[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 21 of about 21
1. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Ependymoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


2. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Ependymoma.
  • Genetic Alliance. consumer health - Glioma.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


3. Hargrave DR, Zacharoulis S: Pediatric CNS tumors: current treatment and future directions. Expert Rev Neurother; 2007 Aug;7(8):1029-42
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


Advertisement
4. Mueller S, Chang S: Pediatric brain tumors: current treatment strategies and future therapeutic approaches. Neurotherapeutics; 2009 Jul;6(3):570-86
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric brain tumors: current treatment strategies and future therapeutic approaches.
  • Pediatric CNS tumors are the most common solid tumors of childhood and the second most common cancer after hematological malignancies accounting for approximate 20 to 25% of all primary pediatric tumors.
  • With over 3,000 new cases per year in the United States, childhood CNS tumors are the leading cause of death related to cancer in this population.
  • The prognosis for these patients has improved over the last few decades, but current therapies continue to carry a high risk of significant side effects, especially for the very young.
  • Currently a combination of surgery, radiation, and chemotherapy is often used in children greater than 3 years of age.
  • This article will outline current and future therapeutic strategies for the most common pediatric CNS tumors, including primitive neuroectodermal tumors such as medulloblastoma, as well as astrocytomas and ependymomas.
  • [MeSH-major] Brain Neoplasms / therapy. Neuroectodermal Tumors / therapy
  • [MeSH-minor] Animals. Astrocytoma / therapy. Child, Preschool. Clinical Trials as Topic. Drug Therapy / methods. Ependymoma / physiopathology. Ependymoma / therapy. Glioma / therapy. Humans. Medulloblastoma / therapy. Neoplasm Staging. Neurosurgical Procedures / methods. Radiotherapy / methods

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19560746.001).
  • [ISSN] 1933-7213
  • [Journal-full-title] Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
  • [ISO-abbreviation] Neurotherapeutics
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 172
  •  go-up   go-down


