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1. Cavazos CM, Keir ST, Yoshinari T, Bigner DD, Friedman HS: Therapeutic activity of the topoisomerase I inhibitor J-107088 [6-N-(1-hydroxymethyla-2-hydroxyl) ethylamino-12,13-dihydro-13-(beta-D-glucopyranosyl) -5H-indolo[2,3-a]-pyrrolo[3,4-c]-carbazole-5,7(6H)-dione]] against pediatric and adult central nervous system tumor xenografts. Cancer Chemother Pharmacol; 2001 Sep;48(3):250-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic activity of the topoisomerase I inhibitor J-107088 [6-N-(1-hydroxymethyla-2-hydroxyl) ethylamino-12,13-dihydro-13-(beta-D-glucopyranosyl) -5H-indolo[2,3-a]-pyrrolo[3,4-c]-carbazole-5,7(6H)-dione]] against pediatric and adult central nervous system tumor xenografts.
  • PURPOSE: The in vivo antitumor activity of a novel topoisomerase I inhibitor, J-107088, was tested in athymic nude mice bearing subcutaneous or intracranial pediatric and adult malignant CNS tumor-derived xenografts.
  • METHODS: J-107088 was administered to animals on days 1-5 and 8-12 via intraperitoneal injection at a dose of 54 mg/kg (162 mg/m2) per day in 10% dimethyl sulfoxide in 0.9% saline.
  • The xenografts evaluated were derived from a childhood glioblastoma multiforme (D-456 MG), a childhood medulloblastoma (D-341 MED), an adult anaplastic astrocytoma (D-54 MG), an adult glioblastoma multiforme (D-245 MG), and a procarbazine-resistant subline of D-245 MG [D-245 MG (PR)].
  • CONCLUSION: These results indicate that J-107088 may be active in the treatment of childhood and adult malignant brain tumors and provide the rationale for initiation of clinical trials with this agent.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Carbazoles / therapeutic use. Enzyme Inhibitors / therapeutic use. Glioma / drug therapy. Glucosides / therapeutic use. Indoles. Topoisomerase I Inhibitors
  • [MeSH-minor] Adult. Animals. Child. Female. Humans. Injections, Intraperitoneal. Injections, Subcutaneous. Male. Mice. Mice, Nude. Neoplasm Transplantation. Survival Rate. Transplantation, Heterologous. Treatment Outcome. Tumor Cells, Cultured

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  • (PMID = 11592348.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / 2RO1-NS30245-12; United States / NINDS NIH HHS / NS / 5P50-NS-20023-17; United States / NCI NIH HHS / CA / CA11898; etc
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbazoles; 0 / Enzyme Inhibitors; 0 / Glucosides; 0 / Indoles; 0 / Topoisomerase I Inhibitors; 1V8X590XDP / edotecarin
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2. Salmaggi A, Riva M, Silvani A, Merli R, Tomei G, Lorusso L, Russo A, Marchioni E, Imbesi F, Lombardia Neuro-oncology Group: A multicentre prospective collection of newly diagnosed glioblastoma patients in Lombardia, Italy. Neurol Sci; 2005 Oct;26(4):227-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A multicentre prospective collection of newly diagnosed glioblastoma patients in Lombardia, Italy.
  • The objective was to set the basis for a prospective, multicentre data collection on newly diagnosed adult glioblastoma patients diagnosed in Lombardia by means of a common database used by neurological and neurosurgical units of various hospitals, providing epidemiological, therapy and follow-up data.
  • All adult patients with a newly diagnosed glioblastoma in 9 Lombardia hospitals from 31 March 2003 to 31 March 2004 were followed prospectively by a form elaborated by the Lombardia Neuro-oncology Group.
  • Demographic data were recorded, as well as symptoms at onset, entity of tumour resection, post-surgical Karnofsky Performance Score, radio- and chemotherapy, presence/absence of venous thrombosis, type of antiepileptic treatment, time to tumour progression and survival time (ST).
  • One hundred and thirty-four newly diagnosed glioblastoma patients were enrolled during the first year of the study.
  • In 71 patients, the tumour involved 1 brain lobe at diagnosis.
  • A very high proportion of patients were treated with antiepileptic drugs, even in the absence of seizures.
  • Data in newly diagnosed glioblastoma patients in Lombardia are in line with other case series reported in other populations.
  • [MeSH-major] Brain Neoplasms / physiopathology. Glioblastoma / physiopathology
  • [MeSH-minor] Adult. Brain / pathology. Cohort Studies. Databases, Factual. Disease Progression. Female. Geography. Humans. Italy. Male. Middle Aged. Prospective Studies. Seizures / etiology. Survival Analysis

