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1. King GD, Kroeger KM, Bresee CJ, Candolfi M, Liu C, Manalo CM, Muhammad AG, Pechnick RN, Lowenstein PR, Castro MG: Flt3L in Combination With HSV1-TK-mediated Gene Therapy Reverses Brain Tumor-induced Behavioral Deficits. Mol Ther; 2008 Apr;16(4):682-690

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Flt3L in Combination With HSV1-TK-mediated Gene Therapy Reverses Brain Tumor-induced Behavioral Deficits.
  • : Glioblastoma multiforme (GBM) is an invasive and aggressive primary brain tumor which is associated with a dismal prognosis.
  • We have earlier developed a macroscopic, intracranial, syngeneic GBM model, in which treatment with adenoviral vectors (Ads) expressing herpes simplex virus type 1 thymidine kinase (HSV1-TK) plus ganciclovir (GCV) resulted in survival of ∼20% of the animals.
  • We hypothesized that the growth of a large intracranial tumor mass would cause behavioral abnormalities that can be reversed by the combined gene therapy.
  • We assessed the behavior and neuropathology of tumor-bearing animals treated with the combined gene therapy, 3 days after treatment, in long-term survivors, and in a recurrent model of glioma.
  • We demonstrate that the intracranial GBM induces behavioral deficits that are resolved after treatment with Ad-Flt3L/Ad-TK (+GCV).
  • The lack of long-term behavioral deficits and limited neuropathological abnormalities demonstrate the efficacy and safety of the combined Ad-Flt3L/Ad-TK gene therapy for GBM.
  • These findings can serve to underpin further developments of this therapeutic modality, leading toward implementation of a Phase I clinical trial.

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  • [Copyright] Copyright © 2008 The American Society of Gene Therapy. Published by Elsevier Inc. All rights reserved.
  • (PMID = 28178463.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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2. Iacob G, Dinca EB: Current data and strategy in glioblastoma multiforme. J Med Life; 2009 Oct-Dec;2(4):386-93
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  • [Title] Current data and strategy in glioblastoma multiforme.
  • Glioblastoma multiforme (GBM) or astrocytoma grade IV on WHO classification is the most aggressive and the most frequent of all primary brain tumors.
  • Glioblastoma is multiforme, resistant to therapeutic interventions illustrating the heterogeneity exhibited by this tumor in its every aspect, including clinical presentation, pathology, genetic signature.
  • Current data and treatment strategy in GBM are presented focusing on basic science data and key clinical aspects like surgery, including personal experience; adjuvant modalities: radiotherapy, chemotherapy, but also for experimental approaches.
  • Therapeutic attitude in recurrent GBM is also widely discussed.
  • [MeSH-major] Brain Neoplasms / surgery. Glioblastoma / surgery

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  • (PMID = 20108752.001).
  • [ISSN] 1844-122X
  • [Journal-full-title] Journal of medicine and life
  • [ISO-abbreviation] J Med Life
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Romania
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Number-of-references] 45
  • [Other-IDs] NLM/ PMC3019011
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3. Machado CM, Ikemori RY, Zorzeto TQ, Nogueira AC, Barbosa SD, Savino W, Schenka AA, Vassallo J, Heinrich JK, Boetcher-Luiz F, Verinaud L: Characterization of cells recovered from the xenotransplanted NG97 human-derived glioma cell line subcultured in a long-term in vitro. BMC Cancer; 2008;8:291
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  • BACKGROUND: In order to elucidate tumoral progression and drug resistance, cultured cell lines are valuable tools applied on tumor related assays provided they are well established and characterized.
  • Our laboratory settled the NG97 cell line derived from a human astrocytoma grade III, which started to develop and express important phenotypical characteristics of an astrocytoma grade IV after injection in the flank of nude mice.
  • Astrocytomas are extremely aggressive malignancies of the Central Nervous System (CNS) and account for 46% of all primary malignant brain tumors.
  • Progression to worse prognosis occurs in 85% of the cases possibly due to changes in cell tumor microenvironment and through biological pathways that are still unclear.
  • Our results emphasize important queries about astrocytomas tumor progression.
  • [MeSH-major] Astrocytoma / pathology
  • [MeSH-minor] Animals. Antigens, CD29 / biosynthesis. Cell Growth Processes / physiology. Cell Line, Tumor. Chromosome Aberrations. Flow Cytometry. Glial Fibrillary Acidic Protein / biosynthesis. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Transplantation, Heterologous. Vimentin / biosynthesis

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  • (PMID = 18840301.001).
  • [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 / Antigens, CD29; 0 / Glial Fibrillary Acidic Protein; 0 / Vimentin
  • [Other-IDs] NLM/ PMC2572634
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4. Isolan GR, Ribas Filho JM, Isolan PM, Giovanini A, Malafaia O, Dini LI, Kummer A Jr, Negrão AW: [Astrocytic neoplasms and correlation with mutate p53 and Ki-67 proteins]. Arq Neuropsiquiatr; 2005 Dec;63(4):997-1004
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Astrocytic neoplasms and correlation with mutate p53 and Ki-67 proteins].
  • The astrocytic neoplasms respond by 60% of the central nervous system tumors, being the study of the molecular biology an important step for the understanding of the genesis and biological behavior of these diseases.
  • The Ki-67 proteins, which are markers of the cellular proliferation, and p53, which is the product of the tumor suppressor gene TP53, are both important tumoral markers.
  • This study intends to identify and quantify the Ki-67 and p53 proteins in astrocytic tumors of different grades of malignancy, as well as to analyze their relations with age and gender.
  • Ki-67 and p53 proteins in 47 patients with surgically resected astrocytic neoplasms were studied through immunohistochemistry.
  • They have been previously classified and reviewed concerning their histological grade, as suggested by the World Health Organization.
  • p53 was present in 14 cases (35.13%) with a higher correlation with astrocytoma grade IV (p=0.59).
  • The hypotheses of a greater presence of Ki-67 and p53 in astrocytic neoplasms with a higher degree of malignancy, except for the correlation between grade III and p53, is corroborated by the results of this study.
  • [MeSH-major] Astrocytoma / chemistry. Central Nervous System Neoplasms / chemistry. Ki-67 Antigen / analysis. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 16400419.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] por
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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5. Shahar T, Nossek E, Blumenthal DT, Bokstein F, Freedman S, Harosh CB, Sitt R, Corn BW, Kanner AA, Ram Z: Trial To Survive: The Impact of Enrollment in Clinical Trials on Survival of Patients with Glioblastoma: 975. Neurosurgery; 2009 Aug 01;65(2):425

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Trial To Survive: The Impact of Enrollment in Clinical Trials on Survival of Patients with Glioblastoma: 975.

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  • (PMID = 28173171.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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6. Larsen C: [Genetic and molecular abnormalities of glioblastomas (GBM)]. Bull Cancer; 2010 Nov;97(11):1389-407
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Genetic and molecular abnormalities of glioblastomas (GBM)].
  • [Transliterated title] Anomalies génétiques et moléculaires des glioblastomes (GBM).
  • This presentation reports a series of data dealing with recurrent genetic abnormalities and gene expression profiles that characterize primary glioblastomas and secondary glioblastomas resulting from the transformation of low grade tumors (grade II and III astrocytomas and oligodendrogliomas).
  • The most recent aspects of the concept of tumor stem cells that may explain the relentless growth of GBM will be reported.
  • Molecular features of tumor neoangiogenesis will be described.
  • Some aspects of tumor predisposition will be also discussed.
  • Finally, a short description of exosomes as vectors of tumor information will be presented.
  • [MeSH-major] Brain Neoplasms / genetics. Exosomes / genetics. Glioblastoma / genetics. Mutation / genetics
  • [MeSH-minor] Chromosome Deletion. DNA Methylation / genetics. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Epigenomics. Gene Deletion. Genomics / methods. Histones / genetics. Humans. Isocitrate Dehydrogenase / genetics. MicroRNAs / genetics. Neoplastic Stem Cells / pathology. Neovascularization, Pathologic / genetics. Proto-Oncogene Proteins B-raf / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 21084244.001).
  • [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] 0 / Histones; 0 / MicroRNAs; 0 / Tumor Suppressor Proteins; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 6.5.1.- / DNA Repair Enzymes
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7. Chong PK, Loo AV: Visual epilepsy in glioblastoma multiforme. Med J Malaysia; 2008 Dec;63(5):406-7
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  • [Title] Visual epilepsy in glioblastoma multiforme.
  • Craniotomy and excision of tumour was done and the histology confirmed glioblastoma multiforme (GBM).
  • [MeSH-major] Brain Neoplasms / pathology. Epilepsies, Partial / pathology. Glioblastoma / pathology. Hallucinations / pathology. Occipital Lobe / pathology

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  • (PMID = 19803301.001).
  • [ISSN] 0300-5283
  • [Journal-full-title] The Medical journal of Malaysia
  • [ISO-abbreviation] Med. J. Malaysia
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Malaysia
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8. 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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  • However, it has become a common practice to accept organs from donors that have low-grade tumors or tumors with low metastatic potential.
  • 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.
  • In conclusion, in our experience, despite violation of the blood-brain barrier and high-grade CNS tumors, recurrence was uncommon.
  • Grafts from these donors are often an overlooked source of high-quality organs from younger donors and can be appropriately used, particularly in patients who, despite low Model for End-Stage Liver Disease scores, carry a high risk of mortality.
  • [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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9. Ehtesham M, Cooper MK, Valadez JG, Thompson RC: 897 Derivation of Tumorigenic Stem-like Cells from Glioblastoma Multiforme. Neurosurgery; 2005 Aug 01;57(2):429

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 897 Derivation of Tumorigenic Stem-like Cells from Glioblastoma Multiforme.

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  • (PMID = 28184825.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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10. Stendel R: Extent of Resection and Survival in Glioblastoma Multiforme. Neurosurgery; 2009 Jun 01;64(6):E1206

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extent of Resection and Survival in Glioblastoma Multiforme.

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  • (PMID = 28175567.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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11. Aghi MK, Rose SD, VandenBerg SR, Bergers G: Identifying Mechanisms of Bevacizumab Evasion in Human Glioblastoma: 971. Neurosurgery; 2009 Aug 01;65(2):424

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identifying Mechanisms of Bevacizumab Evasion in Human Glioblastoma: 971.

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  • (PMID = 28173297.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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12. Allen C, Paraskevakou G, Iankov I, Giannini C, Schroeder M, Sarkaria J, Puri RK, Russell SJ, Galanis E: Interleukin-13 Displaying Retargeted Oncolytic Measles Virus Strains Have Significant Activity Against Gliomas With Improved Specificity. Mol Ther; 2008 Sep;16(9):1556-1564
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  • : The majority of glioblastoma multiforme (GBM) tumors (80%) overexpress interleukin-13 receptor α2 (IL-13Rα2), but there is no expression of IL-13Rα2 in normal brain.

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  • [Copyright] Copyright © 2008 The American Society of Gene Therapy. Published by Elsevier Inc. All rights reserved.
  • (PMID = 28189011.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Larocque M, Syme A, Fallone BG: Sci-Sat AM(1): Imaging-01: Tumour and normal tissue T2 and ADC distributions for a mouse model at 9.4T. Med Phys; 2008 Jul;35(7Part3):3414
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sci-Sat AM(1): Imaging-01: Tumour and normal tissue T2 and ADC distributions for a mouse model at 9.4T.
  • We are currently using mouse models of human glioblastoma multiforme (GBM) to study tumour response to ionizing radiation by MRI at 9.4T.

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  • [Copyright] © 2008 American Association of Physicists in Medicine.
  • (PMID = 28512910.001).
  • [ISSN] 2473-4209
  • [Journal-full-title] Medical physics
  • [ISO-abbreviation] Med Phys
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Cancer / Diffusion / Ionizing radiation / Magnetic resonance / Magnetic resonance imaging / Medical imaging / Radiation therapy / Relaxation times / Time measurement / Tissues
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14. Joiner MC, Mogili N, Marples B, Burmeister J: Significant dose can be lost by extended delivery times in IMRT with x rays but not high-LET radiations. Med Phys; 2010 Jun;37(6Part2):2457-2465

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: The effect of prolonging the delivery time of a treatment fraction was investigatedin vitro using human PC-3 prostate and HGL21 glioblastoma tumor cell lines.
  • More clinically common prolongations of 5-30 and 5-15 min resulted in effective dose reductions of 3.8% and 1.7% for PC-3, and 7.3% and 2.9% for HGL21.

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  • [Copyright] © 2010 American Association of Physicists in Medicine.
  • (PMID = 28513910.001).
  • [ISSN] 2473-4209
  • [Journal-full-title] Medical physics
  • [ISO-abbreviation] Med Phys
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Cancer / Cell cultures / Dosimetry / Dosimetry/exposure assessment / IMRT / Intensity modulated radiation therapy / Neutron radiation effects / Neutrons / Radiation therapy / Radiation treatment / Therapeutic applications, including brachytherapy / X-ray effects / X-ray imaging / X-rays / biological effects of X-rays / biological effects of neutrons / biological organs / cellular effects of radiation / dose protraction / dosimetry / incomplete repair / loss of effectiveness / neutrons / physiological models / radiation therapy / simulation / tumours
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15. Hofstetter CP, Boockvar JA: Recreating Glioblastoma Multiforme in Cell Culture Dish. Neurosurgery; 2009 Sep 01;65(3):N11

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recreating Glioblastoma Multiforme in Cell Culture Dish.

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  • (PMID = 28173235.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Chahlavi A, Daneshvar H, Richmond A, Nishimura F, Okada H, Vogelbaum MA, Barnett GH, Finke J: 895 Desferoxamine Protects T Cells from Glioblastoma Multiforme-mediated Apoptosis and Improves Cytolytic Activity of T Cells in Killing of Tumor Targets. Neurosurgery; 2005 Aug 01;57(2):428-429

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 895 Desferoxamine Protects T Cells from Glioblastoma Multiforme-mediated Apoptosis and Improves Cytolytic Activity of T Cells in Killing of Tumor Targets.

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  • (PMID = 28184901.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Adamson DC, Lin N, Di C, Bortoff K, Fu J, Truszkowski P, Killela P, Duncan C, McLendon R, Bigner D: Genome Mapping of Glioblastoma Identifies a Novel Epigenetically-Silenced, Migration-Related Gene, Adherens Junctional Associated Protein, Whose Restoration of Expression by Demethylating Agents Can Inhibit Cell Migration: 972. Neurosurgery; 2009 Aug 01;65(2):424

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genome Mapping of Glioblastoma Identifies a Novel Epigenetically-Silenced, Migration-Related Gene, Adherens Junctional Associated Protein, Whose Restoration of Expression by Demethylating Agents Can Inhibit Cell Migration: 972.

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  • (PMID = 28173148.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Prados M, Gilbert M, Kuhn J, Lamborn K, Cloughesy T, Lieberman F, Puduvalli V, Robins HI, Lassman A, Wen PY: Phase I/II study of sorefenib and erlotinib for patients with recurrent glioblastoma (GBM) (NABTC 05-02). J Clin Oncol; 2009 May 20;27(15_suppl):2005

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I/II study of sorefenib and erlotinib for patients with recurrent glioblastoma (GBM) (NABTC 05-02).
  • : 2005 Background: Single agent targeted therapy has been disappointing in GBM.
  • METHODS: The NABTC conducted a phase I/II study of sorafenib (VEGFR/PDGFR/Raf inhibitor) in combination with erlotinib (EGFR inhibitor) in recurrent GBM.
  • Eligibility criteria included histologically proven GBM, radiologic progression, > 18 yrs old, KPS > 60, adequate bone marrow reserve, and organ function.
  • Dose-finding used a standard 3 + 3 design and the MTD was defined as the dose with DLTs in 1/6 or fewer patients.
  • If > 4 of the initial 19 patients achieved PFS6, an additional 14 patients would be accrued for a total of 33 patients.
  • At this dose 1/6 evaluable patients had a DLT (grade 4 lipase).
  • Other grade 3 or 4 toxicities included transaminitis, hypertension, hypophosphatemia, and increased lipase.

