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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.
  • Additional experiments conducted against subcutaneous D-245 MG xenografts by using reduced doses of 13.5 or 9.0 mg/kg daily for five days demonstrated tumor growth delays of 82.2 and 53.5 days, with corresponding tumor regressions in 8 of 9 and 9 of 10 treated mice, respectively (all values, p < 0.001), with one toxic death.
  • These findings suggest that VNP40101M is active in the treatment of a wide range of human central nervous system tumors and warrants translation to the clinic.

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  • [Cites] Cancer Chemother Pharmacol. 1994;34(2):171-4 [8194169.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jul;87(14):5368-72 [2164681.001]
  • [Cites] Cancer Res. 1995 Jul 1;55(13):2853-7 [7796412.001]
  • [Cites] Cancer Res. 1997 Jul 15;57(14):2933-6 [9230204.001]
  • [Cites] Invest New Drugs. 2005 Mar;23(2):123-35 [15744588.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] Biochem Pharmacol. 2000 Feb 1;59(3):283-91 [10609557.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):3033-8 [11306484.001]
  • [Cites] Int J Toxicol. 2002 Jan-Feb;21(1):23-38 [11936896.001]
  • [Cites] Cancer Chemother Pharmacol. 2004 Apr;53(4):288-95 [14685775.001]
  • [Cites] Clin Cancer Res. 2004 May 1;10(9):2908-17 [15131024.001]
  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] Neurosurgery. 1979 Apr;4(4):308-14 [450229.001]
  • [Cites] Cancer Res. 1988 Aug 1;48(15):4189-95 [3390813.001]
  • [Cites] J Neurooncol. 1994;20(2):111-20 [7807189.001]
  • (PMID = 17522334.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / P50 NS020023; United States / NINDS NIH HHS / NS / 5P50-NS20023-23
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hydrazines; 0 / Prodrugs; 0 / Sulfonamides; 14J2G0U3NQ / laromustine
  • [Other-IDs] NLM/ PMC1907418
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2. Mahfouz S, Aziz AA, Gabal SM, el-Sheikh S: Immunohistochemical study of CD99 and EMA expression in ependymomas. Medscape J Med; 2008;10(2):41
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  • Tumors of the central nervous system (CNS) represent a unique, heterogeneous population of neoplasms and include both benign and malignant tumors.
  • The present study was carried out on a total of 79 archival cases of ependymal tumors in addition to a variety of other primary CNS tumors.
  • It was found that all 38 ependymoma cases (classic and nonclassic) showed positive membranous and intracytoplasmic CD99 immunoreactivity.
  • Upon comparing with other CNS tumors (41 cases), it was found that CD99 could differentiate between ependymomas and nonependymal tumors, but intensity and pattern of staining were of no consequence in determining variant type or degree of histologic aggressiveness.
  • In regard to EMA immunoreactivity, which was restricted to the ependymoma group, 2 patterns of staining could be detected--the intracytoplasmic dotlike pattern and the ringlike pattern--but some cases were completely negative.
  • Thus, EMA was found to be of little value in the diagnosis of ependymoma and in the differentiation between different types and grades.
  • CD99 can hence be recommended for use as a good marker for differentiation between ependymal and other CNS tumors.
  • EMA expression and pattern of distribution, on the other hand, cannot be employed to determine the type of variant or the degree of tumor aggressiveness, and hence cannot predict the behavior of ependymal neoplasms.
  • [MeSH-major] Antigens, CD / analysis. Biomarkers, Tumor / analysis. Brain Neoplasms / diagnosis. Brain Neoplasms / metabolism. Cell Adhesion Molecules / analysis. Ependymoma / diagnosis. Ependymoma / metabolism. Mucin-1 / analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Female. Gene Expression Profiling. Humans. Infant. Infant, Newborn. Male. Middle Aged. Neoplasm Proteins / analysis. Sensitivity and Specificity

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  • [Cites] Appl Immunohistochem Mol Morphol. 2000 Mar;8(1):25-31 [10937045.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2001 Jun;9(2):125-9 [11396629.001]
  • [Cites] Diagn Cytopathol. 2002 Apr;26(4):247-50 [11933271.001]
  • [Cites] J Neurooncol. 2002 May;58(1):13-9 [12160136.001]
  • [Cites] Exp Mol Med. 2002 Jul 31;34(3):177-83 [12216109.001]
  • [Cites] Acta Neuropathol. 2003 Oct;106(4):385-8 [12898159.001]
  • [Cites] Mod Pathol. 2003 Oct;16(10):980-91 [14559980.001]
  • [Cites] Am J Pathol. 2003 Nov;163(5):1721-7 [14578171.001]
  • [Cites] Curr Treat Options Oncol. 2003 Dec;4(6):517-23 [14585232.001]
  • [Cites] Cancer. 2004 Mar 15;100(6):1230-7 [15022291.001]
  • [Cites] J Neuropathol Exp Neurol. 2004 Mar;63(3):185-92 [15055442.001]
  • [Cites] Neuropathol Appl Neurobiol. 1988 May-Jun;14(3):197-205 [3405393.001]
  • [Cites] Cancer Res. 1988 Nov 1;48(21):6127-31 [2844401.001]
  • [Cites] Acta Neuropathol. 1989;78(3):325-8 [2763805.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1990;417(2):97-103 [1695040.001]
  • [Cites] Arch Pathol Lab Med. 1990 Sep;114(9):956-60 [2390011.001]
  • [Cites] Cancer. 1991 Apr 1;67(7):1886-93 [1848471.001]
  • [Cites] Acta Neuropathol. 1991;82(3):208-16 [1718129.001]
  • [Cites] Am J Surg Pathol. 1994 May;18(5):486-94 [7513503.001]
  • [Cites] J Neurooncol. 2005 Jan;71(2):189-93 [15690137.001]
  • [Cites] Brain Tumor Pathol. 2004;21(1):17-21 [15696964.001]
  • [Cites] Cancer. 2005 Jun 15;103(12):2598-605 [15861411.001]
  • [Cites] Histopathology. 2007 Feb;50(3):365-70 [17257132.001]
  • [Cites] J Neurooncol. 2002 Jul;58(3):255-70 [12187959.001]
  • [Cites] Acta Neuropathol. 1997 Mar;93(3):310-6 [9083565.001]
  • [Cites] Neuropathology. 2004 Dec;24(4):330-5 [15641594.001]
  • [Cites] Pathol Res Pract. 2004;200(10):717-25 [15648610.001]
  • (PMID = 18382710.001).
  • [ISSN] 1934-1997
  • [Journal-full-title] Medscape journal of medicine
  • [ISO-abbreviation] Medscape J Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / CD99 protein, human; 0 / Cell Adhesion Molecules; 0 / Mucin-1; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC2270873
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3. Nicholson HS, Kretschmar CS, Krailo M, Bernstein M, Kadota R, Fort D, Friedman H, Harris MB, Tedeschi-Blok N, Mazewski C, Sato J, Reaman GH: Phase 2 study of temozolomide in children and adolescents with recurrent central nervous system tumors: a report from the Children's Oncology Group. Cancer; 2007 Oct 1;110(7):1542-50
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  • [Title] Phase 2 study of temozolomide in children and adolescents with recurrent central nervous system tumors: a report from the Children's Oncology Group.
  • BACKGROUND: Effective chemotherapy is lacking for most types of central nervous system (CNS) tumors in children.
  • Temozolomide, an agent with activity against adult brain tumors, was investigated in children and adolescents with recurrent CNS tumors.
  • RESULTS: The cohort comprised 122 patients, including 113 with CNS tumors.
  • Among 104 evaluable patients with CNS tumors, 5 PRs and 1 CR were observed.
  • PRs occurred in 1 of 23 evaluable patients with high-grade astrocytoma, 1 of 21 with low-grade astrocytoma, and 3 of 25 with medulloblastoma/primitive neuroectodermal tumor (PNET).
  • No responses were observed in patients with ependymoma, brain-stem glioma, or other CNS tumors.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Administration, Oral. Adolescent. Adult. Astrocytoma / drug therapy. Central Nervous System Neoplasms / drug therapy. Child. Child, Preschool. Drug Administration Schedule. Ependymoma / drug therapy. Female. Humans. Infant. Male. Medulloblastoma / drug therapy. Neuroectodermal Tumors, Primitive / drug therapy. Treatment Outcome


