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1. 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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  • [Title] Activity of VNP40101M (Cloretazine) in the treatment of CNS tumor xenografts in athymic mice.
  • 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%.
  • In mice bearing intracranial D-245 MG xenografts, treatment with VNP40101M at a dose of 18 mg/kg daily for five days produced a 50% increase in median survival compared with controls.
  • Additional experiments conducted against subcutaneous D-245 MG xenografts by using reduced doses of 13.5 or 9.0 mg/kg daily for five days demonstrated tumor growth delays of 82.2 and 53.5 days, with corresponding tumor regressions in 8 of 9 and 9 of 10 treated mice, respectively (all values, p < 0.001), with one toxic death.
  • These findings suggest that VNP40101M is active in the treatment of a wide range of human central nervous system tumors and warrants translation to the clinic.

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  • [Cites] Cancer Chemother Pharmacol. 1994;34(2):171-4 [8194169.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jul;87(14):5368-72 [2164681.001]
  • [Cites] Cancer Res. 1995 Jul 1;55(13):2853-7 [7796412.001]
  • [Cites] Cancer Res. 1997 Jul 15;57(14):2933-6 [9230204.001]
  • [Cites] Invest New Drugs. 2005 Mar;23(2):123-35 [15744588.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] Biochem Pharmacol. 2000 Feb 1;59(3):283-91 [10609557.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):3033-8 [11306484.001]
  • [Cites] Int J Toxicol. 2002 Jan-Feb;21(1):23-38 [11936896.001]
  • [Cites] Cancer Chemother Pharmacol. 2004 Apr;53(4):288-95 [14685775.001]
  • [Cites] Clin Cancer Res. 2004 May 1;10(9):2908-17 [15131024.001]
  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] Neurosurgery. 1979 Apr;4(4):308-14 [450229.001]
  • [Cites] Cancer Res. 1988 Aug 1;48(15):4189-95 [3390813.001]
  • [Cites] J Neurooncol. 1994;20(2):111-20 [7807189.001]
  • (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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2. Gururangan S, Chi SN, Young Poussaint T, Onar-Thomas A, Gilbertson RJ, Vajapeyam S, Friedman HS, Packer RJ, Rood BN, Boyett JM, Kun LE: Lack of efficacy of bevacizumab plus irinotecan in children with recurrent malignant glioma and diffuse brainstem glioma: a Pediatric Brain Tumor Consortium study. J Clin Oncol; 2010 Jun 20;28(18):3069-75
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  • [Title] Lack of efficacy of bevacizumab plus irinotecan in children with recurrent malignant glioma and diffuse brainstem glioma: a Pediatric Brain Tumor Consortium study.
  • PURPOSE: A phase II study of bevacizumab (BVZ) plus irinotecan (CPT-11) was conducted in children with recurrent malignant glioma (MG) and intrinsic brainstem glioma (BSG).
  • PATIENTS AND METHODS: Eligible patients received two doses of BVZ intravenously (10 mg/kg) 2 weeks apart and then BVZ plus CPT-11 every 2 weeks until progressive disease, unacceptable toxicity, or a maximum of 2 years of therapy.
  • Median time to progression for all 34 eligible patients enrolled was 127 days for MG and 71 days for BSG.
  • Toxicities related to BVZ included grade 1 to 3 fatigue in seven patients, grade 1 to 2 hypertension in seven patients, grade 1 CNS hemorrhage in four patients, and grade 4 CNS ischemia in two patients.
  • Vascular permeability parameters did not change significantly after therapy in either stratum.
  • CONCLUSION: BVZ plus CPT-11 was well-tolerated but had minimal efficacy in children with recurrent malignant glioma and brainstem glioma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Brain Stem Neoplasms / drug therapy. Glioma / drug therapy. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adolescent. Adult. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Bevacizumab. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Child. Diffusion Magnetic Resonance Imaging. Humans. Phosphorylation. Survival Rate. Treatment Outcome. Vascular Endothelial Growth Factor Receptor-2 / metabolism. Young Adult

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  • [Cites] Clin Cancer Res. 2007 Feb 15;13(4):1253-9 [17317837.001]
  • [Cites] Cancer Cell. 2007 Jan;11(1):83-95 [17222792.001]
  • [Cites] Nat Rev Cancer. 2008 Apr;8(4):309-16 [18337733.001]
  • [Cites] Neuro Oncol. 2008 Aug;10(4):624-30 [18539884.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2008 Oct 1;72(2):383-9 [18793954.001]
  • [Cites] Pediatr Blood Cancer. 2008 Dec;51(6):806-11 [18802947.001]
  • [Cites] Clin Cancer Res. 2008 Oct 15;14(20):6371-5 [18927275.001]
  • [Cites] J Neurooncol. 2009 Feb;91(3):329-36 [18953493.001]
  • [Cites] J Clin Oncol. 2009 Feb 10;27(5):740-5 [19114704.001]
  • [Cites] J Clin Oncol. 2009 Oct 1;27(28):4733-40 [19720927.001]
  • [Cites] Cancer Res. 2000 Apr 1;60(7):1878-86 [10766175.001]
  • [Cites] Oncogene. 2000 Nov 20;19(49):5598-605 [11114740.001]
  • [Cites] Eur J Cancer. 2001 Nov;37(16):2064-72 [11597385.001]
  • [Cites] NMR Biomed. 2002 Feb;15(1):6-17 [11840548.001]
  • [Cites] J Neurooncol. 2002 Jul;58(3):237-53 [12187958.001]
  • [Cites] J Clin Oncol. 2002 Dec 15;20(24):4684-91 [12488414.001]
  • [Cites] J Clin Oncol. 2003 Sep 15;21(18):3542; author reply 3543 [12972536.001]
  • [Cites] N Engl J Med. 1971 Nov 18;285(21):1182-6 [4938153.001]
  • [Cites] J Natl Cancer Inst. 1990 Jan 3;82(1):4-6 [1688381.001]
  • [Cites] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840.001]
  • [Cites] Cancer. 1993 Jul 1;72(1):271-5 [8508417.001]
  • [Cites] J Clin Oncol. 1999 May;17(5):1516-25 [10334539.001]
  • [Cites] J Neurooncol. 1999 May;43(1):43-7 [10448870.001]
  • [Cites] Am J Health Syst Pharm. 2004 Nov 1;61(21 Suppl 5):S21-6 [15552623.001]
  • [Cites] J Natl Cancer Inst. 2005 Feb 2;97(3):172-87 [15687360.001]
  • [Cites] Neurol Res. 2005 Jun;27(4):371-7 [15949234.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2347-55 [15985545.001]
  • [Cites] Oncology. 2005;69 Suppl 3:25-33 [16301833.001]
  • [Cites] Cancer. 2006 Mar 15;106(6):1364-71 [16463390.001]
  • [Cites] Cancer Cell. 2007 Jan;11(1):69-82 [17222791.001]
  • [Cites] Cancer. 2007 Oct 1;110(7):1542-50 [17705175.001]
  • (PMID = 20479404.001).
  • [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 / NCRR NIH HHS / RR / M01 RR000188; United States / NCI NIH HHS / CA / U01 CA081457; United States / NCRR NIH HHS / RR / M01RR00188; United States / NCI NIH HHS / CA / U01CA81457
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0H43101T0J / irinotecan; 2S9ZZM9Q9V / Bevacizumab; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; XT3Z54Z28A / Camptothecin
  • [Other-IDs] NLM/ PMC2903337
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3. Broniscer A, Ke W, Fuller CE, Wu J, Gajjar A, Kun LE: Second neoplasms in pediatric patients with primary central nervous system tumors: the St. Jude Children's Research Hospital experience. Cancer; 2004 May 15;100(10):2246-52
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  • [Title] Second neoplasms in pediatric patients with primary central nervous system tumors: the St. Jude Children's Research Hospital experience.
  • BACKGROUND: Details on second neoplasms (SNs) following pediatric central nervous system (CNS) tumors are scant, because of the rarity of such SNs.
  • METHODS: The authors reviewed clinical and treatment data on all institutional patients age < 22 years at diagnosis of a primary CNS tumor who developed any type of SN.
  • Patients with neurofibromatosis type 1 were excluded.
  • RESULTS: The SNs investigated in the current study included 10 gliomas (42%), 5 meningiomas (21%), 2 desmoid tumors, 2 myelodysplastic syndromes, 2 basal cell carcinomas, 1 leukemia, 1 malignant fibrous histiocytoma, and 1 thyroid carcinoma.
  • Twenty-one patients had previously received radiotherapy, and 12 patients had received chemotherapy.
  • The estimated 15-year cumulative incidence rate for malignant SNs was 4%.
  • Children with choroid plexus tumors had an estimated 10-year cumulative incidence rate of 20.2%; 2 of those patients had germline TP53 mutations.
  • No significant difference in the estimated cumulative incidence of SNs was found among patients who had received different types of therapy.
  • CONCLUSIONS: The risk of lethal SNs after pediatric CNS tumors is small.
  • Young patients and patients with choroid plexus tumors appear to have an increased risk of SNs that is associated with genetic factors.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / secondary. Neoplasms, Second Primary / pathology. Spinal Cord Neoplasms / pathology. Spinal Cord Neoplasms / secondary
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / therapeutic use. Child. Child, Preschool. Combined Modality Therapy. Female. Humans. Incidence. Infant. Male. Radiotherapy. Retrospective Studies. Risk Factors. Survival Rate

