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1. Hsu TR, Wong TT, Chang FC, Ho DM, Tang RB, Thien PF, Chang KP: Responsiveness of progressive optic pathway tumors to cisplatin-based chemotherapy in children. Childs Nerv Syst; 2008 Dec;24(12):1457-61
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  • BACKGROUND: Though the pathology of optic pathway tumor is mostly pilocytic astrocytoma, the benign tumor behaves like malignant tumor because total resection is not feasible.
  • Adjuvant chemotherapy might be a reasonable strategy for management of these low grade tumors which keep growing.
  • We evaluate the responsiveness of optic pathway tumor to cisplatin-based chemotherapy.
  • Brain MRI was performed every 3 months to evaluate the objective response to chemotherapy.
  • The pathology showed pilocytic astrocytomas in 11 patients, astrocytoma in one patient, and anaplastic astrocytomas in two patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / drug therapy. Optic Nerve Neoplasms / drug therapy
  • [MeSH-minor] Bone Marrow Diseases / chemically induced. Child. Child, Preschool. Cisplatin / administration & dosage. Cisplatin / adverse effects. Disease-Free Survival. Drug Administration Schedule. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Gastrointestinal Diseases / chemically induced. Humans. Infection / chemically induced. Magnetic Resonance Imaging. Male. Treatment Outcome. Vinblastine / administration & dosage. Vinblastine / adverse effects

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  • (PMID = 18769928.001).
  • [ISSN] 1433-0350
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 5V9KLZ54CY / Vinblastine; 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin
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2. Korones DN, Smith A, Foreman N, Bouffet E: Temozolomide and oral VP-16 for children and young adults with recurrent or treatment-induced malignant gliomas. Pediatr Blood Cancer; 2006 Jul;47(1):37-41
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  • BACKGROUND: Children and young adults with recurrent or treatment-induced malignant gliomas have limited responses to temozolomide or oral VP-16 when either is administered as a single agent.
  • We postulated that a combination of these two drugs for patients with recurrent or treatment-induced malignant gliomas might result in better and more prolonged responses.
  • Diagnoses included recurrent brain stem glioma (2), recurrent anaplastic astrocytoma (2), and glioblastoma (7) (3 treatment-induced, 2 malignant transformations of lower grade tumors, 1 recurrence, and 1 second tumor arising 10 months after diagnosis of medulloblastoma).
  • One patient had a complete response (CR), six had partial responses (PR), and four had progressive disease (PD).
  • There was one grade 4 neutropenia, but no other grade 3 or 4 toxicities.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Glioma / drug therapy. Neoplasm Recurrence, Local / drug therapy. Neoplasms, Second Primary / drug therapy
  • [MeSH-minor] Administration, Oral. Adolescent. Adult. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Agents, Phytogenic / adverse effects. Child. Child, Preschool. Dacarbazine / administration & dosage. Dacarbazine / adverse effects. Dacarbazine / analogs & derivatives. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Humans. Male. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16047359.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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3. 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.
  • In previous reports, the alcohol metabolite of IDA, 4-demethoxydaunorubicinol (idarubicinol, or IDOL), had cytotoxic activity and the ability to penetrate the blood-brain barrier.
  • 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.
  • 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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4. Foreman NK, Schissel D, Le T, Strain J, Fleitz J, Quinones R, Giller R: A study of sequential high dose cyclophosphamide and high dose carboplatin with peripheral stem-cell rescue in resistant or recurrent pediatric brain tumors. J Neurooncol; 2005 Jan;71(2):181-7
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  • [Title] A study of sequential high dose cyclophosphamide and high dose carboplatin with peripheral stem-cell rescue in resistant or recurrent pediatric brain tumors.
  • PURPOSE: To determine the maximum tolerated dose (MTD) of carboplatin with autologous hematopoietic stem-cell rescue, in children with poor-prognosis brain tumors.
  • Toxicity and tumor response were recorded.
  • RESULTS: There were two grade IV toxicities at the dose level of 775 mg/m2/day.
  • One child with a metastatic anaplastic astrocytoma had a CR.
  • The median duration of tumor response was 10 months (range: 1.5-87 months) with two children disease free at 66 and 87 months.
  • Sequential stem-cell supported cyclophosphamide and carboplatin was tolerable in children with brain tumors and produced responses in PNETs and Germinomas.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / therapy. Drug Resistance, Neoplasm. Hematopoietic Stem Cell Transplantation. Neoplasm Recurrence, Local / therapy. Salvage Therapy
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / therapeutic use. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / therapeutic use. Carboplatin / administration & dosage. Carboplatin / therapeutic use. Child. Child, Preschool. Cyclophosphamide / administration & dosage. Cyclophosphamide / therapeutic use. Dose-Response Relationship, Drug. Female. Humans. Male

