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1. Santi M, Mena H, Wong K, Koeller K, Olsen C, Rushing EJ: Spinal cord malignant astrocytomas. Clinicopathologic features in 36 cases. Cancer; 2003 Aug 1;98(3):554-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: The authors studied 36 cases to investigate the prognostic effect of the World Health Organization (WHO) tumor grade, tumor localization, cell proliferative activity, p53 expression, and therapy.
  • For two patients, there were no data available regarding surgical treatment.
  • After initial surgery, 10 (29%) patients were treated with radiation therapy alone and 7 (19%) received radiation therapy with chemotherapy.
  • Patterns of disease recurrence included extraneural metastases (two cases), brain metastases (five cases), local extension (one case), and diffuse spread along the neuraxis (six cases).
  • The overall median survival time was 33 months (range, 24-42 months) for A, 10 months (range, 1-84 months) for AA, and 10 months (range, 1-43 months) for GBM.
  • [MeSH-major] Astrocytoma / pathology. Spinal Cord Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Aged, 80 and over. Antineoplastic Agents / therapeutic use. Cell Division. Child. Child, Preschool. Combined Modality Therapy. Female. Humans. Immunoenzyme Techniques. Ki-67 Antigen / metabolism. Male. Middle Aged. Neoplasm Recurrence, Local / pathology. Neoplasm Staging. Prognosis. Radiotherapy Dosage. Survival Rate. Treatment Outcome. Tumor Suppressor Protein p53 / metabolism

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  • [Copyright] Copyright 2003 American Cancer Society.DOI 10.1002/cncr.11514
  • (PMID = 12879473.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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2. Badhe PB, Chauhan PP, Mehta NK: Brainstem gliomas--a clinicopathological study of 45 cases with p53 immunohistochemistry. Indian J Cancer; 2004 Oct-Dec;41(4):170-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The WHO brain tumor classification and Stroink's CT classification were applied.
  • Diffuse astrocytomas were seen in 40 cases (5% were Grade I, 47.5%Grade II, 32.5% Grade III and 15% Grade IV) and pilocytic astrocytomas in 5 cases.
  • Grade II astrocytomas were treated with excision and radiotherapy, while grade III and IV tumors were treated with radiotherapy and chemotherapy (CCNU).
  • It was found in 50 % of glioblastoma multiforme, 28.57% of grade III astrocytoma and 12.5% of grade II astrocytoma, while grade 1 astrocytomas failed to express p53 protein. p53 positivity was more in high grade lesions, decreasing significantly in lower grade lesions.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Brain Stem Neoplasms / metabolism. Glioma / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Humans. Immunohistochemistry. India / epidemiology. Infant. Infant, Newborn. Male. Middle Aged. Retrospective Studies. Survival Rate

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  • (PMID = 15659871.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Protein p53
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3. Tortosa A, Viñolas N, Villà S, Verger E, Gil JM, Brell M, Caral L, Pujol T, Acebes JJ, Ribalta T, Ferrer I, Graus F: Prognostic implication of clinical, radiologic, and pathologic features in patients with anaplastic gliomas. Cancer; 2003 Feb 15;97(4):1063-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: The clinical evolution of anaplastic glioma (anaplastic astrocytoma, oligodendroglioma, and oligoastrocytoma) is variable.
  • Variables included age, gender, clinical manifestations at diagnosis (seizures, focal neurologic deficit, and cognitive changes), computed tomographic (CT) scan characteristics (diffuse, ring, and no enhancement), tumor location, extent of resection, histopathology, postoperative Karnofsky performance status (KPS) score, adjuvant chemotherapy, tumor response, proliferation index (Ki-67 expression), and p53, p16, pRb, and epidermal growth factor receptor immunohistochemical expression.
  • RESULTS: Ninety-five patients with a histologic diagnosis of anaplastic astrocytoma (73%), anaplastic oligoastrocytoma (16.6%), or anaplastic oligodendroglioma (10.4%) constituted the basis of this study.
  • CONCLUSIONS: In addition to previously recognized prognostic variables such as age and KPS score, CT ring enhancement and tumor proliferation index were identified as independent predictors of survival in a homogeneous series of patients with anaplastic gliomas.
  • [MeSH-minor] Adult. Age Factors. Aged. Cholera Toxin. Cyclin-Dependent Kinase Inhibitor p16 / analysis. Female. Humans. Immunohistochemistry. Karnofsky Performance Status. Ki-67 Antigen / analysis. Male. Multivariate Analysis. Prognosis. Survival Analysis. Tumor Suppressor Protein p53 / analysis

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  • [Copyright] Copyright 2003 American Cancer Society
  • (PMID = 12569607.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; 9012-63-9 / Cholera Toxin
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4. Sanson M, Cartalat-Carel S, Taillibert S, Napolitano M, Djafari L, Cougnard J, Gervais H, Laigle F, Carpentier A, Mokhtari K, Taillandier L, Chinot O, Duffau H, Honnorat J, Hoang-Xuan K, Delattre JY, ANOCEF group: Initial chemotherapy in gliomatosis cerebri. Neurology; 2004 Jul 27;63(2):270-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Initial chemotherapy in gliomatosis cerebri.
  • BACKGROUND: Because of the diffuse nature of gliomatosis cerebri (GC), surgery is not suitable, and large field radiotherapy carries the risk of severe toxicity.
  • In this setting, initial chemotherapy warrants further investigation.
  • METHODS: The authors treated 63 consecutive patients with GC with initial chemotherapy consisting of either PCV (procarbazine, 60 mg/m2 on days 8 to 21; CCNU, 110 mg/m2 on day 1; and vincristine, 1.4 mg/m2 on days 8 and 29) or temozolomide (TMZ; 150 to 200 mg/m2 for 5 days every 4 weeks).
  • GC was initially present at diagnosis in 49 patients (primary GC), whereas 14 patients with a circumscribed glioma at onset developed secondary GC after a median follow-up period of 5.11 years.
  • GC was classified based on the predominant tumor cells as astrocytic, oligodendroglial, or mixed GC.
  • Regardless of the chemotherapeutic regimen, oligodendroglial GC had a better prognosis than astrocytic and oligoastrocytic GC in terms of PFS (p < 0.02) and OS (p < 0.0001).
  • CONCLUSION: Initial chemotherapy is useful for some patients with gliomatosis cerebri.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Neoplasms, Neuroepithelial / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Astrocytoma / drug therapy. Astrocytoma / radiotherapy. Combined Modality Therapy. Cranial Irradiation. Disease Progression. Disease-Free Survival. Drug Administration Schedule. Female. Hematologic Diseases / chemically induced. Humans. Karnofsky Performance Status. Lomustine / administration & dosage. Lomustine / adverse effects. Magnetic Resonance Imaging. Male. Middle Aged. Oligodendroglioma / drug therapy. Oligodendroglioma / radiotherapy. Procarbazine / administration & dosage. Procarbazine / adverse effects. Survival Analysis. Treatment Outcome. Vincristine / administration & dosage. Vincristine / adverse effects

