplasms / pathology. Cerebellum / pathology. Glioblastoma / pathology

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  • (PMID = 16622570.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Brazil
  • [Number-of-references] 16
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17. Tunici P, Yu JS: Pituitary adenoma stem cells. Methods Mol Biol; 2009;568:195-201
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  • The identification of a subpopulation of brain tumor cells with potent tumorigenic capacity strengthens the cancer stem cell hypothesis of the origin of the tumors that has recently attracted the attention of many researchers.
  • Reports have been published on the identification of tumor cells with stem cells characteristics in different types of tumors (acute myelogenic leukemia, breast cancer, prostate cancer, bone sarcomas, liver cancer, and melanomas).
  • We and other groups have previously reported the isolation of cancer stem cells from adult glioblastoma multiforme.
  • In vivo they give a tumor that recapitulates the characteristics of the tumor in the patient.
  • More recently we have isolated tumor stem-like cells also from benign tumors like pituitary adenomas.
  • The immunocytochemical analysis revealed that pituitary tumor stem-like cells are positives for nestin and, when grown for ten days in differentiation medium they express GFAP, BIII tubulin, and S-100.
  • In vitro tumor stem-like cells derived from a patient with a somatotroph adenoma showed high production of growth hormone and prolactin, while cells derived from the same patient but grown in presence of fetal bovine serum showed no production of hormones.

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  • (PMID = 19582428.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin
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18. Potter NE, Phipps K, Harkness W, Hayward R, Thompson D, Jacques TS, Harding B, Thomas DG, Rees J, Darling JL, Warr TJ: Astrocytoma derived short-term cell cultures retain molecular signatures characteristic of the tumour in situ. Exp Cell Res; 2009 Oct 1;315(16):2835-46
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  • [Title] Astrocytoma derived short-term cell cultures retain molecular signatures characteristic of the tumour in situ.
  • We have characterised gene expression changes induced by short-term culture in astrocytoma in order to determine whether derived short-term cell cultures are representative of the tumour in situ.
  • We have used the Affymetrix GeneChip U133A to generate gene expression profiles of 6 paediatric pilocytic astrocytoma (PA) biopsies and derived short-term cell cultures and 3 adult glioblastoma multiforme (GBM) biopsies and derived short-term cultures.
  • This gene cohort can distinguish PA and GBM tumours, regardless of the sample source, suggesting that astrocytoma derived short-term cultures do retain key aspects of the global tumour expression profile and are representative of the tumour in situ.
  • Furthermore, these genes are involved in pathways and functions characteristic of adult GBM including VEGF signalling, hypoxia and TP53 signalling.
  • [MeSH-major] Astrocytoma. Biomarkers, Tumor / metabolism. Brain Neoplasms. Tumor Cells, Cultured / metabolism
  • [MeSH-minor] Adult. Animals. Child. Cluster Analysis. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Oligonucleotide Array Sequence Analysis. Signal Transduction / physiology

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  • (PMID = 19523942.001).
  • [ISSN] 1090-2422
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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19. Marumoto T, Tashiro A, Friedmann-Morvinski D, Scadeng M, Soda Y, Gage FH, Verma IM: Development of a novel mouse glioma model using lentiviral vectors. Nat Med; 2009 Jan;15(1):110-6
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  • We report the development of a new method to induce glioblastoma multiforme in adult immunocompetent mice by injecting Cre-loxP-controlled lentiviral vectors expressing oncogenes.
  • Cell type- or region-specific expression of activated forms of the oncoproteins Harvey-Ras and AKT in fewer than 60 glial fibrillary acidic protein-positive cells in the hippocampus, subventricular zone or cortex of mice heterozygous for the gene encoding the tumor suppressor Tp53 were tested.
  • Mice developed glioblastoma multiforme when transduced either in the subventricular zone or the hippocampus.
  • Transplantation of brain tumor cells into naive recipient mouse brain resulted in the formation of glioblastoma multiforme-like tumors, which contained CD133(+) cells, formed tumorspheres and could differentiate into neurons and astrocytes.
  • We suggest that the use of Cre-loxP-controlled lentiviral vectors is a novel way to generate a mouse glioblastoma multiforme model in a region- and cell type-specific manner in adult mice.


20. Umesh S, Tandon A, Santosh V, Anandh B, Sampath S, Chandramouli BA, Sastry Kolluri VR: Clinical and immunohistochemical prognostic factors in adult glioblastoma patients. Clin Neuropathol; 2009 Sep-Oct;28(5):362-72
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  • [Title] Clinical and immunohistochemical prognostic factors in adult glioblastoma patients.
  • OBJECTIVE: Glioblastomas are the commonest and the most malignant of all adult brain tumors, characterized by genetic instability, intratumoral histopathological variability, and unpredictable clinical behavior.
  • The utility of tumor markers that reflect their underlying biology is becoming increasingly important with respect to patient prognostication and their potential role as molecular targets of therapy is being recognized.
  • MATERIALS AND METHODS: We evaluated 54 cases of adult supratentorial glioblastomas operated over a span of 1 year, with respect to clinical features such as age, Karnofsky performance score (KPS), extent of resection, adjuvant therapy, and immunohistochemical expression of p53, EGFR (Epidermal Growth Factor Receptor) and PTEN (Phosphatase and Tensin homolog).
  • CONCLUSIONS: Our study shows that EGFR and p53 overexpression along with loss of PTEN expression are important adjuncts to clinical variables in prognosticating glioblastoma patients.
  • [MeSH-major] Glioblastoma / diagnosis. Supratentorial Neoplasms / diagnosis
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Female. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. PTEN Phosphohydrolase / metabolism. Prognosis. Receptor, Epidermal Growth Factor / metabolism. Severity of Illness Index. Treatment Outcome. Tumor Suppressor Protein p53 / metabolism. Young Adult