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  • (PMID = 15690136.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide; BG3F62OND5 / Carboplatin
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5. Pollack IF, Hamilton RL, Sobol RW, Burnham J, Yates AJ, Holmes EJ, Zhou T, Finlay JL: O6-methylguanine-DNA methyltransferase expression strongly correlates with outcome in childhood malignant gliomas: results from the CCG-945 Cohort. J Clin Oncol; 2006 Jul 20;24(21):3431-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] O6-methylguanine-DNA methyltransferase expression strongly correlates with outcome in childhood malignant gliomas: results from the CCG-945 Cohort.
  • PURPOSE: O6-methylguanine-DNA methyltransferase (MGMT) functions to counteract the cytotoxic effects of alkylating agents, such as nitrosoureas, which play a central role in the treatment of childhood malignant gliomas.
  • Epigenetic silencing of MGMT has been associated with prolonged survival in adults with malignant gliomas, although the association between MGMT expression status and outcome in pediatric malignant gliomas has not been defined.
  • METHODS: We examined the association between MGMT expression and survival duration using tumor samples from the Children's Cancer Group 945 study, the largest randomized trial for childhood malignant gliomas completed to date.
  • RESULTS: Twelve of the 109 samples demonstrated overexpression of MGMT compared with normal brain.
  • The association between MGMT overexpression and adverse outcome remained significant after stratifying for institutional histologic diagnosis (eg, anaplastic astrocytoma or glioblastoma multiforme), as well as age, amount of residual tumor, and tumor location.
  • CONCLUSION: Overexpression of MGMT in childhood malignant gliomas is strongly associated with an adverse outcome in children treated with alkylator-based chemotherapy, independently of a variety of clinical prognostic factors.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Biomarkers, Tumor / metabolism. Brain Neoplasms / drug therapy. Brain Neoplasms / enzymology. Glioma / drug therapy. Glioma / enzymology. O(6)-Methylguanine-DNA Methyltransferase / metabolism

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  • (PMID = 16849758.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA13539; United States / NINDS NIH HHS / NS / NS37704
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Biomarkers, Tumor; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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6. Patel M, McCully C, Godwin K, Balis FM: Plasma and cerebrospinal fluid pharmacokinetics of intravenous temozolomide in non-human primates. J Neurooncol; 2003 Feb;61(3):203-7
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  • Temozolomide is a prodrug that undergoes spontaneous chemical degradation at physiologic pH to form the highly reactive alkylating agent, methyl-triazenyl imidazole carboxamide (MTIC).
  • In clinical trials, temozolomide has activity in gliomas and is approved for recurrent anaplastic astrocytoma.
  • We, therefore, studied the penetration of temozolomide into the cerebrospinal fluid (CSF) as a surrogate for blood-brain barrier penetration in a non-human primate model.
  • In this non-human primate model, temozolomide penetrated readily across the blood-brain barrier.
  • These findings are consistent with the activity of temozolomide in brain tumors.
  • [MeSH-major] Antineoplastic Agents, Alkylating / blood. Antineoplastic Agents, Alkylating / cerebrospinal fluid. Dacarbazine / analogs & derivatives. Dacarbazine / blood. Dacarbazine / cerebrospinal fluid
  • [MeSH-minor] Animals. Area Under Curve. Blood-Brain Barrier / physiology. Half-Life. Infusions, Intravenous. Macaca mulatta. Male

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  • (PMID = 12675312.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; YF1K15M17Y / temozolomide
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7. Yung WK: Future directions for temozolomide therapy. Semin Oncol; 2001 Aug;28(4 Suppl 13):43-6
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  • Although the initial indications of temozolomide (Temodar in the United States, Temodal globally; Schering Corporation, Kenilworth, NJ) therapy are for refractory central nervous system malignancies (anaplastic astrocytoma in the United States and Europe, glioblastoma multiforme in Europe), a number of clinical trials are planned or ongoing to evaluate the efficacy and safety of temozolomide in newly diagnosed glioma, oligodendroglioma, pediatric glioma, brain metastases, metastatic melanoma, and other systemic tumors.
  • Also under investigation are modifications to the temozolomide dosing schedule, other routes of administration, and treatment regimens that include temozolomide in combination with other chemotherapeutic and biologic agents.
  • Temozolomide has the potential to be a useful agent in the treatment of a variety of cancers.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Central Nervous System Neoplasms / drug therapy. Dacarbazine / therapeutic use
  • [MeSH-minor] Clinical Trials as Topic. Drug Administration Schedule. Drug Resistance, Neoplasm. Forecasting. Humans