5. Shim KW, Kim DS, Choi JU: The history of ependymoma management. Childs Nerv Syst; 2009 Oct;25(10):1167-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Ependymoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Strahlentherapie. 1980 Feb;156(2):97-101 [7355422.001]
  • [Cites] Neurosurgery. 1996 Apr;38(4):696-701; discussion 701-2 [8692387.001]
  • [Cites] Acta Oncol. 1988;27(3):261-7 [3415856.001]
  • [Cites] Cancer. 1977 Aug;40(2):907-15 [890671.001]
  • [Cites] Cancer Treat Rep. 1982 Dec;66(12 ):2013-20 [6890409.001]
  • [Cites] Childs Nerv Syst. 1989 Feb;5(1):25-8 [2702673.001]
  • [Cites] Surg Neurol. 1975 Mar;3(3):147-52 [1124485.001]
  • [Cites] J Neurosurg. 1993 Jul;79(1):32-5 [8315466.001]
  • [Cites] Cancer. 1974 Feb;33(2):460-7 [4812764.001]
  • [Cites] Acta Oncol. 2000;39(1):97-100 [10752661.001]
  • [Cites] Surg Neurol. 1988 Apr;29(4):271-81 [3353839.001]
  • [Cites] Br J Cancer. 2002 Mar 18;86(6):929-39 [11953826.001]
  • [Cites] Am J Clin Oncol. 2002 Apr;25(2):117-22 [11943886.001]
  • [Cites] J Neurosurg. 1988 Jan;68(1):99-111 [3275756.001]
  • [Cites] Pediatr Neurosurg. 1998 Apr;28(4):215-22 [9732252.001]
  • [Cites] Neurosurgery. 1984 Nov;15(5):707-9 [6504288.001]
  • [Cites] J Neurooncol. 2002 Jan;56(1):87-94 [11949831.001]
  • [Cites] J Neurosurg. 1977 Jan;46(1):52-5 [830815.001]
  • [Cites] Radiother Oncol. 1997 Jun;43(3):269-73 [9215786.001]
  • [Cites] Med Pediatr Oncol. 1996 Jul;27(1):8-14 [8614396.001]
  • [Cites] Cancer. 2000 Feb 15;88(4):870-5 [10679657.001]
  • [Cites] Neuro Oncol. 2008 Oct;10(5):675-89 [18701711.001]
  • [Cites] Neurosurgery. 1993 Jan;32(1):38-44 [8421555.001]
  • [Cites] Childs Nerv Syst. 1999 Oct;15(10):563-70 [10550587.001]
  • [Cites] Arch Neurol Psychiatry. 1949 Dec;62(6):847-56, illust [15396372.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2008 Jul 15;71(4):972-8 [18337022.001]
  • [Cites] J Neurooncol. 1993 Feb;15(2):125-31 [8509817.001]
  • [Cites] Technol Cancer Res Treat. 2005 Dec;4(6):683-9 [16292889.001]
  • [Cites] Childs Brain. 1983;10(3):145-56 [6872622.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 May 1;53(1):52-7 [12007941.001]
  • [Cites] J Neurosurg. 1963 Mar;20:252-3 [14192105.001]
  • [Cites] Surg Neurol. 2000 Jul;54(1):19-26; discussion 26 [11024503.001]
  • [Cites] Expert Rev Neurother. 2006 Apr;6(4):501-7 [16623649.001]
  • [Cites] Neurology. 1988 Sep;38(9):1374-9 [3412585.001]
  • [Cites] Br J Cancer. 2007 Jan 15;96(1):6-10 [17179988.001]
  • [Cites] Cancer. 1969 May;23(5):1038-45 [5305238.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1990 Apr;18(4):723-45 [2323965.001]
  • [Cites] Cancer Treat Rep. 1987 Nov;71(11):1039-42 [3315195.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1983 Aug;9(8):1121-4 [6874447.001]
  • [Cites] Pediatr Neurosurg. 1990-1991;16(2):57-65 [2132926.001]
  • [Cites] Radiat Med. 1994 Nov-Dec;12(6):269-72 [7724818.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1992;23 (2):313-9 [1587752.001]
  • [Cites] J Clin Oncol. 1999 Nov;17(11):3476-86 [10550145.001]
  • [Cites] Anesth Analg. 2000 May;90(5):1238-40 [10781491.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 Feb 1;52(2):325-32 [11872277.001]
  • [Cites] Pediatr Neurosurg. 1998 Mar;28(3):135-42 [9705591.001]
  • [Cites] Can J Neurol Sci. 1994 Aug;21(3):213-8 [8000976.001]
  • [Cites] Neurosurg Clin N Am. 1992 Oct;3(4):881-91 [1392582.001]
  • [Cites] Neurology. 2000 May 23;54(10):1886-93 [10822423.001]
  • [Cites] Pediatr Hematol Oncol. 2002 Jul-Aug;19(5):295-308 [12078861.001]
  • [Cites] Neurosurgery. 1978 Nov-Dec;3(3):380-4 [740137.001]
  • [Cites] Pediatr Blood Cancer. 2006 Jul;47(1):30-6 [16047361.001]
  • [Cites] J Clin Oncol. 1997 May;15(5):1814-23 [9164190.001]
  • [Cites] J Neurooncol. 1992 Jul;13(3):283-90 [1517804.001]
  • [Cites] Childs Nerv Syst. 1990 Nov;6(7):375-8 [1669244.001]
  • [Cites] Childs Nerv Syst. 1986;2(2):55-9 [3731169.001]
  • [Cites] Cancer. 1984 Sep 1;54(5):825-9 [6744214.001]
  • [Cites] Cancer. 1975 Mar;35(3 suppl):950-6 [1167486.001]
  • [Cites] Neurosurgery. 2005;56(1):130-7; discussion 138 [15617595.001]
  • [Cites] Cancer. 2004 Mar 15;100(6):1230-7 [15022291.001]
  • [Cites] J Neurosurg. 1973 Sep;39(3):306-14 [4354763.001]
  • [Cites] Neurosurgery. 1992 Mar;30(3):325-30 [1620293.001]
  • [Cites] Neurosurgery. 1998 Apr;42(4):899-907; discussion 907-8 [9574655.001]
  • [Cites] J Neurosurg. 1976 Sep;45(3):273-83 [948014.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Jan 15;46(2):287-95 [10661334.001]
  • [Cites] Radiat Oncol Investig. 1998;6(6):276-80 [9885944.001]
  • [Cites] J Neurosurg. 1969 May;30(5):585-94 [5305351.001]
  • [Cites] Anticancer Res. 1990 May-Jun;10(3):689-92 [2369084.001]
  • [Cites] Radiother Oncol. 1997 Oct;45(1):3-10 [9364625.001]
  • [Cites] Cancer. 1985 Oct 1;56(7):1497-501 [4040799.001]
  • [Cites] Neurosurgery. 1998 May;42(5):1044-55; discussion 1055-6 [9588549.001]
  • [Cites] Br J Radiol. 2005 Jun;78(930):548-52 [15900062.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Dec 1;42(5):953-8 [9869215.001]
  • [Cites] Neuropsychology. 2003 Oct;17(4):548-55 [14599268.001]
  • [Cites] Med Pediatr Oncol. 1984;12(1):1-3 [6546602.001]
  • [Cites] Cancer. 1985 Oct 1;56(7 Suppl):1812-6 [4027918.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Mar 1;40(4):845-50 [9531369.001]
  • [Cites] Cancer Res. 2006 Aug 1;66(15):7445-52 [16885340.001]
  • [Cites] Strahlenther Onkol. 1992 Sep;168(9):513-9 [1411924.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2001 Jul 15;50(4):929-35 [11429220.001]