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  • (PMID = 27964562.001).
  • [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
  • [Publication-country] United States
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19. Chi AS, Gerstner ER, Eichler AF, Chea HK, Drappatz J, Wen PY, Ivy SP, Loeffler JS, Sorensen AG, Jain RK, Batchelor TT: Phase Ib study of cediranib in combination with daily temozolomide and radiation in patients with newly diagnosed glioblastoma. J Clin Oncol; 2009 May 20;27(15_suppl):e13010

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase Ib study of cediranib in combination with daily temozolomide and radiation in patients with newly diagnosed glioblastoma.
  • : e13010 Background: Pre-clinical evidence suggests antiangiogenic therapy combined with radiation therapy (RT) and chemotherapy may improve tumor control in patients with glioblastoma (GBM).
  • We conducted a phase Ib study to evaluate the safety and maximum tolerated dose (MTD) of the combination of cediranib, a potent pan-VEGF receptor tyrosine kinase inhibitor, standard RT, and temozolomide (TMZ) in patients with newly diagnosed GBM who were not taking enzyme-inducing antiepileptic drugs (EIAED).
  • METHODS: After undergoing tumor biopsy or resection, six patients with pathologically confirmed GBM were treated with concurrent TMZ (75mg/m2/day), RT (60 Gy) and cediranib (dose level 1 = 20mg/day; dose level 2 = 30mg/day) followed by post-radiation TMZ (150-200 mg/m2 on days 1-5 of each 28 day cycle) and cediranib (45mg/day) for up to 6 monthly cycles.
  • During combined cediranib and TMZ therapy in the post-radiation setting, one patient discontinued cediranib because of toxicity (grade 3 transaminase elevation) and one patient required dose reduction to 15mg/day due to grade 3 proteinuria.
  • CONCLUSIONS: Cediranib given in combination with standard RT and TMZ for newly diagnosed GBM patients not on EIAEDs is well tolerated and the MTD is 30mg/day.

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  • (PMID = 27962847.001).
  • [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
  • [Publication-country] United States
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20. De Groot JF, Prados M, Urquhart T, Robertson S, Yaron Y, Sorensen AG, Norton A, Batchelor T, Drappatz J, Wen P: A phase II study of XL184 in patients (pts) with progressive glioblastoma multiforme (GBM) in first or second relapse. J Clin Oncol; 2009 May 20;27(15_suppl):2047

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of XL184 in patients (pts) with progressive glioblastoma multiforme (GBM) in first or second relapse.
  • Elevated levels of VEGFR2 and its ligand VEGF are found in GBM, and elevated levels of MET and KIT are correlated with poor prognosis in GBM pts.
  • Treatment with XL184 results in potent inhibition of GBM in preclinical models.
  • METHODS: This is a phase II study of 46 pts with recurrent GBM who received XL184 175mg PO qd.
  • At least 1 post-baseline tumor assessment at 4 weeks was available for 26 pts.
  • SAFETY: 6 pts have experienced a total of 9 possibly related grade 3/4 SAEs including increased troponin I and myocarditis (n = 1); dehydration, nausea, and fatigue (n = 1); elevated ALT (n = 1); pulmonary embolism (n = 2); and CNS hemorrhage (n = 1).
  • Based on investigator assessment of bidimensional contrast-enhancing tumor measurements, 10 pts (38%) had a best radiologic response of >= 50% reduction from baseline (including 1 pt with a 100% reduction), 9 pts (35%) had tumor measurement changes ranging from +24% and -49%, and 7 pts (27%) had a >= 25% increase in tumor burden.
  • Of the 17 anti-angiogenic-naïve pts, 9 (53%) had a best radiologic response of >= 50% reduction in tumor burden.
  • CONCLUSIONS: XL184 at a dose of 175 mg PO qd, has demonstrated substantial activity in pts with progressive or recurrent GBM.

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  • (PMID = 27964644.001).
  • [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
  • [Publication-country] United States
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21. Pistollato F, Abbadi S, Rampazzo E, Viola G, Della Puppa A, Cavallini L, Panchision DM, Te Kronnie G, Basso G: Glioblastoma-derived cells exhibit differential responses to glycolysis inhibition under hypoxia. J Clin Oncol; 2009 May 20;27(15_suppl):e13031

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glioblastoma-derived cells exhibit differential responses to glycolysis inhibition under hypoxia.
  • : e13031 It has been suggested that oxygen tension is a crucial component of the brain tumor niche, as hypoxia positively correlates with tumor aggressiveness and over-activity of hypoxia inducible factor-1α (HIF-1α) reinforces tumor progression.
  • Here we investigate the effects mediated by in vitro glycolysis inhibition by using 2-deoxyglucose (2-DG) in glioblastoma (GBM) derived cells maintained under two different oxygen tensions, a lowered oxygen tension (2%) versus a higher non-physiological (20%).
  • GBM account for 50% of all gliomas and arise after age 50 in most patients and it has been seen that younger patients tend to have a better prognosis than the elderly.
  • Our results show that adult GBM displaying a highly immature phenotype manifested the highest resistance to glucose deprivation.
  • Also, hypoxia inhibits the mitochondria-controlled apoptosis induced by 2-DG, by conferring cell resistance through progressive activation of pro-survival NF-kB and induction of tumor cell autophagy.
  • These results indicate differences in tumor cells behavior that may be predictive of cell response to therapy aiming to limit glucose uptake or glucose metabolism.

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  • (PMID = 27962877.001).
  • [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
  • [Publication-country] United States
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22. Wen PY, Cloughesy T, Kuhn J, Lamborn K, Abrey LE, Lieberman F, Robins HI, Wright J, Prados MD, Gilbert M: Phase I/II study of sorafenib and temsirolimus for patients with recurrent glioblastoma (GBM) (NABTC 05-02). J Clin Oncol; 2009 May 20;27(15_suppl):2006

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I/II study of sorafenib and temsirolimus for patients with recurrent glioblastoma (GBM) (NABTC 05-02).
  • : 2006 Background: The activity of targeted molecular therapy with single agents has been disappointing in GBM.
  • METHODS: The North American Brain Tumor Consortium conducted a phase I/II study of sorafenib (VEGFR/PDGFR/Raf inhibitor) in combination with temsirolimus (mTOR inhibitor) in recurrent GBM.
  • Eligibility criteria included histologically proven GBM, radiologic progression, > 18 years old, KPS > 60, adequate bone marrow reserve, and organ function.
  • Dose-finding used a standard 3 + 3 design with the MTD defined as the dose with DLTs in 1/6 or fewer patients.
  • If > 4 of the initial 19 patients achieved PFS6, an additional 14 patients would be accrued for a total of 33 patients.
  • At this dose 1/6 patients had a DLT (grade 3 thrombocytopenia).
  • Other grade 3 or 4 toxicities included transaminitis, hypophosphatemia, fatigue, diarrhea, and hyperlipidemia.
  • One patient was found not to have GBM on central review.
  • CONCLUSIONS: The combination of sorafenib and temsirolimus was moderately well-tolerated but did not demonstrate sufficient efficacy in recurrent GBM to warrant further investigation.

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  • (PMID = 27964559.001).
  • [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
  • [Publication-country] United States
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23. Lesser GJ, Carver KA, Newton SJ, Tallant EA, Gallagher PE: Angiotensin-(1-7), a small molecule inhibitor of glioblastoma growth. J Clin Oncol; 2009 May 20;27(15_suppl):2024

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Angiotensin-(1-7), a small molecule inhibitor of glioblastoma growth.
  • : 2024 Background: Recent studies suggest that anti-angiogenic therapies may be effective in patients with glioblastoma multiforme (GBM), a highly vascular tumor.
  • We have previously demonstrated that angiotensin-(1-7) [Ang-(1-7)], an endogenous heptapeptide with anti-angiogenic properties, significantly reduced the serum-stimulated growth of three human glioblastoma cell lines which contained mRNA for the AT<sub>(1-7)</sub> receptor mas.
  • We now provide the first evidence that Ang-(1-7) markedly decreases the proliferation and growth of human glioblastomas in vivo using a xenograft model.
  • METHODS: Athymic mice with tumors resulting from injection of human U87 glioblastoma cells were treated for 18 days with saline or 1000 μg/kg Ang-(1-7), delivered by subcutaneous injection every 12 h.
  • The Ang-(1-7)-mediated reduction in tumor growth was associated with a significant decrease in immunoreactive Ki67, a proliferation marker.
  • CONCLUSIONS: These results suggest that Ang-(1-7) may reduce the concentration and ratio of proliferative and anti-proliferative prostaglandins to decrease glioblastoma growth as well as attenuate angiogenesis through a reduction in VEGF.
  • Thus, Ang-(1-7) may be a new, first-in-class small molecule inhibitor for the treatment of glioblastoma, providing combination therapy as a selective COX-2/PGES-1 and angiogenic inhibitor, targeting a specific AT<sub>(1-7)</sub> receptor mas.

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  • (PMID = 27964600.001).
  • [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
  • [Publication-country] United States
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24. Baehr O, Herrlinger U, Weller M, Steinbach JP: Very late relapses in glioblastoma long-term survivors. J Clin Oncol; 2009 May 20;27(15_suppl):e13017

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Very late relapses in glioblastoma long-term survivors.
  • : e13017 Background: Long-term survival of patients with histologically confirmed glioblastoma is a rare event with figures in the range of 2-3% for 5-year survival.
  • METHODS: We here report on the extended follow-up (mean, 139.4 months) of a cohort of 10 glioblastoma long-term survivors.
  • Four of these patients died from recurrent tumor.
  • One patient died from leukoencephalopathy-associated complications without evidence of tumor progression.
  • CONCLUSIONS: Very late relapses pose a serious threat for glioblastoma long-term survivors and call for continuous vigilance.
  • The maintenance of a tight control schedule even in patients surviving for more than 10 years should be considered.

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  • (PMID = 27962828.001).
  • [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
  • [Publication-country] United States
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25. Hu J, Wen PY, Abrey LE, Fadul C, Drappatz J, Salem N, Amato A, Carminati P, Supko J, Hochberg F: Phase II trial of oral gimatecan in adults with recurrent glioblastoma. J Clin Oncol; 2009 May 20;27(15_suppl):2009

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II trial of oral gimatecan in adults with recurrent glioblastoma.
  • METHODS: We conducted a multicenter two-stage phase II trial to evaluate the efficacy of gimatecan in adults with recurrent glioblastoma.
  • Eligibility criteria included ≤1 prior treatment for recurrent disease, age ≥18, ECOG performance status 0 or 1, and normal organ function.
  • The daily dose was reduced to 1.0 mg/m<sup>2</sup> after four of the first 10 patients experienced grade 4 hematologic toxicity.
  • One patient was removed from trial due to toxicity (grade 3 leukopenia and thrombocytopenia).
  • Treatment-related grade 3/4 toxicities included thrombocytopenia (17.2%), leukopenia (17.2%), and neutropenia (10.3%).
  • Only 1/19 patients treated with 1.0 mg/m<sup>2</sup>/day experienced grade 3/4 hematologic toxicity.
  • Only one patient had a partial radiographic response by the modified Macdonald criteria and stable disease was the best response in 13 patients.
  • All other patients had progressive disease after two cycles of therapy.

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  • (PMID = 27964558.001).
  • [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
  • [Publication-country] United States
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26. Raizer JJ, Grimm S, Rice L, Muro K, Chandler J, Tellez C, Mellot AL, Newman S, Nicholas MK, Chamberlain M: A phase II trial of single-agent bevacizumab given every 3 weeks for recurrent malignant gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):2044

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: All patients (pts) had to sign an IRB informed consent except six pts who were treated at a different site in a similar fashion.
  • Patients were assessed using Macdonald criteria and continued on trial until tumor progression or toxicity.
  • RESULTS: 61 patients (35 male; 26 female; 50 GBM, 5 AA, 6 AO/AOA) with a median age of 51 were treated.
  • Grade 3+ toxicities were non-fatal intracranial hemorrhage (1), fatal GI perforation (1), DVT (1), fatigue (4), rectal bleeding (1), weakness (1), and lack of drive (1).

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  • (PMID = 27964646.001).
  • [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
  • [Publication-country] United States
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27. Rossi J, McCaffery I, Paweletz K, Tudor Y, Elliott S, Fitzpatrick VD, Patterson SD: Analysis of cell surface erythropoietin receptor (EpoR) expression and function in human epithelial tumor tissues. J Clin Oncol; 2009 May 20;27(15_suppl):11104

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of cell surface erythropoietin receptor (EpoR) expression and function in human epithelial tumor tissues.
  • : 11104 Background: EpoR mRNA and protein expression have been reported at low levels in human tumors implying EpoR may be functional in tumor cells with inferred implications for the use of erythropoiesis stimulating agents in the Oncology setting.
  • However, mRNA studies use bulk tumor tissue which ignores contribution from the stroma and IHC studies have all used Abs that have since been shown to not be specific for EpoR.
  • METHODS: EpoR expression and function was investigated in viable, non-apoptotic primary human tumor cells (using tumor specific Abs) that were disaggregated from at least 30 patients from each of the following tumor types: breast (incl. metastases), NSC lung, colorectal, and ovarian.
  • Additional tumor types included head and neck, GBM, pancreatic and gastric.
  • RESULTS: No expression of cell surface EpoR was detected in tumor cells in any of the over 130 tumors.
  • No induction of EpoR signaling was observed in tumor cells at any [Epo], whereas activation was readily detected in tumor cells treated in parallel with a cocktail of known tumor growth factors.
  • No evidence of EpoR expression or function was observed in tumor endothelial cells.
  • CONCLUSIONS: These data demonstrate that epithelial tumor cells do not express functional cell surface EpoR and are not responsive to physiological, therapeutic or indeed very high levels of Epo (300U/mL).

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  • (PMID = 27963466.001).
  • [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
  • [Publication-country] United States
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28. Rudnick JD, Phuphanich S, Chu R, Mazer M, Wang H, Serrano N, Francisco M, Black KL, Wheeler C, Yu J: A phase I trial of surgical resection with biodegradable carmustine (BCNU) wafer placement followed by vaccination with dendritic cells pulsed with tumor lysate for patients with malignant glioma. J Clin Oncol; 2009 May 20;27(15_suppl):2033

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I trial of surgical resection with biodegradable carmustine (BCNU) wafer placement followed by vaccination with dendritic cells pulsed with tumor lysate for patients with malignant glioma.
  • : 2033 Background: Our prior immunotherapy trials demonstrated efficacy in generating a tumor specific immune response in malignant glioma and the potential for high tumor-specific toxicity and sustained tumoricidal activity.
  • METHODS: We exploited this synergistic effect to maintain a cytotoxic environment around the tumor milieu.
  • Patients with high-grade glioma were eligible after maximal resection with biodegradable carmustine (BCNU) wafer placement.
  • Screening leukapheresis is used to isolate mononuclear cells which are differentiated into dendritic cells, pulsed with tumor lysate, and then 3 intradermal vaccines are administered at 2-week intervals.
  • The histology included 3 newly diagnosed glioblastoma multiforme (GBM), 8 recurrent GBM, 2 newly diagnosed anaplastic astrocytoma (AA), and 2 recurrent AA.
  • Our preliminary data on 15 patients and 39 courses of Dendritic Cell vaccines demonstrate one grade 3 toxicity of fever/chest pain.
  • A stable disease interval of 13 to 90 weeks was observed for patients who received vaccine.
  • The 3 newly diagnosed GBM patients have stable disease (18 to 71 weeks).
  • In the recurrent GBM cohort 7/8 patients had progression within 6 months from the post-vaccination MRI.
  • CONCLUSIONS: This phase I study demonstrates the safety, feasibility of dendritic cell vaccination with biodegradable carmustine (BCNU) wafers with one grade 3 AE.