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  • (PMID = 19788052.001).
  • [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 / Tumor Suppressor Protein p53; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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21. McKean-Cowdin R, Barnholtz-Sloan J, Inskip PD, Ruder AM, Butler M, Rajaraman P, Razavi P, Patoka J, Wiencke JK, Bondy ML, Wrensch M: Associations between polymorphisms in DNA repair genes and glioblastoma. Cancer Epidemiol Biomarkers Prev; 2009 Apr;18(4):1118-26
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  • [Title] Associations between polymorphisms in DNA repair genes and glioblastoma.
  • A pooled analysis was conducted to examine the association between select variants in DNA repair genes and glioblastoma multiforme, the most common and deadliest form of adult brain tumors.
  • Genetic data for approximately 1,000 glioblastoma multiforme cases and 2,000 controls were combined from four centers in the United States that have conducted case-control studies on adult glioblastoma multiforme, including the National Cancer Institute, the National Institute for Occupational Safety and Health, the University of Texas M. D.
  • The C allele of the PARP1 rs1136410 variant was associated with a 20% reduction in risk for glioblastoma multiforme (odds ratio(CT or CC), 0.80; 95% confidence interval, 0.67-0.95).
  • A 44% increase in risk for glioblastoma multiforme was found for individuals homozygous for the G allele of the PRKDC rs7003908 variant (odds ratio(GG), 1.44; 95% confidence interval, 1.13-1.84); there was a statistically significant trend (P = 0.009) with increasing number of G alleles.
  • Few studies have reported on the associations between variants in DNA repair genes and brain tumors, and few specifically have examined their impact on glioblastoma multiforme.
  • Our results suggest that common variation in DNA repair genes may be associated with risk for glioblastoma multiforme.

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  • (PMID = 19318434.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01CA070917; United States / NCI NIH HHS / CA / R01 CA052689-18; United States / NCI NIH HHS / CA / R01 CA052689-19; United States / NCI NIH HHS / CA / CA097257-080001; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / CA052689-19; United States / NCI NIH HHS / CA / P50 CA097257; United States / NCI NIH HHS / CA / R01 CA070917; United States / NCI NIH HHS / CA / P50CA097257; United States / NCI NIH HHS / CA / R01CA52689; United States / NCI NIH HHS / CA / P50 CA097257-080001; United States / NCI NIH HHS / CA / R01 CA070917-09; United States / NCI NIH HHS / CA / CA052689-18; United States / NCI NIH HHS / CA / R01 CA052689
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 6.5.1.- / DNA Repair Enzymes
  • [Other-IDs] NLM/ NIHMS96659; NLM/ PMC2667563
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22. Lesniak MS: Gene therapy for malignant glioma. Expert Rev Neurother; 2006 Apr;6(4):479-88
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  • Glioblastoma multiforme represents the most common primary malignant tumor of the adult CNS.
  • Consequently, efforts aimed at developing new therapies have focused on new treatment strategies that specifically target tumor cells and spare normal cells.
  • One such modality, gene therapy, has shown promise in the spectrum of agents utilized against brain tumors.
  • This review highlights the principles of gene therapy and discusses the results of recent clinical trials in which gene therapy has been employed against malignant brain tumors.
  • [MeSH-major] Brain Neoplasms / genetics. Genetic Therapy / methods. Glioma / genetics
  • [MeSH-minor] Animals. Genetic Vectors / genetics. Genetic Vectors / therapeutic use. Glioblastoma / genetics. Glioblastoma / therapy. Humans

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  • (PMID = 16623647.001).
  • [ISSN] 1744-8360
  • [Journal-full-title] Expert review of neurotherapeutics
  • [ISO-abbreviation] Expert Rev Neurother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 77
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23. Khan MK, Hunter GK, Vogelbaum M, Suh JH, Chao ST: Evidence-based adjuvant therapy for gliomas: current concepts and newer developments. Indian J Cancer; 2009 Apr-Jun;46(2):96-107
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  • Of the 18,820 new cases of primary central nervous system (CNS) tumors diagnosed annually in the United States, gliomas account for over 60% with 30-40% of them being glioblastoma multiforme (GBM), 10% being anaplastic astrocytoma (AA), and 10% being low grade gliomas (LGGs).
  • This is in contrast to one study from West Bengal, India, in which only 7.9% of the brain tumors were GBMs, while 46.8% were astrocytomas.
  • Of all adult primary CNS tumors, GBM is the most common and the most malignant with about 7,000 to 8,000 new cases annually in the United States.
  • Common to these approaches is the use of adjuvant radiation therapy, even as surgery alone, with or without chemotherapy, may be the mainstay for some lower grade and low-risk gliomas.
  • Specifically, the database is searched using the following keywords, with various combinations: glioma, low-grade, anaplastic, astrocytoma, oligodendroglioma, oligoastrocytoma, glioblastoma multiforme, chemotherapy, radiation, new concepts, phase III, MGMT, CDX-110 (Celldex), temozolomide, 1p/19q deletion, and bevacizumab.
  • [MeSH-major] Central Nervous System Neoplasms / therapy. Chemotherapy, Adjuvant. Evidence-Based Medicine. Glioma / therapy. Radiotherapy, Adjuvant
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Astrocytoma / radiotherapy. Astrocytoma / therapy. Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Glioblastoma / therapy. Humans