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  • [Copyright] Copyright 2001 by W.B. Saunders Company.
  • (PMID = 11550138.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
  • [Number-of-references] 16
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8. Wagner S, Csatary CM, Gosztonyi G, Koch HC, Hartmann C, Peters O, Hernáiz-Driever P, Théallier-Janko A, Zintl F, Längler A, Wolff JE, Csatary LK: Combined treatment of pediatric high-grade glioma with the oncolytic viral strain MTH-68/H and oral valproic acid. APMIS; 2006 Oct;114(10):731-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined treatment of pediatric high-grade glioma with the oncolytic viral strain MTH-68/H and oral valproic acid.
  • The case of a 12-year-old boy with anaplastic astrocytoma of the left thalamus is reported.
  • Postoperative irradiation and chemotherapy could not repress tumor progression; therefore, treatment was undertaken with an oncolytic virus, MTH-68/H, an attenuated strain of Newcastle disease virus (NDV), and valproic acid (VPA), an antiepileptic drug, which also has antineoplastic properties.
  • This treatment resulted in a far-reaching regression of the thalamic glioma, but 4 months later a new tumor manifestation, an extension of the thalamic tumor, appeared in the wall of the IVth ventricle, which required a second neurosurgical intervention.
  • Under continuous MTH-68/H - VPA administration the thalamic tumor remained under control, but the rhombencephalic one progressed relentlessly and led to the fatal outcome.
  • In the final stage, a third tumor manifestation appeared in the left temporal lobe.
  • The possible reasons for the antagonistic behavior of the three manifestations of the same type of glioma to the initially most successful therapy are discussed.
  • The comparative histological study of the thalamic and rhombencephalic tumor manifestations revealed that MTH-68/H treatment induces, similar to in vitro observations, a massive apoptotic tumor cell decline.
  • In the rhombencephalic tumor, in and around the declining tumor cells, NDV antigen could be demonstrated immunohistochemically, and virus particles have been found in the cytoplasm of tumor cells at electron microscopic investigation.
  • [MeSH-major] Anticonvulsants / therapeutic use. Astrocytoma / drug therapy. Astrocytoma / therapy. Brain Neoplasms / therapy. Valproic Acid / therapeutic use. Viral Vaccines / therapeutic use
  • [MeSH-minor] Administration, Oral. Antigens, Viral / analysis. Antigens, Viral / metabolism. Brain / virology. Child. Combined Modality Therapy. Cytoplasm / virology. Fatal Outcome. Humans. Male. Newcastle disease virus / immunology. Recurrence. Thalamus / pathology

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  • (PMID = 17004977.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / Antigens, Viral; 0 / Newcastle disease virus vaccine MTH-68-H; 0 / Viral Vaccines; 614OI1Z5WI / Valproic Acid
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9. De Sio L, Milano GM, Castellano A, Jenkner A, Fidani P, Dominici C, Donfrancesco A: Temozolomide in resistant or relapsed pediatric solid tumors. Pediatr Blood Cancer; 2006 Jul;47(1):30-6
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  • [Title] Temozolomide in resistant or relapsed pediatric solid tumors.
  • PURPOSE: We report the off-label study aimed at investigating the use of temozolomide (TMZ) as single agent in relapsed or resistant pediatric solid tumors.
  • The drug was administered at the dose of 215 mg/m2/day x 5 days or 180 mg/m2/day x 5 days in patients with prior craniospinal irradiation (CSI) or autologous bone marrow transplantation (ABMT).
  • Tumor types were: neuroblastoma (NB; n = 17), medulloblastoma (MB; 8), brain stem glioma (BSG; 8), extraosseous Ewing's sarcoma/peripheral neuroectodermal tumor (EOES; 4), Ewing's sarcoma (ES; 4), anaplastic astrocytoma (AA; 3), rhabdomyosarcoma (RMS; 2), ependymoma (EP; 2), cerebral primitive neuroectodermal tumor (cPNET; 2), hepatocarcinoma (HC; 1), and osteosarcoma (OS; 1).
  • RESULTS: Objective response-rate (CR + PR + MR) in our series was 13.4% (1.9% CR, 3.8% PR, and 7.7% MR), SD occurred in 38.4% of patients and 48% had PD.
  • Haematological toxicity grade 3-4 (mainly thrombocytopenia) was observed in 21.4% of administered courses, nausea was reported in 3.1% and respiratory distress in 0.7%.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Dacarbazine / analogs & derivatives. Drug Resistance, Neoplasm. Neoplasm Recurrence, Local / drug therapy. Neoplasms / drug therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease-Free Survival. Dose-Response Relationship, Drug. Female. Humans. Male. Survival Analysis