  • [Cites] Pediatr Neurol. 1996 Apr;14(3):216-19 [8736405.001]
  • [Cites] Neurosurg Clin N Am. 1990 Jan;1(1):65-80 [2135974.001]
  • [Cites] Clin Radiol. 1984 Mar;35(2):163-6 [6697658.001]
  • [Cites] Childs Nerv Syst. 1991 Nov;7(7):368-74 [1794116.001]
  • [Cites] Stroke. 1995 Jan;26(1):131-6 [7839383.001]
  • [Cites] Pediatr Blood Cancer. 2004 May;42(5):457-60 [15049020.001]
  • [Cites] Ann Neurol. 1992 Oct;32(4):551-4 [1456739.001]
  • [Cites] Arch Neurol. 1975 Nov;32(11):731-9 [1180742.001]
  • [Cites] J Neurosurg. 1976 May;44(5):562-6 [1262915.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1990 Dec;19(6):1497-502 [2262372.001]
  • [Cites] J Neurosurg. 1996 Oct;85(4):618-24 [8814165.001]
  • [Cites] Radiother Oncol. 1995 Aug;36(2):101-6 [7501807.001]
  • [Cites] Radiology. 1977 Sep;124(3):805-8 [887779.001]
  • [Cites] JAMA. 1969 Oct 27;210(4):726 [5394410.001]
  • [Cites] J Neurosurg. 1981 Mar;54(3):406-8 [7463145.001]
  • [Cites] Neurosurgery. 1983 Jan;12(1):14-7 [6828220.001]
  • [Cites] Cancer Treat Rep. 1977 Jul;61(4):691-4 [301782.001]
  • [Cites] Cancer. 1991 Jun 1;67(11):2766-71 [2025840.001]
  • [Cites] Anesthesiology. 1982 Oct;57(4):338-9 [7125277.001]
  • [Cites] Childs Nerv Syst. 1998 Mar;14(3):94-6 [9579861.001]
  • [Cites] Neurosurgery. 1981 Sep;9(3):249-52 [7301065.001]
  • [Cites] J Clin Oncol. 1998 May;16(5):1723-8 [9586884.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2008 Jul 15;71(4):987-93 [18258381.001]
  • [Cites] Med Pediatr Oncol. 1997 Aug;29(2):79-85 [9180907.001]
  • [Cites] No Shinkei Geka. 1995 May;23(5):411-5 [7753320.001]
  • [Cites] J Pediatr Hematol Oncol. 1999 May-Jun;21(3):203-11 [10363853.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1987 Oct;13(10):1457-62 [3624024.001]
  • [Cites] J Neurosurg. 1997 Jun;86(6):943-9 [9171172.001]
  • [Cites] J Neurosurg. 1998 Apr;88(4):695-703 [9525716.001]
  • [Cites] Clin Radiol. 1974 Jul;25(3):355-60 [4547600.001]
  • [Cites] Arch Neurol. 1976 Nov;33(11):739-44 [185991.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2001 Mar 1;49(3):757-61 [11172959.001]
  • [Cites] J Neurosurg. 1983 Oct;59(4):652-9 [6886786.001]
  • [Cites] Cancer Res. 1993 Jul 15;53(14):3416-20 [8324751.001]
  • [Cites] Cancer. 1975 Jun;35(6):1563-73 [1148991.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1994 Jan 15;28(2):381-6 [8276653.001]
  • [Cites] N Engl J Med. 1993 Jun 17;328(24):1725-31 [8388548.001]
  • [Cites] J Neurosurg. 1970 Oct;33(4):428-38 [5471932.001]
  • [Cites] J Clin Oncol. 1994 Aug;12(8):1607-15 [8040673.001]
  • [Cites] J Neurosurg. 1989 May;70(5):707-13 [2709111.001]
  • [Cites] Acta Med Croatica. 2008 Feb;62(1):33-40 [18365498.001]
  • [Cites] Neuro Oncol. 2008 Oct;10(5):648-60 [18577562.001]
  • [Cites] Clin Cancer Res. 2002 Oct;8(10):3054-64 [12374672.001]
  • [Cites] Neuropathol Appl Neurobiol. 1994 Apr;20(2):118-21 [7915406.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1982 Jan;8(1):37-43 [7061255.001]
  • [Cites] Neurosurgery. 1991 May;28(5):666-71; discussion 671-2 [1876244.001]
  • [Cites] Radiology. 1964 Jul;83:98-105 [14191663.001]
  • [Cites] Neurosurgery. 2001 Apr;48(4):731-42; discussion 742-4 [11322433.001]
  • [Cites] Am J Clin Oncol. 2006 Feb;29(1):106-7 [16462515.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1995 Feb 1;31(3):561-6 [7852120.001]
  • [Cites] Acta Oncol. 1994;33(1):29-32 [8142120.001]
  • [Cites] Pediatr Neurosurg. 1996 Jul;25(1):7-12 [9055328.001]
  • [Cites] Pediatr Neurosurg. 1996;24(3):119-25 [8870014.001]
  • [Cites] Am J Roentgenol Radium Ther Nucl Med. 1964 Jan;91:167-75 [14113762.001]
  • [Cites] J Neurooncol. 1998 Apr;37(2):135-43 [9524092.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1994 Oct 15;30(3):531-9 [7928483.001]
  • [Cites] J Neurooncol. 1998 Apr;37(2):131-3 [9524091.001]
  • [Cites] Pediatr Pathol Lab Med. 1996 Jul-Aug;16(4):551-61 [9025853.001]
  • [Cites] Childs Nerv Syst. 2000 Mar;16(3):170-5 [10804053.001]
  • [Cites] Cancer. 1991 Jul 15;68(2):309-15 [1712663.001]
  • [Cites] J Neurosurg. 1994 Jul;81(1):115-21 [8207512.001]
  • [Cites] Neurosurgery. 1995 Oct;37(4):655-66; discussion 666-7 [8559293.001]
  • [Cites] Histopathology. 2008 Jul;53(1):39-47 [18613924.001]
  • [Cites] Childs Nerv Syst. 1990 May;6(3):131-4 [2357709.001]
  • [Cites] Neuro Oncol. 1999 Jul;1(3):177-87 [11550312.001]
  • [Cites] Pediatr Neurosurg. 1998 May;28(5):273-8 [9732262.001]
  • [Cites] Childs Brain. 1979;5(4):408-12 [456112.001]
  • [Cites] Cancer. 1975 Mar;35(3 suppl):957-64 [163143.001]
  • [Cites] Pediatr Neurosurg. 1998 Jul;29(1):40-5 [9755311.001]
  • [Cites] Neurol Clin. 1985 Nov;3(4):855-66 [3001491.001]
  • [Cites] Cancer. 1990 Dec 15;66(12):2465-9 [2249186.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1986 Nov;12(11):1937-41 [3771314.001]
  • [Cites] Pediatr Neurol. 1985 Sep-Oct;1(5):311-6 [3916906.001]
  • [Cites] Neurosurgery. 1991 May;28(5):659-64; discussion 664-5 [1876243.001]
  • [Cites] Cancer. 1997 Jul 15;80(2):341-7 [9217048.001]
  • [Cites] J Neurosurg. 1990 Mar;72(3):408-17 [2303876.001]
  • [Cites] Childs Nerv Syst. 1991 Aug;7(4):177-82 [1933913.001]
  • [Cites] J Neurosurg. 1990 Jun;72 (6):959-63 [2187060.001]
  • [Cites] Acta Neurochir (Wien). 1979;50(1-2):103-16 [229698.001]
  • [Cites] Childs Brain. 1977;3(3):154-68 [862469.001]
  • [Cites] Neurosurgery. 1997 Apr;40(4):856-60; discussion 860 [9092863.001]
  • (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
  •  go-up   go-down