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  • (PMID = 19346643.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 64
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24. Lustig R, Mikkelsen T, Lesser G, Grossman S, Ye X, Desideri S, Fisher J, Wright J, New Approaches to Brain Tumor Therapy CNS Consortium: Phase II preradiation R115777 (tipifarnib) in newly diagnosed GBM with residual enhancing disease. Neuro Oncol; 2008 Dec;10(6):1004-9
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  • Glioblastoma multiforme (GBM) is a lethal primary malignant brain tumor in adults.
  • Following surgery, an MRI confirmed the presence of residual enhancing tumor.
  • The primary end point was overall survival; secondary end points were tumor response rate and toxicity.
  • There were no tumor responses.

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  • (PMID = 18725460.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01-CA62475; United States / NCI NIH HHS / CA / U01 CA062475; United States / NCI NIH HHS / CA / P30-CA0516; United States / NCI NIH HHS / CA / U01-CA105689; United States / NCI NIH HHS / CA / U01 CA105689
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / Antineoplastic Agents; 0 / Quinolones; 192185-72-1 / tipifarnib
  • [Other-IDs] NLM/ PMC2718997
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25. Grossman SA, Alavi JB, Supko JG, Carson KA, Priet R, Dorr FA, Grundy JS, Holmlund JT: Efficacy and toxicity of the antisense oligonucleotide aprinocarsen directed against protein kinase C-alpha delivered as a 21-day continuous intravenous infusion in patients with recurrent high-grade astrocytomas. Neuro Oncol; 2005 Jan;7(1):32-40
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  • [Title] Efficacy and toxicity of the antisense oligonucleotide aprinocarsen directed against protein kinase C-alpha delivered as a 21-day continuous intravenous infusion in patients with recurrent high-grade astrocytomas.
  • Aprinocarsen is an antisense oligonucleotide against PKC-alpha that reduces PKC-alphain human cell lines and inhibits a human glioblastoma tumor cell line in athymic mice.
  • In this phase 2 study, aprinocarsen was administered to patients with recurrent high-grade gliomas by continuous intravenous infusion (2.0 mg/kg/day for 21 days per month).
  • Their median age was 46 years (range, 28-68 years), median Karnofsky performance status was 80 (range, 60-100), median tumor volume was 58 cm3 (range, 16-254 cm3), and histology included glioblastoma multiforme (n = 16), anaplastic oligodendroglioma (n = 4), and anaplastic astrocytoma (n = 1).
  • No tumor responses were observed.
  • The observed toxicities were mild, reversible, and uncommon (grade 3 thrombocytopenia [n = 3] and grade 4 AST [n = 1]), and no coagulopathy or CNS bleeding resulted from this therapy.
  • This is the first study to use an antisense oligonucleotide or a specific PKC-alpha inhibitor in patients with high-grade gliomas.
  • The rapid deterioration seen in these patients could result from tumor growth or an effect of aprinocarsen on bloodbrain barrier integrity.

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  • (PMID = 15701280.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA062475; United States / NCI NIH HHS / CA / U01-CA-26406; United States / NCI NIH HHS / CA / UO1CA-62475
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oligonucleotides, Antisense; 0 / Phosphorothioate Oligonucleotides; EC 2.7.11.13 / PRKCA protein, human; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.13 / Protein Kinase C-alpha; FMT95051CQ / aprinocarsen
  • [Other-IDs] NLM/ PMC1871621
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26. Sathornsumetee S, Rich JN, Reardon DA: Diagnosis and treatment of high-grade astrocytoma. Neurol Clin; 2007 Nov;25(4):1111-39, x
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  • [Title] Diagnosis and treatment of high-grade astrocytoma.
  • High-grade astrocytomas include the most common adult central nervous system (CNS) tumor, glioblastoma multiforme, and anaplastic astrocytoma--a highly aggressive cancer with short median survival despite maximal multimodality therapy.
  • Nearly all patients who have high-grade astrocytomas develop tumor recurrence or progression after this multimodality treatment.
  • Two treatment challenges are molecular/genetic heterogeneity of tumors and limited CNS tumor delivery.
  • This article discusses diagnosis and current treatment of high-grade astrocytomas.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Astrocytoma / pathology. Astrocytoma / therapy. Brain Neoplasms / pathology. Brain Neoplasms / therapy. Dacarbazine / analogs & derivatives
  • [MeSH-minor] Brachytherapy. Diagnosis, Differential. Humans. Magnetic Resonance Imaging. Magnetic Resonance Spectroscopy. Neoplasm Staging. Neurosurgical Procedures / methods