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • [ErratumIn] Pediatr Blood Cancer. 2006 Oct 15;47(5):647-8
  • (PMID = 16047361.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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10. Kieran MW, Packer RJ, Onar A, Blaney SM, Phillips P, Pollack IF, Geyer JR, Gururangan S, Banerjee A, Goldman S, Turner CD, Belasco JB, Broniscer A, Zhu Y, Frank E, Kirschmeier P, Statkevich P, Yver A, Boyett JM, Kun LE: Phase I and pharmacokinetic study of the oral farnesyltransferase inhibitor lonafarnib administered twice daily to pediatric patients with advanced central nervous system tumors using a modified continuous reassessment method: a Pediatric Brain Tumor Consortium Study. J Clin Oncol; 2007 Jul 20;25(21):3137-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I and pharmacokinetic study of the oral farnesyltransferase inhibitor lonafarnib administered twice daily to pediatric patients with advanced central nervous system tumors using a modified continuous reassessment method: a Pediatric Brain Tumor Consortium Study.
  • RESULTS: Fifty-three children with progressive or recurrent brain tumors were enrolled, with a median age of 12.2 years (range, 3.9 to 19.5 years).
  • Both radiographic response (one anaplastic astrocytoma) and stable disease (one medulloblastoma, two high-grade and four low-grade gliomas, one ependymoma, and one sarcoma) were noted, and seven patients remained on treatment for 1 year or longer.
  • [MeSH-major] Central Nervous System Neoplasms / drug therapy. Central Nervous System Neoplasms / mortality. Enzyme Inhibitors / pharmacokinetics. Farnesyltranstransferase / antagonists & inhibitors. Neoplasm Invasiveness / pathology. Piperidines / pharmacokinetics. Pyridines / pharmacokinetics
  • [MeSH-minor] Administration, Oral. Adolescent. Adult. Child. Child, Preschool. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Infant. Infant, Newborn. Male. Maximum Tolerated Dose. Neoplasm Staging. Risk Assessment. Survival Analysis. Treatment Outcome

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  • (PMID = 17634493.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01 CA81457
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Piperidines; 0 / Pyridines; 193275-84-2 / lonafarnib; EC 2.5.1.29 / Farnesyltranstransferase
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11. Reddy AT, Wellons JC 3rd: Pediatric high-grade gliomas. Cancer J; 2003 Mar-Apr;9(2):107-12
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  • [Title] Pediatric high-grade gliomas.
  • High-grade gliomas, including glioblastoma multiforme, anaplastic astrocytoma, and intrinsic pontine, are very difficult to treat in children.
  • Almost all patients with high-grade gliomas respond to radiation therapy, and it is the current mainstay of adjuvant therapy.
  • Current and proposed studies are combining radiation therapy and/or chemotherapy with agents that have shown preclinical promise as radiosensitizers, anti-angiogenesis factors, growth factor receptor inhibitors, and free radical inducers.
  • Other biologic therapies, including gene therapy, are also being investigated.
  • [MeSH-major] Brain Neoplasms / therapy. Glioma / therapy