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  • [Copyright] Copyright 2004 American Cancer Society.
  • (PMID = 15139071.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA21765
  • [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 / Antineoplastic Agents
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4. 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.
  • 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.
  • Only 1 patient developed reduced cardiac function.
  • 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.
  • We conclude from this data and from that in nonhuman primates that it is unlikely that IDA, daunomycin, or other related anthracyclines will be useful for treating primary CNS tumors.
  • [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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5. Frühwald MC, Rickert CH, O'Dorisio MS, Madsen M, Warmuth-Metz M, Khanna G, Paulus W, Kühl J, Jürgens H, Schneider P, Müller HL: Somatostatin receptor subtype 2 is expressed by supratentorial primitive neuroectodermal tumors of childhood and can be targeted for somatostatin receptor imaging. Clin Cancer Res; 2004 May 1;10(9):2997-3006
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  • [Title] Somatostatin receptor subtype 2 is expressed by supratentorial primitive neuroectodermal tumors of childhood and can be targeted for somatostatin receptor imaging.
  • PURPOSE: Although gliomas predominate among central nervous system (CNS) neoplasms in adulthood, embryonal tumors are the most common malignant brain tumors in children.
  • Despite novel treatment approaches, including improved radiotherapy and high-dose chemotherapy, survival rates remain unsatisfactory.
  • The timely diagnosis of residual or recurrent embryonal CNS tumors and thus the earliest possible time point for intervention is often hampered by inaccuracies of conventional imaging techniques.
  • Here, we evaluated somatostatin receptor type 2 (sst(2)) expression using an antibody in an array of CNS tumors of childhood.
  • Eight high-grade gliomas, 4 atypical teratoid/rhabdoid tumors, 7 supratentorial primitive neuroectodermal tumors (stPNET), 1 medulloepithelioma (ME), and 8 ependymomas were screened.
  • Tumors positive in vitro were additionally analyzed in vivo using SRI.
  • RESULTS: Abundant expression of somatostatin receptor type 2 in stPNET, a ME, and ependymomas warranted in vivo imaging of 7 stPNET, 1 rhabdomyosarcoma, 3 ependymomas, 1 ME, and 1 glioblastoma.
  • In selected cases SRI was more sensitive in the detection of relapse than conventional imaging by magnetic resonance imaging and computed tomography.
  • CONCLUSIONS: SRI should be considered in the evaluation of residual or recurrent embryonal CNS tumors, especially stPNET.
  • The strengths of SRI lie in the differentiation of reactive tissue changes versus residual or recurrent tumor, the detection of small lesions, and possibly in the distinction of stPNET from gliomas.
  • [MeSH-major] Neuroectodermal Tumors, Primitive / pathology. Receptors, Somatostatin / biosynthesis. Supratentorial Neoplasms / pathology
  • [MeSH-minor] Central Nervous System Neoplasms / metabolism. Central Nervous System Neoplasms / pathology. Central Nervous System Neoplasms / radionuclide imaging. Child. Child, Preschool. Female. Humans. Immunohistochemistry. Infant. Male. Tomography, Emission-Computed, Single-Photon / methods

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  • (PMID = 15131035.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2
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6. da Silva NS, Cappellano AM, Diez B, Cavalheiro S, Gardner S, Wisoff J, Kellie S, Parker R, Garvin J, Finlay J: Primary chemotherapy for intracranial germ cell tumors: results of the third international CNS germ cell tumor study. Pediatr Blood Cancer; 2010 Mar;54(3):377-83
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  • [Title] Primary chemotherapy for intracranial germ cell tumors: results of the third international CNS germ cell tumor study.
  • BACKGROUND: The treatment of central nervous system (CNS) germ cell tumors (GCT) remains controversial.
  • The purpose of this study was to demonstrate efficacy of a chemotherapy only strategy, with less morbidity, when compared to regimens with irradiation.
  • METHODS: Between January 2001 and December 2004 newly diagnosed patients with CNS GCT were treated with one of two risk-tailored chemotherapy regimens.
  • Twenty-five patients aged 4 months to 24.5 years were stratified: Regimen A consisted of 4-6 cycles of carboplatin/etoposide alternating with cyclophosphamide/etoposide for low risk (LR) localized germinoma with normal cerebrospinal fluid (CSF) and serum tumor markers.
  • Regimen B consisted of 4-6 cycles of carboplatin/cyclophosphamide/etoposide for intermediate-risk (IR) germinoma with positive human chorionic gonadotrophin-beta (HCGbeta) and/or CSF HCGbeta <50 mIU/ml and high-risk (HR) biopsy-proven non-germinomatous malignant elements (MMGCT) or elevated serum/CSF alpha-fetoprotein and/or HCGbeta serum/CSF >50 mIU/ml.
  • Seventeen (68%) patients achieved complete radiographic and marker responses after two courses and 19 (76%) after four courses of chemotherapy.
  • CONCLUSION: These intensive chemotherapy regimens proved less effective than irradiation containing regimens.
  • Our results indicate that, at the present time, standard treatment for CNS GCT continues to include irradiation either alone or combined with chemotherapy for pure germinomas and with chemotherapy for those with MMGCT.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Neoplasms, Germ Cell and Embryonal / drug therapy
  • [MeSH-minor] Adolescent. Adult. Carboplatin / administration & dosage. Carboplatin / adverse effects. Child. Child, Preschool. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Humans. Infant. Male. Treatment Outcome. Young Adult

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  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
  • (PMID = 20063410.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; BG3F62OND5 / Carboplatin
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7. Sands SA, Oberg JA, Gardner SL, Whiteley JA, Glade-Bender JL, Finlay JL: Neuropsychological functioning of children treated with intensive chemotherapy followed by myeloablative consolidation chemotherapy and autologous hematopoietic cell rescue for newly diagnosed CNS tumors: an analysis of the Head Start II survivors. Pediatr Blood Cancer; 2010 Mar;54(3):429-36
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  • [Title] Neuropsychological functioning of children treated with intensive chemotherapy followed by myeloablative consolidation chemotherapy and autologous hematopoietic cell rescue for newly diagnosed CNS tumors: an analysis of the Head Start II survivors.
  • PROCEDURES: Forty-nine patients (mean age 2.9 years) diagnosed with a malignant brain tumor underwent baseline neuropsychological assessment prior to autologous hematopoietic cell transplantation (AuHCT).
  • Age at diagnosis was positively correlated with internalizing symptoms and visual immediate memory, while time since diagnosis was inversely correlated with FSIQ, VIQ, PIQ, reading and delayed verbal memory.
  • CONCLUSION: Induction, with or without intensification using intravenous methotrexate, followed by myeloablative consolidation chemotherapy with AuHCT, may avoid or delay CSI, with possible stabilization of neuropsychological functioning, including those younger at diagnosis.
  • [MeSH-major] Brain Neoplasms / drug therapy. Brain Neoplasms / psychology. Hematopoietic Stem Cell Transplantation. Intelligence / drug effects
  • [MeSH-minor] Child. Child, Preschool. Combined Modality Therapy. Cranial Irradiation / adverse effects. Cranial Irradiation / methods. Female. Humans. Male. Methotrexate / adverse effects. Methotrexate / therapeutic use. Neuropsychological Tests. Psychomotor Performance / drug effects. Survivors

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  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
  • [CommentIn] Pediatr Blood Cancer. 2010 Mar;54(3):346-7 [19902522.001]
  • (PMID = 20052775.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] YL5FZ2Y5U1 / Methotrexate
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8. Khatua S, Dhall G, O'Neil S, Jubran R, Villablanca JG, Marachelian A, Nastia A, Lavey R, Olch AJ, Gonzalez I, Gilles F, Nelson M, Panigrahy A, McComb G, Krieger M, Fan J, Sposto R, Finlay JL: Treatment of primary CNS germinomatous germ cell tumors with chemotherapy prior to reduced dose whole ventricular and local boost irradiation. Pediatr Blood Cancer; 2010 Jul 15;55(1):42-6
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  • [Title] Treatment of primary CNS germinomatous germ cell tumors with chemotherapy prior to reduced dose whole ventricular and local boost irradiation.
  • BACKGROUND: The purpose of this study was to evaluate a reduced irradiation dose strategy for newly diagnosed primary central nervous system (CNS) germinomas.
  • In 18 patients, chemotherapy was followed by whole ventricular irradiation to 21.6-25.5 Gy with a simultaneous integrated or sequential primary site boost to 30-30.6 Gy.
  • Initial tumor markers for beta-human chorionic gonadotrophin (HCGbeta) and alpha-fetoprotein (AFP) were evaluated in serum and lumbar cerebrospinal fluid (CSF).
  • Neurocognitive function was evaluated periodically following treatment.
  • RESULTS: Eighteen of 20 patients are without evidence of residual or recurrent tumor.
  • Both relapsing patients were subsequently determined to harbor malignant non-germinomatous germ cell tumor (NGGCT).
  • CONCLUSION: Chemotherapy followed by reduced dose whole ventricular and local boost irradiation appears to be effective in patients with localized pure CNS germinoma with evidence of preservation of neurocognitive function.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / therapy. Central Nervous System Neoplasms / therapy. Germinoma / therapy. Neoplasms, Germ Cell and Embryonal / therapy
  • [MeSH-minor] Adolescent. Adult. Carboplatin / adverse effects. Carboplatin / therapeutic use. Child. Child, Preschool. Chorionic Gonadotropin, beta Subunit, Human / blood. Combined Modality Therapy. Dose-Response Relationship, Radiation. Etoposide / adverse effects. Etoposide / therapeutic use. Female. Humans. Infant. Magnetic Resonance Imaging. Male. Retrospective Studies. Young Adult. alpha-Fetoproteins / analysis