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  • (PMID = 17964028.001).
  • [ISSN] 0733-8619
  • [Journal-full-title] Neurologic clinics
  • [ISO-abbreviation] Neurol Clin
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 P20 CA096890; United States / NCI NIH HHS / CA / CA11898; United States / NINDS NIH HHS / NS / NS20023
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
  • [Number-of-references] 142
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27. Moise D, Madhusoodanan S: Psychiatric symptoms associated with brain tumors: a clinical enigma. CNS Spectr; 2006 Jan;11(1):28-31
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  • [Title] Psychiatric symptoms associated with brain tumors: a clinical enigma.
  • Patients in psychiatric settings may present with medical conditions, such as brain tumors, which may or may not be associated with neurological symptoms.
  • Brain tumors may be detected in patients at their first presentation to mental health services or sometimes in patients with well-established psychiatric diagnoses.
  • Brain imaging showed the presence of a left thalamic tumor, later confirmed as glioblastoma multiforme.
  • With this we show that in some cases, brain tumors can be neurologically silent and only present atypical psychiatric symptoms.
  • [MeSH-major] Brain Neoplasms / complications. Depressive Disorder, Major / etiology. Stress Disorders, Post-Traumatic / etiology
  • [MeSH-minor] Adult. Female. Functional Laterality. Humans. Severity of Illness Index. Thalamus / surgery

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  • (PMID = 16400253.001).
  • [ISSN] 1092-8529
  • [Journal-full-title] CNS spectrums
  • [ISO-abbreviation] CNS Spectr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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28. Agnihotri S, Wolf A, Picard D, Hawkins C, Guha A: GATA4 is a regulator of astrocyte cell proliferation and apoptosis in the human and murine central nervous system. Oncogene; 2009 Aug 27;28(34):3033-46
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  • [Title] GATA4 is a regulator of astrocyte cell proliferation and apoptosis in the human and murine central nervous system.
  • The GATA transcription factors consist of six family members, which bind to the consensus DNA-binding element, W-GATA-R, and are poorly characterized in the central nervous system (CNS).
  • Using retroviral gene trapping on transgenic mouse glioma models, we identified GATA6 to be a novel tumor suppressor gene in glioblastoma multiforme.
  • We now show GATA4, a family member of GATA6, to be expressed in the neurons and glia of normal murine and human embryonic and adult CNS.
  • Furthermore, GATA4 expression was lost in a panel of human malignant astrocytoma cell lines.
  • Collectively, we show that GATA4 is expressed in the embryonic and adult CNS and acts as a negative regulator of astrocyte proliferation and growth.
  • [MeSH-major] Apoptosis. Astrocytes / physiology. Brain / cytology. GATA4 Transcription Factor / physiology
  • [MeSH-minor] Animals. Cell Cycle. Cell Proliferation. Cells, Cultured. Cyclin-Dependent Kinase Inhibitor p15 / genetics. Humans. Mice. Transforming Growth Factor beta / pharmacology. Tumor Suppressor Protein p53 / physiology

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  • (PMID = 19543315.001).
  • [ISSN] 1476-5594
  • [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 / Cyclin-Dependent Kinase Inhibitor p15; 0 / GATA4 Transcription Factor; 0 / GATA4 protein, human; 0 / Gata4 protein, mouse; 0 / Transforming Growth Factor beta; 0 / Tumor Suppressor Protein p53
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29. Mondin V, Ferlito A, Devaney KO, Woolgar JA, Rinaldo A: A survey of metastatic central nervous system tumors to cervical lymph nodes. Eur Arch Otorhinolaryngol; 2010 Nov;267(11):1657-66
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  • [Title] A survey of metastatic central nervous system tumors to cervical lymph nodes.
  • There are, of course, less frequently encountered differential diagnostic possibilities; one of the most uncommon of all is the possibility of metastasis from an intracranial tumor.
  • The present review examines the published experience with 128 tumors that gave rise to cervical node metastases in both adult and in pediatric patients.
  • While it is presumed that the blood-brain barrier blocks the spread of most tumors beyond the intracranial locale, this is speculative.
  • Although many of the cervical node metastases reported here arose after craniotomy (and, presumably, after breaching of the blood-brain barrier), some arose in the absence of any preceding surgical procedure.
  • Cervical node metastases may arise from glial tumors (including glioblastoma multiforme, in both adult and pediatric patients) and non-glial tumors (such as medulloblastoma in pediatric patients).
  • The history of a previous intracranial lesion is often the key to correct diagnosis, since, without prompting, neither the pathologist nor the radiologist is likely to think of a cervical node metastasis from a brain tumor when assessing a cervical mass of unknown etiology.
  • [MeSH-major] Central Nervous System Neoplasms / pathology. Head and Neck Neoplasms / secondary. Lymphatic Metastasis / pathology
  • [MeSH-minor] Blood-Brain Barrier. Humans

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  • (PMID = 20694730.001).
  • [ISSN] 1434-4726
  • [Journal-full-title] European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
  • [ISO-abbreviation] Eur Arch Otorhinolaryngol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
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30. Khattab AZ, Ahmed MI, Fouad MA, Essa WA: Significance of p53 and CD31 in astrogliomas. Med Oncol; 2009;26(1):86-92
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  • BACKGROUND: Astrogliomas are the most common primary brain tumor.
  • Its progression is the result of activation of oncogenes, inactivation of tumor suppressor genes (TSGs), and expression of various growth factors.
  • Sections were stained with hematoxylin and eosin to determine the type and histological grade according to WHO (2007) classification of CNS tumors.
  • Immunostaining was done using anti p53 and CD31 and the results were measured as labeling index (LI) using image analyzer system CAS-200.
  • The expressions of p53 and CD31 were markedly increased in glioblastoma multiforme (GBM) with mean values (59.7 +/- 13.5) (P = 0.0001) and (40.7 +/- 8.9) (P = 0.001), respectively.
  • Obviously, these observations demonstrate that the co-expression and increased levels of p53 and CD31 in astrogliomas are increasing as the tumor grade is increasing.
  • CONCLUSION: The estimation of p53 and CD31 could be used as good tools to assess the grade, prognosis, and aggressiveness of the astroglial tumors.
  • Thus, the two markers can be used as adjunct to the diagnosis and stratification of the high grade from the low-grade intrinsic brain astrogliomas.
  • [MeSH-major] Antigens, CD31 / biosynthesis. Astrocytoma / metabolism. Biomarkers, Tumor. Brain Neoplasms / metabolism. Tumor Suppressor Protein p53 / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Immunohistochemistry. Infant. Male. Middle Aged. Neoplasm Staging

