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1. Struck RF, Tiwari A, Friedman HS, Keir S, Morgan LR, Waud WR: Acyl derivatives of demethylpenclomedine, an antitumor-active, non-neurotoxic metabolites of penclomedine. Cancer Chemother Pharmacol; 2001 Jul;48(1):47-52
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  • PURPOSE: The purpose of this investigation was to compare the antitumor activities of a series of acyl derivatives of 4-demethylpenclomedine (DM-PEN), the major plasma metabolite of penclomedine (PEN) observed to be an active antitumor agent in vivo and non-neurotoxic in a rat model with that of DM-PEN.
  • METHODS: Acyl derivatives were prepared from DM-PEN and evaluated in vivo against human MX-1 breast tumor xenografts implanted subcutaneously (s.c.) or intracerebrally (i.c.).
  • Several derivatives were also evaluated against other human tumor xenografts and murine P388 leukemia cell lines.
  • RESULTS: Several of the acyl derivatives were found to be superior to DM-PEN against MX-1, human ZR-75-1 breast tumor, human U251 CNS tumor and the P388 leukemia parent cell line and lines resistant to cyclophosphamide and carmustine.
  • 4-Demethyl-4-methoxyacetylpenclomedine showed inferior activity to current clinical brain tumor drugs against a glioma cell line, superior activity to temozolomide and procarbazine against the derived mismatch repair-deficient cell line, and superior activity to cyclophosphamide and carmustine but inferior activity to temozolomide against two ependymoma cell lines, all of which were implanted s.c.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Picolines / pharmacology
  • [MeSH-minor] Animals. Brain Neoplasms / drug therapy. Humans. Mice. Neoplasm Transplantation. Structure-Activity Relationship. Transplantation, Heterologous

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  • (PMID = 11488524.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA34200; United States / NCI NIH HHS / CA / R44 CA85021
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Picolines; 108030-77-9 / penclomedine
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2. Fritsch P, Schwinger W, Schwantzer G, Lackner H, Sovinz P, Wendelin G, Benesch M, Sipurzynski S, Urban C: Peripheral blood stem cell mobilization with pegfilgrastim compared to filgrastim in children and young adults with malignancies. Pediatr Blood Cancer; 2010 Jan;54(1):134-7
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  • [Title] Peripheral blood stem cell mobilization with pegfilgrastim compared to filgrastim in children and young adults with malignancies.
  • BACKGROUND: Pegfilgrastim, the long acting agent of rh-GCSF, has been shown to be as effective as Filgrastim in children undergoing cytotoxic chemotherapy by reducing the duration of neutropenia.
  • Recent studies in adults have also shown that Pegfilgrastim is effective to mobilize CD34+ stem cells, resulting in earlier peripheral stem cell collections (PSCC).
  • The aim of the study was to compare the efficacy of Pegfilgrastim with Filgrastim for CD34+ stem cell mobilization in children.
  • PROCEDURE: Three groups of patients were compared: Group 1: six patients with Ewing Sarcoma stimulated with Filgrastim; Group 2: five patients with Ewing Sarcoma, Ependymoma, and Neuroblastoma; Group 3: four patients with relapsed neoplasm.
  • Patients of Group 2 and 3 were stimulated with Pegfilgrastim followed by peripheral stem cell collection.
  • Two patients in Group 3 needed further cytokine stimulation with Filgrastim combined with stem cell factor, Ancestim.
  • RESULTS: In Groups 1-3, a median of 4, 3, and 3 PSCC between day 12-24, 6-13, and 8-30 were performed, yielding a median of 14.2, 24.0, and 10.3 x 10(6) CD34+ stem cells/kg BW, respectively.
  • CONCLUSIONS: Group 2 data show that stem cell mobilization with Pegfilgrastim in children when performed during primary or without previous long lasting chemotherapy seems to produce earlier CD34+ peaks and better CD34+ yields than in Group 1.
  • CD34+ cell mobilization with Pegfilgrastim in Group 3-patients with previous long lasting chemotherapy was possible.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / therapeutic use. Hematopoietic Stem Cell Mobilization. Neoplasm Recurrence, Local / therapy. Neoplasms / therapy. Peripheral Blood Stem Cell Transplantation
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Filgrastim. Humans. Male. Neutropenia / drug therapy. Prognosis. Prospective Studies. Radiotherapy Dosage. Recombinant Proteins. Survival Rate. Treatment Outcome. Young Adult

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  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
  • (PMID = 19785023.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 3A58010674 / pegfilgrastim; PVI5M0M1GW / Filgrastim
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3. Houshmandi SS, Emnett RJ, Giovannini M, Gutmann DH: The neurofibromatosis 2 protein, merlin, regulates glial cell growth in an ErbB2- and Src-dependent manner. Mol Cell Biol; 2009 Mar;29(6):1472-86
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  • [Title] The neurofibromatosis 2 protein, merlin, regulates glial cell growth in an ErbB2- and Src-dependent manner.
  • Individuals with the inherited cancer predisposition syndrome neurofibromatosis 2 (NF2) develop several central nervous system (CNS) malignancies, including glial cell neoplasms (ependymomas).
  • Recent studies have suggested that the NF2 protein, merlin (or schwannomin), may regulate receptor tyrosine kinase signaling, intracellular mitogenic growth control pathways, or adherens junction organization in non-nervous-system cell types.
  • For this report, we used glial fibrillary acidic protein conditional knockout mice and derivative glia to determine how merlin regulates CNS glial cell proliferation.
  • We show that the loss of merlin in glial cells results in increased proliferation in vitro and in vivo.
  • Merlin regulation of glial cell growth reflects deregulated Src activity, such that pharmacologic or genetic inhibition of Src activation reduces Nf2(-/-) glial cell growth to wild-type levels.
  • We further show that Src regulates Nf2(-/-) glial cell growth by sequentially regulating FAK and paxillin phosphorylation/activity.
  • Next, we demonstrate that Src activation results from merlin regulation of ErbB2 activation and that genetic or pharmacologic ErbB2 inhibition reduces Nf2(-/-) glial cell Src/Src effector activation and proliferation to wild-type levels.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Adhesion / drug effects. Cell Adhesion / physiology. Cell Proliferation / drug effects. Cells, Cultured. Enzyme Activation. Focal Adhesion Kinase 1 / metabolism. Glial Fibrillary Acidic Protein / metabolism. Hippocampus / cytology. Hippocampus / physiology. Mice. Mice, Knockout. Paxillin / metabolism. Phosphorylation. Pyrimidines / pharmacology. Signal Transduction / physiology

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  • (PMID = 19103750.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AG 1879; 0 / Glial Fibrillary Acidic Protein; 0 / Neurofibromin 2; 0 / Paxillin; 0 / Pyrimidines; EC 2.7.10.1 / Erbb2 protein, mouse; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.10.2 / Focal Adhesion Kinase 1; EC 2.7.10.2 / Ptk2 protein, mouse; EC 2.7.10.2 / src-Family Kinases
  • [Other-IDs] NLM/ PMC2648234
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4. Morgan RJ, Synold T, Mamelak A, Lim D, Al-Kadhimi Z, Twardowski P, Leong L, Chow W, Margolin K, Shibata S, Somlo G, Yen Y, Frankel P, Doroshow JH: Plasma and cerebrospinal fluid pharmacokinetics of topotecan in a phase I trial of topotecan, tamoxifen, and carboplatin, in the treatment of recurrent or refractory brain or spinal cord tumors. Cancer Chemother Pharmacol; 2010 Oct;66(5):927-33
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  • METHODS: Tamoxifen 100 mg po bid, topotecan 0.25, 0.5, 0.75, or 1.0 mg/m(2)/d IV, administered as a 72 h continuous infusion on days 1-3, followed by carboplatin AUC = 3, IV on day 3.
  • The tumors included glioblastoma (6), anaplastic astrocytoma (2), metastatic non-small cell (3), small cell lung (2), and one each with medulloblastoma, ependymoma, and metastatic breast or colon carcinoma.
  • 4/8 pts with high-grade gliomas had stable disease (median: 3 cycles (range 2-5)).
  • One patient with metastatic non-small cell and one with small cell lung cancer had objective PRs.
  • CONCLUSIONS: The recommended phase II doses are: tamoxifen 100 mg po bid, topotecan 0.75 mg/m(2)/d IV continuous infusion for 72 h, followed by carboplatin AUC = 3 IV on day 3.

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  • (PMID = 20107803.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA033572; United States / NCI NIH HHS / CA / P30 CA033572-26; United States / NCI NIH HHS / CA / CA 33572
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 094ZI81Y45 / Tamoxifen; 7M7YKX2N15 / Topotecan; BG3F62OND5 / Carboplatin
  • [Other-IDs] NLM/ NIHMS335377; NLM/ PMC3265324
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5. de Bont JM, Packer RJ, Michiels EM, den Boer ML, Pieters R: Biological background of pediatric medulloblastoma and ependymoma: a review from a translational research perspective. Neuro Oncol; 2008 Dec;10(6):1040-60
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  • [Title] Biological background of pediatric medulloblastoma and ependymoma: a review from a translational research perspective.
  • Survival rates of pediatric brain tumor patients have significantly improved over the years due to developments in diagnostic techniques, neurosurgery, chemotherapy, radiotherapy, and supportive care.
  • Prognosis is still highly dependent on clinical characteristics, such as the age of the patient, tumor type, stage, and localization, but increased knowledge about the genetic and biological features of these tumors is being obtained and might be useful to further improve outcome for these patients.
  • It has become clear that the deregulation of signaling pathways essential in brain development, for example, sonic hedgehog (SHH), Wnt, and Notch pathways, plays an important role in pathogenesis and biological behavior, especially for medulloblastomas.
  • More recently, data have become available about the cells of origin of brain tumors and the possible existence of brain tumor stem cells.
  • Newly developed array-based techniques for studying gene expression, protein expression, copy number aberrations, and epigenetic events have led to the identification of other potentially important biological abnormalities in pediatric medulloblastomas and ependymomas.
  • [MeSH-major] Brain Neoplasms / genetics. Ependymoma / genetics. Medulloblastoma / genetics

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  • (PMID = 18676356.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 246
  • [Other-IDs] NLM/ PMC2719002
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6. Engels EA, Sarkar C, Daniel RW, Gravitt PE, Verma K, Quezado M, Shah KV: Absence of simian virus 40 in human brain tumors from northern India. Int J Cancer; 2002 Oct 1;101(4):348-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Simian virus 40 (SV40), a monkey polyomavirus, was a contaminant of early poliovirus vaccines administered to millions of individuals in the 1950s and early 1960s.
  • SV40 causes brain tumors in laboratory animals, and SV40 DNA sequences have been variably identified in human choroid plexus tumors and ependymomas.
  • DNA from pathologic specimens from 33 ependymomas, 14 choroid plexus tumors and 18 control brain tissues (contused brain, brain metastases) was extracted and analyzed under masked conditions.
  • SV40 DNA was detected in 1 specimen (an ependymoma).
  • However, few SV40 DNA copies were detected in this sample (<10 copies, equivalent to <1 copy/350 cells, based on simultaneous GAPDH quantification), and SV40 was not detected when this sample was retested.
  • Our findings do not support a role for SV40 in choroid plexus tumors or ependymomas from northern India.
  • [MeSH-minor] Adolescent. Adult. Animals. Antigens, Polyomavirus Transforming / genetics. Brain / virology. Child. Child, Preschool. Choroid Plexus Neoplasms / virology. DNA, Viral / analysis. Drug Contamination. Ependymoma / virology. Glyceraldehyde-3-Phosphate Dehydrogenases / genetics. Humans. India. Macaca mulatta / virology. Nucleic Acid Hybridization. Poliovirus Vaccines. Polymerase Chain Reaction

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • [CommentIn] Int J Cancer. 2003 Aug 10;106(1):140-2; author reply 143-5 [12794770.001]
  • (PMID = 12209959.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Polyomavirus Transforming; 0 / DNA, Viral; 0 / Poliovirus Vaccines; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases
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7. Kim SK, Lim SY, Wang KC, Kim YY, Chi JG, Choi YL, Shin HJ, Cho BK: Overexpression of cyclooxygenase-2 in childhood ependymomas: role of COX-2 inhibitor in growth and multi-drug resistance in vitro. Oncol Rep; 2004 Aug;12(2):403-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of cyclooxygenase-2 in childhood ependymomas: role of COX-2 inhibitor in growth and multi-drug resistance in vitro.
  • The management of ependymomas remains one of the most frustrating issues in pediatric neuro-oncology.
  • Moreover, the chemoresistance of ependymomas may be explained by the expression of membrane transport molecule P-glycoprotein (P-gp).
  • In this study the expression of cyclooxygenase 2 (COX-2) and the role of the specific COX-2 inhibitor NS-398 in growth and multi-drug resistance of ependymomas were investigated.
  • COX-2 protein expression was assessed in 19 ependymomas immunohistochemically, and the effect of NS-398 on growth and multi-drug resistance was investigated using two primary cultured ependymoma cell lines.
  • COX-2 protein expression was observed in 15 (79%) of the 19 ependymomas.
  • NS-398 was found to reduce the proliferation of monolayer cell cultures in a dose- and time-dependent manner and to induce apoptosis and lower bcl-2 protein levels.
  • Our findings demonstrate that COX-2 is overexpressed in ependymomas and that NS-398 is able to induce apoptosis and suppress P-gp expression and activity.
  • [MeSH-major] Brain Neoplasms / metabolism. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Enzyme Inhibitors / pharmacology. Ependymoma / metabolism. Isoenzymes / biosynthesis. Prostaglandin-Endoperoxide Synthases / biosynthesis
  • [MeSH-minor] Annexin A5 / pharmacology. Apoptosis. Blotting, Western. Cell Proliferation. Child. Child, Preschool. Coloring Agents / pharmacology. Cyclooxygenase 2. Dose-Response Relationship, Drug. Female. Flow Cytometry. Humans. Immunohistochemistry. Infant. Male. Membrane Proteins. P-Glycoprotein / metabolism. Rhodamine 123 / pharmacology. Time Factors. Tumor Cells, Cultured

