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1. 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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  • PURPOSE: As favorable outcomes from malignant brain tumors remain limited by poor survival and treatment-related toxicity, novel approaches to cure are essential.
  • Previously, we identified the cyclic AMP phosphodiesterase-4 (PDE4) inhibitor Rolipram as a potent antitumor agent.
  • RESULTS: We found that PDE4A is expressed in medulloblastoma, glioblastoma, oligodendroglioma, ependymoma, and meningioma.
  • 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.

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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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2. Higashino T, Inamura T, Kawashima M, Ikezaki K, Miyazono M, Yoshiura T, Iwaki T, Fukui M: A lateral ventricular gliosarcoma arising in an ependymoma. Clin Neuropathol; 2001 Sep-Oct;20(5):219-23
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  • [Title] A lateral ventricular gliosarcoma arising in an ependymoma.
  • Computed tomography and magnetic resonance imaging localized the tumor to the right lateral ventricle and showed heterogeneous enhancement with administration of contrast agents.
  • Histologic examination disclosed gliosarcoma arising by malignant transformation of an ependymoma.
  • [MeSH-minor] Adult. Cell Transformation, Neoplastic / pathology. Fatal Outcome. Humans. Magnetic Resonance Imaging. Male. Tomography, X-Ray Computed

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  • (PMID = 11594507.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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3. Okcu MF, Selvan M, Wang LE, Stout L, Erana R, Airewele G, Adatto P, Hess K, Ali-Osman F, Groves M, Yung AW, Levin VA, Wei Q, Bondy M: Glutathione S-transferase polymorphisms and survival in primary malignant glioma. Clin Cancer Res; 2004 Apr 15;10(8):2618-25
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  • [Title] Glutathione S-transferase polymorphisms and survival in primary malignant glioma.
  • RESULTS: For patients with anaplastic astrocytoma, anaplastic oligodendroglioma, anaplastic oligoastrocytoma, and anaplastic ependymoma (n = 78), patients with GSTP1*A/*A-M1 null genotype survived longer than did the rest of the group (median survival "not achieved," and 41 months, respectively; P = 0.06).
  • CONCLUSIONS: In patients with anaplastic astrocytoma, anaplastic oligodendroglioma, and anaplastic oligoastrocytoma, combination of germ-line GSTP1*A/*A and GSTM1 null genotype confers a survival advantage.
  • Patients with this genotype also have an increased risk of adverse events secondary to chemotherapy that primarily comprised nitrosourea alkylating agents.
  • [MeSH-minor] Adult. Astrocytoma / genetics. Ependymoma / genetics. Female. Genotype. Glutathione S-Transferase pi. Humans. Logistic Models. Male. Middle Aged. Neoplasm Metastasis. Oligodendroglioma / genetics. Polymerase Chain Reaction. Polymorphism, Restriction Fragment Length. Proportional Hazards Models. Time Factors. Treatment Outcome

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  • (PMID = 15102663.001).
  • [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 / CA70917
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
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4. Badruddoja MA, Keir ST, King I, Zeidner J, Vredenburgh JJ, Muhlbaier LH, Bigner DD, Friedman HS: Activity of VNP40101M (Cloretazine) in the treatment of CNS tumor xenografts in athymic mice. Neuro Oncol; 2007 Jul;9(3):240-4
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  • VNP40101M, or 1,2-bis(methylsulfonyl)-1-(2-choloroethyl)-2-(methylamino)carbonylhydrazine (Cloretazine), is a bifunctional prodrug that belongs to a class of DNA-modifying agents-the sulfonylhydrazines-that has been synthesized and been shown to have activity against a wide spectrum of xenografts.
  • The current study was designed to assess the activity of VNP40101M administered at a dose of 18 mg/kg daily for five days against a panel of human adult and pediatric CNS tumors growing subcutaneously or intracranially in athymic nude mice.
  • The results demonstrated statistically significant (p < 0.05) growth delays of 15.0, 8.3, 51.0, 60+, 60+, and 60+ days in subcutaneous xenografts derived from childhood glioblastoma multiforme (D-456 MG), childhood ependymoma (D-528 EP and D-612 EP), childhood medulloblastoma (D-425 MED), and adult malignant glioma (D-245 MG and D-54 MG), respectively, with corresponding tumor regressions in 10 of 10, 4 of 10, 8 of 10, 9 of 10, 9 of 10, and 10 of 10 treated mice, respectively.
  • Delayed toxicity was seen more than 60 days after treatment, with 23 deaths in 100 treated animals, despite a median weight loss of only 0.06%.