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4. Rajaram V, Gutmann DH, Prasad SK, Mansur DB, Perry A: Alterations of protein 4.1 family members in ependymomas: a study of 84 cases. Mod Pathol; 2005 Jul;18(7):991-7
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  • Ependymomas are common pediatric and adult CNS malignancies with a wide biologic spectrum that is often hard to predict using classic prognostic variables.
  • The majority of cases harbored one or more detectable genetic alterations, but we found that 4.1B gene deletions and 4.1R loss of expression were statistically more common in the pediatric vs adult, intracranial vs spinal, and grade III vs grade I/II subsets (P-values of 0.038 to <0.001).
  • Also, 4.1G deletions were seen in 11/27 (41%) patients who either died of disease or had residual/recurrent tumor vs 5/41 patients with no evidence of disease at last follow-up (P=0.009).
  • [MeSH-major] Ependymoma / pathology. Membrane Proteins / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Blood Proteins / analysis. Blood Proteins / genetics. Brain Neoplasms / genetics. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Child. Child, Preschool. Cohort Studies. Cytoskeletal Proteins / analysis. Cytoskeletal Proteins / genetics. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Infant. Microfilament Proteins. Microtubule-Associated Proteins / analysis. Microtubule-Associated Proteins / genetics. Middle Aged. Neurofibromin 2 / analysis. Neurofibromin 2 / genetics. Spinal Cord Neoplasms / genetics. Spinal Cord Neoplasms / metabolism. Spinal Cord Neoplasms / pathology. Tumor Suppressor Proteins / analysis. Tumor Suppressor Proteins / genetics

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  • (PMID = 15731777.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Proteins; 0 / Cytoskeletal Proteins; 0 / EPB41L3 protein, human; 0 / Membrane Proteins; 0 / Microfilament Proteins; 0 / Microtubule-Associated Proteins; 0 / Neurofibromin 2; 0 / Tumor Suppressor Proteins; 0 / erythrocyte membrane band 4.1 protein
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5. Azarpira N, Rakei M, Mokhtari M: Cytologic findings in malignant ependymoma: a case report. Acta Cytol; 2010 Sep-Oct;54(5 Suppl):1023-6
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  • [Title] Cytologic findings in malignant ependymoma: a case report.
  • BACKGROUND: Intraoperative imprint cytology has proved to be a valuable tool in the diagnosis of central nervous system (CNS) tumors.
  • Ependymomas are uncommon glial neoplasms of the CNS, arising from ependymal lining of the ventricular system and central canal of the spinal cord.
  • Anaplastic ependymoma is a rare tumor that causes diagnostic difficulties in imprint cytology because of variable cytomorphologic findings.
  • Computed tomography of the head showed hydrocephalus with a large parietal lobe tumor with midline structural shift.
  • The tumor showed pseudorosettes with glial fibrillary acidic protein and epithelial membrane antigen expression.
  • [MeSH-major] Central Nervous System Neoplasms / pathology. Ependymoma / pathology
  • [MeSH-minor] Cell Aggregation. Fatal Outcome. Female. Glial Fibrillary Acidic Protein / metabolism. Humans. Rosette Formation. Tomography, X-Ray Computed. Young Adult

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  • (PMID = 21053591.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein
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6. Attard TM, Giglio P, Koppula S, Snyder C, Lynch HT: Brain tumors in individuals with familial adenomatous polyposis: a cancer registry experience and pooled case report analysis. Cancer; 2007 Feb 15;109(4):761-6
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  • [Title] Brain tumors in individuals with familial adenomatous polyposis: a cancer registry experience and pooled case report analysis.
  • They are at an increased risk of brain tumors, including cerebellar medulloblastoma, when compared with the general population (Brain Tumor Polyposis-BTP Type 2).
  • Genotype-phenotype correlations between APC gene mutations and central nervous system (CNS) tumors have, thus far not been successful.
  • METHODS: The authors analyzed their established hereditary CRC Registry for brain tumors in FAP pedigrees (56 families, 213 individuals), pooled their patients with BTP and known APC mutations with those reported thus far elsewhere, and compared the resulting mutation distribution of FAP-BTP with the mutation distribution for APC mutations in the US.
  • RESULTS: Twenty-eight patients from 24 families were accrued, the most common brain tumor in BTP was medulloblastoma (60%) predominantly in females (12:5) under the age of 20 (mean age 14.7 SD 9.2).
  • Other histologic subtypes included astrocytoma and ependymoma.
  • Analysis of the pooled APC mutation data by Chi-square test of association shows an odds ratio of 3.7 (P < .005) for all brain tumor subtypes and 13.1 (P < .001) for medulloblastoma in patients harboring segment 2 APC mutation (codons 679-1224) compared to nonsegment 2 mutation.
  • CONCLUSIONS: In patients with FAP and identifiable APC gene mutation, CNS tumors, especially medulloblastoma which developed in most cases during childhood, are more common in females with FAP and APC gene mutation in codons 686-1217.
  • [MeSH-major] Adenomatous Polyposis Coli / complications. Adenomatous Polyposis Coli Protein / genetics. Brain Neoplasms / complications. Mutation / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Codon. Female. Humans. Male. Pedigree. Registries