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  • [CommentIn] Neurology. 2004 Jul 27;63(2):204-5 [15277608.001]
  • (PMID = 15277619.001).
  • [ISSN] 1526-632X
  • [Journal-full-title] Neurology
  • [ISO-abbreviation] Neurology
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 7BRF0Z81KG / Lomustine; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; PCV protocol
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5. Hall WA, Doolittle ND, Daman M, Bruns PK, Muldoon L, Fortin D, Neuwelt EA: Osmotic blood-brain barrier disruption chemotherapy for diffuse pontine gliomas. J Neurooncol; 2006 May;77(3):279-84
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  • [Title] Osmotic blood-brain barrier disruption chemotherapy for diffuse pontine gliomas.
  • The prognosis for patients with diffuse pontine gliomas (DPG) remains poor.
  • New aggressive innovative treatments are necessary to treat this disease.
  • From 1984 to 1998, eight patients (4M/4F), median age 11 years, with DPG were treated with monthly osmotic blood-brain barrier disruption (BBBD) chemotherapy using intraarterial carboplatin or methotrexate and intravenous cytoxan and etoposide.
  • Two patients had biopsies that showed an astrocytoma and an anaplastic astrocytoma.
  • Three patients had radiation therapy before BBBD chemotherapy and four afterwards.
  • Two patients had chemotherapy (tamoxifen, topotecan) before BBBD chemotherapy and two afterwards.
  • In general, patients were evaluated with MR imaging every 3 months to monitor for a response to treatment.
  • The median number of chemotherapy cycles that were administered by BBBD was 10, mean 10.
  • Three patients also received one, two, or three cycles of intraarterial chemotherapy without BBBD.
  • The median time to tumor progression was 15 months with the range from <1 to 40 months.
  • The median survival from the time of diagnosis was 27 months, ranging from 7 to 80 months.
  • The median survival time from the first BBBD or intraarterial treatment was 16.5 months, ranging from 5 to 69 months.
  • Although the sample size is small, the TTP and survival times are longer than those previously reported in other DPG series.
  • In addition, the ability to demonstrate stable disease or partial responses in DPG on MR imaging argues for the therapeutic benefit of BBBD chemotherapy.
  • The enhanced delivery of chemotherapy afforded by osmotic BBBD supports the further examination of this treatment modality for patients with DPG.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacokinetics. Blood-Brain Barrier / metabolism. Brain Stem Neoplasms / drug therapy. Drug Delivery Systems / methods. Glioma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Carboplatin / administration & dosage. Child. Child, Preschool. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Humans. Male. Methotrexate / administration & dosage. Osmosis / drug effects. Retrospective Studies. Treatment Outcome

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  • (PMID = 16314949.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS33618; United States / NINDS NIH HHS / NS / NS34608; United States / NINDS NIH HHS / NS / NS44687
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; BG3F62OND5 / Carboplatin; YL5FZ2Y5U1 / Methotrexate
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6. Lesser GJ: Chemotherapy of low-grade gliomas. Semin Radiat Oncol; 2001 Apr;11(2):138-44
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  • [Title] Chemotherapy of low-grade gliomas.
  • Histologic subtypes of low-grade gliomas include pilocytic astrocytomas (World Health Organization [WHO] grade I), diffuse infiltrating astrocytomas, oligodendrogliomas, and mixed oligo-astrocytomas (WHO grade II).
  • Although extended survival is typical with these tumors, most patients eventually succumb to recurrent or progressive disease despite receiving either adjuvant radiation therapy or radiation at the time of recurrence.
  • Not surprisingly, chemotherapy for low-grade gliomas has primarily been evaluated in the salvage setting of postradiotherapy progression in both adults and children.
  • Unfortunately, the published body of literature describing chemotherapy for these tumors is small and subject to a number of confounding methodologic limitations.
  • Nonetheless, some guidelines for the use of chemotherapy in these patients can be inferred from the published experience.
  • The data reviewed clearly identifies a potential benefit for PCV chemotherapy (procarbazine, CCNU, and vincristine) in at least a subset of patients with low-grade oligodendroglial tumors.
  • Nitrosoureas and platinum agents appear to have modest efficacy in recurrent oligodendroglial tumors and in some patients with newly diagnosed or progressive low-grade astrocytomas; however, surgery and radiation remain the primary treatment modalities for this group of malignancies.
  • Until new data becomes available, chemotherapy still should be used only as a salvage option in previously irradiated patients with recurrent or progressive low-grade gliomas.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / drug therapy. Oligodendroglioma / drug therapy. Salvage Therapy
  • [MeSH-minor] Adolescent. Adult. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Brain Neoplasms / surgery. Child. Child, Preschool. Humans. Lomustine / administration & dosage. Middle Aged. Neoplasm Staging. Procarbazine / administration & dosage. Vincristine / administration & dosage