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  • (PMID = 17522334.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / P50 NS020023; United States / NINDS NIH HHS / NS / 5P50-NS20023-23
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hydrazines; 0 / Prodrugs; 0 / Sulfonamides; 14J2G0U3NQ / laromustine
  • [Other-IDs] NLM/ PMC1907418
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5. 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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  • 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.
  • 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
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Humans. Infant. Male

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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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6. 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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  • [Title] Epigenetic inactivation of MCJ (DNAJD1) in malignant paediatric brain tumours.
  • 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.
  • [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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7. Turner CD, Gururangan S, Eastwood J, Bottom K, Watral M, Beason R, McLendon RE, Friedman AH, Tourt-Uhlig S, Miller LL, Friedman HS: Phase II study of irinotecan (CPT-11) in children with high-risk malignant brain tumors: the Duke experience. Neuro Oncol; 2002 04;4(2):102-8
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  • [Title] Phase II study of irinotecan (CPT-11) in children with high-risk malignant brain tumors: the Duke experience.
  • A phase II study of irinotecan (CPT-11) was conducted at Duke University Medical Center, Durham, NC, to evaluate the activity of this agent in children with high-risk malignant brain tumors.
  • A total of 22 children were enrolled in this study, including 13 with histologically verified recurrent malignant brain tumors (glioblastoma multiforme [GBM] 4, anaplastic astrocytoma 1, ependymoma 5, and medulloblastoma/primitive neuroectodermal tumor 3), 5 with recurrent diffuse pontine glioma, and 4 with newly diagnosed GBM.
  • Patients with newly diagnosed tumors initially received 3 cycles of treatment to assess tumor response and then were allowed radiotherapy at physician's choice; patients who demonstrated a response to CPT-11 prior to radiotherapy were allowed to continue the drug after radiation until disease progression or unacceptable toxicity.
  • A 25% to 50% dose reduction was made for grade III-IV toxicity.
  • Responses were seen in 4 of 9 patients with GBM or anaplastic astrocytoma (44%; 95% confidence interval, 11%-82%) (complete response in 2 patients with recurrent GBM lasting 9 months and 48+ months; partial response in one patient with a newly diagnosed midbrain GBM lasting 18 months prior to radiotherapy; and partial response lasting 11 months in 1 patient with recurrent anaplastic astrocytoma), 1 of 5 patients with recurrent ependymoma (partial response initially followed by stable disease lasting 11 months), and none of 5 patients with recurrent diffuse pontine glioma.
  • Toxicity was mainly myelosuppression, with 12 of 22 patients (50%) suffering grade II-IV neutropenia.
  • CPT-11, given in this schedule, appears to be active in children with malignant glioma, medulloblastoma, and ependymoma with acceptable toxicity.
  • Ongoing studies will demonstrate if activity of CPT-11 can be enhanced when combined with alkylating agents, including carmustine and temozolomide.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Brain Neoplasms / drug therapy. Camptothecin / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Astrocytoma / drug therapy. Child. Child, Preschool. Drug Administration Schedule. Ependymoma / drug therapy. Female. Glioblastoma / drug therapy. Glioma. Humans. Magnetic Resonance Imaging. Male. Medulloblastoma / drug therapy. Topoisomerase Inhibitors