7. Wang Z, Huang G, Yan P, Liang R, Wang J, Yan Q, Zhang J, Cheng H, Hu P, Ma MJ: Ectopic cervical anaplastic ependymoma. Pathol Int; 2005 Dec;55(12):781-4
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  • [Title] Ectopic cervical anaplastic ependymoma.
  • Ependymomas generally arise in the central nervous system (CNS), although rare primary extraneural ependymomas have been observed.
  • Reported herein for the first time is the case of a patient with primary ectopic cervical anaplastic ependymoma.
  • The tumor was found in the right neck root region of a 35-year-old man.
  • No additional tumor was found in the CNS or in other parts of the body.
  • Microscopically, the tumor consisted of round to oval cells with fine chromatin, distinct nucleoli, moderate nuclear atypia and numerous mitoses (>25/10 high-power fields) in a densely cellular growth pattern with characteristic fibrillary cytoplasm and formation of perivascular pseudorosettes.
  • By immunohistochemistry, the tumor cells were positive for glial fibrillary acidic protein, epithelial membrane antigen (EMA), vimentin and S-100 protein.
  • EMA staining showed a membranous as well as a paranuclear pattern of immunoreactivity.
  • Electron microscopic studies revealed that tumor cells form micro rosettes, into which microvilli and cilia projected.
  • The diagnosis was World Health Organization grade III anaplastic ependymoma.
  • There is no evidence of local tumor recurrence or distant metastasis after 30 months follow up.
  • [MeSH-major] Ependymoma / pathology. Head and Neck Neoplasms / pathology
  • [MeSH-minor] Adult. Glial Fibrillary Acidic Protein / analysis. Humans. Male. Mucin-1 / analysis. Vimentin / analysis

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  • (PMID = 16287493.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Mucin-1; 0 / Vimentin
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8. Kashyap R, Ryan C, Sharma R, Maloo MK, Safadjou S, Graham M, Tretheway D, Jain A, Orloff M: Liver grafts from donors with central nervous system tumors: a single-center perspective. Liver Transpl; 2009 Oct;15(10):1204-8
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  • [Title] Liver grafts from donors with central nervous system tumors: a single-center perspective.
  • The aim of this study was to analyze our experience with the use of liver grafts from donors with central nervous system (CNS) tumors.
  • A retrospective review of 1173 liver transplants performed between 1992 and 2006 identified 42 donors diagnosed with a CNS tumor.
  • Twenty (47.6%) of the CNS tumors were glioblastoma multiforme (astrocytoma grade IV), 11 (26.2%) were other astrocytomas, and 1 (2.4%) was an anaplastic ependymoma.
  • Over 80% of the patients had at least 1 kind of invasive procedure violating the blood-brain barrier.
  • The rate of recurrence for the entire group was 2.4% (all CNS tumors).
  • There was no difference in survival between recipients of grafts from donors with CNS tumors and recipients of grafts from donors without CNS tumors (1 year: 82% versus 83.3%, P = not significant; 3 years: 77.4% versus 72%, P = not significant).
  • In conclusion, in our experience, despite violation of the blood-brain barrier and high-grade CNS tumors, recurrence was uncommon.
  • [MeSH-major] Central Nervous System Neoplasms / diagnosis. Liver Diseases / therapy. Liver Transplantation / methods. Tissue and Organ Procurement / methods
  • [MeSH-minor] Adult. Blood-Brain Barrier. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Retrospective Studies. Time Factors. Tissue Donors. Treatment Outcome

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  • [Copyright] Copyright 2009 AASLD
  • [CommentIn] Liver Transpl. 2010 Jul;16(7):916 [20583090.001]
  • [CommentIn] Liver Transpl. 2010 Jul;16(7):914-5 [20583288.001]
  • (PMID = 19790151.001).
  • [ISSN] 1527-6473
  • [Journal-full-title] Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society
  • [ISO-abbreviation] Liver Transpl.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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9. Marinovic T, Grahovac G, Habek M, Lambasa S, Tomac D: Simultaneous conus medullaris ependymoma and cerebellar astrocytoma in the same patient. Clin Neuropathol; 2009 May-Jun;28(3):173-6
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  • [Title] Simultaneous conus medullaris ependymoma and cerebellar astrocytoma in the same patient.
  • Multiple primary tumors in the central nervous system of different histological cell types are uncommon.
  • We report a patient who had pilocytic astrocytoma in the cerebellum and ependymoma in the cauda equina region, occurring simultaneously.
  • The suggested mechanism of this association is that primitive multipotent cells might have been displaced in the different CNS areas and developed in different tumor cells.
  • Multiplicity of primary CNS tumors should be considered in certain occasions, when clinical symptoms and signs are pointing in that direction.
  • [MeSH-major] Astrocytoma / pathology. Cerebellar Neoplasms / pathology. Ependymoma / pathology. Neoplasms, Multiple Primary / pathology. Spinal Cord Neoplasms / pathology
  • [MeSH-minor] Adult. Cauda Equina / pathology. Cauda Equina / surgery. Female. Humans. Magnetic Resonance Imaging. Neurosurgical Procedures

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  • (PMID = 19537133.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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10. McGuire CS, Sainani KL, Fisher PG: Incidence patterns for ependymoma: a surveillance, epidemiology, and end results study. J Neurosurg; 2009 Apr;110(4):725-9
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  • [Title] Incidence patterns for ependymoma: a surveillance, epidemiology, and end results study.
  • OBJECT: Previous small studies disagree about which clinical risk factors influence ependymoma incidence.
  • The authors analyzed a large, population-based cancer registry to examine the relationship of incidence to patient age, sex, race, and tumor location, and to determine incidence trends over the past 3 decades.
  • For children, the age at diagnosis differed significantly by tumor location, with the mean age for patients with infratentorial tumors calculated as 5 +/- 0.4 years; for supratentorial tumors it was 7.77 +/- 0.6 years, and for spinal lesions it was 12.16 +/- 0.8 years. (Values are expressed as the mean +/- standard error [SE].
  • CONCLUSIONS: Males have a higher incidence of ependymoma than do females.
  • Ependymoma occurs within the CNS at distinct locations at different ages, consistent with hypotheses postulating distinct populations of radial glial stem cells within the CNS.
  • Ependymoma incidence appears to have increased over the past 3 decades, but only in adults.
  • [MeSH-major] Brain Neoplasms / epidemiology. Ependymoma / epidemiology. Spinal Neoplasms / epidemiology
  • [MeSH-minor] Adolescent. Adult. Age Factors. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Male. Middle Aged. SEER Program. Sex Factors. United States / epidemiology