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  • (PMID = 27964627.001).
  • [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
  • [Publication-country] United States
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29. Wadasadawala T, Jalali R, Munshi A, Gupta T, Kalyani N, Menon H, Sarin R, Goel A: Five-year survival data in newly diagnosed glioblastoma treated with radiotherapy along with concurrent and adjuvant temozolomide. J Clin Oncol; 2009 May 20;27(15_suppl):e13009

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Five-year survival data in newly diagnosed glioblastoma treated with radiotherapy along with concurrent and adjuvant temozolomide.
  • : e13009 Background: We report 5-year survival data in patients with newly diagnosed glioblastoma treated with radiotherapy along with concurrent and adjuvant temozolomide (TMZ).
  • METHODS: Between March 2001 to April 2008, 81 patients with newly diagnosed histopathologically proven glioblastoma underwent surgery followed by external radiotherapy to a total dose of 60 Gy in 30 fractions over 6 weeks.
  • Treatment was generally well tolerated with only 2.5% of patients developing grade 3 anemia, leucopoenia, and neutropenia.
  • Grade 3 or 4 thrombocytopenia was seen in 5% patients.

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  • (PMID = 27962766.001).
  • [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
  • [Publication-country] United States
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30. Drappatz J, Norden AD, Wong ET, Lassman AB, Doherty L, LaFrankie D, Gerard M, Phan P, Schiff D, Wen PY: Phase I study of vandetanib with radiation therapy and temozolomide for newly diagnosed glioblastoma. J Clin Oncol; 2009 May 20;27(15_suppl):2031

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I study of vandetanib with radiation therapy and temozolomide for newly diagnosed glioblastoma.
  • : 2031 Background: There is increasing evidence that angiogenesis inhibition may potentiate the effects of radiation therapy (RT) and chemotherapy in patients with glioblastoma (GBM).
  • In addition, inhibition of the epidermal growth factor receptor (EGFR) may be of therapeutic benefit, as EGFR is often upregulated in GBM and contributes to radiation resistance.
  • We conducted a phase I study of vandetanib, an inhibitor of VEGFR2 and EGFR, in patients with newly-diagnosed GBM in combination with RT and temozolomide (TMZ).
  • METHODS: Using a standard 3 + 3 dose escalation design, 13 newly-diagnosed GBM patients received vandetanib with RT (60 Gy) and concurrent TMZ 75 mg/m<sup>2</sup> daily, followed by adjuvant TMZ for up to 12 cycles (150-200 mg/m<sup>2</sup> on days 1-5 of each 28 day cycle).
  • Eligible patients were adults with newly-diagnosed GBM or gliosarcoma, Karnofsky performance status of ≥60%, normal organ function, and not taking enzyme-inducing anti-epileptic drugs.
  • 2/6 patients developed DLTs (grade 5 gastrointestinal hemorrhage and grade 3 thrombocytopenia in one patient and grade 4 neutropenia in one patient).
  • Of 10 evaluable patients, one had a minor response (10%), defined as 25% to <50% reduction in enhancing area for 8 weeks; eight had stable disease (80%), defined as <25% increase or decrease; and one had progressive disease (10%).
  • CONCLUSIONS: These data suggest that vandetanib may be combined with RT and TMZ in GBM patients.

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  • (PMID = 27964631.001).
  • [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
  • [Publication-country] United States
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31. Gerstner ER, Yip S, Wang DL, Louis DN, Iafrate AJ, Batchelor TT: MGMT methylation status may predict survival in elderly patients with newly diagnosed glioblastoma (GBM). J Clin Oncol; 2009 May 20;27(15_suppl):e13023

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MGMT methylation status may predict survival in elderly patients with newly diagnosed glioblastoma (GBM).
  • : e13023 Background: Methylation of the MGMT gene promoter is associated with prolonged survival and response to temozolomide in GBM < 70.
  • However, it is unclear if MGMT is a useful prognostic biomarker in the elderly GBM population who traditionally are viewed as less responsive to treatment.
  • METHODS: We retrospectively reviewed MGMT promoter methylation status and clinical characteristics in patients 70 years or older with newly diagnosed GBM undergoing resection at our institution from 1998-2008.
  • MGMT analysis was performed by extracting tumor genomic DNA for bisulfite conversion.
  • CONCLUSIONS: MGMT methylation status is associated with prolonged PFS and OS in elderly patients with newly diagnosed GBM.

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  • (PMID = 27962794.001).
  • [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
  • [Publication-country] United States
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32. Ursu R, Carpentier A, Metellus P, Barrie M, Meng Y, Laigle-Donadey F, Tibi A, Chinot O, Carpentier AF: Phase II trial of intracerebral administration of CpG oligonucleotide for patients with recurrent glioblastoma. J Clin Oncol; 2009 May 20;27(15_suppl):2043

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II trial of intracerebral administration of CpG oligonucleotide for patients with recurrent glioblastoma.
  • When injected locally, they can induce tumor rejection in animal models.
  • In a phase I clinical trial, intra-tumoral infusions of CpG-ODN in glioblastoma patients were well tolerated at doses up to 20 mg.
  • This multicenter phase II trial was designed to study the efficacy and tolerance of a local treatment by CpG-ODN in patients with recurrent glioblastoma.
  • METHODS: Patients with recurrent GBM occurring at least three months after radiotherapy and previously treated with one at least regimen of chemotherapy received 20mg CpG- ODN (CpG-28) by convection-enhanced delivery.

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  • (PMID = 27964650.001).
  • [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
  • [Publication-country] United States
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33. Sarkaria JN, Galanis E, Wu W, Giannini C, Jaeckle KA, Doyle L, Uhm J, Brown P, Dietz AB, Buckner J: NCCTG phase I trial of temsirolimus (CCI-779) and temozolomide (TMZ) in combination with radiation therapy (RT) in newly diagnosed glioblastoma multiforme (GBM) patients. J Clin Oncol; 2009 May 20;27(15_suppl):2019

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NCCTG phase I trial of temsirolimus (CCI-779) and temozolomide (TMZ) in combination with radiation therapy (RT) in newly diagnosed glioblastoma multiforme (GBM) patients.
  • METHODS: The standard cohorts of 3 design was applied with dose escalation of weekly IV CCI-779 in combination with standard TMZ/RT.
  • Two other patients died of gram-negative sepsis despite prophylaxis: one after their first dose of CCI-779 and one during cycle 4 of adjuvant therapy.
  • In contrast to our 18% grade 5 infection rate, only 4% grade 3 (no grade 4/5) infections were observed in 26 other CTEP-sponsored clinical trials involving 1,006 patients treated with CCI-779.

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  • (PMID = 27964576.001).
  • [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
  • [Publication-country] United States
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34. Gupta S, Sheikh H, Schneider C, Zhang X, Padmanabhan A, Ali A: HER-2/neu expression in glioblastoma multiforme (GBM). J Clin Oncol; 2009 May 20;27(15_suppl):e13035

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HER-2/neu expression in glioblastoma multiforme (GBM).
  • : e13035 Background: Glioblastoma multiforme (GBM) is a disease in which very few cytotoxic chemotherapy agents have been shown to have activity.
  • Trials with bevacizumab, a VEGF inhibitor that disrupts tumor angiogenesis, have demonstrated activity against this otherwise chemotherapy resistant disease.
  • This has led to interest in other biologic agents that target angiogenic pathways for the treatment of GBM.
  • Over-expression of HER-2/neu by human tumor cells is closely associated with increased angiogenesis and expression of VEGF.
  • Limited studies have evaluated HER-2/neu gene expression in GBM and the results are inconsistent.
  • We evaluated the expression of Her-2/neu protein in 41 consecutive GBM cases to explore the potential utility of targeting this pathway.
  • METHODS: Archival histopathologic sections from 41 patients (age 26-89 years) with a diagnosis of GBM from 2004-2008 were reviewed.
  • Three cases demonstrated weak, incomplete membrane staining of rare tumor cells (score 1+) and were interpreted as negative.
  • CONCLUSIONS: Our study indicates that there is no significant immunohistochemical over-expression of HER-2/neu protein in GBM.
  • This suggests that HER-2/neu over-expression is not a significant oncogenic pathway in GBM, and therefore may not be a potential therapeutic target in this disease.

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  • (PMID = 27962861.001).
  • [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
  • [Publication-country] United States
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35. Stankewitz S, Dresemann G: Addition of continuous low dose temozolomide (T) to bevacizumab (Bev) plus irinotecan (Iri) after bevacizumab plus irinotecan failure in heavily pretreated glioblastoma multiforme (GBM). J Clin Oncol; 2009 May 20;27(15_suppl):e13015

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Addition of continuous low dose temozolomide (T) to bevacizumab (Bev) plus irinotecan (Iri) after bevacizumab plus irinotecan failure in heavily pretreated glioblastoma multiforme (GBM).
  • : e13015 Background: In several phase II studies in relapsed GBM, Bev plus Iri showed impressive objective response rates (>50%) with acceptable toxicity rate, duration of response, however, was moderate.
  • METHODS: From April 2007 to October 2008, 35 pretreated patients with confirmed GBM with progressive disease (PD) after Bev (4 mg/kg body weight i.v.) plus Iri (80 mg/m<sup>2</sup> i.v.) were treated with additional continuous low dose T (20 mg per day p.o.) while Bev plus Iri were continued.
  • RESULTS: All 35 patients were eligible for toxicity and efficacy, median follow up was 7 months (2 - 20), 25 patients were male, 10 female, median age was 51 years (29 - 80), 21 patients had primary GBM, 14 patients secondary GBM.
  • 1 patient developed grade 3 leucopenia, and 1 patients grade 3 thrombopenia; 3 patients asymptomatic intracerebral bleeds requiring treatment delay, 1 pat. grade 3 sepsis and 2 patients grade 3 fatigue.
  • In 4/35 patients a partial response (PR) was achieved, in 14/35 patients a disease stabilization for at least 2 months, while 17/35 patients showed primary PD.
  • CONCLUSIONS: The addition of continuous low dose T in combination with Bev plus Iri seems to have activity in GBM patients, after progression on Bev plus Iri treatment, and has an acceptable toxicity profile.
  • Further investigation of the combination Bev plus Iri plus T in GBM patients is necessary.

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  • (PMID = 27962820.001).
  • [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
  • [Publication-country] United States
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36. DePrimo S, Wu B, Huang S, Bautista R, Cancilla B, Vysotskaia V, De Groot J, Prados M, Buller R, Wen P: Correlative tumor molecular profiling and plasma biomarker analysis in a phase II study of XL184 in patients with progressive or recurrent glioblastoma multiforme (GBM). J Clin Oncol; 2009 May 20;27(15_suppl):2049

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Correlative tumor molecular profiling and plasma biomarker analysis in a phase II study of XL184 in patients with progressive or recurrent glioblastoma multiforme (GBM).
  • : 2049 Background: XL184 is an oral inhibitor of MET, RET, KIT, and VEGFR-2 with potent antitumor effects in preclinical models of GBM.
  • Clinically, elevated levels of MET, KIT, VEGFR-2, and VEGF-A are found in GBM, where MET and KIT levels correlate with poor prognosis.
  • XL184-201 is a fully enrolled GBM study (N = 46) which mandated collection of archival tumors and serial plasma samples.
  • The encouraging clinical activity of XL184 in this study is the subject of a separate abstract.
  • METHODS: Tumor profiling focused on genomic alterations prevalent in GBM, reflecting dysregulation of key signaling pathways (Nature 2008; 455:1061), or XL184 targets.
  • RESULTS: Tumor genotyping assessments included EGFR and KIT copy number; PTEN, PIK3CA, PIK3R1, and NF1 sequencing, as well as MGMT and PTEN promoter methylation.
  • In ∼ 80% of samples, tumor cells stained positive for MET with a lower fraction positive for RET and VEGFR-2 in tumor cells (42% and 58%, respectively).
  • RET and VEGFR-2 expression was often seen in tumor-associated blood vessels, while MET signal in blood vessels was more limited (33%).
  • Objective response was observed in the presence or absence of tumor EGFR amplification, PTEN mutation, and MGMT promoter methylation.
  • CONCLUSIONS: Plasma biomarkers confirm pharmacodynamic activity of XL184 in advanced GBM where marked clinical activity has been observed.
  • Upon completed analysis of a full set of biological samples and with mature clinical data, predictive markers for clinical activity of XL184 will be evaluated.

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  • (PMID = 27964640.001).
  • [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
  • [Publication-country] United States
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37. Horbinski C, Mintz A, Engh J, Lieberman F, Hamilton RL, Park DM: Post-therapeutic changes in the molecular profile of glioblastomas. J Clin Oncol; 2009 May 20;27(15_suppl):2026

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Post-therapeutic changes in the molecular profile of glioblastomas.
  • : 2026 Background: Glioblastoma multiforme is the most common and malignant primary brain tumor in adults.
  • While the molecular alterations in pretreated glioblastomas have been the subject of much research in recent years, changes in their genetic profile after adjuvant therapy are largely unknown.
  • METHODS: Herein we describe a cohort of over 40 glioblastomas with characterization of key genetic loci (EGFR, p53, 1p, 19q, 9p, 10q, 17p) using fluorescence in situ hybridization, PCR-based loss of heterozygosity (LOH) analysis, and immunohistochemistry on formalin-fixed, paraffin-embedded tissues.
  • Analyses were performed on tumor tissue obtained at initial diagnosis and at first recurrence.
  • 24% of previously non-EGFR-amplified tumors acquired low-grade amplification (less than 10 copies/chromosome 7 CEP signal) after treatment, and 16% of EGFR-amplified tumors lost amplification after treatment.

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  • (PMID = 27964598.001).
  • [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
  • [Publication-country] United States
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38. Wefel JS, Cloughesy T, Zazzali J, Yi J, Friedman HS, BRAIN Investigators: Neurocognitive function in patients with glioblastoma multiforme in first or second relapse treated with bevacizumab in the BRAIN study. J Clin Oncol; 2009 May 20;27(15_suppl):2056

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neurocognitive function in patients with glioblastoma multiforme in first or second relapse treated with bevacizumab in the BRAIN study.
  • : 2056 Background: Patients with glioblastoma multiforme (GBM) suffer from neurocognitive decline due to both the disease and its treatment.
  • We analyzed neurocognitive function of patients with recurrent GBM who participated in the BRAIN study, a phase II, multicenter, randomized, noncomparative clinical trial which assessed the efficacy and safety of bevacizumab alone or in combination with irinotecan.
  • CONCLUSIONS: Preliminary results suggest that the majority of patients with recurrent GBM who were treated with bevacizumab alone in the BRAIN study demonstrated stable or improved neurocognitive function during the first 6 weeks of treatment.