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  • (PMID = 12784876.001).
  • [ISSN] 1528-9117
  • [Journal-full-title] Cancer journal (Sudbury, Mass.)
  • [ISO-abbreviation] Cancer J
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 25
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12. Nieder C, Andratschke N, Wiedenmann N, Busch R, Grosu AL, Molls M: Radiotherapy for high-grade gliomas. Does altered fractionation improve the outcome? Strahlenther Onkol; 2004 Jul;180(7):401-7
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  • [Title] Radiotherapy for high-grade gliomas. Does altered fractionation improve the outcome?
  • BACKGROUND AND PURPOSE: The publication of Radiation Therapy Oncology Group (RTOG) Study 83-02 in 1996 stimulated further investigations of altered fractionation, i. e., application of more than one fraction per day, in high-grade gliomas.
  • MATERIAL AND METHODS: To identify suitable trials, a Medline search was performed by use of the following key words: brain tumors/astrocytoma/glioma/high-grade glioma/malignant glioma/glioblastoma multiforme and accelerated radiotherapy/hyperfractionated radiotherapy/altered fractionation.
  • Studies in brain stem gliomas, pediatric patients and studies which achieved acceleration by radiosurgery, stereotactic radiotherapy, or brachytherapy rather than conventional external-beam treatment were not included.
  • RESULTS: The authors identified 1,414 patients from 21 studies; two of these were randomized phase III studies.
  • The others provide a very heterogeneous set of data, because a large variety of drugs and administration schedules was used.
  • Seven studies included patients with glioblastoma multiforme only, two were limited to patients with anaplastic gliomas.
  • However, prognostic factors such as tumor histology were not equally distributed and favor the combined-treatment group.
  • CONCLUSION: Altered fractionation shortens the overall treatment time for adult patients with supratentorial high-grade gliomas.
  • [MeSH-major] Brain Neoplasms / radiotherapy. Glioma / radiotherapy

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  • (PMID = 15241527.001).
  • [ISSN] 0179-7158
  • [Journal-full-title] Strahlentherapie und Onkologie : Organ der Deutschen Röntgengesellschaft ... [et al]
  • [ISO-abbreviation] Strahlenther Onkol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 37
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13. Marcus KJ, Goumnerova L, Billett AL, Lavally B, Scott RM, Bishop K, Xu R, Young Poussaint T, Kieran M, Kooy H, Pomeroy SL, Tarbell NJ: Stereotactic radiotherapy for localized low-grade gliomas in children: final results of a prospective trial. Int J Radiat Oncol Biol Phys; 2005 Feb 1;61(2):374-9
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  • [Title] Stereotactic radiotherapy for localized low-grade gliomas in children: final results of a prospective trial.
  • PURPOSE: To evaluate the efficacy of stereotactic radiotherapy (SRT) for small, localized, pediatric brain tumors and to determine the patterns of failure.
  • Of the 81 patients, 50 had low-grade astrocytoma, 23 had residual or recurrent craniopharyngioma, 4 had posterior fossa ependymoma, and 4 had other histologic types.
  • All patients underwent biopsy for diagnosis, with the exception of patients with neurofibromatosis and radiographic evidence of an optic system tumor.
  • This report focused on the patients with low-grade gliomas only.
  • The indications for treatment of patients with low-grade gliomas were progression during or after chemotherapy or progression after surgery alone.
  • The target volume generally included the preoperative tumor plus a 2-mm margin for the planning target volume.
  • Two of the patients with local progression had pathologic progression to anaplastic astrocytoma 3 and 7 years after initial SRT.
  • One patient developed a presumed radiation-induced primitive neuroectodermal tumor 6 years after initial treatment.
  • Six patients died, three of dissemination, two of progression to higher grade tumors, and one of a secondary radiation-induced tumor.
  • All 6 cases of local progression were within the primary tumor bed at the time of progression and had received the full prescription dose.
  • CONCLUSION: Stereotactic radiotherapy provides excellent local control for children with small, localized low-grade glial tumors.
  • [MeSH-major] Astrocytoma / surgery. Brain Neoplasms / surgery. Radiosurgery
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Confidence Intervals. Disease Progression. Disease-Free Survival. Female. Humans. Male. Neoplasm Recurrence, Local / drug therapy. Prospective Studies. Radiotherapy Dosage