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  • (PMID = 11916501.001).
  • [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] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Topoisomerase Inhibitors; 0H43101T0J / irinotecan; XT3Z54Z28A / Camptothecin
  • [Other-IDs] NLM/ PMC1920653
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8. Neuwelt EA, Gilmer-Knight K, Lacy C, Nicholson HS, Kraemer DF, Doolittle ND, Hornig GW, Muldoon LL: Toxicity profile of delayed high dose sodium thiosulfate in children treated with carboplatin in conjunction with blood-brain-barrier disruption. Pediatr Blood Cancer; 2006 Aug;47(2):174-82
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  • PURPOSE: To assess the safety of delayed high dose intravenous (i.v.) sodium thiosulfate (STS) in a case series of 12 children with malignant brain tumors who were treated with intraarterial (i.a.) carboplatin in conjunction with blood-brain-barrier disruption (BBBD).
  • Analogous to results in adult patients, there was mild transient hypernatremia and a trend for improved protection from ototoxicity in children who received STS delayed to 4 hr post-treatment versus 2 hr.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Brain Neoplasms / drug therapy. Carboplatin / adverse effects. Chelating Agents / administration & dosage. Hearing Loss, Sensorineural / prevention & control. Thiosulfates / administration & dosage
  • [MeSH-minor] Auditory Threshold. Blood-Brain Barrier. Child. Child, Preschool. Drug Administration Schedule. Drug-Related Side Effects and Adverse Reactions. Ependymoma / drug therapy. Ependymoma / pathology. Female. Humans. Infant. Infusions, Intravenous. Male. Neuroectodermal Tumors, Primitive / drug therapy. Neuroectodermal Tumors, Primitive / pathology. Survival Analysis. Time Factors

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  • [CommentIn] Pediatr Blood Cancer. 2006 Aug;47(2):120-2 [16206212.001]
  • (PMID = 16086410.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS33618; United States / NINDS NIH HHS / NS / NS34608; United States / NINDS NIH HHS / NS / NS44687
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Chelating Agents; 0 / Thiosulfates; BG3F62OND5 / Carboplatin; HX1032V43M / sodium thiosulfate
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9. 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.
  • 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.
  • [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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10. 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.
  • 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.
  • [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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11. 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).
  • 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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  • Hazardous Substances Data Bank. LOMUSTINE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • Hazardous Substances Data Bank. PROCARBAZINE .
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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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12. Pinker K, Noebauer-Huhmann IM, Stavrou I, Hoeftberger R, Szomolanyi P, Weber M, Stadlbauer A, Grabner G, Knosp E, Trattnig S: High-field, high-resolution, susceptibility-weighted magnetic resonance imaging: improved image quality by addition of contrast agent and higher field strength in patients with brain tumors. Neuroradiology; 2008 Jan;50(1):9-16
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  • [Title] High-field, high-resolution, susceptibility-weighted magnetic resonance imaging: improved image quality by addition of contrast agent and higher field strength in patients with brain tumors.
  • INTRODUCTION: To demonstrate intratumoral susceptibility effects in malignant brain tumors and to assess visualization of susceptibility effects before and after administration of the paramagnetic contrast agent MultiHance (gadobenate dimeglumine; Bracco Imaging), an agent known to have high relaxivity, with respect to susceptibility effects, image quality, and reduction of scan time.
  • METHODS: Included in the study were 19 patients with malignant brain tumors who underwent high-resolution, susceptibility-weighted (SW) MR imaging at 3 T before and after administration of contrast agent.
  • CONCLUSION: The intravenous administration of MultiHance, an agent with high relaxivity, allowed a reduction of scan time from 9 min to 7 min while preserving excellent susceptibility effects and image quality in SW images obtained at 3 T.
  • [MeSH-minor] Adult. Aged. Astrocytoma / diagnosis. Brain / pathology. Efficiency. Ependymoma / diagnosis. Female. Glioblastoma / diagnosis. Humans. Male. Middle Aged. Oligodendroglioma / diagnosis. Plasmacytoma / diagnosis. Sensitivity and Specificity

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  • (PMID = 17876570.001).
  • [ISSN] 1432-1920
  • [Journal-full-title] Neuroradiology
  • [ISO-abbreviation] Neuroradiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Contrast Media; 0 / Organometallic Compounds; 15G12L5X8K / gadobenic acid; 6HG8UB2MUY / Meglumine
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