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  • (PMID = 27964669.001).
  • [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
  • [Publication-country] United States
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39. Wong A, Mitra S, Gupta P: Targeting brain tumor stem cells using a bispecific antibody directed against CD133+ and EGFRvIII. J Clin Oncol; 2009 May 20;27(15_suppl):2022

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting brain tumor stem cells using a bispecific antibody directed against CD133+ and EGFRvIII.
  • : 2022 Background: Using the marker CD133, cancer stem cells (CSCs) have been demonstrated for glioblastomas (GBMs) and medulloblastomas.
  • EGFRvIII is a tumor specific EGF receptor.
  • The BsAb showed the highest binding for cells expressing both epitopes, whereas Di-EGFRvIII and Di-AC133 had the highest affinity for cells expressing high levels of individual antigens.
  • We then explored the efficiency of tumor cell killing.
  • Di-EGFRvIII efficiently induced cytotoxicity in U87-EGFRvIII/CD133 and U87vIII cells but not in U87-CD133 cells.
  • Di-CD133 was the least effective at inducing ADCC.
  • Finally, we studied the ability of the BsAb to induce ADCC on tumor spheres and normal neurospheres.
  • The BsAb showed at least 4X greater lysis on tumor spheres that were CD133+/EGFRvIII+ over normal neurospheres expressing CD133 alone at an E:T of 10:1.

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  • (PMID = 27964602.001).
  • [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
  • [Publication-country] United States
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40. Abacioglu MU, Caglar HB, Yumuk PF, Akgun Z, Atasoy BM, Sengoz M: Efficacy of protracted dose-dense temozolomide (TMZ) in patients with progressive high-grade glioma. J Clin Oncol; 2009 May 20;27(15_suppl):e13018

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Efficacy of protracted dose-dense temozolomide (TMZ) in patients with progressive high-grade glioma.
  • : e13018 Background: The study was aimed to evaluate the efficacy of TMZ on a protracted dose-dense schedule after standard 5-day TMZ regimen in patients with progressive high-grade glioma.
  • METHODS: In this phase II prospective study, patients who had progression on standard 5-day TMZ for recurrence (group 1) or recurrence after concurrent radiotherapy+TMZ and ≥ 2 cycles of adjuvant TMZ (group 2) for high-grade glioma received TMZ 100 mg/m2× 21 q28 days until progression according to MacDonald's criteria.
  • The histopathology was glioblastoma in 18 and grade 3 glioma (anaplastic astrocytoma, anaplastic oligoastrocytoma or anaplastic oligodendroglioma) in 7.
  • The best response during treatment was partial response in 2 (8%), stable disease in 9 (36%), and progression in 9 (36%) out of 20 patients assessed.
  • Out of 80 cycles received there was no anemia; 5 (6%) grade 1, 8 (10%) grade 2, 2 (3%) grade 3 leucopenia; 1 (1%) grade 1, 2 (3%) grade 2, 1 (1%) grade 3, 1 (1%) grade 4 thrombocytopenia; 9 (11%) grade 1, 7 (9%) grade 2, 32 (40%) grade 3, and 11 (14%) grade 4 lymphopenia.
  • Study was terminated in 2 patients (one with grade 4 thrombocytopenia and the other with grade 4 hepatic toxicity).
  • CONCLUSIONS: Protracted dose-dense TMZ after 5-day schedule for recurrent or progressive disease has modest efficacy with tolerable toxicity.

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  • (PMID = 27962826.001).
  • [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
  • [Publication-country] United States
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41. Neyns B, Chaskis C, Dujardin M, Everaert H, Sadones J, Nupponen NN, Michotte A: Phase II trial of sunitinib malate in patients with temozolomide refractory recurrent high-grade glioma. J Clin Oncol; 2009 May 20;27(15_suppl):2038

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II trial of sunitinib malate in patients with temozolomide refractory recurrent high-grade glioma.
  • : 2038 Background: High-grade gliomas (HGG) are characterized by neo-angiogenesis.
  • Decrease in CBV<sub>LTN</sub> and CBF<sub>LTN</sub> was observed in 6/14 evaluable pts after 4 weeks of sunitinib, 5/19 evaluable pts had SD on T1±Gd after 8 weeks; one pt experienced a marked clinical improvement with a reduction in the tumor metabolism on PET.
  • Three pts with a secondary glioblastoma (age <40 year) had an objective PR when administered CCNU at PD under sunitinib (with a TTP of 2, 8 and +9 mths respectively).

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  • (PMID = 27964622.001).
  • [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
  • [Publication-country] United States
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42. Karrasch M, Gillespie GY, Braz E, Liechty PG, Nabors LB, Lakeman AD, Palmer CA, Parker JN, Whitley RJ, Markert JM: Treatment of recurrent malignant glioma with G207, a genetically engineered herpes simplex virus-1, followed by irradiation: Phase I study results. J Clin Oncol; 2009 May 20;27(15_suppl):2042

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Included patients suffered from inoperable pathologically proven recurrent glioblastoma multiforme (GBM) or anaplastic astrocytoma (AA) which was progressive despite radiotherapy or chemotherapy and failed external beam radiotherapy > 5 Gray prior to study enrolment.
  • 5 patients were suffering from relapsed GBM, 4 patients were suffering from relapsed AA.
  • The 2 patients with initial PR (1xGBM, 1xAA) were re-treated with G207/Irradiation at time point of tumor recurrence, showing PR one month after re-treatment again.
  • In patients suffering from relapsed GBM, mOS was 7.4 months, in patients suffering from relapsed AA, mOS was 9.25 months.
  • Within persistent areas of tumor, HSV staining was present by using a polyclonal antibody for HSV, indicating intratumoral G207 replication (proof of concept).
  • CONCLUSIONS: In 9 patients suffering from relapsed GBM or AA, stereotactic intracerebral G207 inoculation followed by radiation therapy was feasible, safe, and induced clinically relevant responses.
  • Therefore, further clinical development of G207 in GBM is medically reasonable.

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  • (PMID = 27964649.001).
  • [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
  • [Publication-country] United States
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43. El-Jawahri AR, Lautenschlaeger T, Patel D, Chakravarti A: Role of Galectin-3 in the activation of p-ERK and in resistance to radiotherapy in glioblastoma through the activation of p-ERK independent of Ras activity. J Clin Oncol; 2009 May 20;27(15_suppl):11073

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of Galectin-3 in the activation of p-ERK and in resistance to radiotherapy in glioblastoma through the activation of p-ERK independent of Ras activity.
  • : 11073 Background: There has been a growing interest in investigating the molecular mechanisms leading to treatment resistance in glioblastoma (GBM).
  • Galectin-3 (Gal3) is commonly overexpressed in astrocytic tumors of the brain and has been associated with adverse clinical outcomes.
  • We investigated the role and mechanisms of Gal3 in mediating treatment resistance in GBM through modulating the MAPK pathway.
  • METHODS: We investigated Gal3 expression in GBM cell lines (U87, LN18, LN229).
  • RESULTS: Gal3 expression was induced in all GBM cell lines following irradiation.
  • CONCLUSIONS: Our results suggest a possible direct novel interaction between Gal3 and ERK in GBMs that is essential for the expression of p-ERK and mediating treatment resistance in GBMs.

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  • (PMID = 27963194.001).
  • [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
  • [Publication-country] United States
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44. Heimberger AB, Archer GE, Mitchell DA, Bigner DD, Schmittling RJ, Herndon JE 2nd, Davis T, Friedman HS, Keler T, Reardon DA, Sampson JH: Epidermal growth factor receptor variant III (EGFRvIII) vaccine (CDX-110) in GBM. J Clin Oncol; 2009 May 20;27(15_suppl):2021

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epidermal growth factor receptor variant III (EGFRvIII) vaccine (CDX-110) in GBM.
  • : 2021 Background: Unlike conventional therapies for GBM, immunologic targeting of tumor-specific gene mutations allows precise eradication of neoplastic cells with reduced toxicity.
  • EGFRvIII is a constitutively activated and immunogenic mutation not expressed in normal tissues, but widely expressed in GBM and other neoplasms.
  • METHODS: A phase II multi-center trial assessed the immunogenicity and efficacy of CDX-110 in patients with newly-diagnosed, EGFRvIII+ GBM.
  • After resection and radiation / TMZ, patients received CDX-110 vaccinations biweekly x 3, then monthly until tumor progression.
  • Despite grade 2 or 3 lymphopenia in all ACT II patients, EGFRvIII-specific immune responses were generated in all patients, and all immune responses were sustained or enhanced during subsequent TMZ cycles.
  • EGFRvIII-specific IgG1 also increased in avidity with vaccination (K<sub>a</sub>>>2x10<sup>9</sup>M<sup>-1</sup>) in a randomly selected subset of 4 patients (p = 0.000068).
  • CONCLUSIONS: CDX-110 vaccination in patients with GBM appears very promising.

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  • (PMID = 27964605.001).
  • [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
  • [Publication-country] United States
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45. Lai A, Nghiemphu P, Green R, Spier L, Peak S, Phuphanich S, Fehrenbacher L, Kolevska T, Polikoff J, Cloughesy T: Phase II trial of bevacizumab in combination with temozolomide and regional radiation therapy for up-front treatment of patients with newly diagnosed glioblastoma multiforme. J Clin Oncol; 2009 May 20;27(15_suppl):2000

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II trial of bevacizumab in combination with temozolomide and regional radiation therapy for up-front treatment of patients with newly diagnosed glioblastoma multiforme.
  • Based on the promising activity of BV in the treatment of recurrent glioblastoma, we are conducting a phase II trial to determine whether up-front treatment of newly diagnosed GBM with BV may be more advantageous than withholding BV until recurrence.
  • In this trial, we evaluate the safety and efficacy of BV combined with standard of care radiation (RT) and temozolomide (TMZ) and radiation (RT) for newly-diagnosed GBM.
  • Newly-diagnosed GBM patients with no prior treatments are eligible.
  • RESULTS: 70 of 70 projected GBM patients have been enrolled between August 2006 and November 2008 at UCLA and Kaiser Permanente (KP) (Northern and Southern California).
  • Preliminary TTP by Kaplan-Meier analysis is promising compared to that of a UCLA/KP control group of patients that received the conventional RT/TMZ regimen.
  • CONCLUSIONS: Addition of BV to the standard regimen of TMZ and RT for newly-diagnosed GBM is well-tolerated and shows promising efficacy.

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  • (PMID = 27964565.001).
  • [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
  • [Publication-country] United States
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46. Soffietti R, Rudà R, Trevisan E, Picco E, Guarneri D, Caroli M, Fabrini M, Scotti V: Phase II study of bevacizumab and nitrosourea in patients with recurrent malignant glioma: A multicenter Italian study. J Clin Oncol; 2009 May 20;27(15_suppl):2012

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The treatment consists of an induction phase with BV at 10 mg/kg intravenously on day 1 and 15 and fotemustine (FTM) (a nitrosourea with elevated lipophilic properties) at 75 mg/m<sup>2</sup> intravenously on day 1 and 8, followed after a 3-week interval by a maintenance phase with BV at 10 mg/kg i.v. and FTM 75 mg/m<sup>2</sup> i.v. every 3 weeks until tumor progression or unacceptable toxicity.
  • The co-primary endpoints are objective response rate (ORR), based on Mc Donald's criteria (CR + PR) and progression-free survival at 6 months (PFS6), with secondary endpoints of safety time to tumor progression (TTP) and overall survival.
  • RESULTS: From April 2008 to December 2008, 34 patients were enrolled and 31 (22 glioblastomas and 9 anaplastic gliomas) are evaluable for response.
  • Overall response rate (2 CR and 9 PR) was 35% (glioblastomas 33%, anaplastic gliomas 41.5%).
  • Fifteen patients are free of tumor progression (from 2 to 8 months).
  • Toxicities included grade III-IV neutropenia in three patients, grade III-IV piastrinopenia in five, and grade III thrombosis in two.
  • Seventeen patients developed mild to moderate fatigue, six arterial hypertension, and three grade I intratumoral haemorrhage.

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  • (PMID = 27964590.001).
  • [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
  • [Publication-country] United States
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47. Kuhn JG, Gilbert M, Wen P, Cloughesy T, Cooper J, Puduvalli V, DeAngelis L, Lieberman F, Lamborn K, Prados M: Interaction between sorafenib and erlotinib. J Clin Oncol; 2009 May 20;27(15_suppl):2500

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 2500 Background: The combination of sorafenib plus erlotinib was evaluated in patients with recurrent glioblastoma (GBM).
  • METHODS: Adults with recurrent GBM with the usual phase I inclusion/exclusion criteria were eligible.

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  • (PMID = 27961962.001).
  • [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
  • [Publication-country] United States
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48. Tosoni A, Franceschi E, Ermani M, Bacci A, Volpin L, Lombardo L, Ravenna G, Pinna G, Poggi R, Brandes AA: MGMT methylation status as a prognostic factor in anaplastic astrocytomas. J Clin Oncol; 2009 May 20;27(15_suppl):2052

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MGMT methylation status as a prognostic factor in anaplastic astrocytomas.
  • : 2052 Background: MGMT methylation status has been found to be an important prognostic factor in glioblastoma patients (pts).
  • However, further data on the epigenetic feature are needed before its role in rare diseases such as anaplastic astrocytomas (AA) can be established.

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  • (PMID = 27964674.001).
  • [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
  • [Publication-country] United States
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49. Potthast L, Chowdhary S, Pan E, Yu D, Zhu W, Brem S: The infiltrative, diffuse pattern of recurrence in patients with malignant gliomas treated with bevacizumab. J Clin Oncol; 2009 May 20;27(15_suppl):2057

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A diffuse, infiltrative pattern of recurrence, as evidenced by MR imaging, was seen manifesting as multifocal disease or presumed CSF dissemination with subependymal spread.
  • Histologies included glioblastoma (GB), anaplastic astrocytomas (AA), anaplastic oligodendrogliomas (AO), anaplastic oligoastrocytomas (AOA), and low-grade astrocytomas.
  • It is unclear why the disparity among this subset of patients occurs, however, we hypothesize that this may once again highlight the distinct tumor biology among young glioma patients.

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  • (PMID = 27964663.001).
  • [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
  • [Publication-country] United States
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50. Ko L, Allalunis-Turner J: Investigation on the mechanism of dichloroacetate (DCA) induced apoptosis in breast cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e14637

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e14637 Background: DCA is a generic, orally available, small molecule metabolic modulator that has an established history in the treatment of mitochondrial diseases and lactic acidosis.
  • Recent studies suggested apoptosis induction by DCA in glioblastoma, endometrial, prostate, and non-small cell lung cancers.

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  • (PMID = 27964196.001).
  • [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
  • [Publication-country] United States
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51. Gribbin TE, Senzer N, Raizer JJ, Shen S, Nabors LB, Wiranowska M, Fiveash JB: A phase I evaluation of intravenous (IV) &lt;sup&gt;131&lt;/sup&gt;I-chlorotoxin delivery to solid peripheral and intracranial tumors. J Clin Oncol; 2009 May 20;27(15_suppl):e14507

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I evaluation of intravenous (IV) <sup>131</sup>I-chlorotoxin delivery to solid peripheral and intracranial tumors.
  • : e14507 Background: Pre-clinical studies demonstrate TM601 binding to glioblastoma, melanoma, and other tumor types in vitro and in vivo (human xenograft tumors in mice).
  • Here we report imaging and safety data from a Phase I clinical trial in patients with recurrent metastatic somatic and/or cerebral solid tumors that received IV <sup>131</sup>I-TM601.
  • METHODS: Patients received an IV imaging test dose of 10 mCi/0.2mg <sup>131</sup>I-TM601.
  • Subjects not showing tumor localization, received a second imaging test dose of 20 mC/0.4mg <sup>131</sup>I-TM601.
  • Subjects without localization at either dose were dropped from study; patients showing tumor localization without toxicity then received a 30 mCi/0.6mg <sup>131</sup>I-TM601 IV injection.
  • 1) determine whole body localization and dosimetry, 2) estimate the maximum tolerated dose based on normal tissue dosimetry and 3) determine the acute toxicity of IV <sup>131</sup>I-TM601.
  • RESULTS: A total of 44 evaluable patients received IV doses of <sup>131</sup>I-TM601 without dose-limiting toxicity.
  • 31/44 (70%) showed tumor specific uptake on follow-up gamma camera or SPECT imaging.
  • Tumor-specific uptake was observed in patients with malignant glioma (7/8), metastatic melanoma (7/7), non-small cell lung cancer (3/4), colon cancer (6/7), pancreatic cancer (2/3), prostate cancer (2/2), breast cancer (1/4) and in one evaluable patient each with transitional cell carcinoma, pleomorphic xanthoastrocytoma and metastatic paraganglioma.
  • Notably, all patients with metastatic cerebral disease showed tumor-specific uptake of systemically injected <sup>131</sup>I-TM601.
  • CONCLUSIONS: Tumor-specific uptake of IV <sup>131</sup>I-TM601 in primary and metastatic (including brain) solid tumors suggests that further dose escalation is warranted.
  • Notably, IV injected <sup>131</sup>I-TM601 crossed the blood brain barrier.