6. Bouffet E, Capra M, Bartels U: Salvage chemotherapy for metastatic and recurrent ependymoma of childhood. Childs Nerv Syst; 2009 Oct;25(10):1293-301
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Salvage chemotherapy for metastatic and recurrent ependymoma of childhood.
  • INTRODUCTION: Chemotherapy has limited role in the up-front management of ependymoma.
  • At the time of recurrence, the role of chemotherapy is also ill defined and the choice of chemotherapeutic agents is often arbitrary, based on anecdotal data and personal experience.
  • METHODS: The purpose of this review is to describe and critically analyze the published literature on chemotherapy in patients with recurrent and metastatic ependymoma.
  • DISCUSSION: The disappointing response rate with single agents (12.9%) and combinations (17.4%) emphasizes the need to re-evaluate the current chemotherapeutic approach of intracranial ependymoma, and biological studies are needed to identify targets that may be considered for clinical trials.
  • [MeSH-major] Ependymoma / drug therapy. Neoplasm Metastasis / drug therapy. Neoplasm Recurrence, Local / drug therapy. Salvage Therapy / methods
  • [MeSH-minor] Brain Neoplasms / drug therapy. Child. Humans. Spinal Cord Neoplasms / drug therapy

  • Genetic Alliance. consumer health - Ependymoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurosurg. 1981 Nov;55(5):749-56 [7310496.001]
  • [Cites] J Neurooncol. 1988 Dec;6(4):319-23 [3221259.001]
  • [Cites] J Neurooncol. 1989 May;7(1):5-11 [2754456.001]
  • [Cites] J Pediatr Hematol Oncol. 2005 Sep;27(9):486-90 [16189442.001]
  • [Cites] J Neurooncol. 2004 Mar-Apr;67(1-2):19-28 [15072444.001]
  • [Cites] Pediatr Neurol. 2001 Feb;24(2):117-21 [11275460.001]
  • [Cites] Med Pediatr Oncol. 1998 Jun;30(6):319-29; discussion 329-31 [9589080.001]
  • [Cites] J Clin Oncol. 2007 Oct 20;25(30):4806-12 [17947729.001]
  • [Cites] J Neurooncol. 1987;5(3):241-4 [3681386.001]
  • [Cites] Neuro Oncol. 2003 Oct;5(4):261-7 [14565163.001]
  • [Cites] Clin Cancer Res. 2007 Nov 15;13(22 Pt 1):6712-8 [18006772.001]
  • [Cites] Clin Cancer Res. 2006 Apr 1;12(7 Pt 1):2070-9 [16609018.001]
  • [Cites] J Clin Oncol. 1992 Feb;10(2):249-56 [1732426.001]
  • [Cites] Pediatr Neurosurg. 2002 Jul;37(1):27-31 [12138216.001]
  • [Cites] Clin Cancer Res. 2006 Jan 15;12(2):516-22 [16428494.001]
  • [Cites] Cancer. 1995 Jun 1;75(11):2762-7 [7743483.001]
  • [Cites] J Clin Oncol. 2008 Oct 20;26(30):4921-7 [18794549.001]
  • [Cites] Pediatr Blood Cancer. 2006 Jul;47(1):30-6 [16047361.001]
  • [Cites] J Neurooncol. 1999;45(1):61-7 [10728911.001]
  • [Cites] J Neurooncol. 2005 Dec;75(3):287-99 [16195801.001]
  • [Cites] J Pediatr Hematol Oncol. 1997 May-Jun;19(3):187-91 [9201138.001]
  • [Cites] J Clin Oncol. 2007 Jul 20;25(21):3137-43 [17634493.001]
  • [Cites] Cancer. 2007 Oct 1;110(7):1542-50 [17705175.001]
  • [Cites] J Pediatr Hematol Oncol. 2000 Jan-Feb;22(1):41-4 [10695820.001]
  • [Cites] J Pediatr Hematol Oncol. 2001 Jun-Jul;23(5):277-81 [11464982.001]
  • [Cites] Cancer Res. 1995 Jul 1;55(13):2853-7 [7796412.001]
  • [Cites] Oncol Rep. 2008 May;19(5):1219-23 [18425379.001]
  • [Cites] J Neurooncol. 1991 Aug;11(1):57-63 [1919647.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Jan 15;46(2):287-95 [10661334.001]
  • [Cites] Br J Cancer. 2008 Oct 7;99(7):1129-35 [18797459.001]
  • [Cites] J Clin Oncol. 2005 Oct 20;23 (30):7646-53 [16234526.001]
  • [Cites] Cancer. 1985 Oct 1;56(7):1497-501 [4040799.001]
  • [Cites] J Clin Oncol. 2008 Feb 20;26(6):919-24 [18281665.001]
  • [Cites] Pediatr Neurol. 1998 Jan;18(1):23-9 [9492087.001]
  • [Cites] Pediatr Blood Cancer. 2006 Jan;46(1):50-5 [15768380.001]
  • [Cites] J Clin Oncol. 2006 Apr 1;24(10):1522-8 [16575002.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2001 Jul 15;50(4):929-35 [11429220.001]
  • [Cites] Cancer. 2005 Jul 1;104(1):143-8 [15912507.001]
  • [Cites] J Neurooncol. 1983;1(1):45-8 [6678305.001]
  • [Cites] Cancer. 1989 Dec 15;64(12):2420-3 [2555038.001]
  • [Cites] J Neurosurg. 1996 Oct;85(4):618-24 [8814165.001]
  • [Cites] Childs Nerv Syst. 2005 Mar;21(3):230-3 [15338180.001]
  • [Cites] Pediatr Blood Cancer. 2007 Jul;49(1):34-40 [16874765.001]
  • [Cites] Acta Cytol. 1964 Mar-Apr;8(2):141-9 [4169713.001]
  • [Cites] Cancer. 1990 Aug 1;66(3):557-63 [2364367.001]
  • [Cites] J Neurooncol. 1986;3(4):341-2 [3958779.001]
  • [Cites] Eur J Cancer. 2006 Sep;42(14 ):2335-42 [16899365.001]
  • [Cites] Pediatr Blood Cancer. 2007 Oct 15;49(5):758-60 [16261561.001]
  • [Cites] J Neurosurg. 1984 Dec;61(6):1063-8 [6502234.001]
  • [Cites] Med Pediatr Oncol. 1997 Jul;29(1):28-32 [9142202.001]
  • [Cites] J Clin Oncol. 1988 Jan;6(1):62-6 [2826716.001]
  • [Cites] Cancer. 2002 Sep 15;95(6):1294-301 [12216098.001]
  • [Cites] Pediatr Blood Cancer. 2009 Feb;52(2):169-76 [19065567.001]
  • [Cites] J Clin Oncol. 2005 Sep 1;23(25):6172-80 [16135484.001]
  • [Cites] AJNR Am J Neuroradiol. 1990 Nov-Dec;11(6):1100-3 [2124036.001]
  • [Cites] Clin Cancer Res. 1999 Dec;5(12):3956-62 [10632325.001]
  • [Cites] Pediatr Hematol Oncol. 1999 May-Jun;16(3):245-50 [10326223.001]
  • [Cites] J Neurooncol. 2007 Jul;83(3):303-6 [17245619.001]
  • [Cites] J Neurooncol. 1999 May;43(1):43-7 [10448870.001]
  • [Cites] Med Pediatr Oncol. 1993;21(1):49-53 [8381203.001]
  • [Cites] J Pediatr Hematol Oncol. 2000 Mar-Apr;22(2):119-24 [10779024.001]
  • [Cites] J Neurooncol. 1990 Aug;9(1):69-76 [2213117.001]
  • [Cites] J Interferon Res. 1988 Dec;8(6):717-25 [3230330.001]
  • [Cites] Med Pediatr Oncol. 2001 Jul;37(1):67-9 [11466729.001]
  • [Cites] Clin Cancer Res. 2002 Oct;8(10):3054-64 [12374672.001]
  • [Cites] Childs Nerv Syst. 2006 Jul;22(7):652-61 [16565851.001]
  • [Cites] Am J Clin Oncol. 2006 Feb;29(1):106-7 [16462515.001]
  • [Cites] Neuro Oncol. 2002 Apr;4(2):102-8 [11916501.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2008 May 1;71(1):87-97 [18406885.001]
  • [Cites] J Clin Oncol. 2003 Jan 1;21(1):143-7 [12506183.001]
  • [Cites] Pediatr Neurosurg. 1996 Jul;25(1):7-12 [9055328.001]
  • [Cites] Cancer. 1993 Jul 1;72(1):271-5 [8508417.001]
  • [Cites] Clin Cancer Res. 1997 Dec;3(12 Pt 1):2459-63 [9815647.001]
  • [Cites] J Neurooncol. 1985;3(3):263-9 [3903064.001]
  • [Cites] J Neurooncol. 1998 Apr;37(2):135-43 [9524092.001]
  • [Cites] J Neurooncol. 1985;3(2):131-5 [2993536.001]
  • [Cites] J Clin Oncol. 1991 May;9(5):783-8 [2016620.001]
  • [Cites] Pediatr Neurosurg. 1998 May;28(5):273-8 [9732262.001]
  • [Cites] Br J Cancer. 2006 Sep 4;95(5):571-80 [16880787.001]
  • [Cites] Radiology. 1996 Jan;198(1):273-8 [8539393.001]
  • [Cites] Cancer. 1990 Dec 15;66(12):2465-9 [2249186.001]
  • [Cites] J Neurooncol. 1995;25(1):77-84 [8523093.001]
  • [Cites] J Neurooncol. 2003 Sep;64(3):239-47 [14558599.001]
  • [Cites] Invest New Drugs. 1990 Nov;8(4):401-6 [2084075.001]
  • [Cites] Neurosurgery. 1997 Apr;40(4):856-60; discussion 860 [9092863.001]
  • (PMID = 19360417.001).
  • [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; Review
  • [Publication-country] Germany
  • [Number-of-references] 85
  •  go-up   go-down


7. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


8. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.