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  • [Copyright] Copyright 2001 by W.B. Saunders Company
  • (PMID = 11285551.001).
  • [ISSN] 1053-4296
  • [Journal-full-title] Seminars in radiation oncology
  • [ISO-abbreviation] Semin Radiat Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 7BRF0Z81KG / Lomustine; PCV protocol
  • [Number-of-references] 32
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7. Turner CD, Gururangan S, Eastwood J, Bottom K, Watral M, Beason R, McLendon RE, Friedman AH, Tourt-Uhlig S, Miller LL, Friedman HS: Phase II study of irinotecan (CPT-11) in children with high-risk malignant brain tumors: the Duke experience. Neuro Oncol; 2002 04;4(2):102-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A total of 22 children were enrolled in this study, including 13 with histologically verified recurrent malignant brain tumors (glioblastoma multiforme [GBM] 4, anaplastic astrocytoma 1, ependymoma 5, and medulloblastoma/primitive neuroectodermal tumor 3), 5 with recurrent diffuse pontine glioma, and 4 with newly diagnosed GBM.
  • All patients with recurrent tumor had prior chemotherapy and/or irradiation.
  • Patients with recurrent tumors received therapy until disease progression or unacceptable toxicity.
  • Patients with newly diagnosed tumors initially received 3 cycles of treatment to assess tumor response and then were allowed radiotherapy at physician's choice; patients who demonstrated a response to CPT-11 prior to radiotherapy were allowed to continue the drug after radiation until disease progression or unacceptable toxicity.
  • Responses were seen in 4 of 9 patients with GBM or anaplastic astrocytoma (44%; 95% confidence interval, 11%-82%) (complete response in 2 patients with recurrent GBM lasting 9 months and 48+ months; partial response in one patient with a newly diagnosed midbrain GBM lasting 18 months prior to radiotherapy; and partial response lasting 11 months in 1 patient with recurrent anaplastic astrocytoma), 1 of 5 patients with recurrent ependymoma (partial response initially followed by stable disease lasting 11 months), and none of 5 patients with recurrent diffuse pontine glioma.
  • Two of 3 patients with medulloblastoma/primitive neuroectodermal tumor had stable disease for 9 and 13 months.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Brain Neoplasms / drug therapy. Camptothecin / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Astrocytoma / drug therapy. Child. Child, Preschool. Drug Administration Schedule. Ependymoma / drug therapy. Female. Glioblastoma / drug therapy. Glioma. Humans. Magnetic Resonance Imaging. Male. Medulloblastoma / drug therapy. Topoisomerase Inhibitors

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  • (PMID = 11916501.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Topoisomerase Inhibitors; 0H43101T0J / irinotecan; XT3Z54Z28A / Camptothecin
  • [Other-IDs] NLM/ PMC1920653
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8. Novillo López ME, Gómez-Ibáñez A, Rosenfeld M, Dalmau J: [Gliomatosis cerebri: review of 22 patients]. Neurologia; 2010 Apr;25(3):168-73
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  • INTRODUCTION: gliomatosis cerebri is a diffuse astrocytic neoplasm that involves more than two lobes of the brain.
  • Treatment is not well defined and the prognosis is considered poor.
  • The most frequent pathological findings were grade III astrocytoma (36.4%), grade II astrocytoma (22.7%), and grade IV astrocytoma (18.3%).
  • Seventeen patients received treatment with chemotherapy, radiotherapy or both, and 12 patients (70.6%) had a clinical or radiological response.
  • The median follow-up was 13 months, median progression free survival 6 months, and median survival 9,5 months (15 months if the patients received treatment).
  • Treatment often results in clinical responses.
  • In this study de median survival of patients who received treatment was similar to that reported in series of glioblastoma multiforme.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Retrospective Studies. Young Adult

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  • [Copyright] Published by Elservier España, S.L. All rights reserved.
  • (PMID = 20492863.001).
  • [ISSN] 0213-4853
  • [Journal-full-title] Neurología (Barcelona, Spain)
  • [ISO-abbreviation] Neurologia
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
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9. Bohner G, Masuhr F, Distl R, Katchanov J, Klingebiel R, Zschenderlein R, von Deimling A, van Landeghem FK: Pilocytic astrocytoma presenting as primary diffuse leptomeningeal gliomatosis: report of a unique case and review of the literature. Acta Neuropathol; 2005 Sep;110(3):306-11
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  • [Title] Pilocytic astrocytoma presenting as primary diffuse leptomeningeal gliomatosis: report of a unique case and review of the literature.
  • We describe a 25-year-old male patient with primary diffuse leptomeningeal gliomatosis (PDLG) presenting with gait ataxia, positive Lhermitte's sign, double vision, and right abducens nerve palsy.
  • Spinal leptomeningeal biopsy revealed a pilocytic astrocytoma WHO grade I.
  • Despite chemotherapy with vincristin and carboplatin, the patient died 2 months after admission.
  • Sequence analysis of tumor protein 53 gene (TP53) revealed a missense mutation in exon 5, and expression of phosphatase and tensin homolog (mutated in multiple advanced cancers 1) (PTEN) protein was not detected, which may have contributed to astrocytoma development.
  • To our knowledge, this is the first definitive case of pilocytic astrocytoma presenting as PDLG.
  • [MeSH-major] Astrocytoma / pathology. Meningeal Neoplasms / pathology. Meninges / pathology. Neoplasms, Neuroepithelial / pathology. Neoplasms, Unknown Primary / pathology. Subarachnoid Space / pathology
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / genetics. Brain / pathology. Brain / physiopathology. Diagnosis, Differential. Fatal Outcome. Humans. Magnetic Resonance Imaging. Male. Mutation / genetics. Spinal Cord / pathology. Spinal Cord / physiopathology. Spinal Cord Compression / etiology. Spinal Cord Compression / pathology. Spinal Cord Compression / physiopathology. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 16003541.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53
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10. Nakasu S, Fukami T, Jito J, Matsuda M: Prognostic significance of loss of O6-methylguanine-DNA methyltransferase expression in supratentorial diffuse low-grade astrocytoma. Surg Neurol; 2007 Dec;68(6):603-8; discussion 608-9
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  • [Title] Prognostic significance of loss of O6-methylguanine-DNA methyltransferase expression in supratentorial diffuse low-grade astrocytoma.
  • If loss of function in MGMT is related to tumor progression, the immunohistochemical method may predict the malignant change of gliomas.
  • METHOD: We investigated the expression of MGMT by immunohistochemical method in 28 supratentorial hemispheric diffuse astrocytomas.
  • Age, sex, extent of surgery, MIB-1 value, and radiation therapy at initial treatment did not correlate with the malignant progression.
  • Two long-term survivors with MGMT-negative tumor responded well to nitrosourea-based chemotherapy and lived more than 8 years after malignant transformation.
  • CONCLUSION: Although the status of MGMT did not affect the overall survival, immunohistochemical evaluation of MGMT expression may be a good marker for tumor progression.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Biomarkers, Tumor / metabolism. O(6)-Methylguanine-DNA Methyltransferase / metabolism. Supratentorial Neoplasms / metabolism. Supratentorial Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Transformation, Neoplastic. Child. Disease Progression. Female. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis