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  • (PMID = 18821037.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Protein p53
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31. Phuphanich S, Carson KA, Grossman SA, Lesser G, Olson J, Mikkelsen T, Desideri S, Fisher JD, New Approaches to Brain Tumor Therapy (NABTT) CNS Consortium: Phase I safety study of escalating doses of atrasentan in adults with recurrent malignant glioma. Neuro Oncol; 2008 Aug;10(4):617-23
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  • Patients were evaluated for response every 8 weeks and remained on the study until the tumor progressed or toxicities occurred.
  • Twenty-two patients had glioblastoma multiforme (GBM), 2 had anaplastic astrocytoma, and 1 had an anaplastic oliogodendroglioma; 24 patients had received one prior chemo therapy regimen before being enrolled in the study.
  • The most common atrasentan-related toxicities were grade 1 or 2 rhinitis, fatigue, and edema.
  • One patient developed grade 3 hypoxia and peripheral edema at a dose of 90 mg/day.

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  • (PMID = 18477765.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA062406; United States / NCI NIH HHS / CA / U01 CA062475; United States / NCI NIH HHS / CA / U01-CA62406; United States / NCI NIH HHS / CA / UO1 CA-62475
  • [Publication-type] Case Reports; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pyrrolidines; V6D7VK2215 / atrasentan
  • [Other-IDs] NLM/ PMC2666236
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32. Kleinschmidt-DeMasters BK, Meltesen L, McGavran L, Lillehei KO: Characterization of glioblastomas in young adults. Brain Pathol; 2006 Oct;16(4):273-86
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  • Most adult glioblastoma multiformes (GBMs) present in patients 45-70 years old; tumors occurring at the extremes of the adult age spectrum are uncommon, and seldom studied.
  • We hypothesized that young-adult GBMs would differ from elderly-adult and from pediatric GBMs.
  • Twenty-eight (74%) of our 38 young-adult GBM patients had primary de novo tumors, two of which occurred in patients with cancer syndromes.
  • GBMs in young adults are a more inhomogeneous tumor group than GBMs occurring in older adult patients and show features that overlap with both pediatric and adult GBMs.
  • [MeSH-major] Brain Neoplasms / mortality. Brain Neoplasms / pathology. Glioblastoma / mortality. Glioblastoma / pathology
  • [MeSH-minor] Adolescent. Adult. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Ki-67 Antigen / metabolism. Male. Mitotic Index. Neoplasms, Radiation-Induced. Neoplasms, Second Primary / mortality. Neoplasms, Second Primary / pathology. Prognosis. Receptor, Epidermal Growth Factor / metabolism. Survival Analysis. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 17107596.001).
  • [ISSN] 1015-6305
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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33. Roche FP, Sheahan BJ, O'Mara SM, Atkins GJ: Semliki Forest virus-mediated gene therapy of the RG2 rat glioma. Neuropathol Appl Neurobiol; 2010 Dec;36(7):648-60
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  • AIMS: Glioblastoma multiforme is the most common and most malignant adult brain tumour.
  • Despite numerous advances in cancer therapy there has been little change in the prognosis of glioblastoma multiforme, which remains invariably fatal.
  • We examined the Semliki Forest virus virus-like particle (SFV VLP) expression system encoding interleukin-12 (IL-12) as a therapeutic intervention against the syngeneic RG2 rat glioma model.
  • High-dose treatment resulted in an 87% reduction in tumour volume, related to the oncolytic capacity of the SFV VLP system.
  • VLP delivery to the central nervous system (CNS) demonstrated the potential of the vector system to induce lethal pathology that was unrelated to replication-competent virus or high-level IL-12 expression.
  • CONCLUSION: The efficacy of an IL-12 gene therapy approach for the treatment of the RG2 glioma model has been demonstrated in addition to the oncolytic capacity of the VLP vector system.
  • Despite this, the broad tropism of the SFV-based expression vector may limit use as a CNS gene therapy vector unless this inherent limitation can be overcome.
  • [MeSH-major] Brain Neoplasms / therapy. Genetic Therapy / methods. Glioma / therapy. Semliki forest virus / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Endpoint Determination. Interleukin-12 / biosynthesis. Interleukin-12 / genetics. Kaplan-Meier Estimate. Male. Neoplasm Transplantation. Rats. Rats, Inbred F344. Stereotaxic Techniques. Virus Replication