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  • (PMID = 20222020.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / alpha-Fetoproteins; 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin
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9. Messing-Jünger AM, Janssen G, Pape H, Bock WJ, Göbel U, Lenard HG, Schmitt G: Interdisciplinary treatment in pediatric patients with malignant CNS tumors. Childs Nerv Syst; 2000 Nov;16(10-11):742-50
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  • [Title] Interdisciplinary treatment in pediatric patients with malignant CNS tumors.
  • Despite sophisticated surgical methods only a few pediatric CNS tumors can be controlled by operation alone.
  • Therefore multimodality treatment regimens are needed to improve quality of life and survival, which is most important in malignant neoplasms.
  • Since 1998 we have treated 16 children with malignant CNS tumors.
  • All 16 patients have been treated on an interdisciplinary basis and are therefore accompanied by a pediatric neurooncology group consisting of a neurosurgeon, pediatric oncologist, and radiotherapist.
  • Depending on tumor histology, child's age, and extent of surgery, further adjuvant therapy is planned by this group.
  • Newly diagnosed tumors are typically treated by a specific chemotherapy protocol according to a multi-institutional study.
  • In recurrent tumors more individual treatment regimens are considered.
  • Data concerning surgery, adjunctive treatment, complications, and outcome of all patients and four case reports are presented.
  • [MeSH-major] Brain Neoplasms / therapy. Patient Care Team
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Male. Survival Rate

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  • (PMID = 11151726.001).
  • [ISSN] 0256-7040
  • [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] Case Reports; Journal Article
  • [Publication-country] Germany
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10. Ronghe MD, Moss TH, Lowis SP: Treatment of CNS malignant rhabdoid tumors. Pediatr Blood Cancer; 2004 Mar;42(3):254-60

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  • [Title] Treatment of CNS malignant rhabdoid tumors.
  • BACKGROUND: Central Nervous System (CNS) rhabdoid tumours are a highly malignant group of neoplasms usually occurring in children under 2 years of age with characteristic histopathologic findings but unclear histiogenesis and almost uniformly fatal outcome.
  • There is still no proven curative therapy available.
  • PROCEDURE: The clinical course and the successful outcome of therapy in two children with primary CNS rhabdoid tumour are described in this context.
  • Both children had subtotal excision of the primary tumour and received chemotherapy based on the SIOP Malignant Mesenchymal Tumour (MMT-95) protocol with addition of triple intrathecal chemotherapy.
  • Following this, one of the patients received high dose therapy (busulphan and thiotepa), whereas the other had craniospinal radiotherapy with a boost to the primary site.
  • RESULTS: The treatment was reasonably well tolerated and both patients are alive with no evidence of disease 52 months and 65 months after the primary diagnosis.
  • CONCLUSIONS: Intensified therapy (with autologous bone marrow transplantation and intrathecal chemotherapy) may improve the prognosis of patients with malignant rhabdoid tumour.
  • [MeSH-major] Central Nervous System Neoplasms / therapy. Rhabdoid Tumor / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Child, Preschool. Combined Modality Therapy. Cranial Irradiation. Female. Humans. Infant. Injections, Spinal. Radiotherapy, Adjuvant. Treatment Outcome

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  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • (PMID = 14752863.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 34
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11. Roland JT Jr, Cosetti M, Liebman T, Waltzman S, Allen JC: Cochlear implantation following treatment for medulloblastoma. Laryngoscope; 2010 Jan;120(1):139-43
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  • [Title] Cochlear implantation following treatment for medulloblastoma.
  • OBJECTIVES/HYPOTHESIS: Medulloblastoma is the most common pediatric malignant tumor of the central nervous system in children.
  • Treatment includes surgical excision, external beam radiation, and multiagent chemotherapy.
  • Otologic sequelae are common and may result from radiation and/or chemotherapy.
  • Profound sensorineural hearing loss (SNHL) is a known complication of neuro-oncologic treatment and may render these patients eligible for cochlear implantation (CI).
  • Issues of CI in this population, including diagnosis, treatment of preoperative middle ear disease, operative and postoperative course, performance data, and long-term tumor surveillance are highlighted and reviewed.
  • METHODS: Three patients treated for pediatric medulloblastoma with surgical resection, postoperative hyperfractioned craniospinal radiotherapy, and multiagent adjuvant chemotherapy who underwent cochlear implantation were identified.
  • Details of neuro-oncologic treatment and associated otologic complications are presented and analyzed.
  • Primary outcome assessment includes treatment of middle ear pathology, perioperative cochlear implant course, and postimplantation performance data.
  • RESULTS: Each patient required surgical treatment of chronic ear disease 4 to 16 years after chemoradiation.
  • All progressed to profound SNHL and were implanted 8 to 17 years post-neuro-oncologic treatment.
  • One patient developed postoperative wound dehiscence requiring operative closure.
  • CONCLUSIONS: Patients treated for pediatric medulloblastoma develop otologic sequelae, including profound SNHL, and may require cochlear implantation.
  • [MeSH-major] Brain Neoplasms / therapy. Cochlear Implantation. Hearing Loss, Sensorineural / surgery. Medulloblastoma / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Combined Modality Therapy. Humans. Retrospective Studies. Treatment Outcome


12. Sajedi M, Wolff JE, Egeler RM, Pinto A, Hughes R, Anderson RA, Coppes MJ: Congenital extrarenal non-central nervous system malignant rhabdoid tumor. J Pediatr Hematol Oncol; 2002 May;24(4):316-20
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  • [Title] Congenital extrarenal non-central nervous system malignant rhabdoid tumor.
  • Malignant rhabdoid tumor (MRT) is a rare tumor occurring mostly in kidneys and central nervous system (CNS).
  • Although the masses in axilla and bone marrow responded rapidly to chemotherapy, the elbow lesion increased in size.
  • Despite intense treatment, the tumor relapsed in lungs and the patient died 12 months after diagnosis.
  • Review of the literature showed twenty additional congenital MRTs arising from sites outside of the kidney and central nervous system were published in the literature.
  • The median overall survival time for all (n = 21) patients was 2.0 months (0-24 months).
  • The only patient who survived had a localized tumor at initial diagnosis.
  • Congenital, extrarenal, non-CNS MRTs are aggressive tumors with poor outcome.
  • [MeSH-major] Brain Neoplasms / pathology. Rhabdoid Tumor / pathology

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  • (PMID = 11972104.001).
  • [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; Review
  • [Publication-country] United States
  • [Number-of-references] 22
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13. Morgenstern DA, Gibson S, Brown T, Sebire NJ, Anderson J: Clinical and pathological features of paediatric malignant rhabdoid tumours. Pediatr Blood Cancer; 2010 Jan;54(1):29-34
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  • [Title] Clinical and pathological features of paediatric malignant rhabdoid tumours.
  • BACKGROUND: Malignant rhabdoid tumours (MRT) and their central nervous system (CNS) counterparts atypical teratoid/rhabdoid tumours (ATRT) are rare, highly aggressive malignant neoplasms of childhood.
  • Although there are isolated reports of long-term survival with intensive, multimodal therapy, outcomes are generally poor.
  • PROCEDURE: We conducted a retrospective review of all patients diagnosed with MRT/ATRT at Great Ormond Street Hospital over the 20 years from 1989 to 2009.
  • There were four long-term survivors (>30 months), all of whom received chemotherapy with or without surgical resection or radiotherapy.
  • CONCLUSIONS: In view of poor outcomes, there is a clear need for new treatment strategies and the identification of novel molecular targets for MRT/ATRT.
  • [MeSH-major] Rhabdoid Tumor / pathology. Teratoma / pathology
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Child. Combined Modality Therapy. Female. Humans. Immunoenzyme Techniques. Infant. Male. Neoplasm Staging. Prognosis. Radiotherapy. Retrospective Studies. Survival Rate. Treatment Outcome

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  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
  • (PMID = 19653294.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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14. Ferri Niguez B, Martínez-Lage JF, Almagro MJ, Fuster JL, Serrano C, Torroba MA, Sola J: Embryonal tumor with abundant neuropil and true rosettes (ETANTR): a new distinctive variety of pediatric PNET: a case-based update. Childs Nerv Syst; 2010 Aug;26(8):1003-8
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  • [Title] Embryonal tumor with abundant neuropil and true rosettes (ETANTR): a new distinctive variety of pediatric PNET: a case-based update.
  • BACKGROUND: Embryonal central nervous system (CNS) tumors are currently classified into three types: medulloblastoma, atypical rhabdoid/teratoid tumors, and primitive neuroectodermal tumor (PNET).
  • A distinctive subtype of PNET called "embryonal tumor with abundant neuropil and true rosettes" (ETANTR) was reported in 2000.
  • It has been suggested that this neoplasm should be considered as a separate entity.
  • ETANTR is an eminently pediatric tumor that has been reported exclusively in children younger than 4 years.
  • ILLUSTRATIVE CASES: A 9-month-old girl underwent subtotal resection of a brainstem neoplasm.
  • A 23-month-old girl was submitted to surgery for a frontoparietal tumor.
  • Both children were treated with chemotherapy and one with radiotherapy.
  • CONCLUSIONS: By reporting these two new instances of ETANTR, we want to contribute to the knowledge of this highly malignant CNS embryonal neoplasm that occurs only in young children, given its present lethal prognosis, the scarcity of reported cases, and the lack of treatment guidelines.
  • [MeSH-major] Brain Neoplasms / pathology. Neuroectodermal Tumors, Primitive / pathology. Neuropil / pathology
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Fatal Outcome. Female. Humans. Infant. Neurosurgical Procedures. Radiotherapy