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  • (PMID = 17825378.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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11. Ewelt C, Stummer W, Klink B, Felsberg J, Steiger HJ, Sabel M: Cordectomy as final treatment option for diffuse intramedullary malignant glioma using 5-ALA fluorescence-guided resection. Clin Neurol Neurosurg; 2010 May;112(4):357-61
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  • [Title] Cordectomy as final treatment option for diffuse intramedullary malignant glioma using 5-ALA fluorescence-guided resection.
  • BACKGROUND: We present a case of an anaplastic astrocytoma (WHO-grade III, AA III) in a 27-year-old woman treated by spinal cordectomy.
  • The patient was pretreated by surgery, radiation therapy and temozolomide chemotherapy and repeat surgery at recurrence.
  • Later on, she developed paraplegia and a diffuse severe pain syndrome.
  • To assess tumor invasion intraoperatively, we used tumor fluorescence derived from 5-aminolevulinic acid (5-ALA).
  • Additional cordectomy was performed because of tumor infiltration at the cut end to T9 as identified by intraoperative tumor fluorescence, and as verified histologically.
  • The final transected level was between T8 and T9, and the cut end did not reveal any tumor invasion intraoperatively by tumor fluorescence and postoperatively by MRI and with regard to the pathological result.
  • She refused additional adjuvant therapy.
  • [MeSH-major] Aminolevulinic Acid. Astrocytoma / surgery. Cordotomy / methods. Neurosurgical Procedures / methods. Spinal Cord Neoplasms / surgery. Surgery, Computer-Assisted / methods
  • [MeSH-minor] Adult. Female. Humans. Magnetic Resonance Imaging. Pain / drug therapy. Pain / etiology. Paraplegia / etiology. Spine / pathology

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  • [Copyright] Copyright 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20061079.001).
  • [ISSN] 1872-6968
  • [Journal-full-title] Clinical neurology and neurosurgery
  • [ISO-abbreviation] Clin Neurol Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 88755TAZ87 / Aminolevulinic Acid
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12. Watanabe T, Komine C, Yokoyama T, Yoshino A, Katayama Y: [Therapeutic efficacy and prognostic factors in diffuse astrocytomas]. No Shinkei Geka; 2003 Jul;31(7):767-73
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  • [Title] [Therapeutic efficacy and prognostic factors in diffuse astrocytomas].
  • Diffuse astrocytomas are slowly growing tumors with a relatively long overall survival.
  • Considerable controversy exists as to the best therapeutic management for patients with such tumors.
  • Gross total resection and interferon-beta therapy were significantly associated with both longer progression free survival (PFS) and overall survival (OS).
  • Immediate postoperative radiation therapy did not prolong either the PFS or OS.
  • Our data suggest that radical surgery plus interferon-beta therapy may offer the best chance for long survival.
  • Since the presence of MGMT methylation is a probable indication of an increased sensitivity to alkylating chemotherapeutic agents, determining the methylation status of MGMT could provide a potential basis for logical therapeutic intervention in identifying a subgroup of patients who could be candidates for early chemotherapy.
  • [MeSH-major] Astrocytoma / therapy. Brain Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Combined Modality Therapy. Disease-Free Survival. Female. Humans. Interferon-beta / therapeutic use. Male. Methylation. Middle Aged. Neurosurgical Procedures. O(6)-Methylguanine-DNA Methyltransferase / genetics. Prognosis. Retrospective Studies

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  • (PMID = 12884791.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 77238-31-4 / Interferon-beta; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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13. Watanabe T, Nakamura M, Kros JM, Burkhard C, Yonekawa Y, Kleihues P, Ohgaki H: Phenotype versus genotype correlation in oligodendrogliomas and low-grade diffuse astrocytomas. Acta Neuropathol; 2002 Mar;103(3):267-75
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  • [Title] Phenotype versus genotype correlation in oligodendrogliomas and low-grade diffuse astrocytomas.
  • Oligodendrogliomas typically show loss of heterozygosity (LOH) on chromosomes 1p and 19q, which correlates with their response to chemotherapy, whereas low-grade astrocytomas are characterized by frequent TP53 mutations and lack of sensitivity to alkylating therapeutic agents.
  • Unequivocal histological distinction of low-grade diffuse astrocytomas from oligodendrogliomas and oligoastrocytomas is often difficult.
  • To elucidate the relationships between morphological phenotype and genetic profile, we screened 19 oligodendrogliomas (WHO grade II) and 23 low-grade diffuse astrocytomas (WHO grade II) for TP53 mutations and LOH on 1p and 19q.
  • In low-grade diffuse astrocytomas, LOH on chromosomes 1p and/or 19q was found in three cases (13%) and TP53 mutation was detected in ten cases (43%).
  • Methylation of the promoter of the gene for O (6)-methylguanine-DNA methyltransferase (MGMT), a DNA repair protein, which confers resistance to chemotherapy with alkylating agents, was detected in 47% of oligodendrogliomas and 48% of low-grade diffuse astrocytomas.
  • [MeSH-major] Astrocytoma / genetics. Astrocytoma / pathology. Genotype. Oligodendroglioma / genetics. Oligodendroglioma / pathology. Phenotype
  • [MeSH-minor] Adult. Aged. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Diagnosis, Differential. Female. Genes, p53 / genetics. Humans. Loss of Heterozygosity / genetics. Male. Middle Aged. Mutation / genetics