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  • [Copyright] © 2010 The Authors. Neuropathology and Applied Neurobiology © 2010 British Neuropathological Society.
  • (PMID = 20649937.001).
  • [ISSN] 1365-2990
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 187348-17-0 / Interleukin-12
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34. Chi AS, Sorensen AG, Jain RK, Batchelor TT: Angiogenesis as a therapeutic target in malignant gliomas. Oncologist; 2009 Jun;14(6):621-36
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  • Currently, adult glioblastoma (GBM) patients have poor outcomes with conventional cytotoxic treatments.
  • Because GBMs are highly angiogenic tumors, inhibitors that target tumor vasculature are considered promising therapeutic agents in these patients.
  • [MeSH-minor] Animals. Cell Movement / drug effects. Clinical Trials as Topic. Drug Resistance, Neoplasm. Edema / drug therapy. Endothelial Cells / drug effects. Humans. Protein Kinase Inhibitors / therapeutic use. Receptors, Platelet-Derived Growth Factor / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors. Signal Transduction / drug effects. Vascular Endothelial Growth Factor A / antagonists & inhibitors

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  • (PMID = 19487335.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA080124
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Protein Kinase Inhibitors; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 175
  • [Other-IDs] NLM/ NIHMS765709; NLM/ PMC4790121
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35. Kunwar S, Prados MD, Chang SM, Berger MS, Lang FF, Piepmeier JM, Sampson JH, Ram Z, Gutin PH, Gibbons RD, Aldape KD, Croteau DJ, Sherman JW, Puri RK, Cintredekin Besudotox Intraparenchymal Study Group: Direct intracerebral delivery of cintredekin besudotox (IL13-PE38QQR) in recurrent malignant glioma: a report by the Cintredekin Besudotox Intraparenchymal Study Group. J Clin Oncol; 2007 Mar 1;25(7):837-44
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  • PURPOSE: Glioblastoma multiforme (GBM) is a devastating brain tumor with a median survival of 6 months after recurrence.
  • PATIENTS AND METHODS: Three phase I clinical studies evaluated intracerebral CED of CB along with tumor resection.
  • All patients underwent tumor resection followed by a single intraparenchymal infusion (in addition to the intraparenchymal one following resection), with a portion of patients who had a preresection intratumoral infusion.
  • The maximum tolerated intraparenchymal concentration was 0.5 microg/mL and tumor necrosis was observed at this concentration.
  • CB- and procedure-related adverse events were primarily limited to the CNS.
  • [MeSH-minor] Adult. Aged. Catheterization. Convection. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Tissue Distribution

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  • (PMID = 17327604.001).
  • [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] Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Exotoxins; 0 / IL13-PE38QQR; 0 / Immunotoxins; 0 / Interleukin-13
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36. Kashyap R, Ryan C, Sharma R, Maloo MK, Safadjou S, Graham M, Tretheway D, Jain A, Orloff M: Liver grafts from donors with central nervous system tumors: a single-center perspective. Liver Transpl; 2009 Oct;15(10):1204-8
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  • [Title] Liver grafts from donors with central nervous system tumors: a single-center perspective.
  • However, it has become a common practice to accept organs from donors that have low-grade tumors or tumors with low metastatic potential.
  • The aim of this study was to analyze our experience with the use of liver grafts from donors with central nervous system (CNS) tumors.
  • A retrospective review of 1173 liver transplants performed between 1992 and 2006 identified 42 donors diagnosed with a CNS tumor.
  • Twenty (47.6%) of the CNS tumors were glioblastoma multiforme (astrocytoma grade IV), 11 (26.2%) were other astrocytomas, and 1 (2.4%) was an anaplastic ependymoma.
  • Twenty (62.5%) neoplasms were grade IV tumors, 8 (25%) were grade II tumors, and 4 (12.5%) were grade III tumors.
  • Over 80% of the patients had at least 1 kind of invasive procedure violating the blood-brain barrier.
  • The rate of recurrence for the entire group was 2.4% (all CNS tumors).
  • There was no difference in survival between recipients of grafts from donors with CNS tumors and recipients of grafts from donors without CNS tumors (1 year: 82% versus 83.3%, P = not significant; 3 years: 77.4% versus 72%, P = not significant).
  • In conclusion, in our experience, despite violation of the blood-brain barrier and high-grade CNS tumors, recurrence was uncommon.
  • [MeSH-major] Central Nervous System Neoplasms / diagnosis. Liver Diseases / therapy. Liver Transplantation / methods. Tissue and Organ Procurement / methods
  • [MeSH-minor] Adult. Blood-Brain Barrier. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Retrospective Studies. Time Factors. Tissue Donors. Treatment Outcome

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  • [Copyright] Copyright 2009 AASLD
  • [CommentIn] Liver Transpl. 2010 Jul;16(7):916 [20583090.001]
  • [CommentIn] Liver Transpl. 2010 Jul;16(7):914-5 [20583288.001]
  • (PMID = 19790151.001).
  • [ISSN] 1527-6473
  • [Journal-full-title] Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society
  • [ISO-abbreviation] Liver Transpl.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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37. Bax DA, Gaspar N, Little SE, Marshall L, Perryman L, Regairaz M, Viana-Pereira M, Vuononvirta R, Sharp SY, Reis-Filho JS, Stávale JN, Al-Sarraj S, Reis RM, Vassal G, Pearson AD, Hargrave D, Ellison DW, Workman P, Jones C: EGFRvIII deletion mutations in pediatric high-grade glioma and response to targeted therapy in pediatric glioma cell lines. Clin Cancer Res; 2009 Sep 15;15(18):5753-61
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  • [Title] EGFRvIII deletion mutations in pediatric high-grade glioma and response to targeted therapy in pediatric glioma cell lines.
  • PURPOSE: The epidermal growth factor receptor (EGFR) is amplified and overexpressed in adult glioblastoma, with response to targeted inhibition dependent on the underlying biology of the disease.
  • We have sought to clarify the role of EGFR in pediatric high-grade glioma (HGG).
  • Pediatric glioblastoma cells transduced with wild-type or deletion mutant EGFRvIII were not rendered more sensitive to erlotinib despite expressing wild-type PTEN.
  • Phosphorylated receptor tyrosine kinase profiling showed a specific activation of platelet-derived growth factor receptor alpha/beta in EGFRvIII-transduced pediatric glioblastoma cells, and targeted coinhibition with erlotinib and imatinib leads to enhanced efficacy in this model.
  • [MeSH-minor] Adolescent. Blotting, Western. Cell Proliferation / drug effects. Child. Erlotinib Hydrochloride. Humans. Prognosis. Quinazolines / pharmacology. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Sensitivity and Specificity. Tumor Cells, Cultured