  • Genetic Alliance. consumer health - Ependymoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurosurg. 1998 Apr;88(4):695-703 [9525716.001]
  • [Cites] J Pediatr Hematol Oncol. 1998 Mar-Apr;20(2):125-30 [9544162.001]
  • [Cites] Cancer Res. 1998 Sep 1;58(17):3932-41 [9731505.001]
  • [Cites] J Pediatr Hematol Oncol. 1999 May-Jun;21(3):203-11 [10363853.001]
  • [Cites] J Pediatr Hematol Oncol. 2005 Sep;27(9):486-90 [16189442.001]
  • [Cites] Neuro Oncol. 2005 Oct;7(4):452-64 [16212810.001]
  • [Cites] Cancer Cell. 2005 Oct;8(4):323-35 [16226707.001]
  • [Cites] Cancer. 2007 Jul 15;110(2):432-41 [17559078.001]
  • [Cites] Cancer. 2007 Oct 1;110(7):1542-50 [17705175.001]
  • [Cites] Pediatr Blood Cancer. 2008 Feb;50(2):231-5 [17610266.001]
  • [Cites] Mol Cancer Ther. 2008 Feb;7(2):418-24 [18245671.001]
  • [Cites] Int J Cancer. 2008 Jul 1;123(1):209-16 [18386816.001]
  • [Cites] Expert Rev Anticancer Ther. 2008 Oct;8(10):1545-57 [18925847.001]
  • [Cites] J Clin Oncol. 2008 Oct 20;26(30):4921-7 [18794549.001]
  • [Cites] Clin Cancer Res. 2009 Jan 15;15(2):701-7 [19147777.001]
  • [Cites] Blood. 1999 Dec 15;94(12):4143-55 [10590059.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Jan 15;46(2):287-95 [10661334.001]
  • [Cites] Carcinogenesis. 2000 Mar;21(3):505-15 [10688871.001]
  • [Cites] Cancer Res. 2000 Apr 1;60(7):1878-86 [10766175.001]
  • [Cites] J Clin Invest. 2000 Apr;105(8):1045-7 [10772648.001]
  • [Cites] Eur J Cancer. 2000 Jun;36(10):1248-57 [10882863.001]
  • [Cites] J Clin Oncol. 2001 Mar 1;19(5):1288-96 [11230470.001]
  • [Cites] J Pediatr Hematol Oncol. 2005 Nov;27(11):573-81 [16282886.001]
  • [Cites] Nature. 2005 Dec 15;438(7070):967-74 [16355214.001]
  • [Cites] J Clin Oncol. 2006 Jan 1;24(1):1-3 [16330665.001]
  • [Cites] Nat Clin Pract Oncol. 2006 Jan;3(1):24-40 [16407877.001]
  • [Cites] Annu Rev Med. 2006;57:83-97 [16409138.001]
  • [Cites] J Clin Oncol. 2006 Apr 1;24(10):1522-8 [16575002.001]
  • [Cites] Clin Cancer Res. 2006 Apr 1;12(7 Pt 1):2070-9 [16609018.001]
  • [Cites] Science. 2006 May 26;312(5777):1171-5 [16728631.001]
  • [Cites] J Chemother. 2006 Apr;18(2):188-91 [16736888.001]
  • [Cites] Cancer Res. 2006 Aug 15;66(16):7843-8 [16912155.001]
  • [Cites] Clin Cancer Res. 2006 Sep 1;12(17):5190-8 [16951238.001]
  • [Cites] Eur J Cancer. 2006 Sep;42(14):2335-42 [16899365.001]
  • [Cites] Nat Rev Cancer. 2006 Nov;6(11):876-85 [17036041.001]
  • [Cites] J Clin Oncol. 2006 Nov 20;24(33):5223-33 [17114655.001]
  • [Cites] J Pediatr Hematol Oncol. 2006 Nov;28(11):720-8 [17114958.001]
  • [Cites] Cancer Cell. 2007 Jan;11(1):69-82 [17222791.001]
  • [Cites] Clin Cancer Res. 2007 Feb 15;13(4):1253-9 [17317837.001]
  • [Cites] Clin Cancer Res. 2007 Mar 1;13(5):1511-5 [17332296.001]
  • [Cites] Pediatr Blood Cancer. 2007 Jul;49(1):34-40 [16874765.001]
  • [Cites] Br J Cancer. 2001 Sep 1;85(5):705-12 [11531256.001]
  • [Cites] J Clin Oncol. 2001 Sep 15;19(18 Suppl):45S-51S [11560971.001]
  • [Cites] Ann Oncol. 2002 Jan;13(1):73-80 [11863115.001]
  • [Cites] J Neurooncol. 2002 Jan;56(1):87-94 [11949831.001]
  • [Cites] Nat Rev Cancer. 2002 Oct;2(10):727-39 [12360276.001]
  • [Cites] Clin Cancer Res. 2002 Oct;8(10):3054-64 [12374672.001]
  • [Cites] Am J Pathol. 2002 Dec;161(6):2133-41 [12466129.001]
  • [Cites] Cancer Res. 2003 Jan 1;63(1):140-8 [12517790.001]
  • [Cites] Semin Oncol. 2003 Feb;30(1 Suppl 1):12-20 [12644980.001]
  • [Cites] Nat Rev Cancer. 2003 Jun;3(6):401-10 [12778130.001]
  • [Cites] Cancer. 2003 Oct 15;98(8):1643-8 [14534880.001]
  • [Cites] Am J Pathol. 2003 Nov;163(5):1721-7 [14578171.001]
  • [Cites] Cancer Chemother Pharmacol. 2003 Nov;52(5):377-82 [12879280.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2004 Mar 1;58(3):941-9 [14967454.001]
  • [Cites] Clin Cancer Res. 2004 Feb 15;10(4):1212-8 [14977817.001]
  • [Cites] Nat Rev Cancer. 2004 Jun;4(6):423-36 [15170445.001]
  • [Cites] N Engl J Med. 2004 Jun 3;350(23):2335-42 [15175435.001]
  • [Cites] J Clin Oncol. 2004 Aug 1;22(15):3156-62 [15284268.001]
  • [Cites] Cancer Treat Rep. 1982 Dec;66(12):2013-20 [6890409.001]
  • [Cites] Cancer. 1985 Oct 1;56(7):1497-501 [4040799.001]
  • [Cites] J Clin Oncol. 1988 Jan;6(1):62-6 [2826716.001]
  • [Cites] J Neurosurg. 1990 Mar;72(3):408-17 [2303876.001]
  • [Cites] Cancer. 1990 Dec 15;66(12):2465-9 [2249186.001]
  • [Cites] Pediatr Neurosurg. 1990-1991;16(2):57-65 [2132926.001]
  • [Cites] J Clin Oncol. 1992 Feb;10(2):249-56 [1732426.001]
  • [Cites] J Neurooncol. 1992 Jul;13(3):283-90 [1517804.001]
  • [Cites] Med Pediatr Oncol. 1993;21(1):49-53 [8381203.001]
  • [Cites] N Engl J Med. 1993 Jun 17;328(24):1725-31 [8388548.001]
  • [Cites] J Clin Oncol. 1994 Aug;12(8):1607-15 [8040673.001]
  • [Cites] Neurosurgery. 1995 Oct;37(4):655-66; discussion 666-7 [8559293.001]
  • [Cites] Med Pediatr Oncol. 1996 Jul;27(1):8-14 [8614396.001]
  • [Cites] Pediatr Neurosurg. 1996;24(3):119-25 [8870014.001]
  • [Cites] J Neurooncol. 1997 May;32(3):243-52 [9049886.001]
  • [Cites] Neurosurgery. 1997 Apr;40(4):856-60; discussion 860 [9092863.001]
  • [Cites] Med Pediatr Oncol. 1997 Jul;29(1):28-32 [9142202.001]
  • [Cites] Med Pediatr Oncol. 1997 Aug;29(2):79-85 [9180907.001]
  • [Cites] Cancer. 1997 Jul 15;80(2):341-7 [9217048.001]
  • [Cites] Eur J Cancer. 1997 Apr;33(4):609-15 [9274443.001]
  • (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
  •  go-up   go-down


9. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.