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  • (PMID = 11907807.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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14. Jayawardena S, Sooriabalan D, Indulkar S, Kim HH, Matin A, Maini A: Regression of grade III astrocytoma during the treatment of CML with imatinib mesylate. Am J Ther; 2006 Sep-Oct;13(5):458-9
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  • [Title] Regression of grade III astrocytoma during the treatment of CML with imatinib mesylate.
  • The cells that demonstrate the greatest degree of anaplasia are used to determine the histologic grade of the tumor.
  • The mean age of survival are approximately 10 years from the time of diagnosis for pilocystic astrocytomas (World Health Organization grade I), more than 5 years for patients with low-grade diffuse astrocytomas (WHO grade II), 2 to 5 years for those with anaplastic astrocytomas (WHO grade III), and less than 1 year for patients with glioblastoma (WHO grade IV).
  • The treatment is a combination of surgery, radiation, and chemotherapy depending of the grade of astrocytoma.
  • We present a case of 31-year-old man with grade III astrocytoma with subsequent chronic myelogenous leukemia treated with imatinib mesylate as part of his chronic myelogenous leukemia treatment failing to show recurrence of the astrocytoma 10 years after standard treatment for astrocytoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Benzamides. Combined Modality Therapy. Humans. Imatinib Mesylate. Magnetic Resonance Imaging. Male

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  • (PMID = 16988542.001).
  • [ISSN] 1075-2765
  • [Journal-full-title] American journal of therapeutics
  • [ISO-abbreviation] Am J Ther
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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15. Smith JS, Perry A, Borell TJ, Lee HK, O'Fallon J, Hosek SM, Kimmel D, Yates A, Burger PC, Scheithauer BW, Jenkins RB: Alterations of chromosome arms 1p and 19q as predictors of survival in oligodendrogliomas, astrocytomas, and mixed oligoastrocytomas. J Clin Oncol; 2000 Feb;18(3):636-45
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  • PURPOSE: A recent report suggests that alterations of chromosome arms 1p and 19q are associated with chemotherapeutic response and overall survival in anaplastic oligodendroglioma patients treated with procarbazine, lomustine, and vincristine chemotherapy.
  • We set out to further clarify the diagnostic and prognostic implications of these alterations in a broader set of diffuse gliomas, including astrocytic neoplasms and low-grade oligodendrogliomas.
  • PATIENTS AND METHODS: Fluorescence in situ hybridization (FISH) signals from DNA probes mapping to 1p and 19q common deletion regions were enumerated in 162 diffuse gliomas (79 astrocytomas, 52 oligodendrogliomas, and 31 mixed oligoastrocytomas), collected as part of an ongoing prospective investigation of CNS tumors.
  • Combined loss of 1p and 19q was identified as a univariate predictor of prolonged overall survival among patients with pure oligodendroglioma (log-rank, P =.03) and remained a significant predictor after adjusting for the effects of patient age and tumor grade (P <.01).
  • This favorable association was not evident in patients with astrocytoma or mixed oligoastrocytoma.
  • CONCLUSION: Combined loss of 1p and 19q is a statistically significant predictor of prolonged survival in patients with pure oligodendroglioma, independent of tumor grade.
  • Given the lack of this association in patients with astrocytic neoplasms and the previously demonstrated chemosensitivity of oligodendrogliomas, a combined approach of histologic and genotypic assessment could potentially improve existing strategies for patient stratification and management.
  • [MeSH-major] Astrocytoma / genetics. Central Nervous System Neoplasms / genetics. Chromosome Deletion. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Oligodendroglioma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Predictive Value of Tests. Prospective Studies. Survival Analysis

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  • (PMID = 10653879.001).
  • [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 / CA50905; United States / NCI NIH HHS / CA / CA50910; United States / NCI NIH HHS / CA / CA64928
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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16. Scott IS, Morris LS, Rushbrook SM, Bird K, Vowler SL, Burnet NG, Coleman N: Immunohistochemical estimation of cell cycle entry and phase distribution in astrocytomas: applications in diagnostic neuropathology. Neuropathol Appl Neurobiol; 2005 Oct;31(5):455-66
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  • An immunohistochemical method for assessing cell cycle phase distribution in neurosurgical biopsies would enable such data to be incorporated into diagnostic algorithms for the estimation of prognosis and response to adjuvant chemotherapy in glial neoplasms, without the requirement for flow cytometric analysis.
  • Paraffin-embedded sections of intracerebral gliomas (n = 48), consisting of diffuse astrocytoma (n = 9), anaplastic astrocytoma (n = 8) and glioblastoma (n = 31), were analysed by immunohistochemistry using markers of cell cycle entry, Mcm-2 and Ki67, and putative markers of cell cycle phase, cyclins D1 (G1-phase), cyclin A (S-phase), cyclin B1 (G2-phase) and phosphohistone H3 (Mitosis).
  • There was a significant increase in Mcm-2 (P < 0.0001), Ki67 (P < 0.0001), cyclin A (P < 0.0001) and cyclin B1 (P = 0.002) expression with increasing grade from diffuse astrocytoma through anaplastic astrocytoma to glioblastoma, suggesting that any of these four markers has potential as a marker of tumour grade.
  • We conclude that it is feasible to obtain detailed cell cycle data by immunohistochemical analysis of tissue biopsies.
  • [MeSH-major] Astrocytoma / pathology. Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Cell Cycle / physiology. Immunohistochemistry / methods
  • [MeSH-minor] Adult. Cell Cycle Proteins / biosynthesis. Cyclin A / biosynthesis. Cyclin B / biosynthesis. Cyclin B1. Cyclin D1 / biosynthesis. Flow Cytometry. Histones / biosynthesis. Humans. Microscopy, Confocal. Prognosis. Reproducibility of Results

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  • (PMID = 16150117.001).
  • [ISSN] 0305-1846
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CCNB1 protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin A; 0 / Cyclin B; 0 / Cyclin B1; 0 / Histones; 136601-57-5 / Cyclin D1
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17. Preusser M, Haberler C, Hainfellner JA: Malignant glioma: neuropathology and neurobiology. Wien Med Wochenschr; 2006 Jun;156(11-12):332-7
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  • The sole unequivocal risk factor is therapeutic ionizing irradiation.
  • Malignant gliomas comprise a spectrum of different tumor subtypes.
  • Within this spectrum, glioblastoma, anaplastic astrocytoma and anaplastic oligodendroglioma share as basic features preferential location in cerebral hemispheres, diffuse infiltration of brain tissue, fast tumor growth with fatal outcome within months or years.
  • Invasion is regarded as one of the main reasons for poor therapeutic success, because it makes complete surgical removal of gliomas impossible.
  • Invasion of glioma cells requires interaction with the extracellular matrix and with surrounding cells of the healthy brain tissue.
  • Vascular proliferates and tissue necrosis are characteristic features of malignant gliomas, in particular glioblastoma.
  • These features are most likely the consequence of rapidly increasing tumor mass that is inadequately oxygenized by the preexisting vasculature.
  • Methylguanine-methyltransferase (MGMT) promoter methylation status in glioblastoma and 1p19q deletion status in anaplastic oligodendroglioma are associated with response to chemotherapy.
  • The role of neuropathology and neurobiology in neurooncology is 1. to provide a clinically meaningful classification of brain tumors on basis of pathobiological factors, 2. to clarify etiology and pathogenesis of brain tumors as rational basis for development of new diagnostic tests and therapies, and 3. to translate testing for new clinically relevant molecular parameters into clinical application.
  • [MeSH-minor] Adult. Brain / pathology. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Child. Chromosome Aberrations. Female. Humans. Infant. Male. Neoplasm Invasiveness / pathology. Prognosis