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  • (PMID = 27963538.001).
  • [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
  • [Publication-country] United States
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52. Conforti R, Ma Y, Morel Y, Paturel C, Terme M, Viaud S, Chaput N, Andre F, Kroemer G, Zitvogel L: Anticancer effects of polyadenylic-polyuridylic acid (poly[A:U]) and uncoupling of chemokine receptor signaling: Role of CCR5 and CXCR3. J Clin Oncol; 2009 May 20;27(15_suppl):3063

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 3063 Background: Several tumor cells express toll-like receptors (TLRs) which constitute putative therapeutic targets.
  • METHODS: To dissect the clinical outcome of the host versus cell autonomous effects of the TLR3 agonist poly(A:U), we took advantage of two murine TLR3 expressing tumor models (melanoma and glioblastoma) that produced large amounts of CCL5 (a CCR5 ligand) and CXCL10 (a CXCR3 ligand) in response to the poly(A:U) and type I IFN in vitro and in vivo.
  • We tested in vivo a triple combination based on vaccine against tumor antigens (V), chemotherapy (C), and TLR3 agonist (poly[A:U]) (T).
  • RESULTS: Single agents (V, C, or T) and combinations of two agents (VC, VT, or CT) failed to improve tumor progression.
  • However, the sequential tritherapy (VCT) significantly retarded tumor growth and prolonged the survival of tumor-bearing C57BL/6 mice.
  • The source of the deleterious CCL5 was the TLR3-activated tumor cells in that stable inhibition of the chemokine production by targeted shRNA CCL5 ameliorated the efficacy of VCT tritherapy.
  • CONCLUSIONS: This study supports the notion that poly(A:U) can act on tumor epithelia to promote the release of beneficial CXCL10 for the recruitment of intratumoral CTLs but also the release of deleterious CCL5 acting on host immunosuppressors.

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  • (PMID = 27962015.001).
  • [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
  • [Publication-country] United States
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53. Lamar RE, Spigel DR, Burris HA, Markus TM, Kuzur M, Ervin T, Fichtel L, Greco FA, Hainsworth JD: Phase II trial of radiation therapy/temozolomide followed by temozolomide/sorafenib in the first-line treatment of glioblastoma multiforme (GBM). J Clin Oncol; 2009 May 20;27(15_suppl):2018

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II trial of radiation therapy/temozolomide followed by temozolomide/sorafenib in the first-line treatment of glioblastoma multiforme (GBM).
  • : 2018 Background: Anti-angiogenesis agents have recently shown activity in the treatment of patients (pts) with GBM.
  • We added sorafenib, a multi-targeted TKI, to the standard first-line treatment of patients with GBM.
  • METHODS: Pts with histologically documented GBM were eligible at diagnosis or after resection.
  • Pts were evaluated every 8 weeks during temozolomide/sorafenib therapy, and every 3 months after therapy ended, until tumor progression.
  • Best responses are as follows: CR, 1 pt (2%); PR, 5 pts (11%); stable disease, 22 pts (49%); progressive disease, 14 pts (31%).
  • Grade 3/4 toxicity during temozolomide/sorafenib was uncommon; 7 pts (16%) required dose reductions of sorafenib during their treatment course.

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  • (PMID = 27964580.001).
  • [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
  • [Publication-country] United States
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54. Kekan M, Fiveash J, Markert JM, Gillespie GY, Kuo H, Meleth S, Gladson CL, Nabors LB: A phase I study of ABT 510 and concurrent temozolamide and radiotherapy for patients with newly diagnosed glioblastoma multiforme. J Clin Oncol; 2009 May 20;27(15_suppl):2023

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I study of ABT 510 and concurrent temozolamide and radiotherapy for patients with newly diagnosed glioblastoma multiforme.
  • This phase I dose escalation trial was designed to study the maximum tolerated dose (MTD) of ABT 510 when used concurrently with temozolomide (TMZ) and radiotherapy (RT) in patients with newly diagnosed glioblastoma multiforme (GBM).
  • METHODS: A total of 23 patients with newly diagnosed, histologically verified GBM were enrolled between April 2005 and January 2007, after obtaining written consent.
  • Patients were monitored with brain MRI along with laboratory values for dose limiting toxicities (DLT) defined as grades 3-4 non-hematological toxicities and grade 4 hematological toxicities (neutropenia or thrombocytopenia).
  • In the absence of a DLT in at least two of the three patients, the dose was increased by 50% in the next cohort of patients.
  • Therapy was discontinued if 14 maintenance cycles were completed, disease progression occurred, or if the patient requested withdrawal.
  • Disease progression and survival statistics were analyzed.
  • RESULTS: During this trial, grade 3/4 DLT were not observed even after the dose was increased to 200 mg/day, hence, the last cohort was expanded to include 14 patients.
  • The median time to tumor progression (TTP) was 220 days and the median overall survival was 422 days.
  • Gene expression analysis of the tumor pathology will be performed to evaluate the relationship between the expression of TSP-1, TSP-2, and patient response to the drug.
  • CONCLUSIONS: ABT 510, at subcutaneous doses up to 200 mg/day, is tolerated well with concurrent TMZ and RT in patients with newly diagnosed GBM.

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  • (PMID = 27964603.001).
  • [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
  • [Publication-country] United States
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55. Green RM, Cloughesy T, Stupp R, DeAngelis LM, Woyshner EA, Ney DE, Lassman AB: Bevacizumab for recurrent ependymoma. J Clin Oncol; 2009 May 20;27(15_suppl):2060

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In recurrent glioblastoma, encouraging responses with bevacizumab have been observed.
  • Five patients achieved a partial response (83%); in one patient the disease was stable.

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  • (PMID = 27964675.001).
  • [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
  • [Publication-country] United States
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56. Desjardins A, Reardon DA, Gururangan S, Peters K, Threatt S, Friedman A, Friedman H, Vredenburgh J: Phase I trial combining SCH 66336 to temozolomide (TMZ) for patients with grade 3 or 4 malignant gliomas (MG). J Clin Oncol; 2009 May 20;27(15_suppl):e13004

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial combining SCH 66336 to temozolomide (TMZ) for patients with grade 3 or 4 malignant gliomas (MG).
  • METHODS: Eligibility included: adult patients with stable or recurrent MG (GBM, anaplastic astrocytoma [AA], anaplastic oligodendroglioma [AO]) previously treated with radiation therapy (RT) and with or without chemotherapy; interval of at least two weeks between prior RT, or four weeks between prior chemotherapy; Karnofsky ≥ 60%; and adequate hematologic, renal and liver function.
  • RESULTS: Thirty-six patients were enrolled (25 GBM, 6 AA, 3 AO).
  • Dose-limiting toxicities were: deep venous thrombosis (1 grade 3); nausea and vomiting (1 grade 3); diarrhea (1 grade 3); elevated ALT (1 grade 3); elevated creatinine (1 grade 3); and fatigue (1 grade 3).
  • Radiographic evaluation reported: 2 partial responses, 14 stable disease for at least 4 cycles, and 11 disease progression after either the first or second cycle.

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  • (PMID = 27962751.001).
  • [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
  • [Publication-country] United States
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57. Sampson JH, Archer GE, Bigner DD, Schmittling RJ, Herndon JE 2nd, Davis T, Friedman HS, Keler T, Reardon DA, Mitchell DA: Effect of daclizumab on T&lt;sub&gt;Reg&lt;/sub&gt; counts and EGFRvIII-specific immune responses in GBM. J Clin Oncol; 2009 May 20;27(15_suppl):2034

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of daclizumab on T<sub>Reg</sub> counts and EGFRvIII-specific immune responses in GBM.
  • : 2034 Background: T<sub>Regs</sub> are increased in patients with GBM and constitutively express the high affinity interleukin-2 receptor (IL-2Rα).
  • EGFRvIII is a constitutively activated and immunogenic mutation not expressed in normal tissues, but widely expressed in GBMs and other neoplasms.
  • In patients with newly-diagnosed, EGFRvIII+ GBM, after resection and radiation/TMZ, patients received CDX-110 vaccinations biweekly x 3, then monthly until tumor progression in combination with TMZ (200 mg/m<sup>2</sup> x 5/28 days).
  • CONCLUSIONS: Daclizumab may reduce T<sub>reg</sub> counts in patients with GBM.

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  • (PMID = 27964629.001).
  • [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
  • [Publication-country] United States
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58. Yu JS, Liu G, Morris-Irvin D, Black KL: 894 Glioblastoma Cancer Stem Cells Exhibit Chemoresistance with Overexpression of Multidrug Resistance Gene BCRP-1. Neurosurgery; 2005 Aug 01;57(2):428

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 894 Glioblastoma Cancer Stem Cells Exhibit Chemoresistance with Overexpression of Multidrug Resistance Gene BCRP-1.

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  • (PMID = 28184783.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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59. Yamada S, Bu XY, Khankaldyyan V, Gonzales-Gomez I, McComb JG, Laug WE: Effect Of The Angiogenesis Inhibitorcilengitide (Emd 121974) On Glioblastoma Growth In Nude Mice. Neurosurgery; 2006 Dec 01;59(6):1304-1312

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect Of The Angiogenesis Inhibitorcilengitide (Emd 121974) On Glioblastoma Growth In Nude Mice.

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  • (PMID = 28180807.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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60. Arbona-Roche EI, Sucre C, Vera-Gimón R, Vera-Gimón A, Vera-Vera R, Gutierrez E, Urdaneta N, Gutierrez M, Somaza S, Tremont-Lukats IW: Treatment of glioblastoma in Venezuela: Limitations using the current standard of care. J Clin Oncol; 2009 May 20;27(15_suppl):e13036

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of glioblastoma in Venezuela: Limitations using the current standard of care.
  • : e13036 Background: The EORTC/NCIC phase III clinical trial using chemoirradiation with temozolomide (TMZ) 75 mg m-2 x 42d, followed by adyuvant TMZ 150-200 mg m-2 daily x 5d q28d x six cycles set a new standard of care for newly diagnosed glioblastoma (GBM).
  • Twelve (40%) patients had stereotactic radiosurgery for recurrent disease during the adjuvant phase.
  • Grade 3-4 hematologic toxicity was seen in two patients (7%).

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  • (PMID = 27962860.001).
  • [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
  • [Publication-country] United States
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61. Uno M, Oba-Shinjo SM, Wakamatsu A, Huang N, Avancini Ferreira Alves V, Rosemberg S, Pires de Aguiar PH, Leite C, Miura F, Marino J R, Scaff M, Nagahashi-Marie SK: Association of TP53 mutation, p53 overexpression, and p53 codon 72 polymorphism with susceptibility to apoptosis in adult patients with diffuse astrocytomas. Int J Biol Markers; 2006 Jan - Mar;21(1):50-57

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of TP53 mutation, p53 overexpression, and p53 codon 72 polymorphism with susceptibility to apoptosis in adult patients with diffuse astrocytomas.
  • : Clarification of TP53 alterations is important to understand the mechanisms underlying the development of diffuse astrocytomas.
  • The aim of this study was to analyze the possible association of TP53 mutation, p53 overexpression, and p53 codon 72 polymorphism with susceptibility to apoptosis in adult Brazilian patients with diffuse astrocytomas.
  • We analyzed 56 surgical specimens of diffuse astrocytomas for alterations of TP53, using polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) direct sequencing. p53 and cleaved caspase 3 protein expression were assessed by immunohistochemistry.
  • We found TP53 mutations in 19.6% (11 out of 56) of tumors tested, with the lowest mutation rate found in the cases of glioblastomas (8.8%) (p = 0.03).
  • We concluded that clarification of the TP53 alterations allows a better understanding of the mechanisms involved in the progression of diffuse astrocytomas, and the allele status at codon 72 was not associated with apoptosis in these tumors.

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  • (PMID = 28207094.001).
  • [ISSN] 1724-6008
  • [Journal-full-title] The International journal of biological markers
  • [ISO-abbreviation] Int. J. Biol. Markers
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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62. Nicholas MK, Lucas RV, Arzbaecher J, Paleologos N, Krouwer H, Malkin M, Omar A, Vick NA: Bevacizumab in combination with temozolomide in the adjuvant treatment of newly diagnosed glioblastoma multiforme: Preliminary results of a phase II study. J Clin Oncol; 2009 May 20;27(15_suppl):2016

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bevacizumab in combination with temozolomide in the adjuvant treatment of newly diagnosed glioblastoma multiforme: Preliminary results of a phase II study.
  • : 2016 Background: Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumor.
  • Because GBM is characterized by vascular proliferation and produces high levels of vascular endothelial growth factor (VEGF), attempts to better control the disease with targeted anti-angiogenesis therapies are underway.
  • Treatment continued until either disease progression or unacceptable toxicity occurred.
  • Best radiographic responses of evaluable subjects, using MacDonald criteria were: 5 complete, 9 partial, 13 stable and 7 progressive disease.
  • Of those taken off study, 13 were due to disease progression.
  • CONCLUSIONS: The co-administration of TMZ/BV following RT/TMZ for newly diagnosed GBM is safe and well-tolerated.

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  • (PMID = 27964582.001).
  • [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
  • [Publication-country] United States
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63. Iuchi T, Hatano K, Sakaida T, Hirono S: Clinical significance of prophylactic intrathecal chemotherapy in the treatment of glioblastoma multiforme. J Clin Oncol; 2009 May 20;27(15_suppl):e13022

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical significance of prophylactic intrathecal chemotherapy in the treatment of glioblastoma multiforme.
  • : e13022 Backgrounds: We previously have reported that hypo-fractionated high-dose irradiation (HdI; 68Gy/8F) showed excellent local control but no effect on prevention of cerebrospinal fluid dissemination (CSFd), resulted in limited efficacy on patients' survival in glioblastoma (GBM).
  • The aim of present analysis is to evaluate the clinical significance of prophylactic intrathecal administration of thiotepa (iT) in the treatment of GBM patients.
  • METHODS: Histologically confirmed GBMs without CSFd at diagnosis were enrolled.
  • RESULTS: Group C and D patients showed significantly longer PFS than Group A and B (p < 0.0001), suggesting the clinical significance of HdI for local control of this tumor.
  • CONCLUSIONS: These data indicated that both of local control and prevention of CSFd were required for better survival of patients with GBM, and iT concurrent with HdI may be one of the treatments that fill these requirements.