  • Genetic Alliance. consumer health - Ependymoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • [Cites] J Clin Oncol. 2004 Aug 1;22(15):3156-62 [15284268.001]
  • [Cites] Neuropsychol Rev. 2004 Mar;14(1):65-86 [15260139.001]
  • [Cites] Med Pediatr Oncol. 1992;20(3):181-91 [1574027.001]
  • [Cites] Neuropsychologia. 1992 Mar;30(3):257-75 [1574161.001]
  • [Cites] N Engl J Med. 1993 Jun 17;328(24):1725-31 [8388548.001]
  • [Cites] Pediatr Res. 1994 Feb;35(2):171-8 [8165051.001]
  • [Cites] J Clin Oncol. 1995 Oct;13(10):2490-6 [7595698.001]
  • [Cites] J Int Neuropsychol Soc. 1997 Nov;3(6):521-7 [9448365.001]
  • [Cites] J Pediatr Psychol. 1997 Dec;22(6):861-70 [9494322.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1999 Aug 1;45(1):137-45 [10477017.001]
  • [Cites] J Pediatr Psychol. 2005 Jan-Feb;30(1):51-63 [15610985.001]
  • [Cites] J Child Neurol. 2005 Feb;20(2):129-33 [15794179.001]
  • [Cites] J Clin Oncol. 2005 Apr 1;23(10):2256-63 [15800316.001]
  • [Cites] J Neurosurg. 2004 Nov;101(2 Suppl):159-68 [15835103.001]
  • [Cites] Pediatr Blood Cancer. 2005 Nov;45(6):814-9 [15924360.001]
  • [Cites] Cancer. 2005 Nov 15;104(10):2222-33 [16206292.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2005 Dec 1;63(5):1546-54 [16115736.001]
  • [Cites] Neuropsychology. 2006 Jan;20(1):105-12 [16460226.001]
  • [Cites] Magn Reson Imaging. 2006 Oct;24(8):1015-22 [16997071.001]
  • [Cites] Neuroradiology. 2007 Nov;49(11):889-904 [17653705.001]
  • [Cites] J Clin Oncol. 2007 Nov 1;25(31):4914-21 [17971588.001]
  • [Cites] Pediatr Clin North Am. 2008 Feb;55(1):121-45, xi [18242318.001]
  • [Cites] BMC Cancer. 2008;8:15 [18208613.001]
  • [Cites] AJNR Am J Neuroradiol. 2008 Apr;29(4):792-7 [18184841.001]
  • [Cites] J Clin Oncol. 2008 Aug 20;26(24):3965-70 [18711186.001]
  • [Cites] Strahlenther Onkol. 2000 Dec;176(12):573-81 [11140152.001]
  • [Cites] J Clin Oncol. 2001 Jan 15;19(2):472-9 [11208841.001]
  • [Cites] J Clin Oncol. 2001 Apr 15;19(8):2302-8 [11304784.001]
  • [Cites] Neuro Oncol. 1999 Jul;1(3):177-87 [11550312.001]
  • [Cites] Appl Neuropsychol. 2001;8(3):129-39 [11686647.001]
  • [Cites] Annu Rev Psychol. 2002;53:309-39 [11752488.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 Feb 1;52(2):325-32 [11872277.001]
  • [Cites] Oncology (Williston Park). 2002 May;16(5):629-42, 644; discussion 645-6, 648 [12108890.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 Aug 1;53(5):1271-8 [12128129.001]
  • [Cites] Child Neuropsychol. 2004 Mar;10(1):14-23 [14977512.001]
  • [Cites] Lancet Oncol. 2004 Jul;5(7):399-408 [15231246.001]
  • [Cites] Am J Clin Oncol. 1982 Dec;5(6):649-55 [7165009.001]
  • (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
  •  go-up   go-down


10. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Ependymoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


11. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Ependymoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


12. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Ependymoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


13. Conklin HM, Li C, Xiong X, Ogg RJ, Merchant TE: Predicting change in academic abilities after conformal radiation therapy for localized ependymoma. J Clin Oncol; 2008 Aug 20;26(24):3965-70
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Predicting change in academic abilities after conformal radiation therapy for localized ependymoma.
  • PURPOSE: Conformal radiation therapy (CRT) aims to limit the highest radiation dose to the tissue volume at risk while sparing surrounding normal tissues.
  • This study investigated whether treatment of childhood ependymoma with CRT would preserve cognitive function.
  • Academic competence was chosen as the primary outcome measure given it is a measure of applied cognitive abilities in a child's natural setting.
  • PATIENTS AND METHODS: Eighty-seven pediatric patients diagnosed with ependymoma received CRT in which doses ranging from 54.0 to 59.4 Gy were prescribed to the postoperative tumor bed with a 10-mm clinical target volume margin.
  • Academic testing included subtests from the Wechsler Individual Achievement Test (WIAT) and the Achenbach Child Behavior Checklist.
  • Supratentorial tumor location and multiple surgeries were predictive of worse reading performance at CRT baseline.
  • Male sex, longer symptomatic interval, pre-CRT chemotherapy, pre-existing endocrine deficiencies, hydrocephalus, and younger age at CRT (< 5 years) were predictive of a significant decline in reading scores over time.
  • CONCLUSION: CRT may result in better long-term cognitive outcomes when compared to conventional radiation therapy approaches.
  • Reading appears more vulnerable than other academic skills and may decline over time despite stable intellectual functioning.

  • Genetic Alliance. consumer health - Ependymoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Ment Retard Dev Disabil Res Rev. 2006;12(3):184-91 [17061287.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2005 Dec 1;63(5):1546-54 [16115736.001]
  • [Cites] J Abnorm Child Psychol. 2008 Apr;36(3):399-410 [17940863.001]
  • [Cites] Magn Reson Imaging. 2008 May;26(4):504-12 [18068933.001]
  • [Cites] J Clin Oncol. 1999 Nov;17(11):3476-86 [10550145.001]
  • [Cites] J Clin Oncol. 2001 Apr 15;19(8):2302-8 [11304784.001]
  • [Cites] Oncology (Williston Park). 2002 May;16(5):629-42, 644; discussion 645-6, 648 [12108890.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 Sep 1;54(1):45-50 [12182973.001]
  • [Cites] Neurosurgery. 2003 Jun;52(6):1348-56; discussion 1356-7 [12762880.001]
  • [Cites] Nat Neurosci. 2003 Jul;6(7):767-73 [12754516.001]
  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):706-13 [14966095.001]
  • [Cites] J Clin Oncol. 2004 Aug 1;22(15):3156-62 [15284268.001]
  • [Cites] Am J Clin Oncol. 1982 Dec;5(6):649-55 [7165009.001]
  • [Cites] Cancer. 1984 Sep 1;54(5):825-9 [6744214.001]
  • [Cites] Neurosurgery. 1987 Nov;21(5):638-44 [3696394.001]
  • [Cites] J Neurosurg. 1989 May;70(5):707-13 [2709111.001]
  • [Cites] J Child Neurol. 1991 Jan;6(1):65-72 [2002204.001]
  • [Cites] J Neurosurg. 1994 Jun;80(6):1004-10 [8189255.001]
  • [Cites] Pediatr Neurosurg. 1994;20(4):248-53 [8043463.001]
  • [Cites] Childs Nerv Syst. 1995 Jun;11(6):340-5; discussion 345-6 [7671269.001]
  • [Cites] J Pediatr Psychol. 1995 Dec;20(6):769-84 [8558377.001]
  • [Cites] J Neurooncol. 1996 Jul;29(1):91-101 [8817420.001]
  • [Cites] J Pediatr Psychol. 1996 Aug;21(4):529-39 [8863462.001]
  • [Cites] J Learn Disabil. 1997 Nov-Dec;30(6):635-42 [9364901.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1999 Aug 1;45(1):137-45 [10477017.001]
  • [Cites] J Clin Oncol. 2005 Apr 1;23(10):2256-63 [15800316.001]
  • [Cites] J Clin Oncol. 2005 Aug 20;23(24):5511-9 [16110011.001]
  • [Cites] Ann Neurol. 2007 Apr;61(4):363-70 [17444510.001]
  • (PMID = 18711186.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA21765
  • [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/ PMC2654312
  •  go-up   go-down