18. Gimenez M, Souza VC, Izumi C, Barbieri MR, Chammas R, Oba-Shinjo SM, Uno M, Marie SK, Rosa JC: Proteomic analysis of low- to high-grade astrocytomas reveals an alteration of the expression level of raf kinase inhibitor protein and nucleophosmin. Proteomics; 2010 Aug;10(15):2812-21
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  • These proteins are not only potential disease biomarkers, but also targets for therapy.
  • The aim of this study was to identify differentially expressed proteins in diffuse astrocytoma grade II, anaplastic astrocytoma grade III and glioblastoma multiforme grade IV in human tumor samples and in non-neoplastic brain tissue as control using 2-DE and MS.
  • Tumor and control brain tissue dissection was guided by histological hematoxylin/eosin tissue sections to provide more than 90% of tumor cells and astrocytes.
  • We report here for the first time the alteration of NPM and RKIP expression in brain cancer.
  • The proteomic data for NPM and RKIP were confirmed by Western blot, quantitative real-time PCR and immunohistochemistry.
  • Due to the participation of NPM and RKIP in uncontrolled proliferation and evasion of apoptosis, these proteins are likely targets for drug development.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Nuclear Proteins / genetics. Phosphatidylethanolamine Binding Protein / genetics. Proteomics
  • [MeSH-minor] Adult. Amino Acid Sequence. Brain / metabolism. Brain / pathology. Electrophoresis, Gel, Two-Dimensional. Female. Humans. Male. Middle Aged. Molecular Sequence Data. Proteins / genetics. Proteins / isolation & purification


19. Iwami K, Arima T, Ooka F, Asai T, Tambara M, Takaoka T: [Bilateral thalamic glioma in an adult: a case report and review of the literature]. No Shinkei Geka; 2009 Mar;37(3):285-90
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  • [Title] [Bilateral thalamic glioma in an adult: a case report and review of the literature].
  • Histological examination of the biopsy specimen identified diffuse astrocytoma (WHO grade II).
  • Death usually occurs within two years after onset, independently of adjuvant therapy such as radiotherapy and chemotherapy.
  • At the time of this writing (5 months after the consultation), there are no neurological symptoms, and no changes on neuroimaging.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Thalamus
  • [MeSH-minor] Adult. Female. Humans

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  • (PMID = 19306649.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 16
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20. Watanabe T, Katayama Y, Yoshino A, Komine C, Yokoyama T, Fukushima T: Treatment of low-grade diffuse astrocytomas by surgery and human fibroblast interferon without radiation therapy. J Neurooncol; 2003 Jan;61(2):171-6
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  • [Title] Treatment of low-grade diffuse astrocytomas by surgery and human fibroblast interferon without radiation therapy.
  • Low-grade diffuse astrocytomas are slowly growing tumors with a relatively long overall survival.
  • Considerable controversy exists as to the best therapeutic management for patients with such tumors.
  • Over the past decade, we have applied human fibroblast interferon (HFIF) therapy without radiation therapy to low-grade astrocytomas.
  • We investigated 28 patients with WHO grade II astrocytomas of the cerebral hemispheres treated by surgery plus HFIF therapy.
  • The overall response rate to the HFIF therapy was 36%.
  • Although our data from small cohort of patients may have modest value, our results suggest that HFIF may be useful in treating low-grade diffuse astrocytomas.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Astrocytoma / surgery. Brain Neoplasms / drug therapy. Brain Neoplasms / surgery. Interferon-beta / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Cohort Studies. Combined Modality Therapy. Female. Fibroblasts / metabolism. Humans. Magnetic Resonance Imaging. Male. Maximum Tolerated Dose. Middle Aged. Survival Rate