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  • (PMID = 16193249.001).
  • [ISSN] 1590-1874
  • [Journal-full-title] Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
  • [ISO-abbreviation] Neurol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Italy
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3. Sivak-Sears NR, Schwartzbaum JA, Miike R, Moghadassi M, Wrensch M: Case-control study of use of nonsteroidal antiinflammatory drugs and glioblastoma multiforme. Am J Epidemiol; 2004 Jun 15;159(12):1131-9
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  • [Title] Case-control study of use of nonsteroidal antiinflammatory drugs and glioblastoma multiforme.
  • Evidence from epidemiologic and experimental studies suggests that use of nonsteroidal antiinflammatory drugs (NSAIDs) reduces risk of colon and breast cancer.
  • The association between use of aspirin and other NSAIDs and risk of adult glioblastoma multiforme (GBM) was evaluated among 236 incident GBM cases and 401 population-based controls frequency-matched on age, gender, and ethnicity from the San Francisco Bay Area Adult Glioma Study.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Brain Neoplasms / etiology. Brain Neoplasms / prevention & control. Glioblastoma / etiology. Glioblastoma / prevention & control
  • [MeSH-minor] Adult. Aged. Case-Control Studies. Epidemiologic Studies. Female. Humans. Incidence. Male. Middle Aged. Odds Ratio

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  • (PMID = 15191930.001).
  • [ISSN] 0002-9262
  • [Journal-full-title] American journal of epidemiology
  • [ISO-abbreviation] Am. J. Epidemiol.
  • [Language] eng
  • [Grant] United States / PHS HHS / / R01-52689
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal
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4. Bax DA, Gaspar N, Little SE, Marshall L, Perryman L, Regairaz M, Viana-Pereira M, Vuononvirta R, Sharp SY, Reis-Filho JS, Stávale JN, Al-Sarraj S, Reis RM, Vassal G, Pearson AD, Hargrave D, Ellison DW, Workman P, Jones C: EGFRvIII deletion mutations in pediatric high-grade glioma and response to targeted therapy in pediatric glioma cell lines. Clin Cancer Res; 2009 Sep 15;15(18):5753-61
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  • [Title] EGFRvIII deletion mutations in pediatric high-grade glioma and response to targeted therapy in pediatric glioma cell lines.
  • PURPOSE: The epidermal growth factor receptor (EGFR) is amplified and overexpressed in adult glioblastoma, with response to targeted inhibition dependent on the underlying biology of the disease.
  • We have sought to clarify the role of EGFR in pediatric high-grade glioma (HGG).
  • Pediatric glioblastoma cells transduced with wild-type or deletion mutant EGFRvIII were not rendered more sensitive to erlotinib despite expressing wild-type PTEN.
  • Phosphorylated receptor tyrosine kinase profiling showed a specific activation of platelet-derived growth factor receptor alpha/beta in EGFRvIII-transduced pediatric glioblastoma cells, and targeted coinhibition with erlotinib and imatinib leads to enhanced efficacy in this model.
  • [MeSH-major] Glioma / drug therapy. Glioma / genetics. Receptor, Epidermal Growth Factor / genetics. Receptor, Epidermal Growth Factor / metabolism. Sequence Deletion
  • [MeSH-minor] Adolescent. Blotting, Western. Cell Proliferation / drug effects. Child. Erlotinib Hydrochloride. Humans. Prognosis. Quinazolines / pharmacology. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Sensitivity and Specificity. Tumor Cells, Cultured

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  • [ErratumIn] Clin Cancer Res. 2009 Nov 15;15(22):7110
  • (PMID = 19737945.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / C1178/A10294; United Kingdom / Cancer Research UK / / C309/A2187; United Kingdom / Cancer Research UK / / C309/A8274
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Quinazolines; 0 / epidermal growth factor receptor VIII; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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5. Zhou WN, Chen ZP, You C, Mu YG, Sai K, Zhang JY, Zhang XH, Cheng JJ, Xu HC: [Individualized therapy and outcomes of microsurgery, radiotherapy, and chemotherapy for astrocytoma]. Ai Zheng; 2004 Nov;23(11 Suppl):1555-60
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  • [Title] [Individualized therapy and outcomes of microsurgery, radiotherapy, and chemotherapy for astrocytoma].
  • BACKGROUND & OBJECTIVE: Astrocytomas, constitute about 75% of neuroepithelial tumors, is one of the most common primary tumors in central nervous system with fairly high incidence and poor prognosis.
  • Individualized multimodality is the hope for improving prognosis of patients with astrocytoma.
  • This study was designed to investigate the efficiency of individualized treatment of microsurgery, radiotherapy, and chemotherapy for 62 patients with astrocytoma.
  • METHODS: Sixty-two patients with astrocytoma in study group were treated with individualized multimodality of microsurgery, postoperative radiotherapy, and/or postoperative chemotherapy according to in vitro sensitivity assay.
  • Fifty patients with astrocytoma in control group were treated with conventional treatment of surgery, chemotherapy, and radiotherapy.
  • Pathologic diagnosis of patients in study group were 19 cases of grade, 32 cases of grade III, and 11 cases of grade IV; in control group were 13 cases of grade II, 28 cases of grade III, and 9 cases of grade IV.
  • RESULTS: Tumor total resection rate in study group was 67.7%, while that in control group was 58.0%.
  • There was no significant difference of KPS and survival rate in patients with low-grade astrocytoma between 2 groups, while the outcome of patients with malignant astrocytoma was significantly improved by individualized treatment.
  • In study group, 2-year expectant survival rate of patients with astrocytoma of grade III, and grade IV were 93.7%, and 36.3%, while in control group were 67.5%, and 22.2% (P< 0.05).
  • In glioblastoma patients, median survival time of study group was 18.68 months, while that of control group was 12.83 months (P< 0.01).
  • CONCLUSION: Individualized microsurgery may improve the total resection of astrocytoma, and benefit to postoperative treatment.Individualized radiotherapy/chemotherapy may prevent patients from some complications.
  • Individualized management may improve prognosis of patients with astrocytoma, particularly malignant astrocytoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / surgery. Brain Neoplasms / surgery. Microsurgery
  • [MeSH-minor] Adolescent. Adult. Combined Modality Therapy. Female. Follow-Up Studies. Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Glioblastoma / surgery. Humans. Male. Middle Aged. Radiotherapy, Conformal. Survival Rate. Treatment Outcome