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  • (PMID = 15254709.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Coloring Agents; 0 / Enzyme Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / P-Glycoprotein; 1N3CZ14C5O / Rhodamine 123; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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8. Tanaka M, Shibui S, Kobayashi Y, Nomura K, Nakanishi Y: A graft-versus-tumor effect in a patient with ependymoma who received an allogenic bone marrow transplant for therapy-related leukemia. Case report. J Neurosurg; 2002 Aug;97(2):474-6
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  • [Title] A graft-versus-tumor effect in a patient with ependymoma who received an allogenic bone marrow transplant for therapy-related leukemia. Case report.
  • The authors report on a 42-year-old man with a recurrent ependymoma who received an allogenic BMT for therapy-related leukemia.
  • After transplantation, the patient developed chronic graft-versus-host disease, which was controlled with steroid agents.
  • Interestingly, the recurrent ependymoma regressed steadily over the next 21 months posttransplant, until the tumor became almost undetectable on magnetic resonance images.
  • This case indicates that the graft-versus-tumor effect, mediated by cytotoxic T cells, may be able to target intraparenchymal neuroepithelial tumors, despite the brain's generally recognized status as an immunoprivileged organ.
  • [MeSH-major] Bone Marrow Transplantation. Brain Neoplasms / physiopathology. Brain Neoplasms / radiotherapy. Ependymoma / physiopathology. Ependymoma / radiotherapy. Graft vs Tumor Effect / physiology. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / surgery. Leukemia, Radiation-Induced / etiology. Leukemia, Radiation-Induced / surgery


9. Haroun RI, Clatterbuck RE, Gibbons MC, Burger PC, Parker R, Fruehauf JP, Brem H: Extreme drug resistance in primary brain tumors: in vitro analysis of 64 resection specimens. J Neurooncol; 2002 Jun;58(2):115-23
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  • [Title] Extreme drug resistance in primary brain tumors: in vitro analysis of 64 resection specimens.
  • Although the literature contains many reports of the application of drug resistance assays, little is known about extreme drug resistance (EDR) in primary brain tumors.
  • From September 1991 to February 1998, we collected 64 brain tumor specimens from patients admitted to the Johns Hopkins Hospital.
  • Brain tumor specimens were tested against 13 different chemotherapeutic agents using an extreme drug resistance assay.
  • Results were reported as percent cell inhibition (PCI) (compared to control cultures).
  • A drug resistance profile (extreme, intermediate, or low) was determined based on statistical comparison to a historical database of tumor specimens tested against the same panel of chemotherapeutic agents.
  • Brain tumor specimens were classified histologically as Grade IV astrocytoma (glioblastoma multiforme, n = 35), Grade II/III astrocytoma (n = 11), oligodendroglioma (n = 6), meningioma (n = 9), hemangiopericytoma (n = 2), and ependymoma (n = 1).
  • A large percentage of glioblastomas displayed extreme drug resistance to paclitaxel (69%, n = 35), SN38 (75%, n = 28), and vincristine (38%, n = 29).
  • The majority of Grade II/III astrocytomas displayed extreme drug resistance to carboplatin (67%, n = 6), cisplatin (60%, n = 10), and paclitaxel (60%, n = 10).
  • In a similar fashion, oligodendrogliomas displayed extreme drug resistance to vincristine (60%, n = 5) and paclitaxel (50% n = 6).
  • Most meningiomas displayed extreme drug resistance to vincristine (75%, n = 8), dacarbazine (63%, n = 8), and 4-HC (50%, n = 8).
  • Through the continued analysis of brain tumor specimens and compilation of data from multiple institutions, chemoresistance profiles could assist in the development of rationale clinical trials and treatment regimens for patients with brain tumors.
  • [MeSH-major] Brain Neoplasms / drug therapy. Drug Resistance, Neoplasm
  • [MeSH-minor] Cell Division / drug effects. Humans

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  • (PMID = 12164682.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-09574; United States / NCI NIH HHS / CA / U19 CA52857
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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10. Benesch M, Siegler N, Hoff Kv, Lassay L, Kropshofer G, Müller H, Sommer C, Rutkowski S, Fleischhack G, Urban C: Safety and toxicity of intrathecal liposomal cytarabine (Depocyte) in children and adolescents with recurrent or refractory brain tumors: a multi-institutional retrospective study. Anticancer Drugs; 2009 Oct;20(9):794-9
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  • Nineteen heavily pretreated patients (males, n = 14; females, n = 5; median age at diagnosis 8.5 years; range, 1.4-22 years) were given intrathecal liposomal cytarabine on a compassionate use basis for recurrent refractory medulloblastoma (n = 12), mixed germ cell tumor (n = 2), central nervous system primitive neuroectodermal tumors of the pons (n = 1), anaplastic ependymoma (n = 1), anaplastic oligodendroglioma (n = 1), atypical teratoid rhabdoid tumor (n = 1), or rhabdoid papillary meningioma (n = 1).
  • Proof of efficacy requires a prospective single-agent phase II study.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Brain Neoplasms / drug therapy. Cytarabine / administration & dosage. Cytarabine / adverse effects
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Compassionate Use Trials. Delayed-Action Preparations. Drug Resistance, Neoplasm. Female. Humans. Infant. Injections, Spinal. Liposomes / administration & dosage. Male. Retrospective Studies. Salvage Therapy. Young Adult

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  • (PMID = 19617818.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Delayed-Action Preparations; 0 / Liposomes; 04079A1RDZ / Cytarabine
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11. Ribalta T, McCutcheon IE, Neto AG, Gupta D, Kumar AJ, Biddle DA, Langford LA, Bruner JM, Leeds NE, Fuller GN: Textiloma (gossypiboma) mimicking recurrent intracranial tumor. Arch Pathol Lab Med; 2004 Jul;128(7):749-58
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  • [Title] Textiloma (gossypiboma) mimicking recurrent intracranial tumor.
  • Resorbable and nonresorbable hemostatic agents have been reported to cause symptomatic mass lesions, most commonly following intra-abdominal surgery.
  • Histologic examination typically shows a core of degenerating hemostatic agent surrounded by an inflammatory reaction.
  • Each agent exhibits distinctive morphologic features that often permit specific identification.
  • OBJECTIVES: The aims of this study were to (1) identify cases of histologically proven cases of textiloma in neurosurgical operations, (2) characterize the specific hemostatic agent associated with textiloma formation, and (3) characterize the preoperative magnetic resonance imaging appearance of textiloma.
  • DESIGN: Cases in which a textiloma constituted the sole finding on repeat surgery for recurrent brain tumor, or was a clinically significant component of a radiologically identified mass lesion together with residual tumor, constituted the study set.
  • The primary neoplasm was different in each case and included pituitary adenoma, tanycytic ependymoma, anaplastic astrocytoma, gliosarcoma, and oligodendroglioma.
  • In all cases, preoperative magnetic resonance imaging suggested recurrent tumor.
  • Textilomas included all categories of resorbable hemostatic agent.
  • Inflammatory reactions included giant cells, granulomas, and fibroblastic proliferation.
  • Microfibrillar collagen (Avitene) textilomas were associated with a striking eosinophil infiltration that was not seen with any other hemostatic agent.
  • CONCLUSIONS: Hemostatic agents may produce clinically symptomatic, radiologically apparent mass lesions.
  • When considering a mass lesion arising after intracranial surgery, the differential diagnosis should include textiloma along with recurrent tumor and radiation necrosis.
  • [MeSH-major] Brain Diseases / diagnosis. Brain Neoplasms / diagnosis. Granuloma, Foreign-Body / diagnosis. Granuloma, Plasma Cell / diagnosis. Hemostasis, Surgical / instrumentation
  • [MeSH-minor] Adolescent. Adult. Cellulose, Oxidized. Collagen. Cotton Fiber. Diagnosis, Differential. Female. Gelatin Sponge, Absorbable. Hemostatics. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Recurrence, Local / diagnosis. Radiation Injuries / diagnosis

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  • (PMID = 15214828.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cellulose, Oxidized; 0 / Hemostatics; 82347-53-3 / Surgicel; 9007-34-5 / Collagen
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12. Kempuraj D, Devi RS, Madhappan B, Conti P, Nazer MY, Christodoulou S, Reginald J, Suthinthirarajan N, Namasivayam A: T lymphocyte subsets and immunoglobulins in intracranial tumor patients before and after treatment, and based on histological type of tumors. Int J Immunopathol Pharmacol; 2004 Jan-Apr;17(1):57-64
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  • [Title] T lymphocyte subsets and immunoglobulins in intracranial tumor patients before and after treatment, and based on histological type of tumors.
  • It has been reported that nervous system and peripheral immune system communicate with each other and the peripheral immune status is depressed in some intracranial tumor (ICT) patients pre operatively.
  • Little is known about the immune status of intracranial tumor patients during the post operative survival period.
  • We thus investigated total T cells (CD 11+), helper/inducer (CD4+) T cells, suppressor/cytotoxic (CD8+) T cells, B cells (CD19+) and serum immunoglobulins in peripheral blood in certain ICT patients before and after treatment, and based on the histological type of the tumors.
  • Post treatment analysis were conducted 30 days after surgical removal of tumor tissue in benign brain tumor patients and 30 days after chemo therapy (CT)/radiotherapy (RT) following surgical removal of tumor tissue in malignant brain tumor patients.
  • Decreased CD11+, CD4+ and increased CD8+ T cell counts were observed in both benign and malignant tumor cases before treatment compared with control subjects.
  • After treatment, CD4+ T cell count increased and CD8+ T cell count decreased than their pre treatment levels.
  • Serum IgA and IgG levels were decreased in both benign and malignant brain tumor patients before treatment than in control subjects.
  • Serum IgM level has been increased in both benign and malignant tumor patients before and after treatment than in control subjects.
  • Anaplastic malignant astrocytoma, medulloblastoma and glioblastoma multiforme patients showed higher IgM level than astrocytoma, meningioma and ependymoma patients.
  • In conclusions, the depressed host cellular immunity in benign and malignant tumor patients before treatment may be due to the changes in CD4+ and CD8+ counts in addition to tumour specific immunosuppressive factors.
  • Treatment procedures such as surgery, CT and RT may play certain role in the post operative depressed immunosuppression in malignant tumor patients.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / immunology. Brain Neoplasms / pathology. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Immunoglobulins / blood
  • [MeSH-minor] Adjuvants, Immunologic / administration & dosage. Adjuvants, Immunologic / therapeutic use. Analysis of Variance. Astrocytoma / drug therapy. Astrocytoma / immunology. Astrocytoma / pathology. Ependymoma / drug therapy. Ependymoma / immunology. Ependymoma / pathology. Humans. Immunosuppressive Agents / administration & dosage. Immunosuppressive Agents / therapeutic use. Meningioma / drug therapy. Meningioma / immunology. Meningioma / pathology. Oligodendroglioma / drug therapy. Oligodendroglioma / immunology. Oligodendroglioma / pathology

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  • (PMID = 15000867.001).
  • [ISSN] 0394-6320
  • [Journal-full-title] International journal of immunopathology and pharmacology
  • [ISO-abbreviation] Int J Immunopathol Pharmacol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antineoplastic Agents; 0 / Immunoglobulins; 0 / Immunosuppressive Agents
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13. Lewandowicz GM, Harding B, Harkness W, Hayward R, Thomas DG, Darling JL: Chemosensitivity in childhood brain tumours in vitro: evidence of differential sensitivity to lomustine (CCNU) and vincristine. Eur J Cancer; 2000 Oct;36(15):1955-64
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  • The aim of this study was to examine the range of sensitivity of a panel of short-term cultures derived from different types of malignant childhood brain tumours including medulloblastoma, ependymoma and glioblastoma multiforme to three cytotoxic drugs, lomustine (CCNU), vincristine (VCR) and procarbazine (PCB).
  • Short-term cell lines derived from ependymomas were considerably more resistant to VCR than other types of childhood brain tumours, while cultures derived from supratentorial primitive neuroectodermal tumour (PNET) displayed marked sensitivity to both lomustine and VCR.
  • Cultures from ependymomas, medulloblastoma and astrocytic gliomas had similar sensitivity to lomustine and PCB as cultures derived from adult malignant astrocytoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy
  • [MeSH-minor] Adult. Astrocytoma / drug therapy. Child. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Ependymoma / drug therapy. Female. Glioblastoma / drug therapy. Humans. Lomustine / therapeutic use. Male. Medulloblastoma / drug therapy. Procarbazine / therapeutic use. Tumor Cells, Cultured / drug effects. Vincristine / therapeutic use