14. Merchant TE: Current management of childhood ependymoma. Oncology (Williston Park); 2002 May;16(5):629-42, 644; discussion 645-6, 648
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Ependymoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


15. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of cyclooxygenase-2 in childhood ependymomas: role of COX-2 inhibitor in growth and multi-drug resistance in vitro.
  • The management of ependymomas remains one of the most frustrating issues in pediatric neuro-oncology.
  • 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

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


16. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


17. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Ependymoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


19. Timmermann B, Kortmann RD, Kühl J, Willich N, Bamberg M: [Interdisciplinary therapy of childhood ependymomas]. Strahlenther Onkol; 2002 Sep;178(9):469-79
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


21. Grill J, Pascal C, Chantal K: Childhood ependymoma: a systematic review of treatment options and strategies. Paediatr Drugs; 2003;5(8):533-43
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Childhood ependymoma: a systematic review of treatment options and strategies.
  • Childhood intracranial ependymoma have a dismal prognosis, especially in young children and when a gross total resection cannot be performed.
  • Adjuvant therapy is therefore necessary for most, if not all, patients.
  • Despite some indication that benign ependymoma (WHO grade II) could show a better outcome, histology cannot be used at present to stratify treatment protocols.Craniospinal irradiation combined with posterior fossa boost has deleterious adverse effects on cognition.
  • Consequently, pediatric oncology teams have, firstly, tried to use chemotherapy to delay or avoid irradiation, and secondly, progressively reduced irradiation fields to the tumor bed without altering the prognosis.
  • Cisplatin, at a dose of 120 mg/m(2) (cumulated response rate of 34% [95% CI 19-54%]) is the only single agent that has reproducibly shown some efficacy in ependymoma.
  • Despite some combinations showing efficacy in the adjuvant setting, childhood intracranial ependymomas can, in general, be considered as chemoresistant.
  • As the use of chemotherapy with current agents is questionable, phase II studies with new agents and combinations are necessary.
  • In this respect, hyperfractionation or radiosensitizers may be valuable therapeutic options.
  • The treatment of children with ependymoma is a challenge for all caregivers.
  • There is no doubt that any possible improvement in the management of this rare tumor will only be the result of well designed cooperative trials.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / therapy. Ependymoma / therapy
  • [MeSH-minor] Adolescent. Chemotherapy, Adjuvant. Child. Child, Preschool. Drug Resistance, Neoplasm. Drug Therapy, Combination. Humans. Infant. Infant, Newborn. Time Factors