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  • (PMID = 27962815.001).
  • [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
  • [Publication-country] United States
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64. Fiveash JB, Chowdhary SA, Peereboom D Jr, Mikkelsen T, Nabors LB, Lesser GJ, Rosenfeld MR, Ye X, Grossman SA: NABTT-0702: A phase II study of R-(-)-gossypol (AT-101) in recurrent glioblastoma multiforme (GBM). J Clin Oncol; 2009 May 20;27(15_suppl):2010

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NABTT-0702: A phase II study of R-(-)-gossypol (AT-101) in recurrent glioblastoma multiforme (GBM).
  • The objectives of this trial were to determine the efficacy and safety of the more active (-) enantiomer of gossypol (AT-101) in patients with recurrent GBM.
  • METHODS: Fifty-six patients with recurrent GBM were enrolled in this multi-institution phase II clinical trial through the NABTT CNS consortium designed to detect a 33% increase in overall survival (OS, primary endpoint) from 5 to 6.65 months with Power/Alpha 80%/0.01.
  • Radiographic assessment of tumor response was made at q 8-week intervals.
  • Grade 3 or greater adverse events possibly or probably related to AT-101 included fatigue (n = 2), ileus (n = 1), elevated cardiac troponin T levels (n = 1), elevated GGT (n = 1), and thrombocytopenia (n = 1).
  • Seven patients (16%) had stable disease as the best response.
  • CONCLUSIONS: AT-101 is well tolerated and without unique toxicities in patients with recurrent GBM.

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  • (PMID = 27964593.001).
  • [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
  • [Publication-country] United States
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65. Sathornsumetee S, Desjardins A, Vredenburgh JJ, Rich JN, Gururangan S, Friedman AH, Friedman HS, Reardon DA: Phase II study of bevacizumab plus erlotinib for recurrent malignant gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):2045

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Erlotinib (E), an EGFR tyrosine kinase inhibitor, may exhibit anti-tumor activity in some malignant glioma (MG) patients.
  • RESULTS: Fifty-six patients with recurrent MG (n = 24 for glioblastoma multiforme [GBM] and n = 32 for anaplastic gliomas [AGs]) were assessable for outcome.
  • The PFS-6 rates were 25% for GBM and 50% for AGs.
  • Rash (54% grade 1-2 and 38% grade 3) was the most common side effect.
  • Nausea, diarrhea, and fatigue were common but mostly grade 1-2.
  • CONCLUSIONS: Among heavily pretreated recurrent MG patients, bevacizumab plus erlotinib is tolerated and associated with encouraging anti-tumor benefit.

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  • (PMID = 27964647.001).
  • [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
  • [Publication-country] United States
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66. Khosla P, Monga V, Taaca A: Pilot study of topotecan and thalidomide in patients with recurrent malignant gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13019

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e13019 Background: Adults with glioblastoma multiforme (GBM) treated with radiation and chemotherapy have median survival of less than 12 months from diagnosis.
  • METHODS: Single-center prospective phase II study of 10 patients (median age 50, range 38-70) with high-grade recurrent glioma treated at Rush University Medical Center between 2002 and 2006 following IRB approval.
  • Dose reductions were made for grade 3 and 4 hematologic or nonhematologic toxicities.

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  • (PMID = 27962824.001).
  • [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
  • [Publication-country] United States
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67. Gupta DK: Efficacy of a Novel Intratumoral Radio Immunotherapeutic Agent Cotara Delivered via Convection-Enhanced Delivery in Recurrent Glioblastoma Multiforme: An Initial Single Institutional Experience with 8 Cases: 980. Neurosurgery; 2009 Aug 01;65(2):427

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Efficacy of a Novel Intratumoral Radio Immunotherapeutic Agent Cotara Delivered via Convection-Enhanced Delivery in Recurrent Glioblastoma Multiforme: An Initial Single Institutional Experience with 8 Cases: 980.

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  • (PMID = 28173215.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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68. Aldape KD, Jones G, Wang M, Hegi M, Janzer RC, Stupp R, Mehta MP, Gilbert MR: MGMT methylation testing in RTOG 0525: A phase III trial of newly diagnosed glioblastoma. J Clin Oncol; 2009 May 20;27(15_suppl):2051

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MGMT methylation testing in RTOG 0525: A phase III trial of newly diagnosed glioblastoma.
  • : 2051 Background: MGMT promoter methylation has been described as a prognostic marker in glioblastoma (GBM) and may be associated with chemosensitivity to alkylating agents.
  • This study determined the feasibility of real-time determination of MGMT promoter methylation testing in a large international phase III clinical trial.
  • METHODS: Paraffin tumor blocks were obtained from patients registered onto RTOG 0525 then distributed to one of two central pathology labs: MD Anderson (Houston TX, K.
  • After histologic confirmation of GBM, unstained slides (40 microns of tumor tissue) were sent to the testing laboratories.
  • Among cases that were evaluable as either methylated or unmethylated (n = 904) the MGMT promoter methylation rate in newly diagnosed GBM was approximately 1/3 (33.4%), a rate that is somewhat lower than prior reports.
  • CONCLUSIONS: The results demonstrate the feasibility of performing real-time MGMT methylation testing, a tumor based assay, as a stratification factor in a multinational clinical trial.
  • This study confirms that treatment decisions based on the molecular characteristics of the tumor are feasible, thereby providing opportunities to develop more molecularly-based tumor stratification or selection, a major advance in developing personalized treatment regimens.

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  • (PMID = 27964673.001).
  • [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
  • [Publication-country] United States
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69. Supko JG, Grossman SA, Peereboom DM, Chowdhary S, Lesser GJ, Nabors LB, Mikkelsen T, Desideri S, Batchelor TT: Feasibility and phase I trial of tandutinib in patients with recurrent glioblastoma. J Clin Oncol; 2009 May 20;27(15_suppl):2039

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Feasibility and phase I trial of tandutinib in patients with recurrent glioblastoma.
  • : 2039 Background: Platelet-derived growth factor signaling is important in gliomagenesis and PDGFR-β is expressed on >90% of endothelial cells in glioblastoma specimens.
  • METHODS: We report the results of a feasibility and phase I study of tandutinib (MLN518), an orally bioavailable, quinazoline-based inhibitor of type III receptor tyrosine kinases including PDGFR-β, FLT-3, and c-Kit, in patients with recurrent glioblastoma (GBM) conducted in the New Approaches to Brain Tumor Therapy (NABTT) consortium.
  • RESULTS: A feasibility study was conducted in 6 recurrent GBM patients in whom resection was clinically indicated.
  • In these patients, the drug was measured in tumor tissue and plasma samples obtained shortly before and after the resection by LC/MS.
  • The mean ± SD concentration of tandutinib in tumor tissue was 7.2 ± 3.2 μg/mL and the mean ratio of its concentration in brain tumor-to-plasma was 9.6 ± 7.7.
  • A phase I study was conducted in 19 patients to determine the MTD in this recurrent GBM population with sequential assessment of the following dose levels: 500-, 600-, and 700-mg BID.
  • Dose limiting toxicities were observed in 1/6 patients at 500-mg BID (grade 3 phosphorous, grade 3 fatigue, grade 3 somnolence in 1 patient); 1/6 patients at 600-mg BID (grade 3 phosphorous); 2/3 patients at 700-mg BID (grade 3 fatigue, grade 3 weakness).
  • CONCLUSIONS: The mean brain tumor tissue-to-plasma ratio of tandutinib in GBM patients receiving 500-mg BID exceeded the estimated threshold ratio of 0.33 that was considered as being necessary to achieve local cytotoxic concentrations in brain tumors.
  • The MTD of tandutinib in the recurrent GBM population is 600-mg BID.

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  • (PMID = 27964617.001).
  • [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
  • [Publication-country] United States
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70. Gilbert MR, Wang M, Aldape K, Lassman A, Sorensen AG, Mikkelson T, Groves M, Werner-Wasik M, Regine W, Mehta M: RTOG 0625: A phase II study of bevacizumab with irinotecan in recurrent glioblastoma (GBM). J Clin Oncol; 2009 May 20;27(15_suppl):2011

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] RTOG 0625: A phase II study of bevacizumab with irinotecan in recurrent glioblastoma (GBM).
  • : 2011 Background: Angiogenesis is a hallmark of GBM, making the tumor vasculature an attractive therapeutic target.
  • In gliomas, vascular endothelial growth factor (VEGF) promotes both angiogenesis and invasion of tumor cells.
  • Irinotecan may enhance efficacy by synergistic tumor endothelial cell death or improved tumor delivery of the chemotherapy via "normalized" tumor vasculature.
  • METHODS: Eligibility included age ≥ 18, centrally confirmed GBM or gliosarcoma, progressive or recurrent disease.
  • Moderate toxicity was noted with 21(37%) grade 3, seven (12%) grade 4, and one (<2%) treatment-related death (intracranial hemorrhage).
  • There were six episodes of venous thrombosis, 14 episodes of grade 3 or 4 hematologic toxicity, predominantly lymphopenia (7), and neutropenia (4), no opportunistic infections or febrile neutropenia were noted.
  • CONCLUSIONS: These results, in the cooperative group context, corroborate the efficacy of the bevacizumab and irinotecan combination for recurrent GBM with the 6m-PFS surpassing the predetermined efficacy threshold.
  • Studies to determine the contribution of the cytotoxic agent to efficacy and the role of bevacizumab in newly diagnosed GBM are planned.

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  • (PMID = 27964588.001).
  • [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 / U10 CA021661
  • [Publication-type] Journal Article
  • [Publication-country] United States
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71. Grossman SA, Ye X, Piantadosi S, Desideri S, Nabors LB, Rosenfeld M, Fisher J, NABTT CNS Consortium: Current survival statistics for patients with newly diagnosed glioblastoma treated with radiation and temozolomide on research studies in the United States. J Clin Oncol; 2009 May 20;27(15_suppl):2003

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current survival statistics for patients with newly diagnosed glioblastoma treated with radiation and temozolomide on research studies in the United States.
  • : 2003 Background: Many novel agents are being studied in combination with radiation and temozolomide (RT+TMZ) in newly diagnosed glioblastoma using survival as the primary endpoint.
  • A total of 281 patients with newly diagnosed glioblastoma were enrolled.
  • CONCLUSIONS: Survival of newly diagnosed glioblastoma patients treated with RT+TMZ + novel agents at 9 NABTT institutions accruing from 2005 to 2008 appears increased compared to RT+TMZ at 85 EORTC institutions accruing from 2000 to 2002.

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  • (PMID = 27964564.001).
  • [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
  • [Publication-country] United States
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72. Quant EC, Silver M, Yip S, Ryg P, Provencher K, McCormack K, Louis DN, Betensky R, Nutt C, Batchelor TT: Case-control study of long-term survivors of glioblastoma. J Clin Oncol; 2009 May 20;27(15_suppl):e13021

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Case-control study of long-term survivors of glioblastoma.
  • : e13021 Background: Survival of patients with glioblastoma (GBM) remains poor.
  • However, a small percentage of GBM patients live ≥ 3 years.
  • Relatively little is known about the patterns of care and outcomes of these long term survivors relative to GBM patients with standard or short-term survival.
  • CONCLUSIONS: Controlling for the well-established prognostic factors of age and performance status, long-term GBM survivors differed significantly from short-term GBM survivors based on tumor location and extent of resection.
  • Short-term GBM survivors differed from standard survivors by tumor location and extent of resection.

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  • (PMID = 27962816.001).
  • [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
  • [Publication-country] United States
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73. Greenfield JP, Hoffman C, Boockvar JA: Fallibility of Glioblastoma Multiforme Cell Lines Overcome by Use of Tumor-Derived Stem. Neurosurgery; 2006 Aug 01;59(2):N9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fallibility of Glioblastoma Multiforme Cell Lines Overcome by Use of Tumor-Derived Stem.

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  • (PMID = 28180630.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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74. Sorensen AG, Jenning D, Wang M, Andronesi O, Chen P, Prados M, Wen P, Jackson E, Cha S, deGroot J: Use of neurovascular imaging in GBM patients (pts) to quantify early physiologic changes after treatment with XL184, an inhibitor of multiple receptor tyrosine kinases: Results from a phase II study. J Clin Oncol; 2009 May 20;27(15_suppl):2048

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Use of neurovascular imaging in GBM patients (pts) to quantify early physiologic changes after treatment with XL184, an inhibitor of multiple receptor tyrosine kinases: Results from a phase II study.
  • : 2048 Background: Treatment of recurrent glioblastoma by targeting VEGF has gained recent attention.
  • XL184 is a potent orally bioavailable inhibitor of MET, RET, KIT, and VEGFR2; MET and VEGFR2 have been shown to play important roles in tumor angiogenesis.
  • In preclinical models, simultaneous inhibition of MET and VEGFR2 with XL184 results in profound regression of tumor vasculature which is qualitatively different from that observed with other antiangiogenic agents.
  • METHODS: A multicenter phase II study of XL184 in 46 pts with relapsed or progressive GBM with primary endpoints of 6-month progression free survival and safety is fully enrolled.
  • Vascular neuroimaging including DCE-MRI, CBV/CBF, diffusion, and magnetic resonance spectroscopy (MRS) is performed in these GBM pts treated with XL184.
  • In all 9 pts with imaging available at Day 28, decreases in tumor size were seen on post-Gd T1 (mean drop 51%, SD 31%, p = 0.03 by t-test) and FLAIR (mean drop 53%, SD 20%, p = 0.001) consistent with an anti-vascular/anti-edema effect.
  • Two of 3 pts with no Day 1 decrease in enhancing lesion volume were bev-pretreated.
  • MRS from 3 pts showed an increase of the NAA/Choline ratio (10-100%) between the baseline and Day 28 scans, and a decrease in lipid levels (50-100%), suggesting inhibition of tumor progression.
  • CONCLUSIONS: Treatment with XL184 results in significant decreases in lesion volume and Ktrans at Day 1 and even greater decreases at Day 28, suggestive of biological activity in GBM.

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  • (PMID = 27964638.001).
  • [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
  • [Publication-country] United States
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75. Keltner L, Chen JC, Wang S, Rakic ML: A phase IIa study of light-activated talaporfin sodium in patients with primary or recurrent glioblastoma multiforme. J Clin Oncol; 2009 May 20;27(15_suppl):e13026

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase IIa study of light-activated talaporfin sodium in patients with primary or recurrent glioblastoma multiforme.
  • : e13026 Background: Preclinical studies have shown that talaporfin sodium (LS11) can concentrate in brain-tumor cells and be activated by red light (664nm wavelength) from light-emitting diodes (LEDs).
  • Singlet oxygen is released that induces blood-vessel occlusion and apoptosis in target tumor cells, which results in direct tumor-cell death and a potential antitumor immunogenic effect on untreated tumors.
  • Preferential talaporfin uptake in tumor and clearance from normal surrounding brain occur by 24 hours after injection.
  • A single center, open label phase IIa study was conducted to establish safety and acute antitumor effect of light-activated drug therapy in glioblastoma patients.
  • METHODS: Nine patients (Karnofsky score >90) with operable glioblastoma, four of which were recurrent in the right frontal or temporal lobe, were recruited at a neurosurgical center in Belgrade, Serbia.
  • Tumor diameter ranged 4-9 cm.
  • Treatment consisted of IV injection of 1mg/kg of LS11 with subsequent craniotomy after a 24-hour wait.
  • A single LED device was inserted into the tumor center followed by different light doses, 250 joules in six patients and 500 joules in three patients.
  • Patients were assessed for 4 weeks with serial CT imaging, intracranial pressure monitoring, and clinical, neurologic, and lab examination.
  • CONCLUSIONS: Treatment of glioblastoma with this light-activated drug therapy was safe and tolerable in this study.
  • An antivascular effect and tumor-cell apoptosis were seen histologically and confined to tumor.