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  • [Cites] Am J Surg Pathol. 2009 Feb;33(2):211-7 [18987548.001]
  • [Cites] Acta Neuropathol. 2009 Apr;117(4):457-64 [19057917.001]
  • [Cites] J Neurooncol. 2007 Aug;84(1):91-8 [17332950.001]
  • [Cites] Brain Pathol. 2010 Jan;20(1):133-9 [19120373.001]
  • [Cites] Acta Neuropathol. 2007 Aug;114(2):97-109 [17618441.001]
  • [Cites] Pediatr Dev Pathol. 2000 Jul-Aug;3(4):346-52 [10890250.001]
  • [Cites] Brain Pathol. 2009 Apr;19(2):343-6 [19291003.001]
  • [Cites] Neuropathology. 2010 Feb 1;30(1):84-91 [19563506.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):978-86 [15758008.001]
  • [Cites] J Neurooncol. 2006 Jul;78(3):317-20 [16598427.001]
  • [Cites] Am J Clin Pathol. 2006 Aug;126(2):277-83 [16891204.001]
  • (PMID = 20499240.001).
  • [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] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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15. Partap S, Murphy PA, Vogel H, Barnes PD, Edwards MS, Fisher PG: Efficacy and tolerability of intrathecal liposomal cytarabine for central nervous system embryonal tumors. J Clin Oncol; 2009 May 20;27(15_suppl):2064

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  • [Title] Efficacy and tolerability of intrathecal liposomal cytarabine for central nervous system embryonal tumors.
  • : 2064 Background: Liposomal cytarabine (DepoCyt) is a sustained-release intrathecal (IT) preparation of cytarabine, formulated by encapsulating the drug in spherical aqueous chambers within a lipid matrix.
  • While proven effective in lymphomatous meningitis, this drug has shown some activity in medulloblastoma (MB) with spinal metastases in limited pediatric phase I study.
  • METHODS: We reviewed all patients at our institution treated with liposomal cytarabine for primary central nervous system (CNS) embryonal tumors-MB, primitive neuroectodermal tumor (PNET), and atypical teratoid rhabdoid tumor (ATRT).
  • RESULTS: A cohort of 17 patients were treated with liposomal cytarabine at diagnosis of CNS embryonal tumor (2 PNET, 3 ATRT) or relapse (12 MB [7 average-risk, 5 high-risk]); nine had leptomeningeal metastases.
  • Drug was dosed at 2 mg/kg up to 50, every 2 weeks to monthly, along with dexamethasone.
  • Concurrent systemic chemotherapy was given in 16 patients.
  • A total of 102 doses were administered (lumbar IT 76, Ommaya intraventricular 36) with a mean of six treatments (range 1-16).
  • All six evaluable patients with malignant cerebrospinal fluid (CSF) cytology and treated with at least two doses cleared their spinal fluid (mean 3 doses, range 1-5).
  • No patient developed malignant CSF cytology while receiving liposomal cytarabine.
  • Ten patients developed progressive disease and died, with only one later recurrence in the spinal fluid.
  • All patients with neoplastic meningitis cleared malignant cells from their spinal fluid after treatment with IT liposomal cytarabine and systemic chemotherapy.
  • Our findings warrant a phase II trial of liposomal cytarabine in newly diagnosed or recurrent CNS embryonal tumors.

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  • (PMID = 27964690.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Raco A, Raimondi AJ, D'Alonzo A, Esposito V, Valentino V: Radiosurgery in the management of pediatric brain tumors. Childs Nerv Syst; 2000 May;16(5):287-95
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  • [Title] Radiosurgery in the management of pediatric brain tumors.
  • A total of 114 patients with benign and malignant intracranial tumors were treated by Valentino at the Flaminia Radiosurgical Center using a Philips 6-MeV linear accelerator between 1987 and 1995.
  • The tumor locations break down as follows: 36 in the cerebral hemispheres, 14 in the region of the hypothalamus/optic chiasm, 21 in the III ventricle/pineal region, 3 in the basal ganglia, 27 in the posterior fossa, 13 in the brain stem.
  • Seventy-nine patients had multivariate/combined treatment consisting of surgery or biopsy followed by chemotherapy, radiotherapy and/or radiosurgery.
  • Thirty-five were not operated on or biopsied but were treated primarily by radiosurgery, which was associated with chemotherapy and conventional radiotherapy.
  • The short- and long-term results were evaluated separately for each pathology in an attempt to derive guidelines for future treatment.
  • For tumors of the pineal region, we are of the opinion that radiosurgery is the treatment of choice in children and that more than one-third of patients can be cured by this means.
  • The remaining patients require surgery and/or chemotherapy in addition.
  • For medulloblastomas radiosurgery may be useful to control local recurrence if coupled with chemotherapy.
  • We fear that limiting treatment to radiosurgery, rather than prescribing conventional radiotherapy when indicated, could permit CNS seeding.
  • In glial tumors radiosurgery helped either to "sterilize" the tumor bed after removal or to treat remnants of the lesions in critical areas; for diffuse brain stem gliomas it should be considered the treatment of choice.
  • [MeSH-major] Brain / surgery. Brain Neoplasms / pathology. Brain Neoplasms / surgery. Radiosurgery / methods
  • [MeSH-minor] Adolescent. Chemotherapy, Adjuvant. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Infant. Karnofsky Performance Status. Male. Neoplasm Recurrence, Local. Neoplasm Seeding. Neoplasm, Residual / surgery. Prognosis. Radiotherapy. Reoperation. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • (PMID = 10883372.001).
  • [ISSN] 0256-7040
  • [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
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17. Zimmerman MA, Goumnerova LC, Proctor M, Scott RM, Marcus K, Pomeroy SL, Turner CD, Chi SN, Chordas C, Kieran MW: Continuous remission of newly diagnosed and relapsed central nervous system atypical teratoid/rhabdoid tumor. J Neurooncol; 2005 Mar;72(1):77-84
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  • [Title] Continuous remission of newly diagnosed and relapsed central nervous system atypical teratoid/rhabdoid tumor.
  • Atypical teratoid/rhabdoid tumors (AT/RT) are highly malignant lesions of childhood that carry a very poor prognosis.
  • AT/RT can occur in the central nervous system (CNS AT/RT) and disease in this location carries an even worse prognosis with a median survival of 7 months.
  • In spite of multiple treatment regimens consisting of maximal surgical resection (including second look surgery), radiation therapy (focal and craniospinal), and multi-agent intravenous, oral and intrathecal chemotherapy, with or without high-dose therapy and stem cell rescue, only seven long-term survivors of CNS AT/RT have been reported, all in patients with newly diagnosed disease.
  • For this reason, many centers now direct such patients, particularly those under 5 years of age, or those with recurrent disease, towards comfort care rather than attempt curative therapy.
  • We now report on four children, two with newly diagnosed CNS AT/RT and two with progressive disease after multi-agent chemotherapy who are long term survivors (median follow-up of 37 months) using a combination of surgery, radiation therapy, and intensive chemotherapy.
  • The chemotherapy component was modified from the Intergroup Rhabdomyosarcoma Study Group (IRS III) parameningeal protocol as three of the seven reported survivors in the literature were treated using this type of therapy.
  • Our four patients, when added to the three reported survivors in the literature using this approach, suggest that patients provided this aggressive therapy can significantly alter the course of their disease.
  • More importantly, we report on the first two survivors after relapse with multi-agent intravenous and intrathecal chemotherapy treated with this modified regimen.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / therapy. Neoplasm Recurrence, Local / therapy. Rhabdoid Tumor / therapy. Teratoma / therapy
  • [MeSH-minor] Chemotherapy, Adjuvant / methods. Child. Child, Preschool. Female. Humans. Infant. Male. Radiotherapy, Adjuvant / methods. Remission Induction. Survival Analysis