11. Mogler C, Kohlhof P, Penzel R, Grenacher L, Haag GM, Schirmacher P, Mueller W: A primary malignant ependymoma of the abdominal cavity: a case report and review of the literature. Virchows Arch; 2009 Apr;454(4):475-8
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  • [Title] A primary malignant ependymoma of the abdominal cavity: a case report and review of the literature.
  • Ependymomas generally arise in the central nervous system (CNS).
  • Here, we describe the first case of an overt malignant primary extraneural ependymoma in a young female patient.
  • Careful reevaluation together with extensive review of the literature and comparison of related cases established the diagnosis after treatment failure and tumor progression.
  • The tumor was large and firm with some small cysts and showed pseudorosettes with strong glial fibrillary acidic protein (GFAP) expression.
  • [MeSH-major] Abdominal Cavity / pathology. Diagnostic Errors. Ependymoma / diagnosis
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Autonomic Pathways / pathology. Combined Modality Therapy. Digestive System Surgical Procedures. Female. Gastrointestinal Neoplasms / pathology. Glial Fibrillary Acidic Protein / biosynthesis. Humans. Immunohistochemistry. Peripheral Nervous System Neoplasms / pathology

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  • (PMID = 19238432.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glial Fibrillary Acidic Protein
  • [Number-of-references] 15
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12. Fassett DR, Pingree J, Kestle JR: The high incidence of tumor dissemination in myxopapillary ependymoma in pediatric patients. Report of five cases and review of the literature. J Neurosurg; 2005 Jan;102(1 Suppl):59-64
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  • [Title] The high incidence of tumor dissemination in myxopapillary ependymoma in pediatric patients. Report of five cases and review of the literature.
  • Only 8 to 20% of these tumors occur in the first two decades of life, making this tumor a rarity in pediatric neurosurgery.
  • Four (80%) of these five patients suffered from disseminated disease of the central nervous system (CNS) at the time of presentation; this incidence is much higher than that reported in the combined adult and pediatric literature.
  • In nine cases (35%) CNS metastases occurred.
  • In those cases in which patients underwent screening for CNS tumor dissemination, however, the incidence of disseminated disease was 58% (seven of 12 patients).
  • In pediatric patients MPEs may spread throughout the CNS via cerebrospinal fluid pathways; therefore, MR imaging of the entire CNS axis is recommended at both presentation and follow-up review to detect tumor dissemination.
  • [MeSH-major] Brain Neoplasms / secondary. Ependymoma / pathology. Ependymoma / secondary. Neoplasm Metastasis. Spinal Cord Neoplasms / pathology


13. Rodríguez D, Cheung MC, Housri N, Quinones-Hinojosa A, Camphausen K, Koniaris LG: Outcomes of malignant CNS ependymomas: an examination of 2408 cases through the Surveillance, Epidemiology, and End Results (SEER) database (1973-2005). J Surg Res; 2009 Oct;156(2):340-51
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  • [Title] Outcomes of malignant CNS ependymomas: an examination of 2408 cases through the Surveillance, Epidemiology, and End Results (SEER) database (1973-2005).
  • BACKGROUND: Determine the role of surgery and radiation therapy for patients with malignant CNS ependymomas.
  • Patients who successfully underwent surgical resection had a considerably longer median survival (237 mo versus 215 mo, P<0.001) as well as a significantly improved five-year survival (72.4% versus 52.6%, P<0.001).
  • Univariate analysis demonstrated that age, gender, ethnicity, primary tumor site, WHO grade and surgical resection were significant predictors of improved survival for ependymoma patients.
  • Multivariate analysis identified that a WHO grade III tumor, male gender, patient age, intracranial tumor locations and failure to undergo surgical resection were independent predictors of poorer outcomes.
  • [MeSH-major] Central Nervous System Neoplasms / radiotherapy. Central Nervous System Neoplasms / surgery. Ependymoma / radiotherapy. Ependymoma / surgery
  • [MeSH-minor] Adult. Female. Humans. Male. SEER Program. Treatment Outcome. United States / epidemiology

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  • (PMID = 19577759.001).
  • [ISSN] 1095-8673
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Engelhard HH, Corsten LA: Leptomeningeal metastasis of primary central nervous system (CNS) neoplasms. Cancer Treat Res; 2005;125:71-85
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  • [Title] Leptomeningeal metastasis of primary central nervous system (CNS) neoplasms.
  • Leptomeningeal dissemination of primary CNS tumors varies widely by histologic subtype.
  • In certain tumors including medulloblastoma, ependymoma, germ cell tumors, and primary CNS lymphoma, seeding of the cerebrospinal fluid space is a critical factor in determining stage, prognosis and appropriate therapy.
  • Other tumor types, such as glioma, may have radiographic evidence of leptomeningeal metastases without clear impact on prognosis or therapy.
  • [MeSH-major] Brain Neoplasms / pathology. Central Nervous System Neoplasms / pathology. Meningeal Neoplasms / secondary
  • [MeSH-minor] Adult. Child. Humans. Incidence

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  • (PMID = 16211884.001).
  • [ISSN] 0927-3042
  • [Journal-full-title] Cancer treatment and research
  • [ISO-abbreviation] Cancer Treat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 86
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15. Rousseau A, Idbaih A, Ducray F, Crinière E, Fèvre-Montange M, Jouvet A, Delattre JY: Specific chromosomal imbalances as detected by array CGH in ependymomas in association with tumor location, histological subtype and grade. J Neurooncol; 2010 May;97(3):353-64
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  • [Title] Specific chromosomal imbalances as detected by array CGH in ependymomas in association with tumor location, histological subtype and grade.
  • Moreover, key molecular events in the pathogenesis of ependymoma are yet to be defined.
  • The main objective of the present study was to identify specific patterns of chromosomal aberrations that correlate with tumor location, histological subtype and grade.
  • Forty-five ependymoma samples were analyzed by 1-megabase resolution array comparative genomic hybridization (CGH).
  • Identification of specific genomic imbalances at a given tumor location suggests that ependymomas from different central nervous system (CNS) regions represent genetically distinct diseases.
  • [MeSH-major] Brain Neoplasms. Chromosome Aberrations. Chromosomes. Ependymoma. Gene Expression Regulation, Neoplastic
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Comparative Genomic Hybridization / methods. Female. Gene Expression Profiling / methods. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis / methods. Young Adult