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  • (PMID = 27962791.001).
  • [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
  • [Publication-country] United States
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76. Wick Wolfgang W, Combs SE, Platten M, Weller M, Ohnmacht U, Stoffregen C, Thornton D: Enzastaurin (ENZ) before and concomitant with radiation therapy (RTX), followed by ENZ maintenance therapy in patients with newly diagnosed glioblastoma (GBM) without hypermethylation of the O6-methylguanyl DNA-methyltransferase (MGMT) promoter: A multicenter, open-label, uncontrolled phase II study. J Clin Oncol; 2009 May 20;27(15_suppl):e13038

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Enzastaurin (ENZ) before and concomitant with radiation therapy (RTX), followed by ENZ maintenance therapy in patients with newly diagnosed glioblastoma (GBM) without hypermethylation of the O6-methylguanyl DNA-methyltransferase (MGMT) promoter: A multicenter, open-label, uncontrolled phase II study.
  • : e13038 Background: There is an unmet need to improve efficacy outcome for GBM patients without hypermethylation of the MGMT promoter.
  • METHODS: Patients (pts) with newly diagnosed supratentorial GBM were entered.
  • No drug-related grade 3/4 toxicity was reported.
  • The only laboratory toxicity CTC grade 3 (low potassium) and 1 serious adverse event (erysipelas) were reported in the BID regimen.

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  • (PMID = 27962863.001).
  • [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
  • [Publication-country] United States
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77. Bullain SS, Szentirmai O, Lin N, Sanchez CE, Mulligan RC, Carter B: Chimeric T-cell Receptor Therapy for Glioblastoma Multiforme 895. Neurosurgery; 2006 Aug 01;59(2):486

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chimeric T-cell Receptor Therapy for Glioblastoma Multiforme 895.

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  • (PMID = 28180724.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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78. Stummer W: Extent of Resection and Survival in Glioblastoma Multiforme. Neurosurgery; 2009 Jun 01;64(6):E1206

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extent of Resection and Survival in Glioblastoma Multiforme.

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  • (PMID = 28175598.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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79. Beyene R, Boockvar JA: Novel Treatment of Glioblastoma Multiforme Tumor Stem Cells with Oncolytic Viruses. Neurosurgery; 2009 Jul 01;65(1):N11-N12

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel Treatment of Glioblastoma Multiforme Tumor Stem Cells with Oncolytic Viruses.

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  • (PMID = 28175600.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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80. Batchelor T, Eichler AF, Plotkin SR, Drappatz J, Wen P, Sorensen AG, Gerstner E: Phase I trial of vatalanib (PTK787) in combination with standard radiation and temozolomide in patients with newly diagnosed glioblastoma. J Clin Oncol; 2009 May 20;27(15_suppl):2035

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial of vatalanib (PTK787) in combination with standard radiation and temozolomide in patients with newly diagnosed glioblastoma.
  • Vatalanib (MW 347, T1/2 4.6 h) is an oral, pan-VEGFR tyrosine kinase inhibitor that has shown activity in patients with recurrent glioblastoma.
  • METHODS: This phase I study was designed to determine the maximal tolerated dose of vatalanib in combination with RT and TMZ for patients with newly diagnosed GBM who were taking enzyme-inducing anti-epileptic drugs.
  • Vatalanib was initiated 5 days prior to the start of RT and continued daily until tumor progression, unacceptable toxicity or a maximum of up to 12 cycles of post-RT TMZ.
  • Cohorts of 3 patients were treated during RT and TMZ at doses of 250mg daily, 250mg BID, or 500mg BID of vatalanib.
  • Potentially related grade 3-4 toxicities included elevated transaminases (2 patients), thrombocytopenia (1 patient), leukopenia (1 patient), neutropenia (1 patient), depressed level of consciousness (1 patient), and fatigue (1 patient).

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  • (PMID = 27964624.001).
  • [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
  • [Publication-country] United States
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81. Synowitz M, Glass R, Waelzlein J, Kronenberg G, Gast D, Wang L, Markovic D, Kempermann G, Kettenmann H: 842 Glioblastoma-induced Neurogenesis. Neurosurgery; 2005 Aug 01;57(2):409

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 842 Glioblastoma-induced Neurogenesis.

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  • (PMID = 28184753.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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82. Allison DL, Glantz M, Werner TL, Kirkegaard SL, Murdock K, Jensen R: Intra-CSF trastuzumab in patients with neoplastic meningitis from breast cancer or primary brain tumors. J Clin Oncol; 2009 May 20;27(15_suppl):2066

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Trastuzumab, a large molecule monoclonal antibody directed against the HER-2/neu receptor (overexpressed on some breast cancers, glioblastomas, and medulloblastomas), has negligible access to the CSF after intravenous administration.
  • METHODS: Sixteen patients with neoplastic meningitis (11 GBM, 4 breast cancer, 1 medulloblastoma) and progressive neurologic deterioration were treated with intra-CSF trastuzumab (20-60 mg per dose, either weekly or every other week) for four treatments.
  • MRI scanning of sites of previously demonstrated leptomeningeal tumor was performed after four treatments and then at 8 week intervals.
  • Seven of 11 patients with GBM have responded (two cytologically, two radiographically, all seven clinically), with response durations ranging from 4 to 12+ weeks.
  • CONCLUSIONS: Trastuzumab can be safely administered into the CSF in patients with solid tumor neoplastic meningitis.

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  • (PMID = 27964686.001).
  • [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
  • [Publication-country] United States
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83. Akella NS, Nabors LB, Rosenfeld SS, Chamberlain MC, Mrugala MM, Jacoby DB, O'Neill AM: A phase I evaluation of intravenous TM601 in recurrent glioblastoma: Use of perfusion MRI to monitor antiangiogenic effects. J Clin Oncol; 2009 May 20;27(15_suppl):2041

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I evaluation of intravenous TM601 in recurrent glioblastoma: Use of perfusion MRI to monitor antiangiogenic effects.
  • Based on this work and previous clinical trials demonstrating tumor-specific uptake of <sup>131</sup>I-TM601 in malignant glioma after IV delivery, a phase I trial was initiated with intravenous unlabeled TM-601.
  • METHODS: Six patients with recurrent glioblastoma have been enrolled.
  • All patients received a test dose of 10 mCi <sup>131</sup>I-TM601 to demonstrate tumor-specific uptake prior to TM601 treatment at doses of 0.04 mg/kg IV weekly for 3 weeks in a 4 week cycle.
  • Treatment continued until tumor progression.
  • Patients were evaluated at week 4 of each cycle with conventional and dynamic susceptibility contrast MRI (DSC-MRI) to assess perfusion.
  • Three other serious adverse events considered to be unrelated to therapy included disease progression on therapy, a hip fracture and renal calculi in a patient with a history of renal calculi.

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  • (PMID = 27964654.001).
  • [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
  • [Publication-country] United States
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84. Komotar RJ, Bruce JN, Connolly ES: EGFR Targeted Treatment of Glioblastoma. Neurosurgery; 2006 Feb 01;58(2):N7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] EGFR Targeted Treatment of Glioblastoma.

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  • (PMID = 28180409.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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85. Khalil M, Wulfkuhle J, Fillmore H, Deng J, Liotta L, Petricoin E 3rd, Watson J, Broaddus W: Functional pathway mapping of human glioblastoma multiforme and brain metastases for patient tailored therapy. J Clin Oncol; 2009 May 20;27(15_suppl):2076

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional pathway mapping of human glioblastoma multiforme and brain metastases for patient tailored therapy.
  • : 2076 Background: Genome scanning analysis of human glioblastoma multiforme (GBM) has suggested that this form of cancer is a protein pathway disease.
  • With the current focus on targeted translational therapeutic modalities, a functional understanding of the GBM signaling repertoire is critical, and yet largely unknown.
  • METHODS: Twelve tumors were included in this study: 10 GBMs (9 primary, 1 recurrent) and two brain metastases (1 breast and 1 lung).
  • Pure tumor cell populations were obtained from fixed frozen tissue sections using Laser Capture Microdissection.
  • The two metastatic tumors clustered separately and distinctly from the GBMs.
  • The GBM specimens clustered according to pathway activity.
  • CONCLUSIONS: This study represents the most comprehensive proteomic analysis of human GBM pathway mapping to date.
  • Since certain pathway biomarkers are themselves being targeted by current investigational therapies, the ability to map pathway activation and identify critical pathway biomarkers can lead to targeted therapeutics tailored to each patient's tumor.

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  • (PMID = 27964379.001).
  • [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
  • [Publication-country] United States
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86. Slotman BJ, Eppinga WS, Reijneveld JC, Noske DP, Buter J, Braam LM, Lagerwaard FJ: Impact of extent of resection of glioblastoma multiforme (GBM) in the era of chemoradiation. J Clin Oncol; 2009 May 20;27(15_suppl):e13029

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of extent of resection of glioblastoma multiforme (GBM) in the era of chemoradiation.
  • : e13029 Background: Controversy remains regarding the impact of the extent of resection (EOR) on survival in patients with GBM (Sanai 2008).
  • We studied the prognostic impact of the EOR using early (<72 hours) po-MRI scans in a cohort of GBM patients treated with CTRT in a single center.
  • EOR was categorized as biopsy (N = 3), partial resection (N = 24), major resection (N = 11; i.e., total resection according to the surgeon's report, but residual tumor on po-MRI), and total resection (N = 10; i.e. no residual tumor on po-MRI).

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  • (PMID = 27962797.001).
  • [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
  • [Publication-country] United States
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87. Rosenfeld MR, Chamberlain M, Grossman SA, Peereboom DM, Lesser GJ, Batchelor TT, Desideri S, Salazar AM, Ye X, New Approaches to Brain Tumor Therapy: A CNS Consortium: A phase II study of chemoradiation followed by adjuvant temozolomide and poly-ICLC in patients with newly diagnosed glioblastoma: 12- and 18-month survival data (NABTT 0501). J Clin Oncol; 2009 May 20;27(15_suppl):2002

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of chemoradiation followed by adjuvant temozolomide and poly-ICLC in patients with newly diagnosed glioblastoma: 12- and 18-month survival data (NABTT 0501).
  • The objective of this study was to determine the safety and efficacy of poly-ICLC when added to adjuvant treatment for newly diagnosed glioblastoma.
  • METHODS: Newly diagnosed patients > 18 years with histologically proven glioblastoma received standard external beam radiation with concurrent low-dose temozolomide (TMZ) (75 mg/m<sup>2</sup>) followed by adjuvant cycles of TMZ for 5 days (150-200 mg/m2) (week 1) then intramuscular injections of poly-ICLC (20 mcg/kg) 3 times a week (weeks 2-8; total 21 injections) with week 9 off and no limit to the number of adjuvant cycles (TMZ + poly-ICLC).
  • Fourteen patients did not start adjuvant treatment (5 patient request and 4 investigator withdrawal; 2 progressive disease; 1 death; 1 toxicity; 1 other).
  • The most frequent CTC grade 3-4 toxicities occurring in > 5% of subjects at least possibly related to poly-ICLC were leukopenia (20%), thrombocytopenia (14%), anemia (13%), neutropenia (10%), and SGPT (9%) or alkaline phosphatase (7%) elevation.

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  • (PMID = 27964563.001).
  • [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
  • [Publication-country] United States
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88. Paldino M, Desjardins A, Friedman HS, Vredenburgh JJ, Barboriak DP: Prognostic significance of early changes in the apparent diffusion coefficient that occurs after treatment of patients with glioblastoma multiforme with bevacizumab. J Clin Oncol; 2009 May 20;27(15_suppl):2058

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of early changes in the apparent diffusion coefficient that occurs after treatment of patients with glioblastoma multiforme with bevacizumab.
  • : 2058 Background: To determine the prognostic significance of changes in parameters derived from diffusion tensor imaging (DTI) that occur in response to combination chemotherapy with the antiangiogenesis agent bevacizumab (BEV) in patients with recurrent glioblastoma multiforme (GBM).
  • METHODS: 16 patients (10 men, 6 women; age range 38-62 years) with recurrent GBM underwent serial 1.5T MR imaging.
  • Based on two pre-treatment scans, the 95% confidence limits for change (95%CL) in ADC and FA were calculated in volumes of tumor-related contrast-enhancement (TRE) and FLAIR signal abnormality (FSA).
  • CONCLUSIONS: In patients with GBM treated with BEV and CPT-11, a change in ADC after therapy in areas of FSA is associated with decreased survival.
  • Parameters derived from DTI may, therefore, potentially serve as early markers of treatment failure in patients with GBM.

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  • (PMID = 27964666.001).
  • [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
  • [Publication-country] United States
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89. Mason WP, MacNeil M, Easaw J, McIntosh L, Lwin Z, Chen E, Eisenhauer EE: A phase I study of temozolomide (TMZ) and RAD001 in patients (pts) with glioblastoma multiforme (GBM). J Clin Oncol; 2009 May 20;27(15_suppl):2036

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I study of temozolomide (TMZ) and RAD001 in patients (pts) with glioblastoma multiforme (GBM).
  • This phase I trial was designed to determine the maximum tolerated dose(s) (MTD) and recommended phase II dose(s) of RAD001 in combination with TMZ in patients with GBM.
  • METHODS: Enrollment was restricted to pts with proven GBM, either newly diagnosed following completion of radiotherapy with concurrent TMZ, or at first progression.
  • In the NEIAEDs group at dose level 2 (RAD001 2.5 mg, TMZ 200 mg/m2) 3 of 4 pts had cycle 2 delays and dose reduction of TMZ because of myelosuppression (neutropenia 2 pts, neutropenia and thrombocytopenia, 1 pt), so further escalation of only RAD001 was undertaken, while fixing TMZ at 150 mg/m2.
  • CONCLUSIONS: RAD001 at a daily dose of 10mg can safely be combined with TMZ at 150 mg/m2/d and is the recommended dose for GBM pts receiving NEIAEDs.

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  • (PMID = 27964625.001).
  • [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
  • [Publication-country] United States
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90. Peters K, Desjardins A, Reardon DA, Perry S, Herndon JE 2nd, Bailey L, Friedman AH, Friedman HS, Bigner DD, Vredenburgh JJ: Temozolomide (TMZ) and bevacizumab (BV) as initial treatment for unresectable or multifocal glioblastoma multiforme (GBM). J Clin Oncol; 2009 May 20;27(15_suppl):e13025

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Temozolomide (TMZ) and bevacizumab (BV) as initial treatment for unresectable or multifocal glioblastoma multiforme (GBM).
  • : e13025 Background: GBMs are vascular tumors and inherently resistant to therapy.
  • Patients with unresectable or multifocal GBMs have an even poorer prognosis, with a median survival of 6-8 months.
  • Given the angiogenic phenotype of GBM, we conducted a phase II trial of upfront BV and 5-day TMZ in newly diagnosed unresectable or multifocal GBMs.
  • METHODS: Patients had histologically documented newly diagnosed GBMs that were unresectable or multifocal.
  • An MRI was performed after every cycle and patients continued on therapy as long as there was no tumor progression, grade 4 non-hematologic toxicity or recurrent grade 4 hematologic toxicity after a dose reduction to 150 mg/m<sup>2</sup>/d.
  • The primary endpoint was tumor response using the modified MacDonald criteria plus FLAIR and T2 sequences to evaluate non-enhancing tumor.
  • As the best response, there were 8 (25.8%) partial responses, 19 (61.3 %) patients with stable disease, and 4(12.9 %) had disease progression.
  • 19 of the 41 patients enrolled completed four cycles without tumor progression.
  • The regimen was tolerable, with 3 grade 4 hematologic toxicities including neutropenia and thrombocytopenia.
  • There were 2 grade 4 non-hematologic toxicities, including pulmonary embolism.
  • CONCLUSIONS: Upfront temozolomide and bevacizumab was well tolerated, but synergistic chemotherapy or growth factor inhibitors need to be added to produce meaningful clinical benefit, particularly for unresectable or multifocal GBM.

