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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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  • (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. Wright KD, Gajjar A: New chemotherapy strategies and biological agents in the treatment of childhood ependymoma. Childs Nerv Syst; 2009 Oct;25(10):1275-82
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  • [Title] New chemotherapy strategies and biological agents in the treatment of childhood ependymoma.
  • INTRODUCTION: With the limited role of current treatment regimens and potential associated side effects of radiation in young children with ependymoma, considerable effort is being focused on new chemotherapeutic strategies and biologic agents.
  • DISCUSSION AND CONCLUSION: Identification of those molecular changes underlying the development of ependymoma may, in time, lead to the development of not only novel therapeutic agents, but also specific patient-tailored therapies directed against known cell-signaling pathways.

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  • (PMID = 19212772.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; None / None / / P30 CA021765-30; United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / P30 CA021765-30
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Quinazolines; 2S9ZZM9Q9V / Bevacizumab; DA87705X9K / Erlotinib Hydrochloride; S65743JHBS / gefitinib
  • [Other-IDs] NLM/ NIHMS85887; NLM/ PMC2738756
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3. Merchant TE: Current management of childhood ependymoma. Oncology (Williston Park); 2002 May;16(5):629-42, 644; discussion 645-6, 648
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  • [Title] Current management of childhood ependymoma.
  • Radiation therapy has long been a mainstay in the treatment of ependymoma.
  • Concerns about the long-term effects of radiation therapy have made many parents and caregivers wary of this treatment modality.
  • However, with the advent of conformal radiation and evidence supporting its use in younger children (ie, < 3 years old), the standard of care for childhood ependymoma is rapidly evolving to include immediate postoperative radiation therapy for all pediatric patients.
  • The role of chemotherapy in the treatment of ependymoma has diminished recently because (1) chemotherapy fails to delay radiation therapy for a meaningful period of time;.
  • (2) tumors that progress during chemotherapy do not respond as well to subsequent irradiation; and (3) the combination of chemotherapy and irradiation does not improve overall survival.
  • However, chemotherapy may make residual tumor more amenable to a second resection.
  • Fewer than 50% of pediatric patients with ependymoma undergo complete resection before receiving radiation therapy.
  • Because the extent of resection is one of the most important prognostic factors in the treatment of this disease, increasing the rate of complete resections is a significant means of increasing long-term survival.
  • By incorporating current concepts of ependymoma, a more uniform approach to the treatment of this disease can be developed.
  • In addition, by combining the best available means of detecting and managing side effects, the future for pediatric patients with ependymoma remains optimistic.
  • This review presents historical and current practices used to treat ependymoma, and is intended to provide an information framework for caregivers so that they can assist parents in the decision-making process.
  • [MeSH-major] Central Nervous System Neoplasms / diagnosis. Central Nervous System Neoplasms / therapy. Ependymoma / diagnosis. Ependymoma / therapy
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / therapeutic use. Child. Child, Preschool. Combined Modality Therapy. Humans. Magnetic Resonance Imaging. Neurosurgical Procedures / methods. Radiotherapy / methods. Reoperation. Treatment Outcome

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  • (PMID = 12108890.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [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.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 51
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4. Wong VC, Morrison A, Tabori U, Hawkins CE: Telomerase inhibition as a novel therapy for pediatric ependymoma. Brain Pathol; 2010 Jul;20(4):780-6
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  • [Title] Telomerase inhibition as a novel therapy for pediatric ependymoma.
  • Ependymomas are the third most common pediatric brain tumor with an overall survival of approximately 50%.
  • Recently, we showed that telomerase [human telomerase reverse transcriptase (hTERT)] expression is a predictor of poor outcome in pediatric ependymoma.
  • Thus, we hypothesized that ependymomas with functional telomerase may behave more aggressively and that these patients may benefit from anti-telomerase therapy.
  • To address our hypothesis, we investigated the effect of telomerase inhibition on primary ependymoma cells harvested at the time of surgery, as no animal models or established cell lines are readily available for this tumor.
  • After 72 h of telomerase inhibition, primary ependymoma cells showed a significant decrease in cell number (P < 0.001), accompanied by increased DNA damage (gammaH2AX expression) (P < 0.01) and decreased proliferative index (MIB-1) (P < 0.01).
  • These data suggest that telomerase inhibition may be an effective adjuvant therapy in pediatric ependymoma, potentially inducing tumor growth arrest in the short term, independent of telomere shortening.
  • [MeSH-major] Brain Neoplasms / metabolism. Ependymoma / metabolism. Telomerase / antagonists & inhibitors. Telomere / metabolism
  • [MeSH-minor] Analysis of Variance. Apoptosis / drug effects. Benzamides / pharmacology. Cell Count. Cell Proliferation / drug effects. Cell Survival / drug effects. Cells, Cultured. Child. DNA Damage / drug effects. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry