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  • (PMID = 19865800.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Sharma MC, Ghara N, Jain D, Sarkar C, Singh M, Mehta VS: A study of proliferative markers and tumor suppressor gene proteins in different grades of ependymomas. Neuropathology; 2009 Apr;29(2):148-55
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  • [Title] A study of proliferative markers and tumor suppressor gene proteins in different grades of ependymomas.
  • Ependymomas are CNS tumors that originate from the spinal canal and walls of the ventricular system.
  • Histopathologic grades show relationship with MIB1 and Topo IIalpha labelling indices and cut-off values of 5% can differentiate between anaplastic and lower grades. p53 and MDM2 proteins expression are not common in ependymomas; however, they are seen in higher grades only and may be involved in the tumor progression.
  • [MeSH-major] Central Nervous System Neoplasms / metabolism. DNA Topoisomerases, Type II / metabolism. Ependymoma / metabolism. Ependymoma / pathology. Ki-67 Antigen / metabolism. Proto-Oncogene Proteins c-mdm2 / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Humans. Immunohistochemistry. Infant. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Young Adult

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  • (PMID = 18721229.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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17. Capper D, Weissert S, Balss J, Habel A, Meyer J, Jäger D, Ackermann U, Tessmer C, Korshunov A, Zentgraf H, Hartmann C, von Deimling A: Characterization of R132H mutation-specific IDH1 antibody binding in brain tumors. Brain Pathol; 2010 Jan;20(1):245-54
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  • [Title] Characterization of R132H mutation-specific IDH1 antibody binding in brain tumors.
  • Here we investigate the capability of this antibody to differentiate wild type and mutated IDH1 protein in central nervous system (CNS) tumors by Western blot and immunohistochemistry.
  • Immunohistochemistry of 345 primary brain tumors demonstrated a strong cytoplasmic and weaker nuclear staining in 122 cases.
  • Intriguing is the ability of mIDH1R132H to detect single infiltrating tumor cells.
  • The very high frequency and the distribution of this mutation among specific brain tumor entities allow the highly sensitive and specific discrimination of various tumors by immunohistochemistry, such as anaplastic astrocytoma from primary glioblastoma or diffuse astrocytoma World Health Organization (WHO) grade II from pilocytic astrocytoma or ependymoma.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / enzymology. Brain Neoplasms / genetics. Ependymoma / genetics. Glioma / enzymology. Glioma / genetics. Isocitrate Dehydrogenase / genetics. Isocitrate Dehydrogenase / immunology
  • [MeSH-minor] Adolescent. Adult. Aged. Antigen-Antibody Reactions. Blotting, Western. Child. Child, Preschool. Cloning, Molecular. DNA, Neoplasm / biosynthesis. DNA, Neoplasm / genetics. Female. Humans. Immunohistochemistry. Infant. Male. Middle Aged. Mutation / genetics. Mutation / physiology. Protein Biosynthesis. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • (PMID = 19903171.001).
  • [ISSN] 1750-3639
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human
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18. Idowu MO, Rosenblum MK, Wei XJ, Edgar MA, Soslow RA: Ependymomas of the central nervous system and adult extra-axial ependymomas are morphologically and immunohistochemically distinct--a comparative study with assessment of ovarian carcinomas for expression of glial fibrillary acidic protein. Am J Surg Pathol; 2008 May;32(5):710-8
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  • [Title] Ependymomas of the central nervous system and adult extra-axial ependymomas are morphologically and immunohistochemically distinct--a comparative study with assessment of ovarian carcinomas for expression of glial fibrillary acidic protein.
  • We reviewed the morphologic and immunohistochemical features of 5 extra-axial ependymomas occurring in adults, 1 arising in an infantile sacrococcygeal teratoma, and a control group of 10 central nervous system (CNS) ependymomas in adults.
  • The adult extra-axial cases demonstrated more architectural variability than the CNS cases.
  • We observed that both the CNS and adult extra-axial ependymomas expressed GFAP diffusely, whereas only 9 stage III, high-grade ovarian serous papillary carcinomas stained with GFAP (2 strongly and diffusely and 7 exhibiting focally weak expression).
  • There were significant immunophenotypic differences between adult extra-axial and CNS ependymomas, with extra-axial cases preferentially expressing 34betaE12 (60% vs. 0%), CK18 (100% vs. 20%), CAM 5.2 (60% vs. 10%), CK7 (80% vs. 10%), ER (100% vs. 10%), and PR (80% vs. 20%).
  • CNS ependymomas more frequently expressed CD99 (100% vs. 20%).
  • The following stains were not differentially expressed: epithelial membrane antigen (expressed in 2 of 15 cases, including both extra-axial and CNS ependymomas), synaptophysin (1/15), chromogranin (0/15), WT1 (8/15), AE1:3 (10/15), and CK20 (0/15).
  • The ependymal elements of the sacrococcygeal tumor failed to express 34betaE12, CK18, CAM 5.2, and CK7, like most CNS ependymomas.
  • The morphologic and immunophenotypic differences between extra-axial and CNS ependymomas suggest that they derive from distinct precursors and/or differentiate along distinct pathways.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Central Nervous System Neoplasms / metabolism. Ependymoma / metabolism. Glial Fibrillary Acidic Protein / metabolism. Ovarian Neoplasms / metabolism
  • [MeSH-minor] Adolescent. Adult. Female. Humans. Immunoenzyme Techniques. Infant. Middle Aged. Neoplasm Recurrence, Local. Neoplasm Staging

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  • (PMID = 18360284.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glial Fibrillary Acidic Protein
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19. Engelhard HH, Villano JL, Porter KR, Stewart AK, Barua M, Barker FG, Newton HB: Clinical presentation, histology, and treatment in 430 patients with primary tumors of the spinal cord, spinal meninges, or cauda equina. J Neurosurg Spine; 2010 Jul;13(1):67-77
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  • OBJECT Patients having a primary tumor of the spinal cord, spinal meninges or cauda equina, are relatively rare.
  • Neurosurgeons encounter and treat such patients, and need to be aware of their clinical presentation, tumor types, treatment options, and potential complications.
  • The purpose of this paper is to report results from a series of 430 patients with primary intraspinal tumors, taken from a larger cohort of 9661 patients with primary tumors of the CNS.
  • METHODS Extensive information on individuals diagnosed (in the year 2000) as having a primary CNS neoplasm was prospectively collected in a Patient Care Evaluation Study conducted by the Commission on Cancer of the American College of Surgeons.
  • Intraspinal tumor cases were identified based on ICD-O-2 topography codes C70.1, C72.0, and C72.1.
  • RESULTS Patients with primary intraspinal tumors represented 4.5% of the CNS tumor group, and had a mean age of 49.3 years.
  • Pain was the most common presenting symptom, while the most common tumor types were meningioma (24.4%), ependymoma (23.7%), and schwannoma (21.2%).
  • [MeSH-major] Cauda Equina / pathology. Meningeal Neoplasms / pathology. Meningeal Neoplasms / surgery. Peripheral Nervous System Neoplasms / pathology. Peripheral Nervous System Neoplasms / surgery. Spinal Cord Neoplasms / pathology. Spinal Cord Neoplasms / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Chemotherapy, Adjuvant. Chi-Square Distribution. Child. Child, Preschool. Ependymoma / epidemiology. Ependymoma / pathology. Ependymoma / surgery. Female. Humans. Infant. Male. Meningioma / epidemiology. Meningioma / pathology. Meningioma / surgery. Middle Aged. Neurilemmoma / epidemiology. Neurilemmoma / pathology. Neurilemmoma / surgery. Postoperative Complications / epidemiology. Prospective Studies. Radiotherapy, Adjuvant. Registries. Risk Factors. Treatment Outcome. United States / epidemiology