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  • [ErratumIn] Clin Cancer Res. 2009 Nov 15;15(22):7110
  • (PMID = 19737945.001).
  • [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 Kingdom / Cancer Research UK / / C1178/A10294; United Kingdom / Cancer Research UK / / C309/A2187; United Kingdom / Cancer Research UK / / C309/A8274
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Quinazolines; 0 / epidermal growth factor receptor VIII; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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38. Paugh BS, Qu C, Jones C, Liu Z, Adamowicz-Brice M, Zhang J, Bax DA, Coyle B, Barrow J, Hargrave D, Lowe J, Gajjar A, Zhao W, Broniscer A, Ellison DW, Grundy RG, Baker SJ: Integrated molecular genetic profiling of pediatric high-grade gliomas reveals key differences with the adult disease. J Clin Oncol; 2010 Jun 20;28(18):3061-8
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  • [Title] Integrated molecular genetic profiling of pediatric high-grade gliomas reveals key differences with the adult disease.
  • PURPOSE: To define copy number alterations and gene expression signatures underlying pediatric high-grade glioma (HGG).
  • Results were compared with publicly available data from adult tumors.
  • RESULTS: Significant differences in copy number alterations distinguish childhood and adult glioblastoma.
  • No IDH1 hotspot mutations were found in pediatric tumors, highlighting molecular differences with adult secondary glioblastoma.
  • Pediatric and adult glioblastomas were clearly distinguished by frequent gain of chromosome 1q (30% v 9%, respectively) and lower frequency of chromosome 7 gain (13% v 74%, respectively) and 10q loss (35% v 80%, respectively).
  • CONCLUSION: Integrated molecular profiling showed substantial differences in the molecular features underlying pediatric and adult HGG, indicating that findings in adult tumors cannot be simply extrapolated to younger patients.

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  • (PMID = 20479398.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / P01 CA096832; United States / NCI NIH HHS / CA / R01 CA135554; United Kingdom / Cancer Research UK / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Other-IDs] NLM/ PMC2903336
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39. Silvestre DC, Gil GA, Tomasini N, Bussolino DF, Caputto BL: Growth of peripheral and central nervous system tumors is supported by cytoplasmic c-Fos in humans and mice. PLoS One; 2010;5(3):e9544
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  • [Title] Growth of peripheral and central nervous system tumors is supported by cytoplasmic c-Fos in humans and mice.
  • Herein we examined phospholipid synthesis status in brain tumors from human patients and from NPcis mice, an animal model of the human disease Neurofibromatosis Type 1 (NF1).
  • PRINCIPAL FINDINGS: In human samples, c-Fos expression was at the limit of detection in non-pathological specimens, but was abundantly expressed associated to ER membranes in tumor cells.
  • This was also observed in CNS of adult tumor-bearing NPcis mice but not in NPcis fos(-/-) KO mice.
  • A glioblastoma multiforme and a malignant PNS tumor from a NF1 patient (MPNST) showed a 2- and 4- fold c-Fos-dependent phospholipid synthesis activation, respectively.
  • They also disclose this protein as a potential target for controlling tumor growth in the nervous system.
  • [MeSH-major] Central Nervous System Neoplasms / pathology. Cytoplasm / metabolism. Proto-Oncogene Proteins c-fos / biosynthesis
  • [MeSH-minor] Animals. Brain / metabolism. Brain / pathology. Cell Proliferation. Disease Models, Animal. Endoplasmic Reticulum / metabolism. Genotype. Humans. Male. Mice. Mice, Inbred C57BL. Mice, Knockout. Neurofibromatosis 1 / metabolism. Phosphorylation

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  • (PMID = 20209053.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-fos
  • [Other-IDs] NLM/ PMC2832012
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40. Salmaggi A, Riva M, Silvani A, Merli R, Tomei G, Lorusso L, Russo A, Marchioni E, Imbesi F, Lombardia Neuro-oncology Group: A multicentre prospective collection of newly diagnosed glioblastoma patients in Lombardia, Italy. Neurol Sci; 2005 Oct;26(4):227-34
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  • [Title] A multicentre prospective collection of newly diagnosed glioblastoma patients in Lombardia, Italy.
  • The objective was to set the basis for a prospective, multicentre data collection on newly diagnosed adult glioblastoma patients diagnosed in Lombardia by means of a common database used by neurological and neurosurgical units of various hospitals, providing epidemiological, therapy and follow-up data.
  • All adult patients with a newly diagnosed glioblastoma in 9 Lombardia hospitals from 31 March 2003 to 31 March 2004 were followed prospectively by a form elaborated by the Lombardia Neuro-oncology Group.
  • One hundred and thirty-four newly diagnosed glioblastoma patients were enrolled during the first year of the study.
  • In 71 patients, the tumour involved 1 brain lobe at diagnosis.
  • Data in newly diagnosed glioblastoma patients in Lombardia are in line with other case series reported in other populations.
  • [MeSH-major] Brain Neoplasms / physiopathology. Glioblastoma / physiopathology
  • [MeSH-minor] Adult. Brain / pathology. Cohort Studies. Databases, Factual. Disease Progression. Female. Geography. Humans. Italy. Male. Middle Aged. Prospective Studies. Seizures / etiology. Survival Analysis