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  • (PMID = 20184588.001).
  • [ISSN] 1750-3639
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / / MOP 82727
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Benzamides; 0 / Glial Fibrillary Acidic Protein; 0 / MST 312; EC 2.7.7.49 / Telomerase
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7. Geoerger B, Gaspar N, Opolon P, Morizet J, Devanz P, Lecluse Y, Valent A, Lacroix L, Grill J, Vassal G: EGFR tyrosine kinase inhibition radiosensitizes and induces apoptosis in malignant glioma and childhood ependymoma xenografts. Int J Cancer; 2008 Jul 1;123(1):209-16
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  • [Title] EGFR tyrosine kinase inhibition radiosensitizes and induces apoptosis in malignant glioma and childhood ependymoma xenografts.
  • Malignant gliomas and childhood ependymomas have a high rate of treatment failure.
  • Epidermal growth factor receptor (EGFR) activation has been implicated in the tumorigenesis and radioresistance of many cancers, including brain tumors.
  • Therefore, combining EGFR targeting with irradiation is a potentially attractive therapeutic option.
  • We evaluated the tyrosine kinase inhibitor gefitinib for its antitumor activity and potential to radio-sensitize in vivo in two xenograft models: an EGFR amplified glioma and an EGFR expressing ependymoma, both derived from primary tumors.
  • When administered at 100 mg/kg for 5 consecutive days, gefitinib-induced partial tumor regression in all treated EGFR amplified IGRG88 glioma xenografts.
  • The addition of 1 Gy of irradiation prior to gefitinib administration resulted in 5 complete and 4 partial regressions for the 9 treated tumors as well as a significant tumor growth delay of 33 days for the combined treatment compared to 19 days for each therapy alone, suggesting additive antitumor activity.
  • Tumor regression was associated with inhibition of AKT and MAPK pathways by gefitinib.
  • In contrast, the ependymoma IGREP83 was sensitive to irradiation, but remained resistant to gefitinib.
  • Combined treatment was associated with inhibition of radiation-induced MAPK phosphorylation and significant induction of apoptotic cell death though radiation-induced AKT phosphorylation was maintained.
  • Depending on the scheduling of both therapies, a trend towards superior antitumor activity was observed with combined treatment.
  • Thus, EGFR targeting through tyrosine kinase inhibition appears to be a promising new approach in the treatment of EGFR-driven glioma, particularly in combination with radiation therapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis. Ependymoma / drug therapy. Ependymoma / radiotherapy. Glioma / drug therapy. Glioma / radiotherapy. Protein Kinase Inhibitors / pharmacology. Quinazolines / pharmacology. Radiation-Sensitizing Agents / pharmacology. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Chemotherapy, Adjuvant. Child. Enzyme Activation / drug effects. Enzyme Activation / radiation effects. Female. Flow Cytometry. G1 Phase / drug effects. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Enzymologic / radiation effects. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / radiation effects. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. In Situ Nick-End Labeling. Mice. Mice, Nude. Middle Aged. Mitogen-Activated Protein Kinase Kinases / drug effects. Mitogen-Activated Protein Kinase Kinases / metabolism. Phosphorylation / drug effects. Proto-Oncogene Proteins c-akt / drug effects. Proto-Oncogene Proteins c-akt / metabolism. RNA, Messenger / metabolism. Radiotherapy, Adjuvant. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / drug effects. Time Factors. Xenograft Model Antitumor Assays

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18386816.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / RNA, Messenger; 0 / Radiation-Sensitizing Agents; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; S65743JHBS / gefitinib
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8. Di Pinto M, Conklin HM, Li C, Xiong X, Merchant TE: Investigating verbal and visual auditory learning after conformal radiation therapy for childhood ependymoma. Int J Radiat Oncol Biol Phys; 2010 Jul 15;77(4):1002-8
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  • [Title] Investigating verbal and visual auditory learning after conformal radiation therapy for childhood ependymoma.
  • PURPOSE: The primary objective of this study was to determine whether children with localized ependymoma experience a decline in verbal or visual-auditory learning after conformal radiation therapy (CRT).
  • The secondary objective was to investigate the impact of age and select clinical factors on learning before and after treatment.
  • METHODS AND MATERIALS: Learning in a sample of 71 patients with localized ependymoma was assessed with the California Verbal Learning Test (CVLT-C) and the Visual-Auditory Learning Test (VAL).
  • There were significant longitudinal effects (improved learning scores after treatment) among older children on the CVLT-C and children that did not receive pre-CRT chemotherapy on the VAL.
  • CONCLUSION: There was no evidence of global decline in learning after CRT in children with localized ependymoma.
  • (1) identification of and differentiation among variables with transient vs. long-term effects on learning, (2) demonstration that children treated with chemotherapy before CRT had greater risk of adverse visual-auditory learning performance, and (3) establishment of baseline and serial assessment as critical in ascertaining necessary sensitivity and specificity for the detection of modest effects.