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  • (PMID = 20594020.001).
  • [ISSN] 1547-5646
  • [Journal-full-title] Journal of neurosurgery. Spine
  • [ISO-abbreviation] J Neurosurg Spine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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20. Kawasaki K, Kohno M, Inenaga C, Sato A, Hondo H, Miwa A, Fujii Y, Takahashi H: Chordoid glioma of the third ventricle: a report of two cases, one with ultrastructural findings. Neuropathology; 2009 Feb;29(1):85-90
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  • Chordoid glioma, which generally occurs in adults, is a rare CNS tumor arising in the anterior part of the third ventricle.
  • Both tumors showed essentially the same histological and immunohistochemical features; the tumors were composed of cords and nests of epithelioid, GFAP-immunoreactive cells in a mucinous stroma with lymphoplasmacytic infiltrates at the tumor periphery.
  • Ultrastructural examination in one case revealed that the tumor cells were characterized by the presence of hemidesmosomes and associated focal basal lamina formation, intermediate junctions, microvilli and cilia, and intercellular microrosettes with microvilli.
  • In the brain, the presence of fenestrated endothelial cells is a feature of the circumventricular organs (except the subcommissural organ), among which the organum vasculosum of the lamina terminalis is located in the anterior part of the third ventricular floor that is lined by specialized ependymal cells known as tanycytes.
  • These findings further strengthen the hypothesis that chordoid glioma may represent a peculiar clinicopathological subtype of ependymoma (chordoid ependymoma) originating from the lamina terminalis area.
  • [MeSH-minor] Adult. Basement Membrane / pathology. Blood Vessels / pathology. Cilia / pathology. Endothelial Cells / pathology. Ependymoma / pathology. Epithelioid Cells / pathology. Female. Glial Fibrillary Acidic Protein / analysis. Hemidesmosomes / pathology. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Microscopy, Electron. Microvilli / pathology. Middle Aged. Tomography, X-Ray Computed

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  • [ErratumIn] Neuropathology. 2009 Apr;29(2):208
  • (PMID = 18498285.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein
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21. Mangels KJ, Johnson MD, Weil RJ: 35-year-old woman with progressive bilateral leg weakness. Brain Pathol; 2006 Apr;16(2):183-4, 187

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  • Serial sections revealed a homogeneous black tumor without necrosis.
  • H&E stained sections showed an occasionally fascicular tumor of melanocytes and small round blue tumor spindle cells with melanin pigmentation and 1-2 mitotic figures per 10 high-powered fields.
  • A diagnosis of primary meningeal melanocytic tumor was made.
  • PMMTs of the CNS consist of a spectrum of tumors ranging from well-differentiated melanocytoma to its overtly malignant counterpart, melanoma.
  • IGMs are more cellular than the well-differentiated variant, with 1-3 mitotic figures per 10 HPFs and MIB-1 labeling of <6%.
  • Once metastasis, including drop metastasis from pigmented medulloblastomas, have been excluded, the differential includes pigmented meningiomas and schwannomas (solitary or as part of Carney complex), as well as other pigmented CNS tumors such as ependymoma and pineoblastoma and systemic diseases such as lymphoma . . .
  • For primary CNS melanocytic neoplasms, complete tumor resection is preferred, as it leads to cure of well-differentiated and intermediate-grade melanocytomas and most melanomas.
  • [MeSH-minor] Adult. Female. Functional Laterality. Humans. Thoracic Vertebrae. Treatment Outcome

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  • (PMID = 16768759.001).
  • [ISSN] 1015-6305
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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22. Lasky JL 3rd, Choe M, Nakano I: Cancer stem cells in pediatric brain tumors. Curr Stem Cell Res Ther; 2009 Dec;4(4):298-305
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  • [Title] Cancer stem cells in pediatric brain tumors.
  • Central nervous system (CNS) tumors remain the leading cause of death among pediatric neoplasms.
  • Although standard therapies cure many pediatric CNS tumors, the long-term cognitive and physical consequences of these therapies are devastating.
  • Although recent studies have focused on molecular mechanisms that underlie the initiation and progression of adult glioblastoma multiforme (GBM), these tumors differ phenotypically and at a molecular level from pediatric brain tumors.
  • Recent investigations have identified a stem cell population, termed "brain tumor stem cells" (BTSC) within the heterogeneous cell populations that comprise malignant brain tumors which may be partly responsible for the resistance to current therapies.
  • By exploiting molecular differences present within these heterogeneous populations of brain tumor cells, we may be able to achieve specific eradication of BTSC and long-lasting remissions, while causing less toxicity to normal tissues.
  • In this review, we describe the issues surrounding the identification and characterization of BTSC, the molecular biology of BTSC for different pediatric brain tumors, and suggest future avenues for the development of treatments for this devastating disease.
  • [MeSH-major] Brain Neoplasms / pathology. Ependymoma / pathology. Medulloblastoma / pathology. Neoplastic Stem Cells / pathology. Optic Nerve Glioma / pathology
  • [MeSH-minor] Adult Stem Cells / pathology. Biomarkers / metabolism. Cell Differentiation. Chemotherapy, Adjuvant. Child. Humans. Surgical Procedures, Operative


23. Onilude OE, Lusher ME, Lindsey JC, Pearson AD, Ellison DW, Clifford SC: APC and CTNNB1 mutations are rare in sporadic ependymomas. Cancer Genet Cytogenet; 2006 Jul 15;168(2):158-61
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  • The ependymoma is the second most common malignant brain tumor of childhood; however, its molecular basis is poorly understood.
  • The formation of multiple ependymomas has been reported as an occasional feature of Turcot syndrome type 2 (TS2), a familial cancer syndrome caused by inherited mutations of the APC tumor suppressor gene, and characterised by the concurrence of a primary CNS tumor (predominantly medulloblastoma) and multiple colorectal adenomas.
  • In summary, although inherited APC mutations may be associated with ependymoma development in certain TS2 cases, these data indicate that somatic mutations affecting APC and CTNNB1 do not play a major role in the pathogenesis of sporadic ependymomas.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Ependymoma / genetics. Mutation / genetics. beta Catenin / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Chromatography, High Pressure Liquid. DNA Mutational Analysis. Female. Humans. Male. Middle Aged