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  • (PMID = 15667955.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Graham C, Tucker C, Creech J, Favours E, Billups CA, Liu T, Fouladi M, Freeman BB 3rd, Stewart CF, Houghton PJ: Evaluation of the antitumor efficacy, pharmacokinetics, and pharmacodynamics of the histone deacetylase inhibitor depsipeptide in childhood cancer models in vivo. Clin Cancer Res; 2006 Jan 1;12(1):223-34
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  • [Title] Evaluation of the antitumor efficacy, pharmacokinetics, and pharmacodynamics of the histone deacetylase inhibitor depsipeptide in childhood cancer models in vivo.
  • PURPOSE: Histone acetyltransferases and histone deacetylases (HDAC) control the acetylation state of histones and other proteins regulating transcription and protein function.
  • Several structurally diverse HDAC inhibitors have been developed as cancer therapeutic agents and in vitro have been shown to cause differentiation, cell cycle arrest, or apoptosis.
  • Here, we have evaluated depsipeptide, a natural tetrapeptide HDAC inhibitor, against a panel of pediatric solid tumor models in vivo and evaluated pharmacokinetic and pharmacodynamic variables with tumor sensitivity.
  • EXPERIMENTAL DESIGN: Depsipeptide was administered at the maximum tolerated dose (4.4 mg/kg administered every 7 days x 3 i.v. repeated q21d for a total of two cycles) to scid mice bearing 39 independently derived childhood tumors (9 brain tumors, 11 kidney cancers, 9 rhabdomyosarcomas, 3 neuroblastomas, and 7 osteosarcomas).
  • RESULTS: Of 39 tumors evaluated, three showed objective tumor regressions [two brain tumors (primitive neuroectodermal tumor and atypical teratoid malignant rhabdoid tumor) and one Wilms' tumor].
  • Depsipeptide inhibited growth of many tumor lines but achieved stable disease (<25% increase in volume during treatment cycle 1) in only two tumor models (anaplastic astrocytoma, two rhabdomyosarcomas, and a Wilms' tumor).
  • In two sensitive tumor lines, IRS56 and BT27 (both wild-type p53) p53 increased in treated tumors being maximal at 8 hours and associated with induction of p21(cip1), whereas p53 was stable in tumors with mutant p53.
  • CONCLUSIONS: Our results show that depsipeptide inhibits its target in vivo causing increased histone acetylation; however, this does not correlate with drug sensitivity.
  • The relatively low objective response rate [3 of 39 (8%) tumor lines showing greater than or equal to partial response and 4 (10%) stable disease] administered at dose levels that give clinically relevant drug exposures suggests that as a single agent depsipeptide may have limited clinical utility against pediatric solid tumors in a first-line setting.
  • [MeSH-major] Depsipeptides / pharmacokinetics. Depsipeptides / therapeutic use. Enzyme Inhibitors / pharmacokinetics. Enzyme Inhibitors / therapeutic use. Histone Deacetylases / drug effects. Neoplasms, Experimental / drug therapy
  • [MeSH-minor] Acetylation / drug effects. Animals. Blotting, Western. Cell Line, Tumor. Child. Disease Models, Animal. Female. Histones / drug effects. Humans. Mice. Mice, SCID. Neoplasm Transplantation. Reverse Transcriptase Polymerase Chain Reaction. Tumor Suppressor Protein p53 / drug effects

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  • (PMID = 16397046.001).
  • [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 / CA21765; United States / NCI NIH HHS / CA / CA23099; United States / NCI NIH HHS / CA / CA96696
  • [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 / Depsipeptides; 0 / Enzyme Inhibitors; 0 / Histones; 0 / Tumor Suppressor Protein p53; EC 3.5.1.98 / Histone Deacetylases
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15. Cavazos CM, Keir ST, Yoshinari T, Bigner DD, Friedman HS: Therapeutic activity of the topoisomerase I inhibitor J-107088 [6-N-(1-hydroxymethyla-2-hydroxyl) ethylamino-12,13-dihydro-13-(beta-D-glucopyranosyl) -5H-indolo[2,3-a]-pyrrolo[3,4-c]-carbazole-5,7(6H)-dione]] against pediatric and adult central nervous system tumor xenografts. Cancer Chemother Pharmacol; 2001 Sep;48(3):250-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic activity of the topoisomerase I inhibitor J-107088 [6-N-(1-hydroxymethyla-2-hydroxyl) ethylamino-12,13-dihydro-13-(beta-D-glucopyranosyl) -5H-indolo[2,3-a]-pyrrolo[3,4-c]-carbazole-5,7(6H)-dione]] against pediatric and adult central nervous system tumor xenografts.
  • PURPOSE: The in vivo antitumor activity of a novel topoisomerase I inhibitor, J-107088, was tested in athymic nude mice bearing subcutaneous or intracranial pediatric and adult malignant CNS tumor-derived xenografts.
  • METHODS: J-107088 was administered to animals on days 1-5 and 8-12 via intraperitoneal injection at a dose of 54 mg/kg (162 mg/m2) per day in 10% dimethyl sulfoxide in 0.9% saline.
  • The xenografts evaluated were derived from a childhood glioblastoma multiforme (D-456 MG), a childhood medulloblastoma (D-341 MED), an adult anaplastic astrocytoma (D-54 MG), an adult glioblastoma multiforme (D-245 MG), and a procarbazine-resistant subline of D-245 MG [D-245 MG (PR)].
  • CONCLUSION: These results indicate that J-107088 may be active in the treatment of childhood and adult malignant brain tumors and provide the rationale for initiation of clinical trials with this agent.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Carbazoles / therapeutic use. Enzyme Inhibitors / therapeutic use. Glioma / drug therapy. Glucosides / therapeutic use. Indoles. Topoisomerase I Inhibitors
  • [MeSH-minor] Adult. Animals. Child. Female. Humans. Injections, Intraperitoneal. Injections, Subcutaneous. Male. Mice. Mice, Nude. Neoplasm Transplantation. Survival Rate. Transplantation, Heterologous. Treatment Outcome. Tumor Cells, Cultured