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 19783376.001).
  • [ISSN] 1879-355X
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA021765-28; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / P30 CA021765-28
  • [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
  • [Other-IDs] NLM/ NIHMS125044; NLM/ PMC3037814
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9. Timmermann B, Kortmann RD, Kühl J, Willich N, Bamberg M: [Interdisciplinary therapy of childhood ependymomas]. Strahlenther Onkol; 2002 Sep;178(9):469-79
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  • [Title] [Interdisciplinary therapy of childhood ependymomas].
  • [Transliterated title] Die interdiszipliäre Therapie von Ependymomen im Kindesalter.
  • BACKGROUND: Ependymomas represent about 10% of CNS tumors in children.
  • Further investigations should clarify the impact of chemotherapy, histological grading, dose, and volume of radiotherapy.
  • MATERIAL AND METHOD: Based on historical reports, the recent literature, present guidelines, and ongoing trials an overview is provided for the management of ependymomas in childhood.
  • RESULTS: Local tumor control is the most important aim.
  • Recurrences occur predominantly at the primary tumor region.
  • The main instrument is surgery to effect maximal tumor resection.
  • Regarding the volume of irradiation there is confidence today that local fields are sufficient for all non-disseminated ependymomas.
  • Regarding chemotherapy in ependymomas trials have shown limited efficacy to date.
  • For metastatic disease standard treatment has shown to be insufficient and high dose chemotherapy regimens to increase survival are in study.
  • In younger children radiotherapy should be delayed using early chemotherapy.
  • With pre-irradiation chemotherapy survival rates of 63.3% for children under age of 3 were achieved.
  • CONCLUSIONS: At present the cooperating clinicians are optimizing treatment procedures to improve results and to reduce toxicity.
  • In radiotherapy reduction of target volume to the involved field for all non-disseminated ependymomas as well as the introduction of hyperfractionated schedules and conformal therapy with dose escalation are important developments.
  • [MeSH-major] Brain Neoplasms / therapy. Ependymoma / therapy
  • [MeSH-minor] Age Factors. Antineoplastic Agents / therapeutic use. Child. Child, Preschool. Clinical Trials as Topic. Combined Modality Therapy. Dose Fractionation. Female. Humans. Infant. Infant, Newborn. Magnetic Resonance Imaging. Male. Neoplasm Recurrence, Local. Prognosis. Radiotherapy Dosage. Survival Analysis. Time Factors

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  • (PMID = 12426832.001).
  • [ISSN] 0179-7158
  • [Journal-full-title] Strahlentherapie und Onkologie : Organ der Deutschen Röntgengesellschaft ... [et al]
  • [ISO-abbreviation] Strahlenther Onkol
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 80
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10. Merchant TE, Mulhern RK, Krasin MJ, Kun LE, Williams T, Li C, Xiong X, Khan RB, Lustig RH, Boop FA, Sanford RA: Preliminary results from a phase II trial of conformal radiation therapy and evaluation of radiation-related CNS effects for pediatric patients with localized ependymoma. J Clin Oncol; 2004 Aug 1;22(15):3156-62
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  • [Title] Preliminary results from a phase II trial of conformal radiation therapy and evaluation of radiation-related CNS effects for pediatric patients with localized ependymoma.
  • PURPOSE: We conducted a phase II trial of conformal radiation therapy (CRT) for localized childhood ependymoma to determine whether the irradiated volume could be reduced to decrease CNS-related side effects without diminishing the rate of disease control.
  • PATIENTS AND METHODS: Between July 1997 and January 2003, 88 pediatric patients (median age, 2.85 +/- 4.5 years) received CRT in which doses (59.4 Gy to 73 patients or 54.0 Gy after gross-total resection to 15 patients younger than 18 months) were administered to the gross tumor volume and a margin of 10 mm.
  • Patients were categorized according to extent of resection (underwent gross total resection, n = 74; near-total resection, n = 6; subtotal resection, n = 8), prior chemotherapy (n = 16), tumor grade (anaplastic, n = 35), and tumor location (infratentorial, n = 68).
  • CONCLUSION: Limited-volume irradiation achieves high rates of disease control in pediatric patients with ependymoma and results in stable neurocognitive outcomes.
  • [MeSH-major] Brain / radiation effects. Brain Neoplasms / radiotherapy. Cognition / radiation effects. Ependymoma / radiotherapy. Radiotherapy, Conformal / adverse effects
  • [MeSH-minor] Child, Preschool. Female. Follow-Up Studies. Humans. Infant. Male. Radiotherapy Dosage. Survival Rate

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  • [Copyright] Copyright 2004 American Society of Clinical Onocology
  • (PMID = 15284268.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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11. Timmermann B, Kortmann RD, Kühl J, Meisner C, Slavc I, Pietsch T, Bamberg M: Combined postoperative irradiation and chemotherapy for anaplastic ependymomas in childhood: results of the German prospective trials HIT 88/89 and HIT 91. Int J Radiat Oncol Biol Phys; 2000 Jan 15;46(2):287-95

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined postoperative irradiation and chemotherapy for anaplastic ependymomas in childhood: results of the German prospective trials HIT 88/89 and HIT 91.
  • PURPOSE: To evaluate the outcome in children with anaplastic ependymomas after surgery, irradiation, and chemotherapy; and to identify prognostic factors for survival.
  • METHODS AND MATERIALS: Fifty-five children (n = 27 girls, 28 boys; median age at diagnosis, 6.2 years) with newly diagnosed anaplastic ependymomas were treated in the multicenter, prospective trials HIT 88/89 and HIT 91.
  • All patients received chemotherapy before (n = 40) or after irradiation (n = 15).
  • The irradiation volume encompassed either the neuraxis followed by a boost to the primary tumor site (n = 40) or the tumor region only (n = 13).
  • The median time to disease progression was 45 months.
  • The only significant prognostic factor was the extent of resection (estimated progression-free survival [EPFS] after 3 years was 83.3% after complete resection and 38.5% after incomplete resection) and the presence of metastases at the time of diagnosis (0% vs. 65.8% 3-year EPFS in localized tumors).
  • Age, sex, tumor site, mode of chemotherapy, and irradiation volume did not influence survival.
  • CONCLUSIONS: Treatment centers should be meticulous about surgery and diagnostic workup.
  • Because the primary tumor region is the predominant site of failure it is important to intensify local treatment.
  • The role of adjuvant chemotherapy requires further study.
  • [MeSH-major] Ependymoma / drug therapy. Ependymoma / radiotherapy. Infratentorial Neoplasms / drug therapy. Infratentorial Neoplasms / radiotherapy. Supratentorial Neoplasms / drug therapy. Supratentorial Neoplasms / radiotherapy
  • [MeSH-minor] Adolescent. Austria. Child. Child, Preschool. Combined Modality Therapy. Disease Progression. Disease-Free Survival. Female. Germany. Humans. Male. Prospective Studies. Radiotherapy Dosage. Survival Rate