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  • (PMID = 16843107.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / CTNNB1 protein, human; 0 / beta Catenin
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24. Mühlisch J, Bajanowski T, Rickert CH, Roggendorf W, Würthwein G, Jürgens H, Frühwald MC: Frequent but borderline methylation of p16 (INK4a) and TIMP3 in medulloblastoma and sPNET revealed by quantitative analyses. J Neurooncol; 2007 May;83(1):17-29
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  • Certain risk groups among tumors of the central nervous system (CNS) in children take an almost inevitably fatal course.
  • Aberrant methylation is common in malignant brain tumors of childhood and may have implications for stratification and therapy.
  • Methylation of p16 (INK4A), p14 (ARF), TIMP3, CDH1, p15 (INK4B )and DAPK1 in medulloblastoma (MB) and ependymoma has been discussed controversially in the literature.
  • We examined methylation in MB, sPNET and ependymoma using methylation-specific PCR (MSP), quantitative Combined Bisulfite Restriction Analysis (COBRA) and direct and clone sequencing of bisulfite PCR products.
  • Therapeutic and diagnostic implications urge into depth analyses of methylation as a mechanism, which might fill some of the gaps of our understanding of brain tumor origin.
  • [MeSH-major] Brain Neoplasms / genetics. Cerebellar Neoplasms / genetics. DNA Methylation. Genes, p16. Medulloblastoma / genetics. Neuroectodermal Tumors, Primitive / genetics. Tissue Inhibitor of Metalloproteinase-3 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Apoptosis Regulatory Proteins / genetics. Calcium-Calmodulin-Dependent Protein Kinases / genetics. Child. Child, Preschool. Death-Associated Protein Kinases. Female. Gene Silencing. Humans. Infant. Male. Middle Aged. Nerve Tissue Proteins / genetics. Receptors, Immunologic / genetics

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  • (PMID = 17206475.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Nerve Tissue Proteins; 0 / Receptors, Immunologic; 0 / TIMP3 protein, human; 0 / Tissue Inhibitor of Metalloproteinase-3; 0 / roundabout protein; EC 2.7.11.1 / DAPK1 protein, human; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
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25. Michalowski MB, de Fraipont F, Michelland S, Entz-Werle N, Grill J, Pasquier B, Favrot MC, Plantaz D: Methylation of RASSF1A and TRAIL pathway-related genes is frequent in childhood intracranial ependymomas and benign choroid plexus papilloma. Cancer Genet Cytogenet; 2006 Apr 1;166(1):74-81
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  • Ependymomas (EP) represent the third most frequent type of central nervous system (CNS) tumor of childhood, after astrocytomas and medulloblastomas.
  • Three adult corteses were used as a control.
  • Although we did not observe a statistical relationship between methylation and clinical outcome, the methylation pattern does not appear to be randomly distributed in ependymoma and may represent a mechanism of tumor development and evolution.
  • [MeSH-major] Apoptosis Regulatory Proteins / genetics. Brain Neoplasms / genetics. DNA Methylation. Ependymoma / genetics. Membrane Glycoproteins / genetics. Papilloma, Choroid Plexus / genetics. Tumor Necrosis Factor-alpha / genetics. Tumor Suppressor Proteins / genetics


26. Kieran MW, Packer RJ, Onar A, Blaney SM, Phillips P, Pollack IF, Geyer JR, Gururangan S, Banerjee A, Goldman S, Turner CD, Belasco JB, Broniscer A, Zhu Y, Frank E, Kirschmeier P, Statkevich P, Yver A, Boyett JM, Kun LE: Phase I and pharmacokinetic study of the oral farnesyltransferase inhibitor lonafarnib administered twice daily to pediatric patients with advanced central nervous system tumors using a modified continuous reassessment method: a Pediatric Brain Tumor Consortium Study. J Clin Oncol; 2007 Jul 20;25(21):3137-43
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I and pharmacokinetic study of the oral farnesyltransferase inhibitor lonafarnib administered twice daily to pediatric patients with advanced central nervous system tumors using a modified continuous reassessment method: a Pediatric Brain Tumor Consortium Study.
  • PURPOSE: A dose-escalation phase I and pharmacokinetic study of the farnesyltransferase inhibitor lonafarnib (SCH66336) was conducted in children with recurrent or progressive CNS tumors.
  • RESULTS: Fifty-three children with progressive or recurrent brain tumors were enrolled, with a median age of 12.2 years (range, 3.9 to 19.5 years).
  • Both radiographic response (one anaplastic astrocytoma) and stable disease (one medulloblastoma, two high-grade and four low-grade gliomas, one ependymoma, and one sarcoma) were noted, and seven patients remained on treatment for 1 year or longer.
  • [MeSH-major] Central Nervous System Neoplasms / drug therapy. Central Nervous System Neoplasms / mortality. Enzyme Inhibitors / pharmacokinetics. Farnesyltranstransferase / antagonists & inhibitors. Neoplasm Invasiveness / pathology. Piperidines / pharmacokinetics. Pyridines / pharmacokinetics
  • [MeSH-minor] Administration, Oral. Adolescent. Adult. Child. Child, Preschool. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Infant. Infant, Newborn. Male. Maximum Tolerated Dose. Neoplasm Staging. Risk Assessment. Survival Analysis. Treatment Outcome

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  • (PMID = 17634493.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01 CA81457
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Piperidines; 0 / Pyridines; 193275-84-2 / lonafarnib; EC 2.5.1.29 / Farnesyltranstransferase
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27. De Sio L, Milano GM, Castellano A, Jenkner A, Fidani P, Dominici C, Donfrancesco A: Temozolomide in resistant or relapsed pediatric solid tumors. Pediatr Blood Cancer; 2006 Jul;47(1):30-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Tumor types were: neuroblastoma (NB; n = 17), medulloblastoma (MB; 8), brain stem glioma (BSG; 8), extraosseous Ewing's sarcoma/peripheral neuroectodermal tumor (EOES; 4), Ewing's sarcoma (ES; 4), anaplastic astrocytoma (AA; 3), rhabdomyosarcoma (RMS; 2), ependymoma (EP; 2), cerebral primitive neuroectodermal tumor (cPNET; 2), hepatocarcinoma (HC; 1), and osteosarcoma (OS; 1).
  • CONCLUSION: Oral TMZ was well tolerated in children with resistant or relapsed solid tumors and showed activity in NB and CNS tumours refractory to standard chemotherapy.
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease-Free Survival. Dose-Response Relationship, Drug. Female. Humans. Male. Survival Analysis