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  • (PMID = 11592348.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / 2RO1-NS30245-12; United States / NINDS NIH HHS / NS / 5P50-NS-20023-17; United States / NCI NIH HHS / CA / CA11898; etc
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbazoles; 0 / Enzyme Inhibitors; 0 / Glucosides; 0 / Indoles; 0 / Topoisomerase I Inhibitors; 1V8X590XDP / edotecarin
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16. López-Aguilar E, Sepúlveda-Vildósola AC, Rivera-Márquez H, Cerecedo-Díaz F, Hernández-Contreras I, Ramón-García G, Diegopérez-Ramírez J, Santacruz-Castillo E: Preirradiation ifosfamide, carboplatin, and etoposide for the treatment of anaplastic astrocytomas and glioblastoma multiforme: a phase II study. Arch Med Res; 2000 Mar-Apr;31(2):186-90
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  • [Title] Preirradiation ifosfamide, carboplatin, and etoposide for the treatment of anaplastic astrocytomas and glioblastoma multiforme: a phase II study.
  • BACKGROUND: Central nervous system (CNS) tumors are the second most common pediatric tumors.
  • Traditional treatment of anaplastic astrocytoma (AA) and glioblastoma multiforme (GM) consisting of surgery-radiotherapy-chemotherapy with nitrosoureas has resulted in a survival rate of 26% at 1 year.
  • Chemotherapy with ifosfamide, carboplatin, and etoposide (ICE) permits synergism among the different drugs and sensitizes the tumor to radiotherapy.
  • Our objective was to evaluate the efficacy, security, and survival rate of postoperative chemotherapy with ICE in pediatric patients with AA or GM.
  • A magnetic resonance image (MRI) study of the tumor was made after surgery to evaluate residual tumor and routine laboratory analysis.
  • AA was the tumor with the greatest reduction of residual tumor after treatment.
  • CONCLUSIONS: Postoperative chemotherapy with ICE reduces the tumor size and increases the survival rate of pediatric patients with malignant astrocytomas with minimal toxicity.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Cranial Irradiation. Glioblastoma / drug therapy. Premedication. Radiotherapy, Adjuvant

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  • (PMID = 10880725.001).
  • [ISSN] 0188-4409
  • [Journal-full-title] Archives of medical research
  • [ISO-abbreviation] Arch. Med. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] MEXICO
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin; NR7O1405Q9 / Mesna; UM20QQM95Y / Ifosfamide; ICE protocol 5
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17. Momota H, Narita Y, Miyakita Y, Hosono A, Makimoto A, Shibui S: Acute lymphoblastic leukemia after temozolomide treatment for anaplastic astrocytoma in a child with a germline TP53 mutation. Pediatr Blood Cancer; 2010 Sep;55(3):577-9
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  • [Title] Acute lymphoblastic leukemia after temozolomide treatment for anaplastic astrocytoma in a child with a germline TP53 mutation.
  • We present a case of a 12-year-old female with a germline TP53 mutation who presented with anaplastic astrocytoma and subsequent acute lymphoblastic leukemia (ALL) 13 months after starting treatment with temozolomide (TMZ).
  • Although alkylating agents such as TMZ are known to induce secondary hematologic malignancy, only several cases of treatment-related acute leukemia have been reported after TMZ-alone chemotherapy for malignant gliomas.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Frontal Lobe. Genes, p53 / genetics. Germ-Line Mutation. Neoplasms, Second Primary / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / chemically induced






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