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  • (PMID = 10661334.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] UNITED STATES
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12. Gaspar N, Grill J, Geoerger B, Lellouch-Tubiana A, Michalowski MB, Vassal G: p53 Pathway dysfunction in primary childhood ependymomas. Pediatr Blood Cancer; 2006 May 1;46(5):604-13
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  • [Title] p53 Pathway dysfunction in primary childhood ependymomas.
  • BACKGROUND: Childhood ependymoma remains a major therapeutic challenge despite surgery, chemotherapy, and irradiation.
  • We hypothesized that p53 function might be abrogated in ependymomas and implicated in their resistance to anti-cancer therapy.
  • PROCEDURE: Primary ependymomas at diagnosis or relapse from 24 children were analyzed for p53 pathway, using a functional assay in yeast, RT-PCR, Western blot analysis, and/or immunohistochemistry for TP53 mutation, p14(ARF) deletion and promoter hypermethylation, MDM2 and PAX5 expression, respectively. p53-mediated response to radiation-induced DNA damage was evaluated using Western blot and flow cytometry analysis in two ependymoma xenograft models, IGREP37 and IGREP83, derived from primary anaplastic childhood ependymomas.
  • RESULTS: No TP53, MDM2, p14(ARF), PAX5 gene abnormalities were detected in the primary ependymomas tumors and xenografts tested.
  • Although irradiation induced necrosis and apoptotic cell death, IGREP37 tumors were moderately sensitive to radiation therapy in vivo.
  • In contrast, irradiation yielded significant tumor growth delays and tumor regressions in the p53 functional IGREP83 xenografts.
  • CONCLUSION: Alterations in p53-mediated growth arrest in ependymomas might be implicated in the radio-resistance of these tumors and demand further evaluation.
  • [MeSH-major] Ependymoma / metabolism. Gene Expression Regulation, Neoplastic. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Animals. B-Cell-Specific Activator Protein / genetics. B-Cell-Specific Activator Protein / metabolism. Blotting, Western. Child. Child, Preschool. DNA Methylation. Female. Humans. Infant. Male. Mice. Promoter Regions, Genetic. Proto-Oncogene Proteins c-mdm2 / genetics. Proto-Oncogene Proteins c-mdm2 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Transplantation, Heterologous. Tumor Cells, Cultured. Tumor Suppressor Protein p14ARF / genetics. Tumor Suppressor Protein p14ARF / metabolism

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  • (PMID = 16086408.001).
  • [ISSN] 1545-5009
  • [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 / B-Cell-Specific Activator Protein; 0 / PAX5 protein, human; 0 / Pax5 protein, mouse; 0 / Tumor Suppressor Protein p14ARF; 0 / Tumor Suppressor Protein p53; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Mdm2 protein, mouse; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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13. van Veelen-Vincent ML, Pierre-Kahn A, Kalifa C, Sainte-Rose C, Zerah M, Thorne J, Renier D: Ependymoma in childhood: prognostic factors, extent of surgery, and adjuvant therapy. J Neurosurg; 2002 Oct;97(4):827-35
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  • [Title] Ependymoma in childhood: prognostic factors, extent of surgery, and adjuvant therapy.
  • OBJECT: The aim of this study was to investigate the effect of patient-related factors, extent of surgery, and adjuvant therapy on survival in children presenting with intracranial ependymoma.
  • METHODS: Between 1980 and 1999, 83 children (mean age 36 months) underwent surgery for intracranial ependymomas.
  • Complete resection, verified on postoperative computerized tomography scans, was achieved in 73%.
  • Adjuvant therapy modalities have changed over the years: before 1990 all patients received radiotherapy, whereas after 1990 the children younger than 3 years of age and later those younger than 5 years of age were treated first with chemotherapy and received radiotherapy only after their first tumor recurrence.
  • The patients in the chemotherapy group did not fare as well as those in the radiotherapy group.
  • A subgroup (36%) within the chemotherapy group, however, survived tumor free after a mean follow-up period of 67 months.
  • It is not clear whether this subgroup either responded well to chemotherapy or needed no adjuvant therapy.
  • [MeSH-major] Brain Neoplasms / surgery. Brain Neoplasms / therapy. Ependymoma / surgery. Ependymoma / therapy
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Child, Preschool. Disease-Free Survival. Educational Status. Female. Follow-Up Studies. Fourth Ventricle. Humans. Hydrocephalus / mortality. Hydrocephalus / surgery. Hydrocephalus / therapy. Infant. Intelligence Tests. Male. Neoplasm Recurrence, Local. Postoperative Complications / mortality. Prognosis. Radiotherapy. Survival Analysis