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  • (PMID = 11000577.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 7BRF0Z81KG / Lomustine
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14. Weggen S, Bayer TA, von Deimling A, Reifenberger G, von Schweinitz D, Wiestler OD, Pietsch T: Low frequency of SV40, JC and BK polyomavirus sequences in human medulloblastomas, meningiomas and ependymomas. Brain Pathol; 2000 Jan;10(1):85-92
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  • [Title] Low frequency of SV40, JC and BK polyomavirus sequences in human medulloblastomas, meningiomas and ependymomas.
  • For the present study, a highly sensitive PCR-assay with fluorescence-labelled primers was developed to search for polyomavirus sequences in human brain tumor and control DNA samples.
  • The assay was shown to detect approximately one viral large T-antigen (TAg) gene per 250 cells.
  • We identified simian virus 40 (SV40)-like sequences in 2/116 medulloblastomas, in 1/131 meningiomas, in 1/25 ependymomas and in 1/2 subependymomas.
  • A single case of ependymoma contained SV40 VP-1 late gene sequences.
  • Immunohistochemical analysis of two SV40 positive tumor biopsies failed to detect large TAg in the tumor cells.
  • In the JC positive meningioma, immunoreactivity for the viral late gene product (VP-1) was not observed.
  • Our data do not entirely rule out SV40 and JC virus as an initiative agent with a hit-and-run mechanism.
  • However the low frequency of virus sequences and the absence of TAg protein expression argue against a major role of these viruses in the pathogenesis of human medulloblastomas, meningiomas and ependymomas.
  • [MeSH-major] BK Virus / genetics. Brain Neoplasms / virology. Cerebellar Neoplasms / virology. Ependymoma / virology. JC Virus / genetics. Medulloblastoma / virology. Meningeal Neoplasms / virology. Meningioma / virology. Simian virus 40 / genetics
  • [MeSH-minor] Humans. Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 10668898.001).
  • [ISSN] 1015-6305
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] SWITZERLAND
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15. Rickert CH: Prognosis-related molecular markers in pediatric central nervous system tumors. J Neuropathol Exp Neurol; 2004 Dec;63(12):1211-24
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  • A survey of publications about prognosis-related molecular features among pediatric brain tumors revealed 74 series, of which 46 presented statistically significant outcome-associated parameters as defined by a p value <0.05.
  • Most investigations revealing significant prognosis-related features were performed on medulloblastomas (34 publications), followed by astrocytic tumors (6 publications) and ependymomas (5 publications).
  • Promising approaches and molecular markers include gene expression profiles, DNA ploidy, loss of heterozygosity and chromosomal aberrations as detected by CGH and FISH (1q, 17p, 17q), as well as oncogenes/ tumor suppressor genes and their proteins (TP53, PTEN, c-erbB2, N-myc, c-myc), growth factor and hormonal receptors (PDGFRA, VEGF, EGFR, HER2, HER4, ErbB-2, hTERT, TrkC), cell cycle genes (p27) and cell adhesion molecules, as well as factors potentially related to therapeutic resistance (multi-drug resistance, DNA topoisomerase IIalpha, metallothionein, P-glycoprotein, tenascin).


16. Karlsson AE, Bergenheim AT, Brännström T, Hedman H, Henriksson R: Distribution of estramustine-binding protein during postnatal development of rat brain. Histochem Cell Biol; 2001 May;115(5):397-401
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  • Estramustine-binding protein (EMBP) is expressed in several types of brain tumors, such as astrocytoma, ependymoma, and meningioma.
  • It binds the cytotoxic drug estramustine with high affinity and is suggested to cause accumulation of the drug in EMBP-expressing tumor cells.
  • In this study, the spatial distribution of EMBP in normal rat brain was studied with immunohistochemistry.
  • EMBP was found in the cytoplasm of ependymal cells, in the leptomeninges, mainly the arachnoid, and in scattered neurons.
  • Moreover, staining was seen in nuclei of choroid plexus cells, in the granular cell layer in the cerebellum, and in a few scattered endothelial cells.
  • The nuclear staining was more frequent in younger animals.
  • Future studies are justified to elucidate the role of EMBP-like proteins in CNS and in brain tumors.
  • [MeSH-major] Brain / growth & development. Brain Chemistry. Neoplasm Proteins / metabolism
  • [MeSH-minor] Age Factors. Animals. Carrier Proteins / genetics. Carrier Proteins / metabolism. Cerebellum / chemistry. Cerebellum / cytology. Choroid Plexus / chemistry. Choroid Plexus / cytology. Ependyma / chemistry. Ependyma / cytology. Estramustine. Female. Immunohistochemistry. Male. Meninges / chemistry. Meninges / cytology. Prostatic Secretory Proteins / genetics. Prostatic Secretory Proteins / metabolism. RNA, Messenger / metabolism. Rats. Reverse Transcriptase Polymerase Chain Reaction. Sex Factors. Tissue Distribution

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  • (PMID = 11449887.001).
  • [ISSN] 0948-6143
  • [Journal-full-title] Histochemistry and cell biology
  • [ISO-abbreviation] Histochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Neoplasm Proteins; 0 / Prostatic Secretory Proteins; 0 / RNA, Messenger; 0 / estramustine-binding protein; 35LT29625A / Estramustine
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17. Borrelli A, Mattiazzi L, Capucchio MT, Biolatti C, Cagnasso A, Gianella P, D'Angelo A: Cachexia secondary to intracranial anaplastic (malignant) ependymoma in a boxer dog. J Small Anim Pract; 2009 Oct;50(10):554-7
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  • [Title] Cachexia secondary to intracranial anaplastic (malignant) ependymoma in a boxer dog.
  • On physical examination, cachexia was the only reported abnormality.
  • Based on the morphological features of the tumour, marked parenchymal invasion, extensive necrosis and cellular atypia, the mass was classified as an anaplastic ependymoma.
  • This case report shows similarities to the diencephalic syndrome reported in human paediatric medicine in which the main clinical sign is a profound emaciation in spite of normal or slightly diminished caloric intake.
  • Weight loss and cachexia are clinically relevant problems in small animals and these clinical signs should raise a suspicion, among the other differentials, of a brain tumour, even in absence of neurologic signs.
  • [MeSH-major] Brain Neoplasms / veterinary. Cachexia / veterinary. Dog Diseases / diagnosis. Ependymoma / veterinary
  • [MeSH-minor] Animals. Diagnosis, Differential. Dogs. Fatal Outcome. Female

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  • (PMID = 19796316.001).
  • [ISSN] 1748-5827
  • [Journal-full-title] The Journal of small animal practice
  • [ISO-abbreviation] J Small Anim Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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18. Ammoun S, Ristic N, Matthies C, Hilton DA, Hanemann CO: Targeting ERK1/2 activation and proliferation in human primary schwannoma cells with MEK1/2 inhibitor AZD6244. Neurobiol Dis; 2010 Jan;37(1):141-6
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  • [Title] Targeting ERK1/2 activation and proliferation in human primary schwannoma cells with MEK1/2 inhibitor AZD6244.
  • Deficiency of the tumor suppressor merlin leads to the development of multiple tumors of the nervous system, such as schwannomas, meningiomas, and ependymomas.
  • Here, we targeted MEK1/2 known as a convergence point for multiple cascades towards ERK1/2 activation and cell proliferation, using MEK1/2 inhibitor AZD6244 (ARRY-142886; Astra Zeneca).
  • We show that AZD6244 at low concentration completely abolished platelet-derived growth factor-DD-mediated ERK1/2 activation and cell proliferation in human primary schwannoma cells.
  • Moreover, this drug was not toxic for either schwannoma or Schwann cells and has been reported to be safe with tolerable side effects.
  • Thus, AZD6244 can be considered as a drug candidate for schwannoma treatment.
  • [MeSH-major] Benzimidazoles / pharmacology. Enzyme Inhibitors / pharmacology. MAP Kinase Kinase 2 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Neurilemmoma / drug therapy. Neurilemmoma / physiopathology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Bromodeoxyuridine. Cell Proliferation / drug effects. Cells, Cultured. Humans. Immunoblotting. Immunohistochemistry. MAP Kinase Signaling System / drug effects. Phosphorylation. Platelet-Derived Growth Factor / metabolism. Schwann Cells / drug effects. Schwann Cells / physiology


19. Keir ST, Hausheer F, Lawless AA, Bigner DD, Friedman HS: Therapeutic activity of 7-[(2-trimethylsilyl)ethyl)]-20 (S)-camptothecin against central nervous system tumor-derived xenografts in athymic mice. Cancer Chemother Pharmacol; 2001 Jul;48(1):83-7
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  • [Title] Therapeutic activity of 7-[(2-trimethylsilyl)ethyl)]-20 (S)-camptothecin against central nervous system tumor-derived xenografts in athymic mice.
  • PURPOSE: Camptothecins have emerged as an important new class of antitumor drugs.
  • Camptothecin derivatives such as CPT-11 and topotecan are commercially available and approved for the treatment of colorectal (CPT-11) and ovarian and small-cell lung cancer (topotecan).
  • This study was designed to test the efficacy of karenitecin, a novel highly lipophilic camptothecin derivative, against a panel of human tumor xenografts derived from adult and pediatric central nervous system malignancies growing in athymic nude mice.
  • METHODS: Xenografts evaluated were derived from childhood high-grade gliomas (D-212 MG, D-456 MG), adult high-grade gliomas (D-54 MG, D-245 MG), medulloblastomas (D-341 MED, D-487 MED), and ependymomas (D-528 EP, D-612 EP), as well as sublines with demonstrated resistance to procarbazine (D-245 MG (PR)) and busulfan (D-456 (BR)).
  • In replicate experiments, karenitecin was given at 1.0 mg/kg per dose via intraperitoneal injection for a period of 10 consecutive days, which is the dosage lethal to 10% of treated animals.
  • Karenitecin also produced statistically significant (P < or = 0.001) increases in survival of animals bearing D-341 MED intracranial xenografts (69% increase) and those bearing D-456 MG xenografts (62% increase).
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Brain Neoplasms / drug therapy
  • [MeSH-minor] Animals. Camptothecin / analogs & derivatives. Camptothecin / pharmacology. Camptothecin / therapeutic use. Female. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Transplantation, Heterologous

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  • (PMID = 11488529.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 24R60NVC41 / cositecan; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
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20. Rooprai HK, Kandanearatchi A, Maidment SL, Christidou M, Trillo-Pazos G, Dexter DT, Rucklidge GJ, Widmer W, Pilkington GJ: Evaluation of the effects of swainsonine, captopril, tangeretin and nobiletin on the biological behaviour of brain tumour cells in vitro. Neuropathol Appl Neurobiol; 2001 Feb;27(1):29-39
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  • [Title] Evaluation of the effects of swainsonine, captopril, tangeretin and nobiletin on the biological behaviour of brain tumour cells in vitro.
  • Hence, attention has now focused on novel therapeutic approaches to combat brain tumours that include the use of anti-invasive and anti-proliferative agents.
  • The effect of four anti-invasive agents, swainsonine (a locoweed alkaloid), captopril (an anti-hypertensive drug), tangeretin and nobiletin (both citrus flavonoids), were investigated on various parameters of brain tumour invasion such as matrix metalloproteinase (MMP) secretion, migration, invasion and adhesion.
  • A standard cytotoxicity assay was used to optimize working concentrations of the drugs on seven human brain tumour-derived cell lines of various histological type and grade of malignancy.
  • A qualitative assessment by gelatin zymography revealed that the effect of these agents varied between the seven cell lines such that the low grade pilocytic astrocytoma was unaffected by three of the agents.
  • In contrast, downregulation of the two gelatinases, MMP-2 and MMP-9 was seen in the grade 3 astrocytoma irrespective of which agent was used.
  • Furthermore, captopril and nobiletin were most efficient at inhibiting invasion, migration and adhesion in four representative cell lines (an ependymoma, a grade II oligoastrocytoma, an anaplastic astrocytoma and a glioblastoma multiforme).
  • Yet again, the effects of the four agents varied between the four cell lines.
  • Nobiletin was, nevertheless, the most effective agent used in these assays.
  • In conclusion, the differential effects seen on the various parameters studied by these putative anti-invasive agents may be the result of interference with MMPs and other mechanisms underlying the invasive phenotype.
  • From these pilot studies, it is possible that these agents, especially the citrus flavonoids, could be of future therapeutic value.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Brain Neoplasms / drug therapy. Captopril / pharmacology. Flavones. Flavonoids / pharmacology. Swainsonine / pharmacology
  • [MeSH-minor] Astrocytoma / drug therapy. Astrocytoma / metabolism. Cell Adhesion / drug effects. Cell Movement / drug effects. Cell Survival / drug effects. Collagen / metabolism. Drug Evaluation, Preclinical. Ependymoma / drug therapy. Ependymoma / metabolism. Glioblastoma / drug therapy. Glioblastoma / metabolism. Humans. Inhibitory Concentration 50. Matrix Metalloproteinases / metabolism. Neoplasm Invasiveness. Tumor Cells, Cultured

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  • (PMID = 11299000.001).
  • [ISSN] 0305-1846
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Flavones; 0 / Flavonoids; 9007-34-5 / Collagen; 9G64RSX1XD / Captopril; D65ILJ7WLY / nobiletin; EC 3.4.24.- / Matrix Metalloproteinases; I4TLA1DLX6 / tangeretin; RSY4RK37KQ / Swainsonine
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21. Nejat F, El Khashab M, Rutka JT: Initial management of childhood brain tumors: neurosurgical considerations. J Child Neurol; 2008 Oct;23(10):1136-48
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  • The infratentorial compartment will be the primary site for 60% to 70% of these tumors, including astrocytomas, medulloblastomas, and ependymomas.
  • Several technological advancements have increased our knowledge of the cell biology of pediatric brain tumors, facilitated earlier diagnosis, and improved neurosurgical resections while minimizing neurological deficits.
  • We review current diagnostic and therapeutic approaches and outcome for children harboring the most common pediatric brain tumors: astrocytomas (low-grade and high-grade glioma), ependymoma, medulloblastoma, and craniopharyngioma.