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  • (PMID = 15566679.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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6. Chi AS, Sorensen AG, Jain RK, Batchelor TT: Angiogenesis as a therapeutic target in malignant gliomas. Oncologist; 2009 Jun;14(6):621-36
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  • Currently, adult glioblastoma (GBM) patients have poor outcomes with conventional cytotoxic treatments.
  • Because GBMs are highly angiogenic tumors, inhibitors that target tumor vasculature are considered promising therapeutic agents in these patients.
  • However, the survival benefits observed to date in uncontrolled trials of antiangiogenic agents have been modest, and several obstacles have limited their effectiveness.
  • This article reviews the rationale for antiangiogenic agents in GBM, their potential mechanisms of action, and their clinical development in GBM patients.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Glioma / blood supply. Glioma / drug therapy. Neovascularization, Pathologic / drug therapy
  • [MeSH-minor] Animals. Cell Movement / drug effects. Clinical Trials as Topic. Drug Resistance, Neoplasm. Edema / drug therapy. Endothelial Cells / drug effects. Humans. Protein Kinase Inhibitors / therapeutic use. Receptors, Platelet-Derived Growth Factor / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors. Signal Transduction / drug effects. Vascular Endothelial Growth Factor A / antagonists & inhibitors

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  • (PMID = 19487335.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA080124
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Protein Kinase Inhibitors; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 175
  • [Other-IDs] NLM/ NIHMS765709; NLM/ PMC4790121
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7. Sung T, Miller DC, Hayes RL, Alonso M, Yee H, Newcomb EW: Preferential inactivation of the p53 tumor suppressor pathway and lack of EGFR amplification distinguish de novo high grade pediatric astrocytomas from de novo adult astrocytomas. Brain Pathol; 2000 Apr;10(2):249-59
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  • [Title] Preferential inactivation of the p53 tumor suppressor pathway and lack of EGFR amplification distinguish de novo high grade pediatric astrocytomas from de novo adult astrocytomas.
  • Classification of high grade astrocytomas of children into genetic subtypes similar to the adult remains to be defined.
  • Here we report an extensive characterization of 29 high grade pediatric astrocytomas, 7 WHO grade III and 22 WHO grade IV, for genetic alterations frequently observed in high grade adult astrocytomas occurring in either the p53/MDM2/p14ARF or Rb/CDK4/p16INK4a tumor suppressor pathways.
  • In addition, we have assessed the contribution of EGFR overexpression and amplification and LOH for chromosome 10, two genetic alterations commonly associated with the development of de novo adult glioblastoma for their roles in the development of de novo astrocytomas of childhood.
  • Our results suggest two major differences in the genetic pathway(s) leading to the formation of de novo high grade astrocytomas in children compared with those of the adult.
  • Our findings show preferential inactivation of the p53 tumor suppressor pathway in >95% of pediatric astrocytomas versus inactivation of the Rb tumor suppressor pathway in <25% of the same tumors.
  • In addition, de novo high grade pediatric astrocytomas lack amplification of the EGFR gene compared with EGFR amplification in one-third of adult glioblastomas.
  • Since drug treatments and gene therapy strategies exploit specific genetic alterations in tumor cells, our findings have important implications for the future development of treatments for high grade pediatric astrocytomas.
  • [MeSH-major] Central Nervous System Neoplasms / genetics. Gene Amplification. Gene Silencing. Genes, Tumor Suppressor / genetics. Glioblastoma / genetics. Nuclear Proteins. Receptor, Epidermal Growth Factor / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Proteins
  • [MeSH-minor] Adolescent. Adult. Carrier Proteins / genetics. Child. Child, Preschool. Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 9 / genetics. Cyclin-Dependent Kinase Inhibitor p16. Diagnosis, Differential. Female. Gene Deletion. Gene Expression. Humans. Male. PTEN Phosphohydrolase. Phosphoric Monoester Hydrolases / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-mdm2

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  • (PMID = 10764044.001).
  • [ISSN] 1015-6305
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 16087
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] SWITZERLAND
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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