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  • (PMID = 12405370.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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14. Massimino M, Gandola L, Giangaspero F, Sandri A, Valagussa P, Perilongo G, Garrè ML, Ricardi U, Forni M, Genitori L, Scarzello G, Spreafico F, Barra S, Mascarin M, Pollo B, Gardiman M, Cama A, Navarria P, Brisigotti M, Collini P, Balter R, Fidani P, Stefanelli M, Burnelli R, Potepan P, Podda M, Sotti G, Madon E, AIEOP Pediatric Neuro-Oncology Group: Hyperfractionated radiotherapy and chemotherapy for childhood ependymoma: final results of the first prospective AIEOP (Associazione Italiana di Ematologia-Oncologia Pediatrica) study. Int J Radiat Oncol Biol Phys; 2004 Apr 1;58(5):1336-45
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  • [Title] Hyperfractionated radiotherapy and chemotherapy for childhood ependymoma: final results of the first prospective AIEOP (Associazione Italiana di Ematologia-Oncologia Pediatrica) study.
  • PURPOSE: A postsurgical "stage-based" protocol for ependymoma was designed.
  • HFRT dose was 70.4 Gy (1.1 Gy/fraction b.i.d.
  • RESULTS: Sixty-three consecutive children were enrolled: 46 NED, 17 ED; the tumor was infratentorial in 47 and supratentorial in 16, with spinal metastasis in 1.
  • Of NED patients, 35 of 46 have been treated with HFRT; 8 received conventionally fractionated radiotherapy, and 3 received no treatment.
  • Of the 17 ED patients, 9 received VEC + HFRT; violations due to postsurgical morbidity were as follows: HFRT only (2), conventionally fractionated radiotherapy (3) + VEC (2), and no therapy (1).
  • CONCLUSIONS: HFRT, despite the high total dose adopted, did not change the prognosis of childhood ependymoma as compared to historical series: New radiotherapeutic approaches are needed to improve local control.
  • Future ependymoma strategies should consider grading when stratifying treatment indications.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Ependymoma / drug therapy. Ependymoma / radiotherapy
  • [MeSH-minor] Adolescent. Adult. Chemotherapy, Adjuvant. Child. Child, Preschool. Cyclophosphamide / administration & dosage. Dose Fractionation. Etoposide / administration & dosage. Feasibility Studies. Humans. Infratentorial Neoplasms / drug therapy. Infratentorial Neoplasms / radiotherapy. Infratentorial Neoplasms / surgery. Patient Compliance. Prospective Studies. Radiotherapy, Adjuvant. Supratentorial Neoplasms / drug therapy. Supratentorial Neoplasms / radiotherapy. Supratentorial Neoplasms / surgery. Survival Analysis. Vincristine / administration & dosage

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  • (PMID = 15050308.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide
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15. Rivarola EG, Chantada GL, Ezcurdia L, Negro A, Gil Deza E, Cascallar D, Santillán D, Carnaval S, Morgenfeld E, Gercovich FG: Adherence to standard therapy for the treatment of childhood CNS tumors in Argentina. An audit perspective. J Clin Oncol; 2004 Jul 15;22(14_suppl):8573

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adherence to standard therapy for the treatment of childhood CNS tumors in Argentina. An audit perspective.
  • : 8573 Background: There are no national protocols for the treatment of children with CNS tumors in Argentina, so patients receive individualized treatment at each center.
  • The aim of this study was to evaluate, from an audit perspective, the treatment prescribed to children with CNS tumors belonging to a large health insurance organization in Argentina.
  • METHODS: The files of all patients with CNS tumors for whom their oncologists requested chemotherapy from 2000 to 2003 were retrieved.
  • The PDQ Cancer Information Treatment Summaries posted at the National Cancer Institute of USA web site was used to define standard therapy.
  • RESULTS: Requests of chemotherapy for 24 children treated at 8 different referral centers were received.
  • There were 10 cases of medulloblastoma, 7 gliomas, 5 ependymomas, 1 malignant rhabdoid-teratoid tumor and 1 anaplastic tumor not otherwise specified.
  • This case was excluded because no standard therapy is available.
  • Seventeen out of 23 patients received standard combinations as first line treatment while in 6/23 patients experimental treatment was prescribed.
  • These included 1 children with brainstem glioma, 3 children with ependymoma and 1 one year old child with glioma that received an experimental combination.
  • Even though the role of temozolomide is not clear in children, this drug was requested for 3 patients with glioma (1 baby) as first line and 2 for second line therapy (ependymoma and glioma).
  • Topotecan was requested for 2 patients with ependymoma.
  • All patients with medulloblastoma received standard therapy.
  • CONCLUSIONS: Despite all patients were treated at prestigious centers, 46% of children with CNS tumors other than medulloblastoma received unproven first line therapy.
  • "Off guidelines" treatments with unproven agents outside a clinical trial such as temozolomide and topotecan were requested for 30% of the cases.
  • According to ethical principles, it is our feeling that all children with malignancies outside a controlled clinical trial should receive standard therapies.

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  • (PMID = 28013925.001).
  • [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. Hargrave DR, Zacharoulis S: Pediatric CNS tumors: current treatment and future directions. Expert Rev Neurother; 2007 Aug;7(8):1029-42

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric CNS tumors: current treatment and future directions.
  • Pediatric CNS tumors are the most common solid tumor of childhood and are the leading cause of cancer-related death in this age group.
  • Current management strategies rely on surgery, radiotherapy and conventional cytotoxic chemotherapy, and although ongoing clinical trials continue to refine these treatments, newer approaches are required.
  • This article will discuss current treatment standards for the most common pediatric CNS tumors: astrocytomas (low- and high-grade glioma), ependymoma and primitive neuroectodermal tumors (medulloblastoma), as well as future biological-based novel therapies.
  • [MeSH-major] Central Nervous System Neoplasms / therapy
  • [MeSH-minor] Child. Forecasting. Humans. Predictive Value of Tests