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  • (PMID = 18952580.001).
  • [ISSN] 1708-8283
  • [Journal-full-title] Journal of child neurology
  • [ISO-abbreviation] J. Child Neurol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R13 NS040925; United States / NINDS NIH HHS / NS / 5R13NS040925-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Number-of-references] 92
  • [Other-IDs] NLM/ NIHMS487102; NLM/ PMC3714852
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22. Kanamori M, Kumabe T, Saito R, Yamashita Y, Sonoda Y, Tominaga T: [The safety of combination chemotherapy with ifosfamide, cisplatin, and etoposide (ICE): single-institution retrospective review of 108 cases]. No Shinkei Geka; 2010 Nov;38(11):997-1005
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  • The histological diagnosis was newly diagnosed or recurrent germ cell tumor in 45 cases, medulloblastoma in 19, primitive neuroectodermal tumor (PNET) in 7, anaplastic ependymoma in 6, recurrent glioblastoma in 13, and others in 18 cases.
  • 3.0 (CTCAE v3.0) grade 4 neutropenia, anemia, and thrombocytopenia occurred in 81.4%, 14.8%, and 35.2% of patients, respectively.
  • The proportion of ICE cycles associated with CTCAE v3.0 grade 4 neutropenia, transfusion of platelets, and elevated AST/ALT significantly decreased after enforcement of dose reduction criteria.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Brain Neoplasms / drug therapy
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Agents, Phytogenic / adverse effects. Child. Child, Preschool. Cisplatin / administration & dosage. Cisplatin / adverse effects. Ependymoma / drug therapy. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Glioblastoma / drug therapy. Hematologic Diseases / chemically induced. Humans. Ifosfamide / administration & dosage. Ifosfamide / adverse effects. Infant. Male. Medulloblastoma / drug therapy. Middle Aged. Neoplasms, Germ Cell and Embryonal / drug therapy. Neuroectodermal Tumors, Primitive / drug therapy. Retrospective Studies

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  • (PMID = 21081811.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin; UM20QQM95Y / Ifosfamide
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23. Lindsey JC, Lusher ME, Strathdee G, Brown R, Gilbertson RJ, Bailey S, Ellison DW, Clifford SC: Epigenetic inactivation of MCJ (DNAJD1) in malignant paediatric brain tumours. Int J Cancer; 2006 Jan 15;118(2):346-52
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  • MCJ (DNAJD1) is a recently discovered member of the DNAJ protein family whose expression is controlled epigenetically by methylation of a CpG island located within the 5' transcribed region of its gene.
  • Methylation-dependent transcriptional silencing of MCJ has been observed in ovarian cancers and associated with increased resistance to chemotherapeutic agents; however, its role in other cancer types has not been widely investigated.
  • We examined the status of MCJ in intracranial primitive neuroectodermal tumours [PNETs, comprising cerebellar PNETs (medulloblastomas) and supratentorial PNETs (stPNETs)] and ependymomas, together representing the most common malignant brain tumours of childhood.
  • Evidence of MCJ hypermethylation was found in all 3 tumour types [medulloblastomas, 3/9 (33%) cell lines, 2/28 (7%) primary tumours; stPNETs, 2/2 (100%) cell lines, 3/10 (30%) primary tumours; and ependymomas, 2/20 (10%) primary tumours] but not in nonneoplastic brain tissues (n = 11), indicating that MCJ methylation is a tumour-specific event.
  • In methylated cases, the distribution of methylated CpG sites across the CpG island could be broadly divided into 2 patterns: (i) extensive methylation of the majority of CpG sites across the island or (ii) limited methylation of individual CpG sites concentrated towards the 5' end of the island.
  • Extensive methylation patterns were associated with the methylation-dependent transcriptional silencing of MCJ in medulloblastoma and stPNET cell lines.
  • These data indicate that epigenetic inactivation of MCJ may play a role in the development of a range of paediatric brain tumour types, and its role in disease pathogenesis and chemotherapeutic resistance should now be investigated further.
  • [MeSH-major] Brain Neoplasms / genetics. Ependymoma / genetics. Epigenesis, Genetic. HSP40 Heat-Shock Proteins / biosynthesis. Membrane Proteins / biosynthesis. Neuroectodermal Tumors, Primitive / genetics
  • [MeSH-minor] Adolescent. Adult. Biomarkers, Tumor. Child. Child, Preschool. DNA Methylation. Female. Gene Expression Profiling. Gene Silencing. Humans. Male. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16049974.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNAJC1 protein, human; 0 / HSP40 Heat-Shock Proteins; 0 / Membrane Proteins
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24. Thorarinsdottir HK, Rood B, Kamani N, Lafond D, Perez-Albuerne E, Loechelt B, Packer RJ, MacDonald TJ: Outcome for children &lt;4 years of age with malignant central nervous system tumors treated with high-dose chemotherapy and autologous stem cell rescue. Pediatr Blood Cancer; 2007 Mar;48(3):278-84
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  • [Title] Outcome for children <4 years of age with malignant central nervous system tumors treated with high-dose chemotherapy and autologous stem cell rescue.
  • In an attempt to delay or obviate radiation therapy (XRT) and improve outcome, our institution has treated children <4 yo with newly diagnosed malignant CNS tumors with high-dose chemotherapy (HDC) and autologous stem cell rescue (ASCR) followed by selective XRT.
  • Histology included five medulloblastomas, four primitive neuroectodermal tumors (PNET), five malignant gliomas, and one ependymoma.
  • Ten patients are alive and disease free 3-77 months (median 18 months) after having completed HDC/ASCR, thereoff five received XRT.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / therapy. Oligodendroglioma / therapy. Peripheral Blood Stem Cell Transplantation
  • [MeSH-minor] Carboplatin / administration & dosage. Child, Preschool. Cisplatin / administration & dosage. Cognition Disorders / etiology. Cranial Irradiation / adverse effects. Cyclophosphamide / administration & dosage. Developmental Disabilities / etiology. Disease-Free Survival. Ependymoma / drug therapy. Ependymoma / mortality. Ependymoma / surgery. Etoposide / administration & dosage. Follow-Up Studies. Ganglioglioma / drug therapy. Ganglioglioma / metabolism. Ganglioglioma / radiotherapy. Ganglioglioma / surgery. Glioma / drug therapy. Glioma / mortality. Glioma / radiotherapy. Glioma / surgery. Humans. Infant. Medulloblastoma / drug therapy. Medulloblastoma / mortality. Medulloblastoma / radiotherapy. Medulloblastoma / surgery. Mitotic Index. Neuroectodermal Tumors, Primitive / drug therapy. Neuroectodermal Tumors, Primitive / mortality. Neuroectodermal Tumors, Primitive / radiotherapy. Neuroectodermal Tumors, Primitive / surgery. Quadriplegia / etiology. Retrospective Studies. Sensation Disorders / etiology. Spinal Cord Neoplasms / drug therapy. Spinal Cord Neoplasms / surgery. Thiotepa / administration & dosage. Transplantation, Autologous. Treatment Outcome. Vincristine / administration & dosage

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16456857.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; 905Z5W3GKH / Thiotepa; BG3F62OND5 / Carboplatin; Q20Q21Q62J / Cisplatin
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25. Wolff JE, Finlay JL: High-dose chemotherapy in childhood brain tumors. Onkologie; 2004 Jun;27(3):239-45
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  • Early attempts to use high-dose chemotherapy technology in order to improve the effect of nitrosourea on high-grade gliomas resulted in minimal benefit as well as in severe toxicity.
  • Since then, other drugs have been applied in conjunction with either autologous bone marrow or peripheral blood stem cells, including thiotepa, etoposide, melphalan, cyclophosphamide, and busulfan.
  • The data suggest benefit in recurrent primitive neuroectodermal tumors (PNET), in newly diagnosed young children with PNET and possibly in young children with newly diagnosed ependymoma, as a strategy not only to improve tumor-free survival but also to avoid exposure of the young brain to irradiation.
  • In other tumors such as recurrent ependymoma and newly diagnosed or recurrent brain stem glioma, high-dose chemotherapy remains ineffective.
  • New protocols under evaluation include new agents, multiple cycles of high-dose chemotherapy and allogeneic transplantation as immunotherapeutic approach.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Drug Therapy / methods
  • [MeSH-minor] Child. Child, Preschool. Combined Modality Therapy / methods. Ependymoma / drug therapy. Ependymoma / surgery. Glioma / drug therapy. Glioma / surgery. Humans. Infant. Infant, Newborn. Medulloblastoma / drug therapy. Medulloblastoma / surgery. Neuroectodermal Tumors / drug therapy. Neuroectodermal Tumors / surgery. Practice Patterns, Physicians'


26. Widera D, Kaus A, Kaltschmidt C, Kaltschmidt B: Neural stem cells, inflammation and NF-kappaB: basic principle of maintenance and repair or origin of brain tumours? J Cell Mol Med; 2008 Apr;12(2):459-70
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  • [Title] Neural stem cells, inflammation and NF-kappaB: basic principle of maintenance and repair or origin of brain tumours?
  • Several recent reports suggest that inflammatory signals play a decisive role in the self-renewal, migration and differentiation of multipotent neural stem cells (NSCs).
  • NSCs are believed to be able to ameliorate the symptoms of several brain pathologies through proliferation, migration into the area of the lesion and either differentiation into the appropriate cell type or secretion of anti-inflammatory cytokines.
  • Although NSCs have beneficial roles, current evidence indicates that brain tumours, such as astrogliomas or ependymomas are also caused by tumour-initiating cells with stem-like properties.
  • However, little is known about the cellular and molecular processes potentially generating tumours from NSCs.
  • Most pro-inflammatory conditions are considered to activate the transcription factor NF-kappaB in various cell types.
  • Moreover, NF-kappaB is constitutively active in most tumour cells described so far.
  • Thus, NF-kappaB might provide a novel mechanistic link between chronic inflammation, stem cells and cancer.
  • [MeSH-major] Inflammation. NF-kappa B / metabolism. Neurons / metabolism. Stem Cells / metabolism
  • [MeSH-minor] Animals. Brain Neoplasms / pathology. Humans. Models, Neurological

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  • (PMID = 18182066.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / NF-kappa B
  • [Number-of-references] 125
  • [Other-IDs] NLM/ PMC3822535
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27. Peyre M, Commo F, Dantas-Barbosa C, Andreiuolo F, Puget S, Lacroix L, Drusch F, Scott V, Varlet P, Mauguen A, Dessen P, Lazar V, Vassal G, Grill J: Portrait of ependymoma recurrence in children: biomarkers of tumor progression identified by dual-color microarray-based gene expression analysis. PLoS One; 2010;5(9):e12932
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  • [Title] Portrait of ependymoma recurrence in children: biomarkers of tumor progression identified by dual-color microarray-based gene expression analysis.
  • BACKGROUND: Children with ependymoma may experience a relapse in up to 50% of cases depending on the extent of resection.
  • Key biological events associated with recurrence are unknown.
  • METHODOLOGY/PRINCIPAL FINDINGS: To discover the biology behind the recurrence of ependymomas, we performed CGHarray and a dual-color gene expression microarray analysis of 17 tumors at diagnosis co-hybridized with the corresponding 27 first or subsequent relapses from the same patient.
  • Eighty-seven genes showed an absolute fold change ≥2 in at least 50% of relapses and were defined as the gene expression signature of ependymoma recurrence.
  • Immunohistochemistry on an independent series of 24 tumor pairs at diagnosis and at relapse confirmed the decrease of MT3 expression at recurrence in 17/24 tumor pairs (p = 0.002).
  • Promoter sequencing after bisulfite treatment of DNA from primary tumors and recurrences as well as treatment of short-term ependymoma cells cultures with a demethylating agent showed that methylation was not involved in MT3 downregulation.
  • CONCLUSIONS/SIGNIFICANCE: The most frequent molecular events associated with ependymoma recurrence were over-expression of kinetochore proteins and down-regulation of metallothioneins.
  • [MeSH-major] Ependymoma / genetics. Ependymoma / pathology. Gene Expression Profiling. Gene Expression Regulation, Neoplastic
  • [MeSH-minor] Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Child. Child, Preschool. Disease Progression. Female. Follow-Up Studies. Humans. Infant. Male. Metallothionein / genetics. Metallothionein / metabolism. Oligonucleotide Array Sequence Analysis / instrumentation. Recurrence

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  • (PMID = 20885975.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 9038-94-2 / Metallothionein
  • [Other-IDs] NLM/ PMC2945762
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28. Brisson C, Lelong-Rebel I, Mottolèse C, Jouvet A, Fèvre-Montange M, Saint Pierre G, Rebel G, Belin MF: Establishment of human tumoral ependymal cell lines and coculture with tubular-like human endothelial cells. Int J Oncol; 2002 Oct;21(4):775-85
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  • [Title] Establishment of human tumoral ependymal cell lines and coculture with tubular-like human endothelial cells.
  • Ependymomas, rare neoplasms of the central nervous system, occur predominantly in children.
  • They are highly vascularized, and histological findings show many perivascular rosettes of tumoral cells radially organized around capillaries.
  • Treatment of ependymomas relies on surgery combined with radio- or chemotherapy, but the efficiency of chemotherapy is limited, probably because of their multidrug resistance (MDR) phenotype.
  • Progress in the therapy of these neoplasms is dramatically limited by the absence of cell line models.
  • We established conditions for the long-term culture of human tumoral ependymocytes and their 3D coculture in Matrigel with endothelial cells.
  • Histological, immunological, and ultrastructural studies showed that the morphological features (microvilli, cilia, and caveolae) of these cultured cells were similar to those of the tumor in vivo.
  • The cells expressed potential oncological markers related to the immature state of tumoral cells (nestin and Notch-1), their tumorigenicity [caveolae and epidermal growth factor-receptor (EGF-R)], or the MDR phenotype [P-glycoprotein (P-gp)].
  • The expression of P-gp, EGF-R, and caveolin-1 by these tumoral ependymocytes could be useful in studies on new drugs.
  • This coculture model might represent a new powerful tool to study new therapeutic delivery strategies in tumoral cells.
  • [MeSH-major] Brain Neoplasms / pathology. Cell Culture Techniques / methods. Endothelium, Vascular / cytology. Ependymoma / pathology. Tumor Cells, Cultured
  • [MeSH-minor] Adolescent. Adult. Aged. Cells, Cultured. Child. Child, Preschool. Coculture Techniques. Collagen / pharmacology. Drug Combinations. Female. Humans. Immunohistochemistry. Infant. Laminin / pharmacology. Male. Microscopy, Electron. Microscopy, Fluorescence. Middle Aged. P-Glycoprotein / metabolism. Proteoglycans / pharmacology. Time Factors. Umbilical Veins / cytology