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  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1988;412(4):393-7 [3125680.001]
  • [Cites] Childs Nerv Syst. 1993 Jun;9(3):185-90; discussion 190 [8397069.001]
  • [Cites] J Neurooncol. 2001 Mar;52(1):49-56 [11451202.001]
  • [Cites] J Neurooncol. 2003 Jan;61(2):121-6 [12622450.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Jul 15;41(5):1013-9 [9719110.001]
  • [Cites] Genes Chromosomes Cancer. 2000 May;28(1):31-7 [10738300.001]
  • [Cites] Arch Ophthalmol. 1967 Dec;78(6):709-13 [4294312.001]
  • [Cites] Surg Neurol. 1992 May;37(5):410-4 [1631771.001]
  • [Cites] Cancer. 1981 Jan 1;47(1):37-40 [7459813.001]
  • [Cites] J Neurooncol. 1995;24(1):21-8 [8523069.001]
  • [Cites] Childs Nerv Syst. 1997 Jul;13(7):418-21 [9298280.001]
  • [Cites] Surv Ophthalmol. 1994 Jan-Feb;38(4):365-70 [8160109.001]
  • [Cites] Neuroradiology. 2000 May;42(5):363-7 [10872158.001]
  • [Cites] Semin Diagn Pathol. 1986 May;3(2):151-63 [3616219.001]
  • [Cites] J Neurooncol. 1999 May;43(1):63-70 [10448873.001]
  • [Cites] Med Pediatr Oncol. 1991;19(4):310-7 [2056976.001]
  • [Cites] J Neurosurg. 1990 Nov;73(5):710-4 [2213160.001]
  • [Cites] Zhonghua Min Guo Xiao Er Ke Yi Xue Hui Za Zhi. 1989 Sep-Oct;30(5):316-22 [2484056.001]
  • [Cites] Acta Neuropathol. 1992;83(4):445-8 [1575023.001]
  • [Cites] J Neurooncol. 2000 May;48(1):41-5 [11026695.001]
  • [Cites] Can J Neurol Sci. 1994 Aug;21(3):273-7 [8000986.001]
  • [Cites] AJNR Am J Neuroradiol. 1993 Jan-Feb;14 (1):107-15 [8427070.001]
  • [Cites] J Pediatr Hematol Oncol. 2002 Jun-Jul;24(5):337-42 [12142780.001]
  • [Cites] Surg Neurol. 1993 Nov;40(5):429-34 [8211663.001]
  • [Cites] Neuropathol Appl Neurobiol. 2003 Jun;29(3):254-61 [12787322.001]
  • [Cites] J Neurooncol. 1998 Dec;40(3):265-75 [10066100.001]
  • [Cites] J Neurooncol. 1995;25(3):193-203 [8592169.001]
  • [Cites] AJNR Am J Neuroradiol. 1995 Sep;16(8):1727-8 [7502982.001]
  • [Cites] Pediatr Neurol. 1995 Jul;13(1):65-8 [7575853.001]
  • [Cites] Acta Neuropathol. 1996;91(6):578-86 [8781656.001]
  • [Cites] J Korean Med Sci. 2002 Oct;17(5):723-6 [12378033.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1993;422(1):81-5 [7679853.001]
  • [Cites] J Neurooncol. 2003 Feb;61(3):219-25 [12675315.001]
  • [Cites] Pediatr Radiol. 2003 Apr;33(4):275-7 [12709762.001]
  • [Cites] J Neurosurg. 1996 Jul;85(1):56-65 [8683283.001]
  • [Cites] Med Pediatr Oncol. 1999 May;32(5):389-91 [10219345.001]
  • [Cites] Cancer. 1991 Apr 15;67(8):2058-61 [2004323.001]
  • [Cites] Pediatr Neurosurg. 1995;22(4):214-22 [7619723.001]
  • [Cites] Ultrastruct Pathol. 1994 Jan-Apr;18(1-2):23-8 [8191632.001]
  • [Cites] J Neurooncol. 2001 Aug;54(1):53-6 [11763423.001]
  • [Cites] Neurology. 1991 Nov;41(11):1847-8 [1944923.001]
  • [Cites] Clin Neuropathol. 1991 Jan-Feb;10(1):1-10 [2015720.001]
  • [Cites] Childs Nerv Syst. 1987;3(6):379-81 [3450389.001]
  • [Cites] J Pediatr Hematol Oncol. 1995 Feb;17(1):71-5 [7743242.001]
  • [Cites] J Comput Assist Tomogr. 1990 May-Jun;14 (3):461-3 [2335617.001]
  • [Cites] Pediatr Neurosurg. 1994;21(4):232-6 [7865408.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Dec 5;97(25):13796-800 [11095756.001]
  • [Cites] Pediatr Pathol. 1989;9(3):307-19 [2546137.001]
  • [Cites] Childs Nerv Syst. 2003 Apr;19(4):244-8 [12682757.001]
  • [Cites] Hum Pathol. 1987 Apr;18(4):332-7 [3030922.001]
  • [Cites] Am J Surg Pathol. 1998 Sep;22(9):1083-92 [9737241.001]
  • [Cites] Postgrad Med J. 1998 Jun;74(872):369-70 [9799897.001]
  • [Cites] Childs Nerv Syst. 2000 Apr;16(4):228-34 [10855521.001]
  • [Cites] Med Pediatr Oncol. 1992;20(3):258 [1637409.001]
  • (PMID = 15803379.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 37
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18. 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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  • [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.
  • 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)].
  • Growth delays ranged from 7.6 days with D-245 MG to 62.1 days with D-456 MG (P < 0.001).
  • 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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19. 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.
  • Astrocytomas represent 35% of all CNS tumors in children.
  • 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.
  • Neoadjuvant chemotherapy has proven good results in the treatment of other solid tumors.
  • 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.
  • We evaluated 11 children with AA or GM who had received no prior treatment.
  • A magnetic resonance image (MRI) study of the tumor was made after surgery to evaluate residual tumor and routine laboratory analysis.
  • Chemotherapy with carboplatin, ifosfamide and etoposide was given every 3 weeks for four courses.
  • Each patient then received hyperfractionated radiotherapy and a final MRI was done at the end of the treatment.
  • Supratentorial and infratentorial tumors had a good response to chemotherapy.
  • Brainstem tumors had an initial response after two courses and then increased in size.
  • 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.
  • Brainstem responded poorly to treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Cranial Irradiation. Glioblastoma / drug therapy. Premedication. Radiotherapy, Adjuvant
  • [MeSH-minor] Adolescent. Carboplatin / administration & dosage. Child. Child, Preschool. Combined Modality Therapy. Disease-Free Survival. Etoposide / administration & dosage. Female. Humans. Ifosfamide / administration & dosage. Life Tables. Male. Mesna / administration & dosage. Prospective Studies. Survival Analysis. Survival Rate. Treatment Outcome

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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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20. Lassaletta A, Lopez-Ibor B, Mateos E, Gonzalez-Vicent M, Perez-Martinez A, Sevilla J, Diaz MA, Madero L: Intrathecal liposomal cytarabine in children under 4 years with malignant brain tumors. J Neurooncol; 2009 Oct;95(1):65-69
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  • [Title] Intrathecal liposomal cytarabine in children under 4 years with malignant brain tumors.
  • Infants and very young children with malignant brain tumors usually have unfavourable locations and are not candidates for craniospinal irradiation.
  • New therapeutic approaches must be attempted to improve poor survival rates.
  • The primary goal of the present study was to report on the safety profile and toxicity of intrathecal administration of liposomal cytarabine in children <4 years with malignant brain tumors.
  • The diagnoses were ependymoma (3), peripheral neuroectodermic tumor (PNET) (2), meduloblastoma, atypical teratoid rhabdoid tumor (ATRT), cerebral lymphoma, and rhabdomyosarcoma with CNS invasion.
  • Eight of the patients (89%) experienced an initial improvement of clinical symptoms after initiation treatment, confirmed by MRI.
  • This study demonstrates the feasibility of using intrathecal liposomal cytarabine in children under 4 years of age with malignant brain tumors.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Brain Neoplasms / drug therapy. Cytarabine / therapeutic use. Phospholipids / administration & dosage

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  • [Cites] J Pediatr Hematol Oncol. 2007 Apr;29(4):222-6 [17414563.001]
  • [Cites] Leuk Lymphoma. 2008 Aug;49(8):1427-30 [18766957.001]
  • [Cites] Leuk Lymphoma. 2008 Aug;49(8):1553-9 [18766969.001]
  • [Cites] J Clin Oncol. 2004 Oct 1;22(19):3916-21 [15459213.001]
  • [Cites] Br J Haematol. 2007 Sep;138(6):812-3 [17655727.001]
  • [Cites] Leuk Lymphoma. 2007 Sep;48(9):1849-51 [17786723.001]
  • [Cites] J Neurooncol. 2005 Dec;75(3):287-99 [16195801.001]
  • [Cites] Haematologica. 2006 Mar;91(3):ECR02 [16533729.001]
  • [Cites] J Neurooncol. 2002 May;57(3):231-9 [12125986.001]
  • [Cites] Int J Hematol. 2007 Jul;86(1):33-6 [17675264.001]
  • [Cites] Ann Pharmacother. 2000 Oct;34(10):1173-8 [11054987.001]
  • [Cites] J Clin Oncol. 2004 Aug 1;22(15):3156-62 [15284268.001]
  • [Cites] J Clin Oncol. 1999 Oct;17(10):3110-6 [10506606.001]
  • [Cites] Ann Hematol. 2008 Nov;87(11):887-90 [18575860.001]
  • [Cites] Ann Hematol. 2008 Dec;87(12):1009-12 [18704421.001]
  • [Cites] Leuk Lymphoma. 2007 Sep;48(9):1672-3 [17786701.001]
  • [Cites] Clin Cancer Res. 1999 Nov;5(11):3394-402 [10589750.001]
  • [Cites] J Neurooncol. 2007 Jul;83(3):303-6 [17245619.001]
  • [Cites] N Engl J Med. 1993 Jun 17;328(24):1725-31 [8388548.001]
  • [Cites] Expert Opin Pharmacother. 2008 Feb;9(2):301-9 [18201152.001]
  • [Cites] Clin Transl Oncol. 2005 Jul;7(6):232-8 [16131445.001]
  • (PMID = 19381444.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Phospholipids; 0 / liposom; 04079A1RDZ / Cytarabine
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21. Makuria AT, Rushing EJ, McGrail KM, Hartmann DP, Azumi N, Ozdemirli M: Atypical teratoid rhabdoid tumor (AT/RT) in adults: review of four cases. J Neurooncol; 2008 Jul;88(3):321-30
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  • [Title] Atypical teratoid rhabdoid tumor (AT/RT) in adults: review of four cases.
  • Atypical teratoid/rhabdoid (AT/RT) tumor is a rare, highly malignant tumor of the central nervous system (CNS) most commonly found in children less than 5 years of age.
  • Since its histological appearance can be confused with other tumors, especially in adults, separating AT/RT from other neoplasms may be difficult.
  • Radiographically, two tumors were localized in the right fronto-parietal region, one was frontal and the other was found in the left temporal lobe.
  • Immunohistochemical staining showed that the tumor cells were positive for vimentin and reacted variably for keratin, epithelial membrane antigen (EMA), synaptophysin, neurofilament protein, CD34, and smooth muscle actin (SMA).
  • In adult examples of AT/RT, the diagnosis requires a high index of suspicion, with early tissue diagnosis and a low threshold for investigation with INI1 immunohistochemistry to differentiate this entity from other morphologically similar tumors.
  • Although the prognosis is dismal in pediatric population, long term survival is possible in adult AT/RT cases after surgery and adjuvant radiotherapy and chemotherapy.
  • [MeSH-major] Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Rhabdoid Tumor / metabolism. Rhabdoid Tumor / pathology