  • Genetic Alliance. consumer health - Ependymoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurooncol. 1988 Dec;6(4):319-23 [3221259.001]
  • [Cites] Cancer Treat Rep. 1982 Dec;66(12 ):2013-20 [6890409.001]
  • [Cites] J Natl Cancer Inst. 2001 Jun 20;93(12):889-90 [11416101.001]
  • [Cites] J Neurooncol. 1989 May;7(1):5-11 [2754456.001]
  • [Cites] J Clin Oncol. 2001 Mar 1;19(5):1288-96 [11230470.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Jun 1;47(3):585-9 [10837939.001]
  • [Cites] Am J Clin Oncol. 2002 Apr;25(2):117-22 [11943886.001]
  • [Cites] Pediatr Neurosurg. 1998 Apr;28(4):215-22 [9732252.001]
  • [Cites] J Neurooncol. 2002 Jan;56(1):87-94 [11949831.001]
  • [Cites] Pediatr Neurosurg. 1996 Jun;24(6):299-305 [8988495.001]
  • [Cites] Radiother Oncol. 1997 Jun;43(3):269-73 [9215786.001]
  • [Cites] Med Pediatr Oncol. 1996 Jul;27(1):8-14 [8614396.001]
  • [Cites] Cancer. 2000 Feb 15;88(4):870-5 [10679657.001]
  • [Cites] Childs Nerv Syst. 1999 Oct;15(10):563-70 [10550587.001]
  • [Cites] Pediatr Neurol. 2001 Feb;24(2):117-21 [11275460.001]
  • [Cites] Childs Nerv Syst. 1999 Oct;15(10):498-505 [10550581.001]
  • [Cites] Childs Brain. 1983;10(3):145-56 [6872622.001]
  • [Cites] Surg Neurol. 2000 Jul;54(1):19-26; discussion 26 [11024503.001]
  • [Cites] Med Pediatr Oncol. 1998 Jun;30(6):319-29; discussion 329-31 [9589080.001]
  • [Cites] Acta Neurochir (Wien). 1991;111(3-4):96-102 [1950695.001]
  • [Cites] Cancer Chemother Pharmacol. 1997;39(3):187-91 [8996518.001]
  • [Cites] J Clin Oncol. 2001 Aug 1;19(15):3588-9 [11481371.001]
  • [Cites] Pediatr Neurosurg. 1990-1991;16(2):57-65 [2132926.001]
  • [Cites] J Neurooncol. 1987;5(3):241-4 [3681386.001]
  • [Cites] J Pediatr Hematol Oncol. 1998 Mar-Apr;20(2):125-30 [9544162.001]
  • [Cites] Radiat Med. 1994 Nov-Dec;12(6):269-72 [7724818.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1992;23 (2):313-9 [1587752.001]
  • [Cites] Acta Neurochir (Wien). 1990;106(3-4):93-8 [2178314.001]
  • [Cites] Cancer Chemother Pharmacol. 1994;35(2):127-31 [7987988.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 Feb 1;52(2):325-32 [11872277.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1982 Jul;8(7):1083-113 [6288633.001]
  • [Cites] Pediatr Neurosurg. 1998 Mar;28(3):135-42 [9705591.001]
  • [Cites] J Clin Oncol. 1987 Aug;5(8):1221-31 [3040919.001]
  • [Cites] Cancer Res. 1989 Feb 1;49(3):736-41 [2491958.001]
  • [Cites] J Clin Oncol. 1992 Feb;10(2):249-56 [1732426.001]
  • [Cites] J Neurosurg. 2000 Oct;93(4):605-13 [11014538.001]
  • [Cites] Cancer. 1995 Jun 1;75(11):2762-7 [7743483.001]
  • [Cites] J Clin Oncol. 1998 Jan;16(1):210-21 [9440745.001]
  • [Cites] Neurology. 1984 May;34(5):615-9 [6538653.001]
  • [Cites] J Clin Oncol. 1997 May;15(5):1814-23 [9164190.001]
  • [Cites] J Pediatr Hematol Oncol. 2000 Jan-Feb;22(1):41-4 [10695820.001]
  • [Cites] Arch Fr Pediatr. 1988 Apr;45(4):249-54 [3408307.001]
  • [Cites] Cancer Res. 1995 Jul 1;55(13):2853-7 [7796412.001]
  • [Cites] Pediatr Neurosci. 1988;14 (6):277-85 [3270047.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Jan 15;46(2):287-95 [10661334.001]
  • [Cites] Klin Padiatr. 1998 Jul-Aug;210(4):227-33 [9743957.001]
  • [Cites] J Clin Oncol. 1996 Feb;14(2):382-8 [8636747.001]
  • [Cites] Cancer. 1985 Oct 1;56(7):1497-501 [4040799.001]
  • [Cites] Pediatr Neurosurg. 2001 Feb;34(2):77-87 [11287807.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Mar 1;40(4):845-50 [9531369.001]
  • [Cites] Childs Nerv Syst. 1998 Oct;14(10):590-5 [9840385.001]
  • [Cites] Neurosurgery. 1993 Feb;32(2):169-75 [8437653.001]
  • [Cites] Pediatr Neurol. 1996 Apr;14(3):216-19 [8736405.001]
  • [Cites] J Neurooncol. 1987;5(3):217-29 [3316521.001]
  • [Cites] Cancer Res. 1991 Jan 15;51(2):619-23 [1824685.001]
  • [Cites] Pediatr Neurosurg. 1998 Jun;28(6):314-9 [9782208.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1990 Dec;19(6):1497-502 [2262372.001]
  • [Cites] Radiother Oncol. 1995 Aug;36(2):101-6 [7501807.001]
  • [Cites] Eur J Cancer. 2001 Nov;37(16):1981-93 [11597375.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1999 Aug 1;45(1):137-45 [10477017.001]
  • [Cites] J Neurooncol. 1986;3(4):341-2 [3958779.001]
  • [Cites] Cancer. 1991 Jun 1;67(11):2766-71 [2025840.001]
  • [Cites] J Clin Oncol. 2003 Mar 15;21(6):1074-81 [12637473.001]
  • [Cites] Br J Cancer. 1994 Mar;69(3):452-6 [8123472.001]
  • [Cites] Med Pediatr Oncol. 1997 Aug;29(2):79-85 [9180907.001]
  • [Cites] Med Pediatr Oncol. 1997 Jul;29(1):28-32 [9142202.001]
  • [Cites] J Clin Oncol. 1988 Jan;6(1):62-6 [2826716.001]
  • [Cites] J Pediatr Hematol Oncol. 1999 May-Jun;21(3):203-11 [10363853.001]
  • [Cites] Cancer. 1998 Aug 15;83(4):813-6 [9708950.001]
  • [Cites] J Neurosurg. 1997 Jun;86(6):943-9 [9171172.001]
  • [Cites] J Neurosurg. 1998 Apr;88(4):695-703 [9525716.001]
  • [Cites] Semin Oncol. 2001 Oct;28(5 Suppl 17):34-9 [11740805.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2001 Mar 1;49(3):757-61 [11172959.001]
  • [Cites] Cancer Res. 1993 Jul 15;53(14):3416-20 [8324751.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1994 Jan 15;28(2):381-6 [8276653.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1991 Aug;21(3):825-30 [1831193.001]
  • [Cites] N Engl J Med. 1993 Jun 17;328(24):1725-31 [8388548.001]
  • [Cites] J Neurooncol. 1999 May;43(1):43-7 [10448870.001]
  • [Cites] J Clin Oncol. 1994 Aug;12(8):1607-15 [8040673.001]
  • [Cites] Med Pediatr Oncol. 1993;21(1):49-53 [8381203.001]
  • [Cites] J Neurooncol. 1990 Aug;9(1):69-76 [2213117.001]
  • [Cites] Biochem Pharmacol. 1989 Mar 15;38(6):929-34 [2930593.001]
  • [Cites] Cancer. 1996 Aug 1;78(3):527-31 [8697400.001]
  • [Cites] Neuropathol Appl Neurobiol. 1994 Apr;20(2):118-21 [7915406.001]
  • [Cites] Neurosurgery. 1991 May;28(5):666-71; discussion 671-2 [1876244.001]
  • [Cites] Med Pediatr Oncol. 1998;Suppl 1:1-9 [9659940.001]
  • [Cites] Med Pediatr Oncol. 1995 Feb;24(2):104-8 [7990757.001]
  • [Cites] Acta Oncol. 1994;33(1):29-32 [8142120.001]
  • [Cites] Neuro Oncol. 2002 Apr;4(2):102-8 [11916501.001]
  • [Cites] Brain Pathol. 1997 Apr;7(2):807-22 [9161731.001]
  • [Cites] J Neuropathol Exp Neurol. 1996 May;55(5):540-8 [8627345.001]
  • [Cites] Pediatr Neurosurg. 1997 Aug;27(2):84-91 [9520080.001]
  • [Cites] Pediatr Neurosurg. 1996 Jul;25(1):7-12 [9055328.001]
  • [Cites] Pediatr Neurosurg. 1996;24(3):119-25 [8870014.001]
  • [Cites] Clin Cancer Res. 1997 Dec;3(12 Pt 1):2459-63 [9815647.001]
  • [Cites] J Chronic Dis. 1961 Apr;13:346-53 [13704181.001]
  • [Cites] J Neurooncol. 1985;3(3):263-9 [3903064.001]
  • [Cites] J Neurooncol. 1998 Apr;37(2):135-43 [9524092.001]
  • [Cites] Pediatr Pathol Lab Med. 1996 Jul-Aug;16(4):551-61 [9025853.001]
  • [Cites] J Neurooncol. 1997 May;32(3):243-52 [9049886.001]
  • [Cites] Neurosurgery. 1995 Oct;37(4):655-66; discussion 666-7 [8559293.001]
  • [Cites] J Neurooncol. 1996 Jan;27(1):87-98 [8699230.001]
  • [Cites] Pediatr Neurosurg. 1998 May;28(5):273-8 [9732262.001]
  • [Cites] Pediatr Neurosurg. 1998 Jul;29(1):40-5 [9755311.001]
  • [Cites] Cancer. 1990 Dec 15;66(12):2465-9 [2249186.001]
  • [Cites] Neurosurgery. 1991 May;28(5):659-64; discussion 664-5 [1876243.001]
  • [Cites] Cancer. 1997 Jul 15;80(2):341-7 [9217048.001]
  • [Cites] J Neurooncol. 1995;25(1):77-84 [8523093.001]
  • [Cites] J Neurosurg. 1990 Mar;72(3):408-17 [2303876.001]
  • [Cites] Invest New Drugs. 1990 Nov;8(4):401-6 [2084075.001]
  • [Cites] Neurosurgery. 1997 Apr;40(4):856-60; discussion 860 [9092863.001]
  • (PMID = 12895136.001).
  • [ISSN] 1174-5878
  • [Journal-full-title] Paediatric drugs
  • [ISO-abbreviation] Paediatr Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 120
  •  go-up   go-down






Advertisement