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  • (PMID = 17678498.001).
  • [ISSN] 1744-8360
  • [Journal-full-title] Expert review of neurotherapeutics
  • [ISO-abbreviation] Expert Rev Neurother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 147
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17. Ramachandran C, Khatib Z, Petkarou A, Fort J, Fonseca HB, Melnick SJ, Escalon E: Tamoxifen modulation of etoposide cytotoxicity involves inhibition of protein kinase C activity and insulin-like growth factor II expression in brain tumor cells. J Neurooncol; 2004 Mar-Apr;67(1-2):19-28
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  • [Title] Tamoxifen modulation of etoposide cytotoxicity involves inhibition of protein kinase C activity and insulin-like growth factor II expression in brain tumor cells.
  • Tamoxifen, a non-steroidal anti-estrogen widely used against breast cancer, is also useful for treatment of other malignancies, due to its sensitizing effect on other chemotherapeutic agents and radiation.
  • We have investigated the advantages of combining tamoxifen with one of the commonly used cancer chemotherapeutic drug, etoposide (VP-16) in brain tumor cell lines.
  • While tamoxifen (10 microM) increased etoposide cytotoxicity 8.3-fold in the human glioma cell line (HTB-14), it increased etoposide cytotoxicity 47.5- and 40-fold in two primary cell lines established from pediatric medulloblastoma patients (MCH-BT-31 and MCH-BT-39), respectively.
  • Similarly, in the pediatric ependymoma cell lines (MCH-BT-30 and MCH-BT-52), tamoxifen enhanced etoposide cytotoxicity 6- and 2.68-fold, respectively.
  • CalcuSyn analysis of cytotoxicity data showed that tamoxifen and etoposide combinations were synergistic with combination index values ranging from 0.243 to 0.369 at IC50 level among different pediatric brain tumor cell lines.
  • Tamoxifen is also cytotoxic at higher concentrations (> 20 microM) in brain tumor cells.
  • While P-gp, IGF-IR and IGF-I were not affected, enhanced inhibition of PKC, and IGF-II were observed in brain tumor cells treated with tamoxifen and etoposide combination as compared to cells treated with either drug alone.
  • IGF-II expression decreased to 48.6% of the untreated control in the combination treatment as compared to 31.2% for etoposide alone and 26.2% for tamoxifen alone treatments.
  • These results suggest that inhibitory effect of tamoxifen on brain tumor cells manifest through different mechanisms involving inhibition of targets such as PKC and IGF-II.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Brain Neoplasms / drug therapy. Etoposide / administration & dosage. Protein Kinase C / drug effects. Tamoxifen / administration & dosage
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols. Cell Line, Tumor. Child. Drug Synergism. Humans. Insulin-Like Growth Factor II / biosynthesis. Insulin-Like Growth Factor II / drug effects

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  • (PMID = 15072444.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 094ZI81Y45 / Tamoxifen; 67763-97-7 / Insulin-Like Growth Factor II; 6PLQ3CP4P3 / Etoposide; EC 2.7.11.13 / Protein Kinase C
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18. Wu X, Dagar V, Algar E, Muscat A, Bandopadhayay P, Ashley D, Wo Chow C: Rhabdoid tumour: a malignancy of early childhood with variable primary site, histology and clinical behaviour. Pathology; 2008 Dec;40(7):664-70
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  • [Title] Rhabdoid tumour: a malignancy of early childhood with variable primary site, histology and clinical behaviour.
  • In these 13 patients, the primary tumour was in the central nervous system (CNS) in seven, in the soft tissue in three, in the liver in two and in the kidney in one.
  • In two an alternative diagnosis, ependymoma or myoepithelial carcinoma of soft tissue, was initially suggested.
  • All the CNS tumours were positive for EMA, GFAP, and SMA.
  • There were no long term survivors, but an occasional patient showed excellent response to intensive chemotherapy.
  • As relatively few tumours showed uniform populations of rhabdoid cells, and some showed features suggesting another diagnosis, INI1 staining should be checked in all high grade CNS tumours and malignant extraCNS tumours where the diagnosis is unclear.
  • The prognosis of RT is poor but medium term remission can be achieved in some patients with aggressive treatment.
  • [MeSH-major] Biomarkers, Tumor / genetics. Chromosomal Proteins, Non-Histone / genetics. DNA-Binding Proteins / genetics. Rhabdoid Tumor / genetics. Rhabdoid Tumor / pathology. Transcription Factors / genetics
  • [MeSH-minor] Blotting, Southern. Child. Child, Preschool. DNA Mutational Analysis. Female. Humans. Immunohistochemistry. Infant. Infant, Newborn. Male. Mutation