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  • [Cites] Hum Pathol. 1981 Jul;12(7):646-57 [7275104.001]
  • [Cites] Semin Cell Dev Biol. 1999 Apr;10 (2):189-95 [10441072.001]
  • [Cites] J Neurooncol. 2001 Mar;52(1):49-56 [11451202.001]
  • [Cites] J Neurooncol. 2003 Jan;61(2):121-6 [12622450.001]
  • [Cites] Mod Pathol. 2005 Jul;18(7):951-8 [15761491.001]
  • [Cites] Genes Dev. 1998 Aug 1;12(15):2278-92 [9694794.001]
  • [Cites] Am J Surg Pathol. 1993 Jul;17(7):729-37 [8391222.001]
  • [Cites] J Clin Oncol. 2004 Jul 15;22(14):2877-84 [15254056.001]
  • [Cites] Neuro Oncol. 2006 Jan;8(1):79-82 [16443951.001]
  • [Cites] Can J Neurol Sci. 1996 Nov;23(4):257-63 [8951203.001]
  • [Cites] Neuroradiology. 2000 May;42(5):363-7 [10872158.001]
  • [Cites] Pathol Int. 1999 Dec;49(12):1114-8 [10632935.001]
  • [Cites] Clin Cancer Res. 2002 Nov;8(11):3461-7 [12429635.001]
  • [Cites] Acta Neuropathol. 1992;83(4):445-8 [1575023.001]
  • [Cites] J Neurooncol. 2005 Sep;74(3):311-9 [16132523.001]
  • [Cites] J Pediatr Hematol Oncol. 2002 Jun-Jul;24(5):337-42 [12142780.001]
  • [Cites] Am J Surg Pathol. 1994 Oct;18(10):1010-29 [8092393.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Oct 26;96(22):12311-5 [10535918.001]
  • [Cites] Cancer Res. 2000 Nov 1;60(21):6171-7 [11085541.001]
  • [Cites] Med Pediatr Oncol. 1997 Mar;28(3):223-7 [9024522.001]
  • [Cites] Brain Pathol. 2005 Jan;15(1):23-8 [15779233.001]
  • [Cites] J Neurosurg. 1996 Jul;85(1):56-65 [8683283.001]
  • [Cites] Acta Neurochir (Wien). 2004 Sep;146(9):1033-8; discussion 1038 [15340816.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1999 Aug 1;45(1):247 [10477033.001]
  • [Cites] Neuropathology. 2002 Dec;22(4):252-60 [12564764.001]
  • [Cites] Am J Surg Pathol. 2004 May;28(5):644-50 [15105654.001]
  • [Cites] Pediatr Radiol. 2006 Feb;36(2):126-32 [16341528.001]
  • [Cites] Cancer Res. 2002 Jan 1;62(1):323-8 [11782395.001]
  • [Cites] Cancer. 1978 May;41(5):1937-48 [206343.001]
  • [Cites] Hum Pathol. 2001 Feb;32(2):156-62 [11230702.001]
  • [Cites] Cancer Res. 2004 May 15;64(10 ):3406-13 [15150092.001]
  • [Cites] Neuropathology. 2006 Feb;26(1):57-61 [16521480.001]
  • [Cites] J Neurooncol. 2007 Aug;84(1):49-55 [17377740.001]
  • [Cites] Cancer Res. 1999 Jan 1;59(1):74-9 [9892189.001]
  • [Cites] Neurol India. 2003 Jun;51(2):273-4 [14571026.001]
  • [Cites] Ultrastruct Pathol. 1997 Jul-Aug;21(4):361-8 [9206001.001]
  • [Cites] Science. 1994 Dec 23;266(5193):2002-6 [7801128.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jul 5;97(14):7748-53 [10884406.001]
  • [Cites] Mol Cell. 1999 Feb;3(2):247-53 [10078207.001]
  • (PMID = 18369529.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / DNA-Binding Proteins; 0 / SMARCB1 Protein; 0 / SMARCB1 protein, human; 0 / Transcription Factors
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22. Sklar CA: Childhood brain tumors. J Pediatr Endocrinol Metab; 2002 May;15 Suppl 2:669-73
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  • [Title] Childhood brain tumors.
  • Primary malignant tumors of the central nervous system (CNS) account for about 16% of all childhood malignancies.
  • These tumors are the second most common type of childhood cancer and the most frequent of the solid tumors.
  • CNS tumors are diverse, representing many histological types and arising in a variety of anatomic sites.
  • The most common malignant tumors include astrocytomas (52%), medulloblastomas/primitive neuroectodermal tumors (PNETs) (21%), gliomas (19%), and ependymomas (9%).
  • The current 5-year survival rate for all pediatric CNS tumors is 67%, but rates differ considerably among tumor types.
  • Treatment modalities also differ according to histological type.
  • Currently, about 25% of patients are treated with surgery alone, 40% undergo surgery plus radiation, and 30% are treated with surgery, radiation, and chemotherapy.
  • Survivors of childhood brain tumors are at substantial risk for increased morbidity and late mortality.
  • Five-year survivors of brain tumors are 13 times more likely to die than healthy age- and sex-matched peers.
  • Neurological, neurocognitive, and endocrine disturbances are the most prevalent disabilities observed among long-term survivors of pediatric brain tumors.
  • [MeSH-major] Brain Neoplasms / epidemiology
  • [MeSH-minor] Child. Humans. Hypothalamus / pathology. Pituitary Neoplasms / pathology. Treatment Outcome

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  • (PMID = 12092679.001).
  • [ISSN] 0334-018X
  • [Journal-full-title] Journal of pediatric endocrinology & metabolism : JPEM
  • [ISO-abbreviation] J. Pediatr. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 20
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23. Gardner SL: Application of stem cell transplant for brain tumors. Pediatr Transplant; 2004 Jun;8 Suppl 5:28-32
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  • [Title] Application of stem cell transplant for brain tumors.
  • Brain tumors are the second most common malignancy in children and the most common solid tumor.
  • The majority of children are treated with surgery alone or in combination with radiation and/or chemotherapy.
  • Recently investigators have used high dose chemotherapy with autologous stem cell rescue (ASCR) in patients with malignant brain tumors.
  • This approach has been most successful in chemosensitive tumors including medulloblastoma, supratentorial primitive neuroectodermal tumors (SPNET) and central nervous system germ cell tumors (CNS GCT).
  • In addition, the use of high dose chemotherapy has enabled the reduction and in many cases elimination of radiation therapy to very young children.
  • To date there have been no prospective randomized studies comparing high dose chemotherapy and ASCR with conventional therapy.
  • Radiation therapy is often not an option for patients with recurrent disease and conventional dose chemotherapy rarely if ever results in long-term survival.
  • Unfortunately, the majority of studies using conventional therapy in order to delay irradiation in young children newly diagnosed with malignant brain tumors have been unsuccessful.
  • Although the numbers are small, preliminary data suggest that not only is survival but also quality of life is superior with the use of high dose chemotherapy.
  • In addition, through the use of peripheral blood stem cells and improvements in supportive care, multiple courses of high dose chemotherapy can be administered.
  • High dose chemotherapy with ASCR is a foundation upon which many different types of therapies can be built.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / therapy. Hematopoietic Stem Cell Transplantation
  • [MeSH-minor] Combined Modality Therapy. Humans. Pediatrics

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  • (PMID = 15125703.001).
  • [ISSN] 1397-3142
  • [Journal-full-title] Pediatric transplantation
  • [ISO-abbreviation] Pediatr Transplant
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
  • [Number-of-references] 25
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24. Göbel U, Calaminus G, Schneider DT, Schmidt P, Haas RJ, MAKEI and MAHO Study Groups of the German Society of Pediatric Oncology and Hematology, and the SIOP CNS GCT Study Group: Management of germ cell tumors in children: approaches to cure. Onkologie; 2002 Feb;25(1):14-22
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  • [Title] Management of germ cell tumors in children: approaches to cure.
  • The introduction of cisplatinum chemotherapy and current advances in the surgical treatment have resulted in a dramatic improvement of the prognosis of children with malignant germ cell tumors (GCT).
  • Cisplatinum chemotherapy generally results in sufficient systemic tumor control, but local relapses may still occur in patients who did not receive adequate local treatment.
  • Therefore, the therapeutic consideration must take into account age, primary site of the tumor, and its histology.
  • In gonadal tumors, there is a high chance of primary complete resection since these tumors tend to be encapsulated, and particularly testicular GCT are often detected at a low tumor stage.
  • In contrast, a primary complete resection may be impossible in large nongonadal tumors such as sacrococcygeal or mediastinal GCT.
  • In these tumors, a neoadjuvant or preoperative chemotherapy after clinical diagnosis by imaging and evaluation of tumor markers significantly facilitates complete resection on delayed surgery.
  • In addition, the impact of chemotherapy on local tumor control may be enhanced by locoregional hyperthermia.
  • Nevertheless, biopsy is essential for diagnosis in nonsecreting tumors.
  • In intracranial GCT, radiotherapy significantly contributes to local tumor control, and doses are stratified according to histology.
  • These general considerations have been integrated into national and international cooperative treatment protocols.
  • In most current protocols, treatment is stratified according to an initial risk assessment that includes the parameters age, site, histology, stage, completeness of resection and the tumor markers alpha(1)-fetoprotein (AFP) and human choriogonadotropin (beta-HCG).
  • Moreover, the previously high-risk groups may now expect a favorable prognosis with this risk-adapted treatment, whereas an increasing number of low-risk patients are treated expectantly or with significantly reduced chemotherapy.
  • As current biologic studies reveal distinct genetic patterns in childhood GCT, it can be expected that further combined clinical and genetic studies will be valuable for risk assessment of childhood GCT.
  • [MeSH-major] Neoplasms, Germ Cell and Embryonal / therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Chorionic Gonadotropin, beta Subunit, Human / blood. Cisplatin / administration & dosage. Cisplatin / adverse effects. Combined Modality Therapy. Female. Humans. Infant. Infant, Newborn. Male. Neoadjuvant Therapy. Neoplasm Staging. Prognosis. alpha-Fetoproteins / metabolism