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  • (PMID = 16193249.001).
  • [ISSN] 1590-1874
  • [Journal-full-title] Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
  • [ISO-abbreviation] Neurol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Italy
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41. Benesch M, Wagner S, Berthold F, Wolff JE: Primary dissemination of high-grade gliomas in children: experiences from four studies of the Pediatric Oncology and Hematology Society of the German Language Group (GPOH). J Neurooncol; 2005 Apr;72(2):179-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary dissemination of high-grade gliomas in children: experiences from four studies of the Pediatric Oncology and Hematology Society of the German Language Group (GPOH).
  • PURPOSE: Clinical data on central nervous system (CNS) dissemination of high-grade gliomas (HGG) at initial presentation in children are rare.
  • PATIENTS AND METHODS: We conducted a retrospective data analysis of all patients enrolled into four consecutive HGG protocols of the Pediatric Oncology and Hematology Society of the German Language Group (GPOH) to determine the incidence of primary CNS dissemination of HGG and to describe clinical characteristics and outcome of children with HGG who were diagnosed with CNS dissemination at initial presentation.
  • Data concerning tumor dissemination are available from 324 patients.
  • RESULTS: A total of 10 patients (3.1%) (anaplastic astrocytoma: n=3, glioblastoma multiforme: n=6, diffuse intrinsic pontine glioma: n=1) had primary tumor dissemination.
  • The most frequent primary tumor sites were the cortex (n=4), followed by the ventricles (n=2), cerebellum (n=1), spinal cord (n=1), and pons (n=1).
  • Median progression-free and overall survival was 0.8 years (95% CI 0.2-1.4) and 1.5 years (95% CI 0.67-2.29) for patients with primary tumor dissemination, respectively, with no statistically significant differences between the group with and the group without primary tumor dissemination.
  • CONCLUSIONS: Initial diagnostic evaluation should include complete CNS imaging as well as cerebrospinal fluid examination in all patients with HGG.
  • As prognosis of children with HGG and primary CNS dissemination was not inferior to patients without dissemination in our population, these patients should be treated in the same way as patients without primary CNS dissemination.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Central Nervous System Neoplasms / pathology. Central Nervous System Neoplasms / therapy. Glioma / pathology. Glioma / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cyclophosphamide / analogs & derivatives. Disease-Free Survival. Etoposide / administration & dosage. Female. Humans. Male. Neoplasm Invasiveness. Radiotherapy. Retrospective Studies. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 15925999.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; H64JRU6GJ0 / trofosfamide
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42. Loh KC, Willert J, Meltzer H, Roberts W, Kerlin B, Kadota R, Levy M, White G, Geddis A, Schiff D, Martin L, Yu A, Kung F, Spear MA: Temozolomide and radiation for aggressive pediatric central nervous system malignancies. J Pediatr Hematol Oncol; 2005 May;27(5):254-8
Hazardous Substances Data Bank. DACARBAZINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Temozolomide and radiation for aggressive pediatric central nervous system malignancies.
  • This study describes the outcomes of children treated with combinations of temozolomide and radiation therapy for various aggressive central nervous system malignancies.
  • Toxicities observed included low-grade neutropenia, thrombocytopenia, and lymphopenia.
  • The combination of temozolomide and radiotherapy appears to be well tolerated in a variety of treatment schemas for aggressive pediatric central nervous system malignancies.
  • This information is of particular use in designing future studies, given the recent positive results in a randomized study examining the use of temozolomide concomitant with radiation in the treatment of adult glioblastoma.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Central Nervous System Neoplasms / drug therapy. Central Nervous System Neoplasms / radiotherapy. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use

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  • (PMID = 15891559.001).
  • [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] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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43. Lobão CA, Barbosa AS, Nogueira J, Aversa A: Cerebellar glioblastoma multiforme in an adult. Arq Neuropsiquiatr; 2008 Dec;66(4):879-80
Genetic Alliance. consumer health - Glioblastoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cerebellar glioblastoma multiforme in an adult.
  • [MeSH-major] Cerebellar Neoplasms / diagnosis. Glioblastoma / diagnosis

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  • (PMID = 19099130.001).
  • [ISSN] 1678-4227
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
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44. Pediatric and adult glioblastoma have different gene expression profiles. Nat Clin Pract Neurol; 2009 Mar;5(3):122-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric and adult glioblastoma have different gene expression profiles.

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  • [CommentOn] Neuro Oncol. 2009 Jun;11(3):274-80 [18981259.001]
  • (PMID = 20387321.001).
  • [ISSN] 1745-8358
  • [Journal-full-title] Nature clinical practice. Neurology
  • [ISO-abbreviation] Nat Clin Pract Neurol
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] England
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