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  • (PMID = 18985520.001).
  • [ISSN] 0031-3025
  • [Journal-full-title] Pathology
  • [ISO-abbreviation] Pathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chromosomal Proteins, Non-Histone; 0 / DNA-Binding Proteins; 0 / SMARCB1 protein, human; 0 / Transcription Factors
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20. Massimino M, Giangaspero F, Garrè ML, Genitori L, Perilongo G, Collini P, Riva D, Valentini L, Scarzello G, Poggi G, Spreafico F, Peretta P, Mascarin M, Modena P, Sozzi G, Bedini N, Biassoni V, Urgesi A, Balestrini MR, Finocchiaro G, Sandri A, Gandola L, AIEOP Neuro-Oncology Group: Salvage treatment for childhood ependymoma after surgery only: Pitfalls of omitting "at once" adjuvant treatment. Int J Radiat Oncol Biol Phys; 2006 Aug 1;65(5):1440-5
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  • [Title] Salvage treatment for childhood ependymoma after surgery only: Pitfalls of omitting "at once" adjuvant treatment.
  • PURPOSE: To discuss the results obtained by giving adjuvant treatment for childhood ependymoma (EPD) at relapse after complete surgery only.
  • METHODS AND MATERIALS: Between 1993 and 2002, 63 children older than 3 years old entered the first Italian Association for Pediatric Hematology and Oncology protocol for EPD (group A), and another 14 patients were referred after relapsing after more tumor excisions only (group B).
  • RESULTS: Mean time to first local progression in group B had been 14 months.
  • All received radiotherapy (RT) to tumor bed and 5 also had pre-RT chemotherapy.
  • Considering only PF tumors and setting time 0 as at the last surgery for group B, progression-free survival and overall survival were 32% and 50% for group B and 52% (p < 0.20)/70% (p < 0.29) for the 46 patients in group A with PF tumors.
  • CONCLUSIONS: Relapsers after surgery only, especially if with PF-EPD, do worse than those treated after first diagnosis; subsequent surgery for tumor relapse has severe neurologic sequelae.
  • [MeSH-major] Brain Neoplasms / radiotherapy. Ependymoma / radiotherapy. Salvage Therapy / methods
  • [MeSH-minor] Adolescent. Chemotherapy, Adjuvant. Child. Child, Preschool. Female. Humans. Neoplasm, Residual. Radiotherapy, Adjuvant. Treatment Outcome

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  • (PMID = 16863927.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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21. Kim SK, Lim SY, Wang KC, Kim YY, Chi JG, Choi YL, Shin HJ, Cho BK: Overexpression of cyclooxygenase-2 in childhood ependymomas: role of COX-2 inhibitor in growth and multi-drug resistance in vitro. Oncol Rep; 2004 Aug;12(2):403-9
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  • [Title] Overexpression of cyclooxygenase-2 in childhood ependymomas: role of COX-2 inhibitor in growth and multi-drug resistance in vitro.
  • The management of ependymomas remains one of the most frustrating issues in pediatric neuro-oncology.
  • Gross total resection is not always possible, and intensive chemotherapy and craniospinal radiotherapy have made no clear advances.
  • Moreover, the chemoresistance of ependymomas may be explained by the expression of membrane transport molecule P-glycoprotein (P-gp).
  • In this study the expression of cyclooxygenase 2 (COX-2) and the role of the specific COX-2 inhibitor NS-398 in growth and multi-drug resistance of ependymomas were investigated.
  • COX-2 protein expression was assessed in 19 ependymomas immunohistochemically, and the effect of NS-398 on growth and multi-drug resistance was investigated using two primary cultured ependymoma cell lines.
  • COX-2 protein expression was observed in 15 (79%) of the 19 ependymomas.
  • NS-398 was found to reduce the proliferation of monolayer cell cultures in a dose- and time-dependent manner and to induce apoptosis and lower bcl-2 protein levels.
  • After NS-398 treatment, Western blotting showed reduced P-gp expression and a rhodamine 123 efflux assay demonstrated a significant decrease in P-gp activity.
  • Our findings demonstrate that COX-2 is overexpressed in ependymomas and that NS-398 is able to induce apoptosis and suppress P-gp expression and activity.
  • [MeSH-major] Brain Neoplasms / metabolism. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Enzyme Inhibitors / pharmacology. Ependymoma / metabolism. Isoenzymes / biosynthesis. Prostaglandin-Endoperoxide Synthases / biosynthesis
  • [MeSH-minor] Annexin A5 / pharmacology. Apoptosis. Blotting, Western. Cell Proliferation. Child. Child, Preschool. Coloring Agents / pharmacology. Cyclooxygenase 2. Dose-Response Relationship, Drug. Female. Flow Cytometry. Humans. Immunohistochemistry. Infant. Male. Membrane Proteins. P-Glycoprotein / metabolism. Rhodamine 123 / pharmacology. Time Factors. Tumor Cells, Cultured

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  • (PMID = 15254709.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Coloring Agents; 0 / Enzyme Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / P-Glycoprotein; 1N3CZ14C5O / Rhodamine 123; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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22. Yoffe R, Khakoo Y, Dunkel IJ, Souweidane M, Lis E, Sklar C: Recurrent ependymoma treated with high-dose tamoxifen in a peripubertal female: Impact on tumor and the pituitary-ovarian axis. Pediatr Blood Cancer; 2007 Oct 15;49(5):758-60
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  • [Title] Recurrent ependymoma treated with high-dose tamoxifen in a peripubertal female: Impact on tumor and the pituitary-ovarian axis.
  • Due to high rates of recurrence, the prognosis of childhood ependymoma remains guarded.
  • Anecdotal evidence suggests that tamoxifen may have a role in the treatment of these tumors.
  • We present a case of a child with recurrent ependymoma treated with tamoxifen who showed tumor regression on two separate occasions.
  • However, treatment with tamoxifen resulted in the development of large ovarian cysts associated with supraphysiological plasma concentrations of estradiol.
  • [MeSH-major] Ependymoma / complications. Ependymoma / drug therapy. Ovarian Cysts / chemically induced. Tamoxifen / pharmacology
  • [MeSH-minor] Child. Estradiol / blood. Female. Humans. Puberty. Recurrence. Tumor Burden / drug effects