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  • [Copyright] Copyright 2002 S. Karger GmbH, Freiburg
  • (PMID = 11893878.001).
  • [ISSN] 0378-584X
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / alpha-Fetoproteins; Q20Q21Q62J / Cisplatin
  • [Number-of-references] 66
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25. Mulne AF, Ducore JM, Elterman RD, Friedman HS, Krischer JP, Kun LE, Shuster JJ, Kadota RP: Oral methotrexate for recurrent brain tumors in children: a Pediatric Oncology Group study. J Pediatr Hematol Oncol; 2000 Jan-Feb;22(1):41-4
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  • [Title] Oral methotrexate for recurrent brain tumors in children: a Pediatric Oncology Group study.
  • PURPOSE: Children with recurrent or progressive central nervous system (CNS) tumors have an unfavorable prognosis.
  • Based on Pediatric Oncology Group (POG) institutional pilot data, low-dose oral methotrexate (MTX) was studied.
  • Patients in six different brain tumor strata were accrued.
  • RESULTS: The response rates (complete or partial responses) were as follows: astrocytoma 2 of 10, malignant glioma 1 of 19, medulloblastoma 0 of 18, brainstem tumor 0 of 12, ependymoma 1 of 7, and miscellaneous histologic types 0 of 12.
  • CONCLUSION: Low-dose oral MTX showed no significant activity against malignant glioma, medulloblastoma, brainstem tumors, and miscellaneous histologic types.
  • This regimen will not be recommended for front-line therapy.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Brain Neoplasms / drug therapy. Methotrexate / therapeutic use. Neoplasm Recurrence, Local / drug therapy

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  • (PMID = 10695820.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-03161; United States / NCI NIH HHS / CA / CA-29691; United States / NCI NIH HHS / CA / CA-69177; etc
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate
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26. Kantar M, Cetingül N, Kansoy S, Anacak Y, Demirtaş E, Erşahin Y, Mutluer S: Radiotherapy-induced secondary cranial neoplasms in children. Childs Nerv Syst; 2004 Jan;20(1):46-9
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  • [Title] Radiotherapy-induced secondary cranial neoplasms in children.
  • BACKGROUND: Secondary malignant neoplasms (SMN) in CNS tumor survivors has become problem of increasing concern over the last 20 years.
  • These tumors usually occur in a different site from the primary brain tumor several years after treatment.
  • CASE REPORT: We report secondary cranial malignant neoplasms in three patients who were treated with irradiation and chemotherapy for their primary brain tumors.
  • The first case is a male survivor of an orbital rhabdomyosarcoma who developed a meningioma 8 years later.
  • The other two cases are female survivors of ependymomas who were irradiated at the age of 3 and developed secondary gliomas 8 and 17 years after therapy respectively.
  • CONCLUSION: Patients carry a risk of developing SMNs many years later since irradiation is still an important part of the treatment.

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  • [Cites] Pediatr Radiol. 2001 Sep;31(9):607-9 [11511997.001]
  • [Cites] J Neurosurg Sci. 1989 Jul-Sep;33(3):271-9 [2693630.001]
  • [Cites] Cancer. 1987 Apr 15;59(8):1506-8 [3545441.001]
  • [Cites] Med Pediatr Oncol Suppl. 1996;1:29-34 [8643045.001]
  • [Cites] Cancer. 1993 Jun 15;71(12):4091-5 [8508374.001]
  • [Cites] J Clin Oncol. 1993 Feb;11(2):262-70 [8426203.001]
  • [Cites] J Neurosurg. 2002 Nov;97(5):1078-82 [12450029.001]
  • [Cites] Acta Neurochir (Wien). 1998;140(8):763-70 [9810442.001]
  • [Cites] Acta Paediatr Scand. 1991 Dec;80(12):1220-8 [1785295.001]
  • [Cites] Neoplasma. 2001;48(6):442-4 [11949834.001]
  • [Cites] Ophthal Plast Reconstr Surg. 2001 Sep;17(5):362-8 [11642493.001]
  • [Cites] J Neurosurg. 1993 Jul;79(1):28-31 [8315464.001]
  • [Cites] N Engl J Med. 1991 Nov 7;325(19):1330-6 [1922234.001]
  • [Cites] J Neurosurg. 1989 Jul;71(1):77-82 [2661743.001]
  • (PMID = 14714135.001).
  • [ISSN] 0256-7040
  • [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] Case Reports; Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Antinuclear; 0 / Antibodies, Monoclonal; 0 / Desmin; 0 / Glial Fibrillary Acidic Protein; 0 / Ki-67 Antigen; 0 / MIB-1 antibody; 0 / S100 Proteins
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27. Pollack IF, Okada H, Chambers WH: Exploitation of immune mechanisms in the treatment of central nervous system cancer. Semin Pediatr Neurol; 2000 Jun;7(2):131-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Exploitation of immune mechanisms in the treatment of central nervous system cancer.
  • Malignant gliomas are among the most common intrinsic brain tumors of both children and adults, and, because of unique aspects of their biology and anatomic site, they are the most refractory to conventional therapeutic strategies involving surgery, radiotherapy, or chemotherapy.
  • Given the failure of standard therapies to improve the outlook of affected patients, significant attention has been focused on development of alternative treatments, particularly immunotherapy.
  • Attempts have been made to treat gliomas using a variety of immunologically based strategies, including passive immunization, adoptive cellular immunotherapy, local and systemic delivery of biological response modifiers, and vaccination with tumor cells.
  • Although preclinical modeling of these therapies provided an impetus for translation of their results into clinical protocols, these therapies have failed to yield consistently promising results in initial trials.
  • However, significant insights into the immunobiology of the central nervous system (CNS) and gliomas have been gained from these studies, and have established that a number of immunobiological features of the brain and of gliomas themselves may be critical determinants in regulating efficacious treatment of these tumors.
  • (1) the presence of a blood-brain barrier that, although partially disrupted by the tumor, functions to exclude elements of the immune system from the tumor or brain parenchyma;.
  • (2) a lack of organized secondary lymphatic tissues supporting efficient immune responses locally in the CNS;.
  • (3) low levels of expression of major histocompatibility complex proteins in the CNS;.
  • (4) an apparent paucity of the most efficient antigen-presenting cells; and (5) glioma-derived immunosuppressive factors, such as transforming growth factor-beta, that interfere with the induction of local as well as systemic immune responses to the tumor.
  • Recognition of these factors, and an appreciation of the underlying need for and validity of developing immunologically based therapies for gliomas, supports continued development of novel immunotherapeutic approaches, particularly those attempting to enhance the immunogenicity of glioma cells.
  • [MeSH-major] Central Nervous System Neoplasms / immunology. Central Nervous System Neoplasms / therapy. Glioma / immunology. Glioma / therapy
  • [MeSH-minor] Adult. Child. Child, Preschool. Combined Modality Therapy. Cytokines / immunology. Humans. Immunotherapy / methods. T-Lymphocytes / immunology. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 10914414.001).
  • [ISSN] 1071-9091
  • [Journal-full-title] Seminars in pediatric neurology
  • [ISO-abbreviation] Semin Pediatr Neurol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA65880; United States / NINDS NIH HHS / NS / NS01810; United States / NINDS NIH HHS / NS / NS37704
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Cytokines; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 123
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28. Schiavetti A, Clerico A, De Pasquale MD, Bernardini L, Moleti ML: Medulloblastoma as a secondary malignancy after radiotherapy-free treatment for acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2003 Jul;25(7):562-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Medulloblastoma as a secondary malignancy after radiotherapy-free treatment for acute lymphoblastic leukemia.
  • Malignant brain tumors have been reported to occur in survivors of childhood acute lymphoblastic leukemia (ALL) more frequently than in the noncancer control population.
  • The strongest risk factor seems to be cranial radiotherapy, used as central nervous system (CNS) prophylaxis.
  • We report the case of a 9-year-old girl affected with metastatic medulloblastoma that developed 6 years after a diagnosis of acute lymphoblastic leukemia.
  • CNS prophylaxis for ALL consisted of intrathecal methotrexate plus cytarabine (20 administrations) and 4 courses of high-dose methotrexate (5g/m2).
  • The child, in first complete remission, was well until the occurrence of a second tumor.
  • She was treated for medulloblastoma with craniospinal radiotherapy and chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cerebellar Neoplasms / radiotherapy. Medulloblastoma / radiotherapy. Neoplasms, Second Primary / radiotherapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Child. Child, Preschool. Combined Modality Therapy. Female. Humans. Time Factors. Treatment Outcome

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  • (PMID = 12847325.001).
  • [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
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29. Spiller SE, Ravanpay AC, Hahn AW, Olson JM: Suberoylanilide hydroxamic acid is effective in preclinical studies of medulloblastoma. J Neurooncol; 2006 Sep;79(3):259-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, little information has been reported on the effects of SAHA on central nervous system (CNS) tumors including medulloblastoma, the most common malignant brain tumor in children.
  • EXPERIMENTAL DESIGN AND RESULTS: Tissue culture studies were performed treating primary human fibroblasts, established medulloblastoma cell lines, and primary human medulloblastoma tumors with SAHA.
  • In athymic mice with medulloblastoma xenograft tumors, oral SAHA resulted in apoptosis of tumor tissue and significantly slowed tumor growth.
  • In the ND2:Smo transgenic mouse medulloblastoma model, SAHA treatment caused significant apoptosis in these cerebellar tumors.
  • CONCLUSIONS: SAHA effectively induces cell death in established medulloblastoma cell lines, human patient primary tumor cultures, medulloblastoma xenografts and intracranial spontaneous medulloblastomas.
  • These findings support the advancement of SAHA to pediatric clinical trials.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cerebellar Neoplasms / drug therapy. Hydroxamic Acids / pharmacology. Medulloblastoma / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cells, Cultured. Child. Fibroblasts / drug effects. Humans. In Situ Nick-End Labeling. Mice. Mice, Nude. Neoplasm Transplantation. Neoplasms, Experimental / drug therapy