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  • (PMID = 12239616.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Laminin; 0 / P-Glycoprotein; 0 / Proteoglycans; 119978-18-6 / matrigel; 9007-34-5 / Collagen
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29. Buccoliero AM, Castiglione F, Rossi Degl'Innocenti D, Paglierani M, Maio V, Gheri CF, Garbini F, Moncini D, Taddei A, Sardi I, Sanzo M, Giordano F, Mussa F, Genitori L, Taddei GL: O6-Methylguanine-DNA-methyltransferase in recurring anaplastic ependymomas: PCR and immunohistochemistry. J Chemother; 2008 Apr;20(2):263-8
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  • [Title] O6-Methylguanine-DNA-methyltransferase in recurring anaplastic ependymomas: PCR and immunohistochemistry.
  • Ependymomas are the third most common brain tumor in children.
  • We evaluated the MGMT gene promoter methylation and the immunohistochemical MGMT protein expression in 12 recurrent anaplastic ependymomas affecting children.
  • Our purpose was to investigate the molecular rationale of the administration of alkylating agents to children affected by recurrent anaplastic ependymomas.
  • All ependymomas lacked MGMT promoter hypermethylation and 9 (75%) showed high MGMT protein expression (>50% tumoral cells).
  • These results may indicate MGMT as a factor of chemoresistance to alkylating drugs in anaplastic ependymomas and support the uncertainties regarding the actual benefit of chemotherapy for patients with anaplastic ependymomas.
  • [MeSH-major] Brain Neoplasms / enzymology. DNA Modification Methylases / biosynthesis. DNA Repair Enzymes / biosynthesis. Ependymoma / enzymology. Neoplasm Recurrence, Local / enzymology. Tumor Suppressor Proteins / biosynthesis
  • [MeSH-minor] Adolescent. Anaplasia. Child. Child, Preschool. DNA Methylation. Drug Resistance, Neoplasm. Female. Humans. Immunohistochemistry. Male. Polymerase Chain Reaction. Promoter Regions, Genetic

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  • (PMID = 18467255.001).
  • [ISSN] 1973-9478
  • [Journal-full-title] Journal of chemotherapy (Florence, Italy)
  • [ISO-abbreviation] J Chemother
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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30. Kawakami M, Kawakami K, Takahashi S, Abe M, Puri RK: Analysis of interleukin-13 receptor alpha2 expression in human pediatric brain tumors. Cancer; 2004 Sep 1;101(5):1036-42
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  • BACKGROUND: Compared with normal brain tissue cells, human malignant glioma cells express higher levels of interleukin-13 receptor (IL-13R).
  • With IL-13R-targeted cytotoxin (IL13-PE38QQR, comprising IL-13 and a mutated form of Pseudomonas exotoxin [PE]) being tested in three Phase I/II clinical trials for the treatment of adult human glioma, and with pediatric studies being planned, the authors set out to analyze pediatric brain tumor tissue specimens for the expression of IL-13R.
  • METHODS: Using in situ hybridization and immunohistochemical staining, the authors examined 58 pediatric brain tumor specimens for expression of the predominant IL-13 binding and internalizing protein (IL-13Ralpha2) chain at the mRNA and protein levels.
  • RESULTS: Overall, approximately 83% of pediatric brain tumor samples expressed IL-13Ralpha2.
  • One hundred percent (11 of 11) high-grade astrocytoma, 79% (26 of 33) low-grade astrocytoma, 67% (4 of 6) medulloblastoma, and 67% (2 of 3) ependymoma samples were positive for IL-13Ralpha2.
  • Among IL-13Ralpha2-positive samples, 88% (42 of 48 samples) had positive expression in > or = 50% of all tumor fields.
  • CONCLUSIONS: The current study established that pediatric brain tumor specimens expressed the IL-13Ralpha2 chain.
  • [MeSH-minor] Adolescent. Adult. Astrocytoma / metabolism. Astrocytoma / pathology. Child. Child, Preschool. Ependymoma / metabolism. Ependymoma / pathology. Female. Humans. Immunoenzyme Techniques. In Situ Hybridization. Infant. Interleukin-13 / metabolism. Interleukin-13 Receptor alpha1 Subunit. Male. Medulloblastoma / metabolism. Medulloblastoma / pathology. RNA Probes. Receptors, Interleukin-13. Receptors, Interleukin-4 / metabolism

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  • [Copyright] Copyright 2004 American Cancer Society.
  • (PMID = 15329913.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IL13RA1 protein, human; 0 / Interleukin-13; 0 / Interleukin-13 Receptor alpha1 Subunit; 0 / RNA Probes; 0 / Receptors, Interleukin; 0 / Receptors, Interleukin-13; 0 / Receptors, Interleukin-4
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31. Mrak RE: The Big Eye in the 21st century: the role of electron microscopy in modern diagnostic neuropathology. J Neuropathol Exp Neurol; 2002 Dec;61(12):1027-39
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  • [Title] The Big Eye in the 21st century: the role of electron microscopy in modern diagnostic neuropathology.
  • Electron microscopy (EM) remains a powerful and even essential tool in modern diagnostic neuropathology. tumors are still encountered that defy histological or immunohistochemical classification, and EM can often provide answers in these cases.
  • Tumors of the CNS for which EM is useful include unusual or atypical variants of meningioma, ependymoma, and schwannoma; oligodendroglioma-like tumors composed of small "clear" cells; and small "blue cell" tumors of childhood.
  • EM is of great value in identifying site of origin for metastatic adenocarcinomas of unknown origin-an under-recognized and under-utilized potential for this technique.
  • EM is also important in the evaluation of certain congenital, inherited and metabolic diseases-including ceroid lipofuscinoses, CADASIL syndrome, certain myopathies, and mitochondrial encephalomyopathies--and of certain toxic and drug-induced peripheral neuropathies.
  • An important application of EM is its utility in initiating a workup of an atypical tumor or metabolic condition, for which clinical and histological clues point in no obvious direction.
  • In these situations, EM may provide either an answer outright (including answers to questions not asked) or important clues that guide further workup and narrow the range of diagnostic possibilities.
  • [MeSH-major] Central Nervous System Diseases / pathology. Central Nervous System Neoplasms / pathology. Microscopy, Electron
  • [MeSH-minor] Diagnosis, Differential. Humans. Muscular Diseases / congenital. Muscular Diseases / physiopathology. Skull Neoplasms / diagnosis. Skull Neoplasms / pathology

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  • (PMID = 12484565.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 60
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32. Rooprai HK, Rucklidge GJ, Panou C, Pilkington GJ: The effects of exogenous growth factors on matrix metalloproteinase secretion by human brain tumour cells. Br J Cancer; 2000 Jan;82(1):52-5
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  • [Title] The effects of exogenous growth factors on matrix metalloproteinase secretion by human brain tumour cells.
  • In this study, we investigated the effects of five exogenous growth factors known to be expressed by gliomas [epidermal growth factor (EGF), basic growth factor (bFGF), transforming growth factor beta (TGF-beta1,2) and vascular endothelial growth factor (VEGF)].on MMP-2 and MMP-9 expression in an ependymoma, two grade III astrocytomas, a grade III oligoastrocytoma and a benign meningioma.
  • Zymogram analysis revealed that the effects of the growth factors depended upon the cell lines used in the study.
  • Growth factors generally up-regulated MMP-2 and MMP-9 expression in the gliomas but were least effective in the meningioma; the effect being most prominent with TGF-beta1 and TGF-beta2 in all the cell lines.
  • It is hypothesized that paracrine growth factor interplay may be crucial in the regulation of MMP expression by glioma invasion of the normal brain.
  • [MeSH-major] Brain Neoplasms / enzymology. Growth Substances / pharmacology. Matrix Metalloproteinase 2 / metabolism. Matrix Metalloproteinase 9 / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Endothelial Growth Factors / pharmacology. Epidermal Growth Factor / pharmacology. Fibroblast Growth Factor 2 / pharmacology. Glioma / enzymology. Humans. Lymphokines / pharmacology. Meningeal Neoplasms / enzymology. Meningioma / enzymology. Transforming Growth Factor alpha / pharmacology. Transforming Growth Factor beta / pharmacology. Tumor Cells, Cultured / drug effects. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • (PMID = 10638966.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] SCOTLAND
  • [Chemical-registry-number] 0 / Endothelial Growth Factors; 0 / Growth Substances; 0 / Lymphokines; 0 / Neoplasm Proteins; 0 / Transforming Growth Factor alpha; 0 / Transforming Growth Factor beta; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 103107-01-3 / Fibroblast Growth Factor 2; 62229-50-9 / Epidermal Growth Factor; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ PMC2363180
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33. Wong VC, Morrison A, Tabori U, Hawkins CE: Telomerase inhibition as a novel therapy for pediatric ependymoma. Brain Pathol; 2010 Jul;20(4):780-6
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  • [Title] Telomerase inhibition as a novel therapy for pediatric ependymoma.
  • Ependymomas are the third most common pediatric brain tumor with an overall survival of approximately 50%.
  • Recently, we showed that telomerase [human telomerase reverse transcriptase (hTERT)] expression is a predictor of poor outcome in pediatric ependymoma.
  • Thus, we hypothesized that ependymomas with functional telomerase may behave more aggressively and that these patients may benefit from anti-telomerase therapy.
  • To address our hypothesis, we investigated the effect of telomerase inhibition on primary ependymoma cells harvested at the time of surgery, as no animal models or established cell lines are readily available for this tumor.
  • The cells were characterized for glial fibrillary acidic protein (GFAP) and hTERT expression, initial telomere length and telomerase activity.
  • They were then subjected to telomerase inhibition (MST-312, 1 microM) and tested for effects on cell viability (MTT assay), proliferation (MIB-1), apoptosis (cleaved caspase 3) and DNA damage (gammaH2AX).
  • After 72 h of telomerase inhibition, primary ependymoma cells showed a significant decrease in cell number (P < 0.001), accompanied by increased DNA damage (gammaH2AX expression) (P < 0.01) and decreased proliferative index (MIB-1) (P < 0.01).
  • These data suggest that telomerase inhibition may be an effective adjuvant therapy in pediatric ependymoma, potentially inducing tumor growth arrest in the short term, independent of telomere shortening.
  • [MeSH-major] Brain Neoplasms / metabolism. Ependymoma / metabolism. Telomerase / antagonists & inhibitors. Telomere / metabolism
  • [MeSH-minor] Analysis of Variance. Apoptosis / drug effects. Benzamides / pharmacology. Cell Count. Cell Proliferation / drug effects. Cell Survival / drug effects. Cells, Cultured. Child. DNA Damage / drug effects. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry

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  • (PMID = 20184588.001).
  • [ISSN] 1750-3639
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / / MOP 82727
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Benzamides; 0 / Glial Fibrillary Acidic Protein; 0 / MST 312; EC 2.7.7.49 / Telomerase
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34. Reyes S, Rembao D, Sotelo J: The antimalarials quinacrine and chloroquine potentiate the transplacental carcinogenic effect of ethylnitrosourea on ependymal cells. Brain Tumor Pathol; 2001;18(2):83-7
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  • [Title] The antimalarials quinacrine and chloroquine potentiate the transplacental carcinogenic effect of ethylnitrosourea on ependymal cells.
  • When compared with controls, no significant differences were observed in tumor incidence.
  • However, early tumor growth was observed in both rats treated with quinacrine (P < 0.0004) and rats treated with chloroquine (P < 0.02).
  • These differences were due mostly to rapid development of ependymomas of the spinal cord.
  • Moreover, the antimalarials studied seem to promote the carcinogenic effects of ethylnitrosourea on ependymal cells.
  • [MeSH-major] Antimalarials / toxicity. Brain Neoplasms / chemically induced. Carcinogens / toxicity. Chloroquine / toxicity. Ependyma / drug effects. Ependymoma / chemically induced. Ethylnitrosourea / toxicity. Prenatal Exposure Delayed Effects. Quinacrine / toxicity. Spinal Cord Neoplasms / chemically induced
  • [MeSH-minor] Animals. Drug Synergism. Female. Glial Fibrillary Acidic Protein / analysis. Immunoenzyme Techniques. Male. Pregnancy. Rats. Rats, Wistar. Synaptophysin / analysis