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  • (PMID = 12622456.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 77238-31-4 / Interferon-beta
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21. Yamada SM, Hayashi Y, Takahashi H, Teramoto A, Matsumoto K, Yamada S: Histological and genetic diagnosis of gliomatosis cerebri: case report. J Neurooncol; 2001 May;52(3):237-40
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  • Gliomatosis cerebri is considered grade III astrocytoma because of the short survival period of patients with this tumor, while the tumor histologically consists of widespread low grade astrocytoma cells.
  • The authors tried to clarify this discrepancy by applying genetic analysis of the tumor.
  • A 29-year-old man originally presented with mild headache and showed diffuse high intensity areas in both hemispheres and in the cerebellum by T2-weighted magnetic resonance imaging (MRI) without gadolinium-dimeglumine (Gd)-enhancement in T1-weighted imaging.
  • Histological diagnosis was gliomatosis cerebri with diffuse grade II astrocytoma.
  • Seven months after temporary improvement following irradiation and chemotherapy, he developed progressive mental deterioration, and died in one year after the surgery.
  • At this time T1-weighted imaging showed Gd-enhanced lesions with enlargement only of the cerebellar tumor.
  • Genetic analysis demonstrated positive FGFR 1 and less FGFR 2 mRNA in the tumor tissue, and FGFR 1 mRNA was beta type dominant.
  • These results indicated that the genetic features of this tumor are similar to those of glioblastoma multiforme concerning FGFR expression.
  • The authors conclude that genetic investigation of the tumor tissue is required to predict the prognosis of gliomatosis cerebri patients, in addition to imaging and histological examinations.
  • [MeSH-minor] Adult. Antigens, Nuclear. Biomarkers, Tumor / genetics. Cerebellar Neoplasms / chemistry. Cerebellar Neoplasms / diagnosis. Cerebellar Neoplasms / genetics. Cerebellar Neoplasms / pathology. Cerebellar Neoplasms / surgery. Combined Modality Therapy. Contrast Media. Fatal Outcome. Gadolinium DTPA. Humans. Magnetic Resonance Imaging. Male. Neoplasm Proteins / genetics. Nuclear Proteins / analysis. RNA, Messenger / analysis. RNA, Neoplasm / analysis. Receptor Protein-Tyrosine Kinases / genetics. Receptor, Fibroblast Growth Factor, Type 1. Receptor, Fibroblast Growth Factor, Type 2. Receptors, Fibroblast Growth Factor / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 11519853.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Biomarkers, Tumor; 0 / Contrast Media; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Fibroblast Growth Factor; EC 2.7.10.1 / FGFR1 protein, human; EC 2.7.10.1 / FGFR2 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 2; K2I13DR72L / Gadolinium DTPA
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22. Sandri A, Sardi N, Genitori L, Giordano F, Peretta P, Basso ME, Bertin D, Mastrodicasa L, Todisco L, Mussa F, Forni M, Ricardi U, Cordero di Montezemolo L, Madon E: Diffuse and focal brain stem tumors in childhood: prognostic factors and surgical outcome. Experience in a single institution. Childs Nerv Syst; 2006 Sep;22(9):1127-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diffuse and focal brain stem tumors in childhood: prognostic factors and surgical outcome. Experience in a single institution.
  • OBJECTIVE: Brainstem tumors (BSTs) are usually gliomas and are divided into diffuse BSTs (DBSTs) and focal BSTs (FBSTs).
  • Patients with DBSTs were treated with locoregional radiotherapy (1.8 Gy/day for 54 Gy) and weekly vincristine for radiosensitization (1.5 mg/sm for six total doses).
  • Chemotherapy and/or radiotherapy were considered in progression.
  • The responses to treatment were ten cases of partial response, three of stable disease, and one of progressive disease.
  • The median time from diagnosis to progression and to death were, nonetheless, 8 (range of 3-13) and 13 (range of 4-25) months, respectively, with a 2-year overall survival rate of 12.3% [standard error (SE) 11.2].
  • Eight out of 17 patients had adjuvant chemo- and/or radiotherapy after progression: 6/8 are without neurological symptoms and 2/8 have died due to tumor progression.
  • The 4-year overall and disease-free survival rates are 87.4 (SE 8.4) and 58.8% (SE 11.9), respectively, the extent of resection being the most important prognostic factor (p=0.012).
  • DBSTs continue to carry a dismal prognosis, thus demanding new treatment modalities; FBSTs can be treated surgically and patients benefit from a better prognosis.
  • [MeSH-major] Astrocytoma / surgery. Brain Stem Neoplasms / surgery. Ganglioglioma / surgery
  • [MeSH-minor] Adolescent. Adult. Brain Stem / pathology. Brain Stem / surgery. Chemotherapy, Adjuvant. Child. Child, Preschool. Combined Modality Therapy. Cranial Irradiation. Disease Progression. Disease-Free Survival. Female. Follow-Up Studies. Humans. Infant. Male. Prognosis. Radiation-Sensitizing Agents / administration & dosage. Radiotherapy, Adjuvant. Survival Rate. Vincristine / administration & dosage

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  • (PMID = 16568342.001).
  • [ISSN] 0256-7040
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Radiation-Sensitizing Agents; 5J49Q6B70F / Vincristine
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23. Cohen KJ, Broniscer A, Glod J: Pediatric glial tumors. Curr Treat Options Oncol; 2001 Dec;2(6):529-36
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  • Glial neoplasms in children comprise many heterogeneous tumors that include pilocytic and fibrillary astrocytomas, ependymomas, and the diffuse intrinsic pontine gliomas.
  • In contrast to adults, most of whom present with high-grade fibrillary neoplasms, alternate histologies represent most cases seen in the pediatric setting.
  • In addition, although most adult gliomas are supratentorial in location, in pediatrics infratentorial tumors (posterior fossa and brain stem) predominate.
  • We discuss three specific tumors: diffuse intrinsic pontine gliomas; pilocytic astrocytomas; and ependymomas.
  • Maximal surgical resection is the mainstay of therapy for both pilocytic astrocytomas and ependymomas.
  • Failure to achieve an optimal resection often results in progression and the need for further therapy for patients with pilocytic astrocytomas, and is ultimately fatal in most children with subtotally resected ependymomas.
  • Surgical resection has no role in the treatment of pontine gliomas.
  • Focal radiation therapy is included routinely in the treatment of ependymomas, and it has been shown to improve event-free survival.
  • This therapy also is used in the treatment of pontine gliomas because radiation treatment appears to slow inevitable tumor progression.
  • Radiation therapy in pilocytic astrocytomas is generally reserved for patients who progress after an initial surgical resection or for those patients with midline tumors; these patients are poor candidates for aggressive surgical resection.
  • The role of chemotherapy in these tumors is in evolution.
  • Chemotherapy for pilocytic astrocytomas, particularly in young children (for whom radiation therapy is avoided), appears to be effective in the treatment of a subset of patients.
  • Up-front chemotherapy is generally reserved for the youngest children who present with ependymoma.
  • In the recurrence setting, chemotherapy has shown some activity, although this approach is never curative.
  • Despite the application of various chemotherapeutics and other biologic agents, none of these therapies has improved the prognosis for patients with the uniformly lethal pontine glioma.
  • [MeSH-major] Brain Neoplasms / therapy. Glioma / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / mortality. Astrocytoma / therapy. Cerebrospinal Fluid Shunts. Chemotherapy, Adjuvant. Child. Child, Preschool. Combined Modality Therapy. Cranial Irradiation. Craniotomy. Disease Progression. Ependymoma / mortality. Ependymoma / therapy. Epidemiologic Methods. Humans. Hydrocephalus / etiology. Hydrocephalus / surgery. Infant. Infratentorial Neoplasms / mortality. Infratentorial Neoplasms / therapy. Palliative Care. Pons. Prognosis. Radiotherapy, Adjuvant. Treatment Outcome