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  • [Cites] Clin Cancer Res. 2003 Sep 1;9(10 Pt 1):3578-88 [14506144.001]
  • [Cites] Cancer Cell. 2004 May;5(5):455-63 [15144953.001]
  • [Cites] Anticancer Res. 1999 Nov-Dec;19(6B):4999-5005 [10697502.001]
  • [Cites] FEBS Lett. 2003 Nov 20;554(3):347-50 [14623092.001]
  • [Cites] Cancer Lett. 2002 Dec 15;188(1-2):127-40 [12406558.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 29;97(18):10014-9 [10954755.001]
  • [Cites] Nat Med. 2003 Aug;9(8):1033-8 [12872164.001]
  • [Cites] J Biol Chem. 1979 Mar 10;254(5):1716-23 [762168.001]
  • [Cites] J Clin Oncol. 2006 Jan 1;24(1):166-73 [16330674.001]
  • [Cites] Eur Urol. 2004 Mar;45(3):382-9; author reply 389 [15036687.001]
  • [Cites] Cancer. 2002 Jan 15;94(2):552-60 [11900240.001]
  • [Cites] Lancet Oncol. 2004 Jul;5(7):399-408 [15231246.001]
  • [Cites] Science. 2002 Aug 30;297(5586):1559-61 [12202832.001]
  • [Cites] J Clin Oncol. 1999 Jul;17(7):2127-36 [10561268.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 3;101(5):1241-6 [14734806.001]
  • [Cites] Neurosci Lett. 2005 Jun 10-17;381(1-2):69-73 [15882792.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 18;100(4):2041-6 [12576549.001]
  • [Cites] Cancer. 2003 Aug 15;98(4):841-53 [12910530.001]
  • [Cites] Mol Cancer Ther. 2002 Apr;1(6):385-92 [12477051.001]
  • [Cites] Lancet Oncol. 2004 Apr;5(4):209-18 [15050952.001]
  • [Cites] Oncogene. 1998 Apr 30;16(17):2283-5 [9619837.001]
  • [Cites] Prostate. 2004 May 1;59(2):177-89 [15042618.001]
  • [Cites] J Natl Cancer Inst. 2000 Aug 2;92(15):1210-6 [10922406.001]
  • [Cites] J Cell Sci. 2004 Sep 1;117(Pt 19):4481-94 [15316072.001]
  • [Cites] J Neurochem. 2005 May;93(4):992-9 [15857402.001]
  • [Cites] Cancer Res. 2004 Nov 1;64(21):7794-800 [15520185.001]
  • (PMID = 16645722.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA112350-01
  • [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 / Hydroxamic Acids; 58IFB293JI / vorinostat
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30. Rice SC, Vacek PM, Homans AH, Kendall H, Rivers J, Messier T, Finette BA: Comparative analysis of HPRT mutant frequency in children with cancer. Environ Mol Mutagen; 2003;42(1):44-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Yet there is a paucity of data on the relationship between gene-environment interactions and the mechanisms associated with the somatic mutational events involved with malignant transformation, especially in children.
  • To gain insight into somatic mutational mechanisms in children who develop cancer, we determined the background mutant frequency (Mf) in the hypoxanthine phosphoribosyl transferase (HPRT) reporter gene of peripheral blood lymphocytes from pediatric cancer patients at the time of diagnosis and prior to therapeutic intervention.
  • We studied 23 children with hematologic malignancies and 31 children with solid tumors prior to initial therapeutic intervention.
  • Children with solid tumors, specifically sarcomas, and Hodgkin's disease were significantly older and had elevated HPRT Mfs (6.1 x 10(-6) and 3.7 x 10(-6), respectively) at the time of diagnosis, compared to normal controls (2.3 x 10(-6)) and other pediatric tumor groups including children with acute lymphocytic leukemia and non-Hodgkin's lymphoma (ALL/NHL, 1.7 x 10(-6)), central nervous system tumors (CNS, 3.6 x 10(-6)), and neuroblastoma (1.9 x 10(-6)).
  • In addition, these data demonstrate the importance of correcting for the effect of age when comparing the frequency of somatic mutations in children and should provide baseline data for future longitudinal biomonitoring studies on the genetic effects of chemotherapy in children treated for cancer.
  • [MeSH-major] Hypoxanthine Phosphoribosyltransferase / genetics. Mutation. Neoplasms / genetics

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  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • (PMID = 12874812.001).
  • [ISSN] 0893-6692
  • [Journal-full-title] Environmental and molecular mutagenesis
  • [ISO-abbreviation] Environ. Mol. Mutagen.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / 1F32ES058701ZRG4; United States / NCI NIH HHS / CA / 1K01CA77737; United States / NICHD NIH HHS / HD / 1K11HD01010; United States / NICHD NIH HHS / HD / 1R29HD35309-01A1
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; EC 2.4.2.8 / Hypoxanthine Phosphoribosyltransferase
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31. Tamburrini G, Colosimo C Jr, Giangaspero F, Riccardi R, Di Rocco C: Desmoplastic infantile ganglioglioma. Childs Nerv Syst; 2003 Jun;19(5-6):292-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Desmoplastic infantile gangliogliomas are rare intracranial tumors that mostly occur in the first 2 years of life.
  • Histologically they are characterized by a divergent astrocytic and ganglionic differentiation and a prominent desmoplastic stroma; more primitive cells may be observed, which present a higher number of mitoses and these areas can mimic the features of malignant astrocytomas.
  • Surgery is the treatment of choice.
  • Data available from the literature suggest that no complimentary treatment is needed in cases of complete tumor resection.
  • Chemotherapy is an option in infants with infiltration of eloquent CNS structures and progressive disease after surgery.
  • DIGs have generally a good prognosis: recurrence-free intervals of up to 14 years have been reported and spontaneous disappearance of tumor residuals has also been described.
  • The first child underwent a staged partial removal of a huge right fronto-temporo-parietal tumor when she was 2 months old.
  • At that time histological diagnosis was anaplastic astrocytoma and on these grounds she underwent six chemotherapy cycles, with a partial reduction of the tumor residual.
  • When she was 16 months old a new operation and complete removal of the tumor residual was performed; histological diagnosis was DIG.
  • Twenty-two months after surgery no tumor recurrence has been documented.
  • MRI control 9 months after surgery showed the disappearance of the tumor residual.
  • Eleven years after surgery no tumor recurrence has been documented.
  • The history of this patient confirms that tumor residuals do not need complimentary treatment; indeed they do not usually grow and, as in our patient, they can spontaneously disappear.
  • [MeSH-major] Brain Neoplasms / pathology. Ganglioglioma / pathology
  • [MeSH-minor] Astrocytes / pathology. Child, Preschool. Female. Fibroblasts / pathology. Frontal Lobe / pathology. Frontal Lobe / surgery. Functional Laterality. Humans. Infant. Magnetic Resonance Imaging. Male. Neuroglia / pathology. Neurosurgical Procedures. Parietal Lobe / pathology. Parietal Lobe / surgery. Prognosis. Supratentorial Neoplasms / pathology. Supratentorial Neoplasms / surgery. Temporal Lobe / pathology. Temporal Lobe / surgery

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  • [CommentIn] Childs Nerv Syst. 2007 Jun;23(6):619-20; author reply 621 [17450367.001]
  • [Cites] Childs Nerv Syst. 2000 Jan;16(1):8-14 [10672423.001]
  • [Cites] Histol Histopathol. 2001 Apr;16(2):613-22 [11332717.001]
  • [Cites] Pediatr Neurosurg. 1993 Mar-Apr;19(2):57-62 [8443097.001]
  • [Cites] AJNR Am J Neuroradiol. 1991 Nov-Dec;12 (6):1195-7 [1763751.001]
  • [Cites] Histopathology. 1992 Jul;21(1):43-9 [1634201.001]
  • [Cites] Mod Pathol. 1997 Sep;10(9):945-51 [9310960.001]
  • [Cites] Radiographics. 2001 Nov-Dec;21(6):1533-56 [11706224.001]
  • [Cites] Pediatr Neurosurg. 2002 Jan;36(1):29-32 [11818743.001]
  • [Cites] Pediatr Radiol. 1995;25(7):540-3 [8545186.001]
  • [Cites] Brain Pathol. 1993 Jul;3(3):275-81 [8293187.001]
  • [Cites] Cancer. 1979 Nov;44(5):1839-52 [498051.001]
  • [Cites] Neurosurgery. 1994 Apr;34(4):583-9; discussion 589 [8008154.001]
  • [Cites] Childs Nerv Syst. 1994 Sep;10 (7):458-62; discussion 462-3 [7842437.001]
  • [Cites] Neurosurg Rev. 2001 Jul;24(2-3):114-8 [11485231.001]
  • [Cites] Acta Oncol. 1997;36(6):655-7 [9408160.001]
  • [Cites] J Neurosurg. 1987 Jan;66(1):58-71 [3097276.001]
  • (PMID = 12750935.001).
  • [ISSN] 0256-7040
  • [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] Case Reports; Journal Article
  • [Publication-country] Germany
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