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  • (PMID = 11908878.001).
  • [ISSN] 1433-7398
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimalarials; 0 / Carcinogens; 0 / Glial Fibrillary Acidic Protein; 0 / Synaptophysin; 886U3H6UFF / Chloroquine; H0C805XYDE / Quinacrine; P8M1T4190R / Ethylnitrosourea
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35. Patel R, Shervington L, Lea R, Shervington A: Epigenetic silencing of telomerase and a non-alkylating agent as a novel therapeutic approach for glioma. Brain Res; 2008 Jan 10;1188:173-81
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  • [Title] Epigenetic silencing of telomerase and a non-alkylating agent as a novel therapeutic approach for glioma.
  • While treatment with 5azadC downregulated hTERT and upregulated MGMT expression in two glioma cell lines, there was no change in the expression of these two genes in the normal cell line.
  • However, cell viability was reduced as a result of 5azadC treatment in all three cell lines.
  • 5azadC treatment reduced telomerase expression and activity and subsequently enhanced chemosensitivity towards cisplatin, taxol and tamoxifen but not with the alkylating agents temozolomide (TMZ), carmustine and chlorambucil.
  • To further evaluate the effect of these findings, the level of hTERT and MGMT expression was measured in a recurrent anaplastic ependymoma, seven glioblastoma and two normal brain tissues.
  • While four of eight gliomas and one of the normal tissues expressed MGMT, hTERT was expressed in all gliomas but not in the normal brain tissue.
  • Results of this study suggest that taxol together with 5azadC may be a good therapeutic combination for glioma.
  • In addition, the work on cell lines can be repeated on tissues utilizing hTERT as the therapeutic target for demethylation using 5azadC in glioma.
  • [MeSH-major] Azacitidine / analogs & derivatives. Brain Neoplasms / drug therapy. Brain Neoplasms / genetics. Gene Silencing / drug effects. Glioma / drug therapy. Glioma / genetics. Telomerase / genetics
  • [MeSH-minor] Antimetabolites, Antineoplastic / pharmacology. Antimetabolites, Antineoplastic / therapeutic use. Antineoplastic Agents, Phytogenic / pharmacology. Antineoplastic Agents, Phytogenic / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Aging / drug effects. Cell Aging / genetics. Cell Line, Tumor. DNA Methylation / drug effects. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Down-Regulation / genetics. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Enzymologic / genetics. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / genetics. Humans. Methyltransferases / antagonists & inhibitors. Methyltransferases / metabolism. Paclitaxel / pharmacology. Paclitaxel / therapeutic use. RNA, Messenger / drug effects. RNA, Messenger / metabolism

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  • (PMID = 18021753.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Phytogenic; 0 / RNA, Messenger; 776B62CQ27 / decitabine; EC 2.1.1.- / Methyltransferases; EC 2.7.7.49 / Telomerase; M801H13NRU / Azacitidine; P88XT4IS4D / Paclitaxel
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36. Noll EN, Lin J, Nakatsuji Y, Miller RH, Black PM: GM3 as a novel growth regulator for human gliomas. Exp Neurol; 2001 Apr;168(2):300-9
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  • The simple ganglioside GM3 inhibits proliferation and induces apoptosis in proliferating immature rodent CNS cells.
  • Here we demonstrate that GM3 treatment dramatically reduces cell numbers in primary cultures of high-grade human glioblastoma multiforme (GBM) tumors and the rat 9L cell gliosarcoma cell line.
  • By contrast, GM3 treatment had little effect on cell number in cultures of normal human brain.
  • A single injection of GM3 3 days after intracranial implantation of 9L tumor cells in a murine xenograft model system resulted in a significant increase in the symptom-free survival period of host animals.
  • The effects of GM3 were not restricted to GBMs and 9L cells.
  • Cultures of high-grade ependymomas, mixed gliomas, astrocytomas, oligodendrogliomas, and gangliogliomas were all susceptible to GM3 treatment.
  • These results suggest that GM3 may have considerable value as a selectively toxic chemotherapeutic agent for human high-grade gliomas.
  • [MeSH-major] Brain Neoplasms / drug therapy. G(M3) Ganglioside / therapeutic use. Glioma / drug therapy
  • [MeSH-minor] Animals. Cell Death / drug effects. Cell Death / physiology. Cell Division / drug effects. Cell Division / physiology. Cell Survival / drug effects. Cell Survival / physiology. Child, Preschool. Drug Screening Assays, Antitumor. Glioblastoma / drug therapy. Glioblastoma / pathology. Humans. Male. Mice. Rats. Transplantation, Heterologous. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / physiology

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  • (PMID = 11259118.001).
  • [ISSN] 0014-4886
  • [Journal-full-title] Experimental neurology
  • [ISO-abbreviation] Exp. Neurol.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS 36674
  • [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 / G(M3) Ganglioside
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37. Dreyer ZE, Kadota RP, Stewart CF, Friedman HS, Mahoney DH, Kun LE, McCluggage CW, Burger PC, Kepner J, Heideman RL, Pediatric Oncology Group: Phase 2 study of idarubicin in pediatric brain tumors: Pediatric Oncology Group study POG 9237. Neuro Oncol; 2003 Oct;5(4):261-7
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  • [Title] Phase 2 study of idarubicin in pediatric brain tumors: Pediatric Oncology Group study POG 9237.
  • For this reason, the Pediatric Oncology Group conducted a Phase 2 trial of IDA for children with recurrent or progressive brain tumors.
  • Patients were stratified by tumor types into 6 categories: stratum 1, low-grade astrocytoma; stratum 2, malignant glioma (glioblastoma multiforme and anaplastic astrocytoma); stratum 3, medulloblastoma; stratum 4, brainstem glioma; stratum 5, ependymoma; and stratum 6, miscellaneous malignant tumors not included in the previous diagnoses.
  • G-CSF was continued until blood cell count recovery.
  • Cycles were repeated at approximately 21-day intervals until patients developed progressive disease or had completed 6 cycles with stable or improved disease.
  • Most patients developed progressive disease; however, in 21 patients with medulloblastoma there was 1 partial response, and 6 patients had stable disease (SD) that in 4 patients lasted more than 20 weeks.
  • The systemic clearance data for IDA and IDOL were nearly identical to those published on patients with leukemia, and the plasma elimination of the IDOL metabolite was substantially longer than that of the parent drug IDA.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Idarubicin / therapeutic use

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  • (PMID = 14565163.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] ZRP63D75JW / Idarubicin
  • [Other-IDs] NLM/ PMC1920677
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38. Chamberlain MC: Recurrent intracranial ependymoma in children: salvage therapy with oral etoposide. Pediatr Neurol; 2001 Feb;24(2):117-21
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  • [Title] Recurrent intracranial ependymoma in children: salvage therapy with oral etoposide.
  • Chronic oral VP-16 (etoposide) is a chemotherapy regimen with a wide application in oncology and documented efficacy against germ cell tumors, lymphomas, Kaposi's sarcoma, and primary brain tumors.
  • This study was performed to assess the toxicity and activity of chronic oral etoposide in the management of children with recurrent intracranial nondisseminated ependymoma.
  • Twelve children (median age of 8 years) with recurrent ependymoma who were refractory to surgery, radiotherapy, and chemotherapy (carboplatinum or the combination of procarbazine, lomustine, and vincristine) were treated with chronic oral etoposide (50 mg/m(2)/day).
  • Three children required transfusion (two with packed red blood cells; two with platelets), and two children developed neutropenic fever.
  • Six children (50%) demonstrated either a radiographic response (two children, both with partial response) or stable disease (four children) with a median duration of response or stable disease of 7 months.
  • In this small cohort of children with recurrent intracranial ependymoma, oral etoposide was well tolerated, produced modest toxicity, and had apparent activity.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / administration & dosage. Brain Neoplasms / drug therapy. Ependymoma / drug therapy. Etoposide / administration & dosage
  • [MeSH-minor] Administration, Oral. Adolescent. Child. Child, Preschool. Drug Administration Schedule. Female. Humans. Male. Neoplasm Recurrence, Local. Prospective Studies. Salvage Therapy. Survival Analysis. Treatment Outcome

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  • (PMID = 11275460.001).
  • [ISSN] 0887-8994
  • [Journal-full-title] Pediatric neurology
  • [ISO-abbreviation] Pediatr. Neurol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide
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39. Ishii K, Zaitsu M, Yonemitsu N, Kan Y, Hamasaki Y, Matsuo M: 5-lipoxygenase pathway promotes cell proliferation in human glioma cell lines. Clin Neuropathol; 2009 Nov-Dec;28(6):445-52
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  • [Title] 5-lipoxygenase pathway promotes cell proliferation in human glioma cell lines.
  • METHODS: We immunohistochemically evaluated the profile of 5-LO expression in various types of brain tumors obtained from 42 patients, and examined the proliferative effects of the 5-LO pathway in human glioma cell lines using a proliferation assay.
  • RESULTS: Immunohistochemistry of glioblastomas, astrocytomas, meningiomas, medulloblastomas, craniopharyngiomas, ependymomas, neurinomas, oligodendrogliomas, malignant lymphomas, dysembryoplastic neuroepithelial and metastatic brain tumors revealed 5-LO expression in the cytoplasm and nuclei or nuclear envelopes of tumor cells.
  • The 5-LO inhibitor A861 and the LTA4 hydrolase inhibitor Bestatin dose-dependently suppressed the proliferation of A172 cells, a glioma cell line.
  • CONCLUSIONS: We confirmed the expression of 5-LO in various human brain tumors and demonstrated the partial suppression of tumor growth by inhibitors of the 5-LO-LTA4 hydrolase pathway in human glioma cell lines.
  • The 5-LO-LTA4 pathway might play roles in the proliferation of human glioma cells.
  • [MeSH-major] Arachidonate 5-Lipoxygenase / physiology. Brain Neoplasms / pathology. Cell Proliferation. Glioma / pathology. Signal Transduction / physiology
  • [MeSH-minor] Adolescent. Adult. Aged. Astrocytoma / pathology. Astrocytoma / physiopathology. Child. Child, Preschool. Dose-Response Relationship, Drug. Female. Glioblastoma / pathology. Glioblastoma / physiopathology. Humans. Leucine / analogs & derivatives. Leucine / pharmacology. Leukotriene A4 / antagonists & inhibitors. Leukotriene A4 / physiology. Lipoxygenase Inhibitors. Male. Meningioma / pathology. Meningioma / physiopathology. Middle Aged. Protease Inhibitors / pharmacology. Tumor Cells, Cultured. Young Adult

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  • (PMID = 19919819.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Leukotriene A4; 0 / Lipoxygenase Inhibitors; 0 / Protease Inhibitors; EC 1.13.11.34 / Arachidonate 5-Lipoxygenase; GMW67QNF9C / Leucine; I0J33N5627 / ubenimex
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40. Karajannis M, Allen JC, Newcomb EW: Treatment of pediatric brain tumors. J Cell Physiol; 2008 Dec;217(3):584-9
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  • Here we review four of the most common subtypes of pediatric brain tumors, low-grade and high-grade astrocytomas, medulloblastomas and ependymomas, highlighting their molecular features regarding their tumor biology, and promising potential therapeutic targets that may hold promise for finding new "molecular targeted" drugs.

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  • (PMID = 18651562.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS057829-02; United States / NINDS NIH HHS / NS / R21 NS057829; United States / NINDS NIH HHS / NS / NS057829; United States / NINDS NIH HHS / NS / R21 NS057829-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Number-of-references] 80
  • [Other-IDs] NLM/ NIHMS66020; NLM/ PMC2574972
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41. Matsuo M, Yonemitsu N, Zaitsu M, Ishii K, Hamasaki Y, Fukuyama K, Tabuchi K, Miyazaki S: Expression of prostaglandin H synthase-2 in human brain tumors. Acta Neuropathol; 2001 Aug;102(2):181-7
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  • Numerous studies have demonstrated that prostaglandin H synthase-2 (PHS-2) is involved in gastrointestinal carcinogenesis, and that nonsteroidal anti-inflammatory drugs (NSAIDs), which inhibit PHS, can reduce the risk of colon cancer.
  • In brain tumors, elevated prostaglandin production and its correlation to anaplastic grade of gliomas have been demonstrated.
  • To determine whether the increased prostaglandin production is due to enhanced expression of PHS-2 and whether the up-regulation of PHS-2 has any correlation to histopathological findings in brain tumors, we evaluated the profile of PHS expression in several human glioma cell lines and surgical specimens from patients with various types of brain tumors.
  • In glioma cell lines, five out of six cell lines showed constitutive expression of PHS-2, whereas PHS-1 was weakly expressed in all of them.
  • All surgical specimens, except an ependymoma, which expressed both isozymes equally, expressed PHS-2 mRNA predominantly.
  • Immunohistochemistry of various types of brain tumors, including six glioblastomas, nine astrocytomas, six meningiomas, five medulloblastomas, four craniopharyngiomas, three ependymomas, three neurinomas, two oligodendrogliomas, two malignant lymphomas, two dysembryoplastic neuroepitherial tumors and one metastatic brain tumor showed PHS-2 staining in most cases.
  • In gliomas, astrocytomas (grade 2 and 3) were strongly stained, but the staining intensity of glioblastomas was relatively weak.
  • Meningiomas and a metastatic brain tumor were also strongly stained.
  • [MeSH-minor] Adolescent. Adult. Aged. Brain / enzymology. Brain / pathology. Cell Compartmentation / genetics. Child. Child, Preschool. Cyclooxygenase 1. Cyclooxygenase 2. Female. Humans. Immunohistochemistry. Male. Membrane Proteins. Middle Aged. Neuroglia / enzymology. Neuroglia / pathology. Neurons / enzymology. Neurons / pathology. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 11563634.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Prostaglandins; 0 / RNA, Messenger; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS1 protein, human; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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42. Ramachandran C, Khatib Z, Petkarou A, Fort J, Fonseca HB, Melnick SJ, Escalon E: Tamoxifen modulation of etoposide cytotoxicity involves inhibition of protein kinase C activity and insulin-like growth factor II expression in brain tumor cells. J Neurooncol; 2004 Mar-Apr;67(1-2):19-28
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  • [Title] Tamoxifen modulation of etoposide cytotoxicity involves inhibition of protein kinase C activity and insulin-like growth factor II expression in brain tumor cells.
  • Tamoxifen, a non-steroidal anti-estrogen widely used against breast cancer, is also useful for treatment of other malignancies, due to its sensitizing effect on other chemotherapeutic agents and radiation.
  • We have investigated the advantages of combining tamoxifen with one of the commonly used cancer chemotherapeutic drug, etoposide (VP-16) in brain tumor cell lines.
  • While tamoxifen (10 microM) increased etoposide cytotoxicity 8.3-fold in the human glioma cell line (HTB-14), it increased etoposide cytotoxicity 47.5- and 40-fold in two primary cell lines established from pediatric medulloblastoma patients (MCH-BT-31 and MCH-BT-39), respectively.
  • Similarly, in the pediatric ependymoma cell lines (MCH-BT-30 and MCH-BT-52), tamoxifen enhanced etoposide cytotoxicity 6- and 2.68-fold, respectively.
  • CalcuSyn analysis of cytotoxicity data showed that tamoxifen and etoposide combinations were synergistic with combination index values ranging from 0.243 to 0.369 at IC50 level among different pediatric brain tumor cell lines.
  • Tamoxifen is also cytotoxic at higher concentrations (> 20 microM) in brain tumor cells.
  • To understand the mechanism underlying the tamoxifen modulation of etoposide cytotoxicity, we analyzed expression of P-glycoprotein (P-gp), insulin-like growth factor-I receptor (IGF-IR), IGF-I, IGF-II and estrogen receptor as well as protein kinase C (PKC) activity.
  • While P-gp, IGF-IR and IGF-I were not affected, enhanced inhibition of PKC, and IGF-II were observed in brain tumor cells treated with tamoxifen and etoposide combination as compared to cells treated with either drug alone.
  • IGF-II expression decreased to 48.6% of the untreated control in the combination treatment as compared to 31.2% for etoposide alone and 26.2% for tamoxifen alone treatments.
  • These results suggest that inhibitory effect of tamoxifen on brain tumor cells manifest through different mechanisms involving inhibition of targets such as PKC and IGF-II.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Brain Neoplasms / drug therapy. Etoposide / administration & dosage. Protein Kinase C / drug effects. Tamoxifen / administration & dosage
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols. Cell Line, Tumor. Child. Drug Synergism. Humans. Insulin-Like Growth Factor II / biosynthesis. Insulin-Like Growth Factor II / drug effects