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • [ErratumIn] Pediatr Blood Cancer. 2006 Oct 15;47(5):647-8
  • (PMID = 16047361.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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28. Barresi V, Tuccari G, Barresi G: NGAL immunohistochemical expression in brain primary and metastatic tumors. Clin Neuropathol; 2010 Sep-Oct;29(5):317-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NGAL immunohistochemical expression in brain primary and metastatic tumors.
  • Thus NGAL urinary detection has been proposed as a method for the early diagnosis of brain tumors.
  • In view of this, the objective of this study was to investigate whether NGAL expression differs according to brain tumor type or in primary vs. metastatic brain neolasias.
  • 42 surgically resected formalin fixed and paraffin embedded neoplasias, including 15 cases of brain metastasis and 27 cases of primary central nervous system (CNS) tumors (11 meningiomas; 1 pilocytic astrocytoma, 2 diffuse astrocytomas, 2 oligoastrocytomas, 2 oligodendrogliomas, 1 anaplastic oligoastrocytoma, 7 glioblastomas, 1 ependymoma) were submitted to the immunohistochemical procedure.
  • In conclusion, our findings suggest that NGAL expression is restricted to high grade gliomas among primary brain tumors, and that brain metastases do not express this protein.
  • Considering the correlation between NGAL expression in tumors and its urinary levels, if our observations will be further validated, NGAL urinary detection might be used as an additional tool in the pre-surgical definition of brain lesions involving difficult differential diagnosis.
  • [MeSH-major] Acute-Phase Proteins / metabolism. Brain Neoplasms / metabolism. Brain Neoplasms / secondary. Lipocalins / metabolism. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Young Adult

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  • (PMID = 20860895.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Acute-Phase Proteins; 0 / LCN2 protein, human; 0 / Lipocalins; 0 / Proto-Oncogene Proteins
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29. Gonçalves MI, Radzinsky TC, da Silva NS, Chiari BM, Consonni D: Speech-language and hearing complaints of children and adolescents with brain tumors. Pediatr Blood Cancer; 2008 Mar;50(3):706-8
MedlinePlus Health Information. consumer health - Speech and Language Problems in Children.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Speech-language and hearing complaints of children and adolescents with brain tumors.
  • Central nervous system (CNS) tumors generally leave sequelae that may compromise speech, language, swallowing, hearing, and voice functions.
  • This report describes the incidence of speech-language and hearing complaints and disorders in children and adolescents with CNS tumor under treatment at one of the most important Brazilian reference center for pediatric cancer.
  • [MeSH-major] Brain Neoplasms / complications. Hearing Loss / etiology. Language Disorders / etiology. Speech Disorders / etiology
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Astrocytoma / complications. Astrocytoma / drug therapy. Child. Child, Preschool. Craniopharyngioma / complications. Craniopharyngioma / drug therapy. Deglutition Disorders / etiology. Ependymoma / complications. Ependymoma / drug therapy. Facial Paralysis / etiology. Female. Humans. Infant. Male. Medulloblastoma / complications. Medulloblastoma / drug therapy

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17534932.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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30. Fuller CE, Perry A: Molecular diagnostics in central nervous system tumors. Adv Anat Pathol; 2005 Jul;12(4):180-94
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular diagnostics in central nervous system tumors.
  • Central nervous system (CNS) neoplasms can be diagnostically challenging, due to remarkably wide ranges in histologic appearance, biologic behavior, and therapeutic approach.
  • In this regard, the field is primed by recent advances in basic research, elucidating the molecular mechanisms of tumorigenesis and progression in the most common adult and pediatric brain tumors.
  • The goal of this article is to highlight the most common genetic alterations currently implicated in CNS tumors, focusing most on those that are either already in common use in ancillary molecular diagnostics testing or are likely to become so in the near future.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Central Nervous System Neoplasms / genetics. Ependymoma / genetics. Oligodendroglioma / genetics
  • [MeSH-minor] Animals. Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Chromosome Aberrations. Humans. In Situ Hybridization, Fluorescence. Meningeal Neoplasms / diagnosis. Meningeal Neoplasms / genetics. Meningioma / diagnosis. Meningioma / genetics. Neoplasms, Germ Cell and Embryonal / diagnosis. Neoplasms, Germ Cell and Embryonal / genetics. Polymerase Chain Reaction. Prognosis

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  • (PMID = 16096380.001).
  • [ISSN] 1072-4109
  • [Journal-full-title] Advances in anatomic pathology
  • [ISO-abbreviation] Adv Anat Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 260
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31. Wentworth S, Pinn M, Bourland JD, Deguzman AF, Ekstrand K, Ellis TL, Glazier SS, McMullen KP, Munley M, Stieber VW, Tatter SB, Shaw EG: Clinical experience with radiation therapy in the management of neurofibromatosis-associated central nervous system tumors. Int J Radiat Oncol Biol Phys; 2009 Jan 1;73(1):208-13
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical experience with radiation therapy in the management of neurofibromatosis-associated central nervous system tumors.
  • PURPOSE: Patients with neurofibromatosis (NF) develop tumors of the central nervous system (CNS).
  • METHODS AND MATERIALS: Eighteen patients with NF with CNS tumors were treated from 1986 to 2007.
  • Progression was defined as growth or recurrence of an irradiated tumor on serial imaging.
  • Tumor types included acoustic neuroma (16%), ependymoma (6%), low-grade glioma (11%), meningioma (60%), and schwanomma/neurofibroma (7%).
  • Five-year PFS rates were 75% (acoustic neuroma), 100% (ependymoma), 75% (low-grade glioma), 86% (meningioma), and 100% (schwanomma/neurofibroma).
  • Radiation therapy should be considered in NF patients with imaging progression of CNS tumors.
  • [MeSH-major] Brain Neoplasms / mortality. Brain Neoplasms / radiotherapy. Neurofibromatoses / mortality. Neurofibromatoses / radiotherapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Humans. Middle Aged. North Carolina / epidemiology. Survival Analysis. Survival Rate. Treatment Outcome. Young Adult


32. Lopez-Gines C, Gil-Benso R, Faus C, Monleon D, Mata M, Morales JM, Cigudosa JC, Gonzalez-Darder J, Celda B, Cerda-Nicolas M: Metastasizing anaplastic ependymoma in an adult. Chromosomal imbalances, metabolic and gene expression profiles. Histopathology; 2009 Mar;54(4):500-4
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metastasizing anaplastic ependymoma in an adult. Chromosomal imbalances, metabolic and gene expression profiles.
  • [MeSH-major] Brain Neoplasms / pathology. Ependymoma / pathology
  • [MeSH-minor] Adult. Anaplasia. Biomarkers, Tumor / metabolism. Chromosome Aberrations. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Gene Expression Profiling. Genes, p53. Humans. In Situ Hybridization, Fluorescence. Magnetic Resonance Imaging. Male. Mutation. Oligonucleotide Array Sequence Analysis

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  • (PMID = 19309408.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cyclin-Dependent Kinase Inhibitor p16
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