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 16261561.001).
  • [ISSN] 1545-5009
  • [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] 094ZI81Y45 / Tamoxifen; 4TI98Z838E / Estradiol
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23. Houghton PJ, Morton CL, Tucker C, Payne D, Favours E, Cole C, Gorlick R, Kolb EA, Zhang W, Lock R, Carol H, Tajbakhsh M, Reynolds CP, Maris JM, Courtright J, Keir ST, Friedman HS, Stopford C, Zeidner J, Wu J, Liu T, Billups CA, Khan J, Ansher S, Zhang J, Smith MA: The pediatric preclinical testing program: description of models and early testing results. Pediatr Blood Cancer; 2007 Dec;49(7):928-40
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  • [Title] The pediatric preclinical testing program: description of models and early testing results.
  • BACKGROUND: The Pediatric Preclinical Testing Program (PPTP) is an initiative supported by the National Cancer Institute (NCI) to identify novel therapeutic agents that may have significant activity against childhood cancers.
  • The PPTP has established panels of childhood cancer xenografts and cell lines to be used for in vivo and in vitro testing.
  • These include panels for Wilms tumor, sarcomas (rhabdomyosarcoma, Ewing sarcoma, and osteosarcoma), neuroblastoma, brain tumors (glioblastoma, ependymoma, and medulloblastoma), rhabdoid tumors (CNS and renal), and acute lymphoblastic leukemia (ALL).
  • Here, we describe the characteristics of the in vivo tumor panels and report results for the in vivo evaluation of two standard agents, vincristine and cyclophosphamide.
  • PROCEDURES: Solid tumors were grown subcutaneously in immune-deficient mice and tumor dimensions were measured weekly.
  • RESULTS: Vincristine-induced objective responses in 6 of 24 (25%) and cyclophosphamide-induced objective responses in 18 of 28 (64%) solid tumor models.
  • Comparable assessments of high levels of activity for these two agents were obtained using a tumor growth delay (TGD) measure.
  • CONCLUSIONS: We have established 51 solid tumor and 10 ALL in vivo models.
  • The PPTP tumor panels appear to generally recapitulate the activity of these agents against specific childhood cancers and to have the potential for identifying novel agents having significant clinical activity.
  • [MeSH-major] Cyclophosphamide / administration & dosage. Neoplasms / drug therapy. Vincristine / administration & dosage. Xenograft Model Antitumor Assays
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Disease Models, Animal. Disease-Free Survival. Drug Administration Schedule. Female. Humans. Injections, Intraperitoneal. Mice. Mice, Inbred BALB C. Mice, Inbred NOD. Mice, Nude. Mice, SCID. Treatment Outcome

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  • [Copyright] 2007 Wiley-Liss, Inc
  • (PMID = 17066459.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CM / N01-CM-42216
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide
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24. Shim KW, Kim DS, Choi JU: The history of ependymoma management. Childs Nerv Syst; 2009 Oct;25(10):1167-83
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  • [Title] The history of ependymoma management.
  • INTRODUCTION: The ependymomas are relatively not a common tumor.
  • However, most clinicians agree that the radical removal of the tumor is the most important prognostic factor.
  • MORBIDITY OF TREATMENT: Tumor removal was not sufficient before the era of magnetic resonance imaging (MRI) and resulted in a considerable operative morbidity and mortality.
  • As the microneurosurgical techniques and microsurgical anatomy become popular and the MRI provide more detailed anatomical information preoperatively, radical removal of this complex and complicated tumor can be more feasible.
  • In childhood ependymoma, the treatment-related morbidity and mortality can be the special issues, which can modify the policy of management safe tumor removal and minimal adjuvant treatment, which are extremely important.
  • RADIATION THERAPY: Radiation treatment has been the option for disseminated disease and residual tumor.
  • PROGNOSTIC FACTORS: Although many clinicians believe that the ependymomas are inheritably chemoresistant, the new targets for the treatment are under investigation or clinically tried.
  • Also, the genetic alterations of ependymoma are developing and might be a promising target.
  • CONCLUSION: The surgical techniques and assistant modalities for tumor removal are still advancing.
  • So, the outcome of ependymoma is still improving.
  • Unfortunately, newer treatment modalities, such as new chemotherapeutic agent and gene modification agent, are still not promising.
  • The history of ependymoma management is still in progress.
  • [MeSH-major] Ependymoma / diagnosis. Ependymoma / therapy
  • [MeSH-minor] Brain Neoplasms / diagnosis. Brain Neoplasms / mortality. Brain Neoplasms / therapy. Child. Drug Therapy / mortality. Humans. Neurosurgical Procedures / mortality. Prognosis. Radiotherapy / mortality. Spinal Cord Neoplasms / diagnosis. Spinal Cord Neoplasms / mortality. Spinal Cord Neoplasms / therapy

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  • (PMID = 19458954.001).
  • [ISSN] 1433-0350
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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25. Hamstra DA: Primary radiotherapy for childhood ependymoma? Lancet Oncol; 2007 Sep;8(9):758-9; author reply 760-1
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary radiotherapy for childhood ependymoma?
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Ependymoma / drug therapy
  • [MeSH-minor] Age Factors. Chemotherapy, Adjuvant. Child, Preschool. Cognition / drug effects. Cognition / radiation effects. Humans. Infant. Research Design. Treatment Outcome

  • Genetic Alliance. consumer health - Ependymoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
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  • [CommentOn] Lancet Oncol. 2007 Aug;8(8):696-705 [17644039.001]
  • (PMID = 17765188.001).
  • [ISSN] 1470-2045
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] England
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