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  • (PMID = 15072444.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 094ZI81Y45 / Tamoxifen; 67763-97-7 / Insulin-Like Growth Factor II; 6PLQ3CP4P3 / Etoposide; EC 2.7.11.13 / Protein Kinase C
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43. Yu L, Baxter PA, Voicu H, Gurusiddappa S, Zhao Y, Adesina A, Man TK, Shu Q, Zhang YJ, Zhao XM, Su JM, Perlaky L, Dauser R, Chintagumpala M, Lau CC, Blaney SM, Rao PH, Leung HC, Li XN: A clinically relevant orthotopic xenograft model of ependymoma that maintains the genomic signature of the primary tumor and preserves cancer stem cells in vivo. Neuro Oncol; 2010 Jun;12(6):580-94
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  • [Title] A clinically relevant orthotopic xenograft model of ependymoma that maintains the genomic signature of the primary tumor and preserves cancer stem cells in vivo.
  • Limited availability of in vitro and in vivo model systems has hampered efforts to understand tumor biology and test novel therapies for ependymoma, the third most common malignant brain tumor that occurs in children.
  • To develop clinically relevant animal models of ependymoma, we directly injected a fresh surgical specimen from a 9-year-old patient into the right cerebrum of RAG2/severe complex immune deficiency (SCID) mice.
  • All five mice receiving the initial transplantation of the patient tumor developed intracerebral xenografts, which have since been serially subtransplanted in vivo in mouse brains for 4 generations and can be cryopreserved for long-term maintenance of tumorigenicity.
  • The xenograft tumors shared nearly identical histopathological features with the original tumors, harbored 8 structural chromosomal abnormalities as detected with spectral karyotyping, maintained gene expression profiles resembling that of the original patient tumor with the preservation of multiple key genetic abnormalities commonly found in human ependymomas, and contained a small population (<2.2%) of CD133(+) stem cells that can form neurospheres and display multipotent capabilities in vitro.
  • The permanent cell line (BXD-1425EPN), which was derived from a passage II xenograft tumor and has been passaged in vitro more than 70 times, expressed similar differentiation markers of the xenograft tumors, maintained identical chromosomal abnormalities, and formed tumors in the brains of SCID mice.
  • In conclusion, direct injection of primary ependymoma tumor cells played an important role in the generation of a clinically relevant mouse model IC-1425EPN and a novel cell line, BXD-1425EPN.
  • This cell line and model will facilitate the biological studies and preclinical drug screenings for pediatric ependymomas.
  • [MeSH-major] Brain Neoplasms / genetics. Ependymoma / genetics. Gene Expression Profiling / methods. Neoplastic Stem Cells / physiology. Xenograft Model Antitumor Assays / methods
  • [MeSH-minor] Animals. Child. Female. Humans. Male. Mice. Mice, SCID


44. Hodozuka A, Hayashi Y, Annei R, Hiroshima S, Saito M, Orimoto R, Sato M, Tanaka T: [Intrathecal infusion of the antineoplastic agents for meningeal dissemination]. Gan To Kagaku Ryoho; 2008 Jun;35(6):900-5
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  • [Title] [Intrathecal infusion of the antineoplastic agents for meningeal dissemination].
  • Meningeal dissemination is a condition in which tumor cells migrate to the brain surface and sub arachnoid space via cerebrospinal fluid and then infiltrate there.
  • Meningeal dissemination frequently arises from germinoma, medulloblastoma, ependymoma and glioblastoma in cases of primary brain tumors and frequently arises from breast cancer, lung cancer and gastric cancer in cases of metastatic brain tumors, known as meningeal carcinomatosis.
  • Intrathecal infusion of anti neoplastic agents is one of the options for treatment of meningeal dissemination.
  • The advantage of intrathecal chemotherapy is that the anti neoplastic agent is rapidly diffused in the sub arachnoid space, and its duration of activity is long due to its slow clearance and metabolism.
  • Commonly used drugs include methotrexate (MTX), cytarabine (Ara-C), and 3-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-1-(2-chloroethyl)- 1-nitrosourea hydrochloride (ACNU), and some new drugs have also begun to be used clinically.
  • Although there are differences depending on the histological type of the tumor, the anti neoplastic agent administered and the method of administration, the response rate is about 40-80% and mean survival time is about 4-25 months.
  • Although side effects of the anti neoplastic agents are not as severe as with agents used for systemic chemotherapy, specific side effects include nonspecific drug-induced meningitis or ventriculitis, transient or permanent paralysis and leukoencephalopathy.
  • These side effects can be alleviated by reducing the dose or discontinuing the anti neoplastic agents, and a small dose of an adrenocorticosteroid is sometimes administered simultaneously.
  • Bacterial meningitis is another complication and requires discontinuation of anti neoplastic agents, removal of the Ommaya reservoir, or systemic or intrathecal administration of antibiotic agents.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / therapeutic use. Meningeal Neoplasms / drug therapy. Meningeal Neoplasms / secondary

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  • (PMID = 18633217.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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45. Batra S, Perelman N, Luck LR, Shimada H, Malik P: Pediatric tumor cells express erythropoietin and a functional erythropoietin receptor that promotes angiogenesis and tumor cell survival. Lab Invest; 2003 Oct;83(10):1477-87
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  • [Title] Pediatric tumor cells express erythropoietin and a functional erythropoietin receptor that promotes angiogenesis and tumor cell survival.
  • We found erythropoietin receptor and erythropoietin expression in common pediatric tumor cells: neuroblastomas, Ewing's sarcoma family of tumors, pediatric brain tumors (medulloblastoma, astrocytoma, and ependymoma), Wilms tumors, rhabdomyosarcomas, and hepatoblastomas (n = 24), and in cell lines derived from some of these tumors (n = 25).
  • Expression of erythropoietin in tumor cell lines was hypoxia-inducible.
  • Addition of exogenous erythropoietin to tumor cell lines expressing erythropoietin receptor increased nuclear DNA binding activity of nuclear factor kappa B and increased the expression of the antiapoptotic genes bcl-1, bcl-xL, and mcl-1.
  • Additionally, exogenous erythropoietin increased production and secretion of angiogenic growth factors, vascular endothelial growth factor, or placenta growth factor from the tumor cell lines, which promoted endothelial cell proliferation and chemotaxis.
  • Erythropoietin receptor expression that promotes tumor cell survival and releases angiogenic growth factors in pediatric tumors has not been previously described.
  • [MeSH-major] Erythropoietin / metabolism. Neoplasms, Germ Cell and Embryonal / metabolism. Neovascularization, Pathologic / physiopathology. Receptors, Erythropoietin / metabolism
  • [MeSH-minor] Cell Hypoxia / physiology. Cell Survival. Child, Preschool. Dose-Response Relationship, Drug. Endothelial Growth Factors / metabolism. Fluorescent Antibody Technique, Indirect. Gene Expression Regulation, Neoplastic. Humans. Infant. Intercellular Signaling Peptides and Proteins / metabolism. Lymphokines / metabolism. Pregnancy Proteins / metabolism. RNA, Messenger / metabolism. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • (PMID = 14563949.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL-P01-48484
  • [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 / Endothelial Growth Factors; 0 / Intercellular Signaling Peptides and Proteins; 0 / Lymphokines; 0 / Pregnancy Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Erythropoietin; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 11096-26-7 / Erythropoietin; 144589-93-5 / placenta growth factor
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46. Sardi I, Cetica V, Massimino M, Buccoliero AM, Giunti L, Genitori L, Aricò M: Promoter methylation and expression analysis of MGMT in advanced pediatric brain tumors. Oncol Rep; 2009 Oct;22(4):773-9
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  • Insufficient response to oral temozolomide (TMZ) in children with brain tumor may depend on the repair-action of inducible O6-methylguanine-DNA methyltransferase (MGMT).
  • To investigate the clinical relevance of MGMT expression, we analyzed MGMT levels by qRT-PCR and immunohistochemistry, and the methylation of gene promoter in patients with relapsed or refractory brain tumor, enrolled in an off-label trial with oral temozolomide.
  • The drug was administered at the dose of 200 mg/m(2)/day in patients with no prior cranio-spinal irradiation, and 180 mg/m(2)/day in those with previous radiotherapy and/or high-dose chemotherapy followed by autologous hematopoietic stem cell rescue.
  • Nine patients with recurrent ependymoma (n=3), low grade glioma (n=3), glioblastoma (n=1), relapsed medulloblastoma (n=2) were enrolled in the study.
  • By immunohistochemistry, the score was 2+ in 6 of the 9 tumor samples, and 1+ in 3, while none was MGMT negative.
  • Methylation of MGMT promoter was detected in only one ependymoma sample.
  • [MeSH-major] Brain Neoplasms / genetics. DNA Methylation / genetics. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Drug Resistance, Neoplasm / genetics. Promoter Regions, Genetic / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Adolescent. Antineoplastic Agents, Alkylating / therapeutic use. Child. Child, Preschool. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Disease-Free Survival. Female. Humans. Immunohistochemistry. Infant. Male. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / genetics. Neoplasm Recurrence, Local / pathology. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19724855.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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47. Houghton PJ, Morton CL, Tucker C, Payne D, Favours E, Cole C, Gorlick R, Kolb EA, Zhang W, Lock R, Carol H, Tajbakhsh M, Reynolds CP, Maris JM, Courtright J, Keir ST, Friedman HS, Stopford C, Zeidner J, Wu J, Liu T, Billups CA, Khan J, Ansher S, Zhang J, Smith MA: The pediatric preclinical testing program: description of models and early testing results. Pediatr Blood Cancer; 2007 Dec;49(7):928-40
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  • BACKGROUND: The Pediatric Preclinical Testing Program (PPTP) is an initiative supported by the National Cancer Institute (NCI) to identify novel therapeutic agents that may have significant activity against childhood cancers.
  • The PPTP has established panels of childhood cancer xenografts and cell lines to be used for in vivo and in vitro testing.
  • These include panels for Wilms tumor, sarcomas (rhabdomyosarcoma, Ewing sarcoma, and osteosarcoma), neuroblastoma, brain tumors (glioblastoma, ependymoma, and medulloblastoma), rhabdoid tumors (CNS and renal), and acute lymphoblastic leukemia (ALL).
  • Here, we describe the characteristics of the in vivo tumor panels and report results for the in vivo evaluation of two standard agents, vincristine and cyclophosphamide.
  • PROCEDURES: Solid tumors were grown subcutaneously in immune-deficient mice and tumor dimensions were measured weekly.
  • ALL xenografts were inoculated intravenously and human CD45-positive cells were enumerated weekly.
  • RESULTS: Vincristine-induced objective responses in 6 of 24 (25%) and cyclophosphamide-induced objective responses in 18 of 28 (64%) solid tumor models.
  • Comparable assessments of high levels of activity for these two agents were obtained using a tumor growth delay (TGD) measure.
  • Both agents induced regressions in each of the ALL models evaluated.
  • CONCLUSIONS: We have established 51 solid tumor and 10 ALL in vivo models.
  • The PPTP tumor panels appear to generally recapitulate the activity of these agents against specific childhood cancers and to have the potential for identifying novel agents having significant clinical activity.
  • [MeSH-major] Cyclophosphamide / administration & dosage. Neoplasms / drug therapy. Vincristine / administration & dosage. Xenograft Model Antitumor Assays
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Disease Models, Animal. Disease-Free Survival. Drug Administration Schedule. Female. Humans. Injections, Intraperitoneal. Mice. Mice, Inbred BALB C. Mice, Inbred NOD. Mice, Nude. Mice, SCID. Treatment Outcome

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  • [Copyright] 2007 Wiley-Liss, Inc
  • (PMID = 17066459.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CM / N01-CM-42216
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide
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48. Goldhoff P, Warrington NM, Limbrick DD Jr, Hope A, Woerner BM, Jackson E, Perry A, Piwnica-Worms D, Rubin JB: Targeted inhibition of cyclic AMP phosphodiesterase-4 promotes brain tumor regression. Clin Cancer Res; 2008 Dec 1;14(23):7717-25
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  • [Title] Targeted inhibition of cyclic AMP phosphodiesterase-4 promotes brain tumor regression.
  • Previously, we identified the cyclic AMP phosphodiesterase-4 (PDE4) inhibitor Rolipram as a potent antitumor agent.
  • EXPERIMENTAL DESIGN: Immunohistochemistry was used to evaluate the expression pattern of a subfamily of PDE4, PDE4A, in multiple brain tumor types.
  • To evaluate the effect of PDE4A on growth, a brain-specific isoform, PDE4A1 was overexpressed in xenografts of Daoy medulloblastoma and U87 glioblastoma cells.
  • RESULTS: We found that PDE4A is expressed in medulloblastoma, glioblastoma, oligodendroglioma, ependymoma, and meningioma.
  • Moreover, when PDE4A1 was overexpressed in Daoy medulloblastoma and U87 glioblastoma cells, in vivo doubling times were significantly shorter for PDE4A1-overexpressing xenografts compared with controls.
  • In long-term survival and bioluminescence studies, Rolipram in combination with first-line therapy for malignant gliomas (temozolomide and conformal radiation therapy) enhanced the survival of mice bearing intracranial xenografts of U87 glioblastoma cells.
  • Bioluminescence imaging indicated that whereas temozolomide and radiation therapy arrested intracranial tumor growth, the addition of Rolipram to this regimen resulted in tumor regression.
  • CONCLUSIONS: This study shows that PDE4 is widely expressed in brain tumors and promotes their growth and that inhibition with Rolipram overcomes tumor resistance and mediates tumor regression.