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  • (PMID = 27962792.001).
  • [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
  • [Publication-country] United States
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91. Vredenburgh JJ, Desjardins A, Reardon DA, Peters K, Herndon JE 2nd, Kirkpatrick J, Gururangan S, Bailey L, Friedman AH, Friedman HS: Safety and efficacy of the addition of bevacizumab (BV) to temozolomide (TMZ) and radiation therapy (RT) followed by BV, TMZ, and irinotecan (CPT-11) for newly diagnosed glioblastoma multiforme (GBM). J Clin Oncol; 2009 May 20;27(15_suppl):2015

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Safety and efficacy of the addition of bevacizumab (BV) to temozolomide (TMZ) and radiation therapy (RT) followed by BV, TMZ, and irinotecan (CPT-11) for newly diagnosed glioblastoma multiforme (GBM).
  • : 2015 Background: Standard GBM treatment includes TMZ and RT, and results in a median progression-free survival and median survival of 6.9 and 15.8 months, respectively.
  • GBM have high concentrations of vascular endothelial growth factor (VEGF), higher levels are associated with poorer prognosis.
  • BV is a humanized antibody to VEGF with activity in recurrent GBMs.
  • This study aims to improve the survival of newly diagnosed GBM patients by incorporating an anti-angiogenic agent with RT and TMZ, and adding a topoisomerase I inhibitor, and an anti-angiogenic agent to TMZ post-RT therapy.
  • Twenty-two patients have completed 6 cycles of BV, TMZ, and CPT-11; 17 of them had a cold PET One patient developed a CNS hemorrhage (grade 2) necessitating stopping BV.
  • Five patients developed thrombocytopenia for which TMZ was held (grade 3, n = 1; grade 4, n = 4).
  • There were no other ≥ grade 3 toxicities, including no wound dehiscence during RT.
  • Twelve patients had tumor progression, and 14 stopped because of toxicity, including: 6 with fatigue; 3 with PEs; 2 with grade 4 thrombocytopenia; the patient with CNS hemorrhage, and one each with a rectal abscess and sepsis.
  • There have been 7 deaths: 5 from tumor progression; one each from sepsis and PEs.

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  • (PMID = 27964581.001).
  • [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
  • [Publication-country] United States
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92. Reardon D, Desjardins A, Vredenburgh JJ, Gururangan S, Peters KB, Norfleet JA: Bevacizumab plus etoposide among recurrent malignant glioma patients: Phase II study final results. J Clin Oncol; 2009 May 20;27(15_suppl):2046

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: Fifty-nine patients (GBM, n = 27; grade 3 MG, n = 32) with a median of 2 prior progressions have enrolled.
  • With a median follow-up of 45 weeks, median overall survival (OS) for GBM and grade 3 MG patients were 46 and 47 weeks, while the 6-PFS is 44% and 40.6%, respectively.
  • The most common toxicities were neutropenia (41%), fatigue (22%), and infection (20%) and were grade 2 in most cases.
  • One patient developed grade 1 intracranial hemorrhage and 1 patient had a grade 4 GI perforation.
  • CONCLUSIONS: Combination of bevacizumab and etoposide is well tolerated in recurrent MG patients and is associated with encouraging anti-tumor benefit.

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  • (PMID = 27964642.001).
  • [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
  • [Publication-country] United States
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93. Bredel M, Renfrow J, Yadav A, Alvarez A, Lin D, Scholtens D, He X, Chandler J, Scheck A, Harsh G: Role of IκBα as a negative regulator of EGFR and a molecular determinant of prognosis in glioblastoma multiforme. J Clin Oncol; 2009 May 20;27(15_suppl):2028

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of IκBα as a negative regulator of EGFR and a molecular determinant of prognosis in glioblastoma multiforme.
  • : 2028 Background: Glioblastoma multiforme is a complex disease that involves the deregulation of overlapping signaling pathways.
  • Constitutive activation of the transcription factor nuclear factor-κB (NF-κB) has been broadly associated with various human cancers, including glioblastomas, and their therapy resistance and may be due to cross-coupling with other oncogenic pathways, such as epidermal growth factor signaling.
  • METHODS: Multidimensional analysis involving gene and transcript data for the endogenous NF-κB modulator IκBα/NFKBIA and clinical patient profiles of 482 glioblastomas/high-grade gliomas from multiple institutions in the United States and The Cancer Genome Atlas Pilot Project.
  • Functional analyses using LN229, U87, and U118 glioblastoma cells, and human embryonic kidney 293T cells with transgene phenotypes for IκBα.
  • IκBα promoter and coding sequence and promoter methylation analyses in a resistance model of 15 glioblastomas cell lines with in vitro and/or in vivo resistance to O6-alkylating agents.
  • RESULTS: We have identified a regulatory circuit between NF-κB and EGFR signaling in glioblastomas, where IκBα binds to EGFR and attenuates EGFR signaling by immobilizing its kinase domain into an inactive conformation.
  • We found the NFKBIA gene at 14q13.2 deleted in 25% of glioblastomas and its occurrence mutually exclusive with EGFR amplification.
  • Functional analyses uncover a bona fide tumor suppressor role for IκBα in glioblastoma cells, where it functions to constrain tumorigenic and migratory potential, and induce spontaneous cellular senescence, and apoptosis in response to treatment.
  • IκBα expression is an independent predictor of patient prognosis in multiple glioblastoma populations.
  • Glioblastomas with initially high IκBα expression significantly repress IκBα upon tumor recurrence, suggesting an acquired mechanism to evade its tumor-suppressive and/or chemo-sensitizing effects during tumor progression.
  • CONCLUSIONS: IκBα is a molecular determinant of biological tumor behavior and patient survival in glioblastoma multiforme.
  • Deletion of NFKBIA could present an alternate mechanism to activate EGFR signaling in EGFR non-amplified glioblastomas.

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  • (PMID = 27964596.001).
  • [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
  • [Publication-country] United States
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94. Chang SM, Kuhn J, Lamborn K, Cloughesy T, Robins I, Lieberman F, Yung A, Dancey J, Prados M, Wen P: Phase I/II study of erlotinib and temsirolimus for patients with recurrent malignant gliomas (MG) (NABTC 04-02). J Clin Oncol; 2009 May 20;27(15_suppl):2004

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 2004 Background: Glioblastomas (GBM) frequently have EGFR amplification/mutations and inactivation of PTEN.
  • METHODS: The North American Brain Tumor Consortium conducted a phase I/II study of the EGFR inhibitor erlotinib in combination with the mTOR inhibitor temsirolimus in recurrent MG.
  • Eligibility criteria were histologically proven GBM and anaplastic gliomas (AG), radiologic progression, >18 years old, KPS >60, adequate bone marrow and organ function.
  • RESULTS: In phase I, 22 patients were enrolled (15 GBM; 7 AG).
  • In phase II, there were 56 patients (including 12 phase I patients treated at the MTD): 40 GBM; 16 AG, median age 47 years (20-72); median KPS 90 (range 60-100), median prior relapses 1 (range 1-3).
  • For GBM patients, there was no PR, 30% SD, and PFS6 was 12.5%.

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  • (PMID = 27964561.001).
  • [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
  • [Publication-country] United States
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95. Del Maestro RF, Siu V, Seyed Sadr M, Alshami J, Sabau C, Seyed Sadr E, Samani A, Assadian S, Greaves K, Pouliot J: The temozolomide O6-methylguanine-DNA methyltransferase (MGMT) study: A phase II trial to evaluate the effect of low-dose preoperative neoadjuvant temozolomide on brain tumour MGMT activity in glioma patients. J Clin Oncol; 2009 May 20;27(15_suppl):e13027

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e13027 Background: Epigenetic methylation of the O6-methylguanine-DNA methyltransferase (MGMT) DNA repair gene promoter in tumor tissue from glioblastoma multiforme patients is associated with improved survival after treatment with radiotherapy plus concomitant and adjuvant temozolomide (TMZ).
  • The primary goal of the study was to evaluate the effect of TMZ 75 mg/m<sup>2</sup> daily prior to surgery on the brain tumor MGMT expression.
  • Samples were obtained from multiple regions of each tumor intra-operatively and were analyzed by methylation specific PCR.
  • RESULTS: Our results on MGMT promoter methylation demonstrate that three groups of patients can be identified: Type I: all sites assessed in the tumor demonstrate no methylation of the MGMT promoter; Type II: all sites demonstrate high levels of MGMT promoter methylation; and Type III: a mixed promoter methylation pattern is observed.
  • This experimental paradigm may be a useful experimental platform for the assessment of the effect of new drugs at the tumor level.

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  • (PMID = 27962800.001).
  • [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
  • [Publication-country] United States
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96. Zitron IM, Norkina O, Al-Kadhimi Z, Barger GR, Lum LG, Mittal S: Targeting of glioblastoma with activated T cells armed with anti-CD3xanti-HER2/neu (HER2Bi) and anti-CD3xanti-EGFR (EGFRBi) bispecific antibodies. J Clin Oncol; 2009 May 20;27(15_suppl):3038

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting of glioblastoma with activated T cells armed with anti-CD3xanti-HER2/neu (HER2Bi) and anti-CD3xanti-EGFR (EGFRBi) bispecific antibodies.
  • The prognosis for patients with glioblastoma remains poor despite aggressive multimodality treatment including surgery and chemoradiotherapy.
  • The receptor tyrosine kinases EGFR, mutant EGFR (EGFRvIII), and HER2/neu are expressed on the majority of glioblastomas and are potential targets for activated T cells (ATCs) armed with bispecific antibodies (BiAbs).
  • HER2Bi- and/or EGFRBi-armed ATCs were examined for in vitro cytotoxicity (MTT and <sup>51</sup>Cr release assays) against long-term malignant glioma lines (U87MG, U118MG, and U251MG) as well as primary glioblastoma lines derived from surgical specimens.
  • Cytotoxicity exhibited by either HER2Bi- or EGFRBi-armed ATCs against four primary glioblastoma cell lines was 50-80%.
  • CONCLUSIONS: BiAbs efficiently target ATCs to kill EGFR and/or HER2/neu expressing glioblastomas.

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  • (PMID = 27962074.001).
  • [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
  • [Publication-country] United States
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97. Ochsenbein AF, Schubert AD, Vassella E, Mariani L: Quantitative analysis of 0&lt;sup&gt;6&lt;/sup&gt;-methylguanine-DNA methyltransferase (MGMT) promoter methylation in patients with low-grade gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):2069

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitative analysis of 0<sup>6</sup>-methylguanine-DNA methyltransferase (MGMT) promoter methylation in patients with low-grade gliomas.
  • : 2069 Background: Loss of heterozygosity (LOH) on the chromosomes 1p and 19q is associated with sensitivity to alkylating agents like temozolomide (TMZ) in patients with low-grade gliomas; whether methylation of the MGMT-promoter, a predictive factor in glioblastoma patients, also correlates with tumor response to TMZ in low-grade gliomas is unclear.
  • METHODS: We performed a retrospective analysis of patients with histologically verified low-grade gliomas (WHO Grade II) who were treated with TMZ for tumor progression at our hospital between November 1999 and November 2007.
  • Objective tumor response was assessed by MRI at 6-month intervals.
  • LOH of microsatellite markers on chromosomes 1p and 19q was determined by polymerase chain reaction (PCR) amplification of the matched pairs of blood and tumor DNA.
  • Seven patients had prior surgical resection of the tumor.
  • Histological classification revealed 10 oligodendrogliomas, 7 oligoastrocytomas, and 5 astrocytomas.
  • All patients were treated with TMZ 200mg/m2 day1-5 in a 4 wk cycle.
  • Grade 3-4 hematological toxicity occurred in 32% of the patients (9% leucopenia, 23% thrombocytopenia).
  • CONCLUSIONS: Quantitative methylation-specific PCR of the MGMT promoter correlates with radiological response to chemotherapy with temozolomide in WHO grade II gliomas.

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  • (PMID = 27964685.001).
  • [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
  • [Publication-country] United States
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98. Neuwelt EA, Frenkel E: The paradoxical effect of targeted antivascular agents in the therapy of CNS malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):2013

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 2013 Background: The rationale of vascular targeted agents (i.e., inhibitors of vascular endothelial growth factors [VEGF] or endothelial intergrins) in the therapy of central nervous system (CNS) malignancies is based upon the concept that normalization of tumor vasculature, with a decrease in tumor interstitial pressure, will improve access of cytoreductive drugs.
  • METHODS: To evaluate this, we studied the effects of bevacizumab, an anti-VEGF agent on tumor vasculature by MRI, using gadolinium-enhanced T1 weighted sequences to assess permeability and the blood pool agent ferumoxytol to assess blood volume.
  • RESULTS: Utilizing two rat brain tumor models, we documented that bevacizumab rapidly decreases tumor enhancement, a pattern equivalent to administration of high dose steroid therapy.
  • Correlative studies in rats and humans exploiting T2 weighted imaging, demonstrated resolution of tumor enhancement with occasional concomitant increase in tumor volume.
  • In a parallel evaluation, pseudo-progression was seen in 9 of 14 glioblastoma patients treated with combined chemo-radiation.
  • These inflammatory responses to treatment, when examined by dynamic MRI, were associated with a transient increase in tumor permeability and decreased cerebral blood volume.
  • CONCLUSIONS: These animal and human studies provide evidence that anti-vascular agents have a steroid-like effect; and in the CNS, may result in reduced delivery of cytoreductive agents to the tumor, thereby compromising standard chemo-radiotherapy.

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  • (PMID = 27964584.001).
  • [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
  • [Publication-country] United States
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99. Herndon J 2nd, Vredenburgh J, Reardon D, Desjardins A, Peters K, Gururangan S, Norfleet J, Friedman A, Bigner D, Friedman HS: Phase I trial of vendetanib and oral etoposide for recurrent malignant gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13016

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e13016 Background: Recurrent malignant gliomas have a poor prognosis, with a median survival of 6-15 months, with grade 4 glioblastomas more aggressive than grade 3 anaplastic astrocytomas or oligodendrogliomas.
  • METHODS: Patients with histologically documented recurrent grade 3 or grade 4 malignant glioma were eligible.
  • There was more hematologic toxicity than expected, with 3/6 of the patients enrolled at dose level 1 developing grade 4 neutropenia.

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  • (PMID = 27962830.001).
  • [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
  • [Publication-country] United States
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100. Franceschi E, Tosoni A, Ermani M, Spagnolli F, La Torre L, Galzio RJ, Pozzati E, Talacchi A, Benevento F, Brandes AA: Impact of MGMT methylation status on 1p/19q intact anaplastic gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13003

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e13003 Background: Chromosomes 1p/19q codeletion has been recognized as a prognostic and predictive factor in patients (pts) with grade 3 gliomas.
  • Non-codeleted (intact) anaplastic oligodendroglioma showed a survival comparable to that usually observed in pts with anaplastic astrocytomas; MGMT methylation status, moreover, has been found to be a prognostic factor in glioblastoma and anaplastic gliomas (AG).
  • Histology was anaplastic oligodendroglioma in 17 pts, anaplastic oligoastrocytoma in 20 pts, and anaplastic astrocytoma in 30 pts; all these pts were 1p19q intact and received surgery, RT, and CT.

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  • (PMID = 27962754.001).
  • [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
  • [Publication-country] United States
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