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  • (PMID = 19047098.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA094056; United States / NINDS NIH HHS / NS / P30 NS057105; United States / NCI NIH HHS / CA / P30 CA91842; United States / NCI NIH HHS / CA / P30 CA091842; United States / NCI NIH HHS / CA / R21 CA108677; United States / NCI NIH HHS / CA / P50 CA94056; United States / NCI NIH HHS / CA / P50 CA094056-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Phosphodiesterase Inhibitors; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 3.1.4.17 / Cyclic Nucleotide Phosphodiesterases, Type 4; K676NL63N7 / Rolipram
  • [Other-IDs] NLM/ NIHMS82831; NLM/ PMC2615415
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49. Geoerger B, Gaspar N, Opolon P, Morizet J, Devanz P, Lecluse Y, Valent A, Lacroix L, Grill J, Vassal G: EGFR tyrosine kinase inhibition radiosensitizes and induces apoptosis in malignant glioma and childhood ependymoma xenografts. Int J Cancer; 2008 Jul 1;123(1):209-16
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  • [Title] EGFR tyrosine kinase inhibition radiosensitizes and induces apoptosis in malignant glioma and childhood ependymoma xenografts.
  • Malignant gliomas and childhood ependymomas have a high rate of treatment failure.
  • We evaluated the tyrosine kinase inhibitor gefitinib for its antitumor activity and potential to radio-sensitize in vivo in two xenograft models: an EGFR amplified glioma and an EGFR expressing ependymoma, both derived from primary tumors.
  • When administered at 100 mg/kg for 5 consecutive days, gefitinib-induced partial tumor regression in all treated EGFR amplified IGRG88 glioma xenografts.
  • The addition of 1 Gy of irradiation prior to gefitinib administration resulted in 5 complete and 4 partial regressions for the 9 treated tumors as well as a significant tumor growth delay of 33 days for the combined treatment compared to 19 days for each therapy alone, suggesting additive antitumor activity.
  • Tumor regression was associated with inhibition of AKT and MAPK pathways by gefitinib.
  • In contrast, the ependymoma IGREP83 was sensitive to irradiation, but remained resistant to gefitinib.
  • Combined treatment was associated with inhibition of radiation-induced MAPK phosphorylation and significant induction of apoptotic cell death though radiation-induced AKT phosphorylation was maintained.
  • Thus, EGFR targeting through tyrosine kinase inhibition appears to be a promising new approach in the treatment of EGFR-driven glioma, particularly in combination with radiation therapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis. Ependymoma / drug therapy. Ependymoma / radiotherapy. Glioma / drug therapy. Glioma / radiotherapy. Protein Kinase Inhibitors / pharmacology. Quinazolines / pharmacology. Radiation-Sensitizing Agents / pharmacology. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Chemotherapy, Adjuvant. Child. Enzyme Activation / drug effects. Enzyme Activation / radiation effects. Female. Flow Cytometry. G1 Phase / drug effects. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Enzymologic / radiation effects. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / radiation effects. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. In Situ Nick-End Labeling. Mice. Mice, Nude. Middle Aged. Mitogen-Activated Protein Kinase Kinases / drug effects. Mitogen-Activated Protein Kinase Kinases / metabolism. Phosphorylation / drug effects. Proto-Oncogene Proteins c-akt / drug effects. Proto-Oncogene Proteins c-akt / metabolism. RNA, Messenger / metabolism. Radiotherapy, Adjuvant. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / drug effects. Time Factors. Xenograft Model Antitumor Assays

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18386816.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / RNA, Messenger; 0 / Radiation-Sensitizing Agents; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; S65743JHBS / gefitinib
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50. Grundy RG, Wilne SH, Robinson KJ, Ironside JW, Cox T, Chong WK, Michalski A, Campbell RH, Bailey CC, Thorp N, Pizer B, Punt J, Walker DA, Ellison DW, Machin D, Children's Cancer and Leukaemia Group (formerly UKCCSG) Brain Tumour Committee: Primary postoperative chemotherapy without radiotherapy for treatment of brain tumours other than ependymoma in children under 3 years: results of the first UKCCSG/SIOP CNS 9204 trial. Eur J Cancer; 2010 Jan;46(1):120-33
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  • [Title] Primary postoperative chemotherapy without radiotherapy for treatment of brain tumours other than ependymoma in children under 3 years: results of the first UKCCSG/SIOP CNS 9204 trial.
  • We aimed to assess the role of a primary chemotherapy strategy in avoiding or delaying radiotherapy in children younger than 3 years with malignant brain tumours other than ependymoma, the results of which have already been published.
  • METHODS: Ninety-seven children were enrolled between March 1993 and July 2003 and, following diagnostic review, comprised: medulloblastoma (n=31), astrocytoma (26), choroid plexus carcinoma [CPC] (15), CNS PNET (11), atypical teratoid/rhabdoid tumours [AT/RT] (6) and ineligible (6).
  • Following maximal surgical resection, chemotherapy was delivered every 14 d for 1 year or until disease progression.
  • FINDINGS: Over all diagnostic groups the cumulative progression rate was 80.9% at 5 years while the corresponding need-for-radiotherapy rate for progression was 54.6%, but both rates varied by tumour type.
  • Patients with medulloblastoma presented as a high-risk group, 83.9% having residual disease and/or metastases at diagnosis.
  • The 5-year OS for desmoplastic/nodular medulloblastoma was 52.9% (95% confidence interval (CI): 27.6-73.0) and for classic medulloblastoma 33.3% (CI: 4.6-67.6); the 5-year EFS were 35.3% (CI: 14.5-57.0) and 33.3% (CI: 4.6-67.6), respectively.
  • All children with large cell or anaplastic variants of medulloblastoma died within 2 years of diagnosis.
  • The 5-year EFS for non-brainstem high-grade gliomas [HGGs] was 13.0% (CI: 2.2-33.4) and the OS was 30.9% (CI: 11.5-52.8).
  • For CPC the 5-year OS was 26.67% (CI: 8.3-49.6) without RT.
  • This treatment strategy was less effective for AT/RT with 3-year OS of 16.7% (CI: 0.8-51.7) and CNS PNET with 1-year OS of 9.1% (CI: 0.5-33.3).
  • INTERPRETATION: The outcome for very young children with brain tumours is dictated by degree of surgical resection and histological tumour type and underlying biology as an indicator of treatment sensitivity.
  • Desmoplastic/nodular sub-type of medulloblastoma has a better prognosis than classic histology, despite traditional adverse clinical features of metastatic disease and incomplete surgical resection.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy
  • [MeSH-minor] Astrocytoma / drug therapy. Astrocytoma / radiotherapy. Astrocytoma / surgery. Child, Preschool. Choroid Plexus Neoplasms / drug therapy. Choroid Plexus Neoplasms / radiotherapy. Choroid Plexus Neoplasms / surgery. Disease Progression. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Infant. Male. Medulloblastoma / drug therapy. Medulloblastoma / radiotherapy. Medulloblastoma / surgery. Neuroectodermal Tumors, Primitive / drug therapy. Neuroectodermal Tumors, Primitive / radiotherapy. Neuroectodermal Tumors, Primitive / surgery. Radiotherapy, Adjuvant / methods. Survival Analysis. Teratoma / drug therapy. Teratoma / radiotherapy. Teratoma / surgery. Treatment Outcome

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  • (PMID = 19818598.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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51. Drabko K, Choma M, Zaucha-Prazmo A, Wójcik B, Gorczyńska E, Kałwak K, Turkiewicz D, Słociak M, Ussowicz M, Dyla A, Chybicka A, Styczyński J, Debski R, Wysocki M, Goździk J, Ratajczak M, Kowalczyk JR: [Megachemotherapy and autologous hematopoietic stem cell transplantation in children with solid tumours excluding neuroblastoma--experience of Polish paediatric centres]. Med Wieku Rozwoj; 2006 Jul-Sep;10(3 Pt 1):785-92
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  • [Title] [Megachemotherapy and autologous hematopoietic stem cell transplantation in children with solid tumours excluding neuroblastoma--experience of Polish paediatric centres].
  • AIM OF THE STUDY was to present the experience of four Polish transplantation centres (Wroclaw, Bydgoszcz, Kraków and Lublin) with use of megachemotherapy (MCT) and autologous hematopoietic stem cell transplantation (autoHSCT) in children with high risk solid tumours.
  • 25 children were treated for Ewing Sarcoma, 13 for rhabdomyosarcoma embryonale (RMS), 7 for germinal tumours, 6 for medulloblastoma, 4 for PNET, 4 for Wilm's tumours, 2 for glioblastoma and single patients with mesenchymoma, astrocytoma, ependymoma, angioblastoma, carcinoma ovarian and carcinoma embryonale glutei.
  • Most common megachemotherapy protocols consisted of: Melphalan, Etopozyd i Carboplatin (MEC)--applied in 24 children and Busulfan plus Melphalan (Bu Mel) administered in 19 patients.
  • RESULTS: 30 children are alive (44%), 28 of them in complete remission of disease.
  • 39 patients relapsed at a median time 11 months after MCT and 37 of them subsequently died of disease at a median time of 16 months.
  • One toxic death was noted--it was a boy, transplanted with progressive disease.
  • Megachemotherapy with autologous stem cell can rescue children with high risk solid tumours.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Neoplasms / drug therapy. Neoplasms / surgery
  • [MeSH-minor] Academic Medical Centers. Adolescent. Antineoplastic Agents, Alkylating / administration & dosage. Bone Neoplasms / drug therapy. Bone Neoplasms / surgery. Child. Child, Preschool. Combined Modality Therapy. Disease-Free Survival. Dose-Response Relationship, Drug. Ependymoma / drug therapy. Ependymoma / surgery. Female. Glioblastoma / drug therapy. Glioblastoma / surgery. Glioma / drug therapy. Glioma / surgery. Humans. Infant. Male. Meningeal Neoplasms / drug therapy. Meningeal Neoplasms / surgery. Meningioma / drug therapy. Meningioma / surgery. Neoplasm Staging. Oncology Service, Hospital. Poland. Remission Induction. Retrospective Studies. Sarcoma, Ewing / drug therapy. Sarcoma, Ewing / surgery. Transplantation, Autologous. Treatment Outcome


52. Inaba H, Rabah R, Meert KL, BhamBhani K: Herpes simplex virus pneumonia in a patient with ependymoma. J Pediatr Hematol Oncol; 2004 Feb;26(2):108-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Herpes simplex virus pneumonia in a patient with ependymoma.
  • The authors report a fatal outcome in a 4-year-old boy with herpes simplex virus (HSV) pneumonia and ependymoma.
  • Bronchoalveolar lavage showed intranuclear viral inclusions, and culture was positive for HSV type 1.
  • His T-cell count was significantly decreased.
  • HSV must be considered in the differential diagnosis of patients with interstitial pneumonia and T-cell deficiency, especially after craniospinal irradiation.
  • [MeSH-major] Brain Neoplasms / pathology. Ependymoma / pathology. Herpes Simplex / diagnosis. Herpesvirus 1, Human / isolation & purification. Pneumonia, Viral / diagnosis
  • [MeSH-minor] Acyclovir / therapeutic use. Antiviral Agents / therapeutic use. Child, Preschool. Drug Therapy, Combination. Fatal Outcome. Foscarnet / therapeutic use. Humans. Immunity, Cellular. Male. Neoplasm Recurrence, Local. T-Lymphocytes / metabolism

  • Genetic Alliance. consumer health - Ependymoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • MedlinePlus Health Information. consumer health - Herpes Simplex.
  • Hazardous Substances Data Bank. Foscarnet .
  • Hazardous Substances Data Bank. ACYCLOVIR .
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  • (PMID = 14767198.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 364P9RVW4X / Foscarnet; X4HES1O11F / Acyclovir
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