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  • (PMID = 12057098.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 30
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24. Capper D, Mittelbronn M, Meyermann R, Schittenhelm J: Pitfalls in the assessment of MGMT expression and in its correlation with survival in diffuse astrocytomas: proposal of a feasible immunohistochemical approach. Acta Neuropathol; 2008 Feb;115(2):249-59
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  • [Title] Pitfalls in the assessment of MGMT expression and in its correlation with survival in diffuse astrocytomas: proposal of a feasible immunohistochemical approach.
  • Implementation of this data in routine clinical diagnostics is limited due to often inappropriate study designs, e.g. pooling of tumor entities, WHO grades or primary and secondary glioblastomas, disregard concerning the infiltration zone or various epidemiological factors.
  • For this, 162 astrocytic tumors WHO II-IV (36 diffuse astrocytomas WHO II, 51 anaplastic astrocytomas, 75 primary glioblastomas) as well as 25 glioblastoma infiltration zones and 19 glioblastoma relapses were analyzed for immunohistochemical MGMT protein expression using tissue microarray technique.
  • We conclude that immunohistochemical MGMT assessment has potential as a powerful diagnostic tool but analysis should only be performed in a grade dependent manner, before radio-/chemotherapy and with special attention to the infiltration zone of diffuse astrocytomas.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / mortality. Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Brain Neoplasms / mortality. DNA Modification Methylases / biosynthesis. DNA Repair Enzymes / biosynthesis. Tumor Suppressor Proteins / biosynthesis
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Neurosurgical Procedures. Prognosis. Radiotherapy. Tissue Array Analysis

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  • (PMID = 17965865.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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25. Marcus KJ, Dutton SC, Barnes P, Coleman CN, Pomeroy SL, Goumnerova L, Billett AL, Kieran M, Tarbell NJ: A phase I trial of etanidazole and hyperfractionated radiotherapy in children with diffuse brainstem glioma. Int J Radiat Oncol Biol Phys; 2003 Apr 1;55(5):1182-5
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  • [Title] A phase I trial of etanidazole and hyperfractionated radiotherapy in children with diffuse brainstem glioma.
  • PURPOSE: To determine the toxicity and maximum tolerated dose of etanidazole administered concurrently with hyperfractionated radiation therapy (HRT) for children with brainstem glioma.
  • All patients had MRI confirmation of diffuse pontine glioma and signs/symptoms of cranial nerve deficit, ataxia, or long tract signs of <6 months' duration.
  • Patients (median age: 8.5 years; 11 males, 7 females) received HRT to the tumor volume plus a 2-cm margin with parallel-opposed 6-15-MV photons.
  • The total dose was 66 Gy in 44 fractions (1.5 Gy b.i.d., with at least 6 h between fractions) for the first 3 patients and 63 Gy in 42 fractions for the subsequent 15 patients.
  • Two patients were treated at this level, and both patients experienced Grade 3 toxicity in the form of a diffuse cutaneous rash.
  • The median survival from the start of treatment was 8.5 months (range: 3-58 months).
  • This is in contrast to the adult experience, which demonstrates a 24% lower MTD of 34 g/m(2) limited by peripheral neuropathy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Stem Neoplasms / radiotherapy. Cranial Irradiation. Dose Fractionation. Etanidazole / therapeutic use. Glioma / radiotherapy. Radiation-Sensitizing Agents / therapeutic use. Radiotherapy, High-Energy
  • [MeSH-minor] Adolescent. Adult. Astrocytoma / drug therapy. Astrocytoma / radiotherapy. Child. Child, Preschool. Combined Modality Therapy. Dose-Response Relationship, Radiation. Drug Administration Schedule. Female. Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Humans. Male. Survival Analysis. Treatment Outcome

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  • (PMID = 12654425.001).
  • [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; Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Radiation-Sensitizing Agents; 30DKA3Q1HL / Etanidazole
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26. Benesch M, Wagner S, Berthold F, Wolff JE: Primary dissemination of high-grade gliomas in children: experiences from four studies of the Pediatric Oncology and Hematology Society of the German Language Group (GPOH). J Neurooncol; 2005 Apr;72(2):179-83
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  • 546 patients with newly diagnosed HGG (n=348) or diffuse intrinsic pontine gliomas (n=198) were enrolled in these four studies.
  • Data concerning tumor dissemination are available from 324 patients.
  • RESULTS: A total of 10 patients (3.1%) (anaplastic astrocytoma: n=3, glioblastoma multiforme: n=6, diffuse intrinsic pontine glioma: n=1) had primary tumor dissemination.
  • The most frequent primary tumor sites were the cortex (n=4), followed by the ventricles (n=2), cerebellum (n=1), spinal cord (n=1), and pons (n=1).
  • One patient had diffuse gliomatosis cerebri.
  • Following surgery eight patients received local radiotherapy and eight additional chemotherapy.
  • Median progression-free and overall survival was 0.8 years (95% CI 0.2-1.4) and 1.5 years (95% CI 0.67-2.29) for patients with primary tumor dissemination, respectively, with no statistically significant differences between the group with and the group without primary tumor dissemination.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Central Nervous System Neoplasms / pathology. Central Nervous System Neoplasms / therapy. Glioma / pathology. Glioma / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cyclophosphamide / analogs & derivatives. Disease-Free Survival. Etoposide / administration & dosage. Female. Humans. Male. Neoplasm Invasiveness. Radiotherapy. Retrospective Studies. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 15925999.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; H64JRU6GJ0 / trofosfamide
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27. Burzynski SR, Janicki TJ, Weaver RA, Burzynski B: Targeted therapy with antineoplastons A10 and AS2-1 of high-grade, recurrent, and progressive brainstem glioma. Integr Cancer Ther; 2006 Mar;5(1):40-7
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  • [Title] Targeted therapy with antineoplastons A10 and AS2-1 of high-grade, recurrent, and progressive brainstem glioma.
  • Most patients with brainstem glioma fail standard radiation therapy and chemotherapy and do not survive longer than 2 years.
  • Treatment is even more challenging when an inoperable tumor is of high-grade pathology (HBSG).
  • Fourteen patients had diffuse intrinsic tumors.
  • Twelve patients suffered from recurrence, and 6 patients did not have radiation therapy or chemotherapy.
  • Responses were assessed by gadolinium-enhanced magnetic resonance imaging and positron emission tomography.
  • RESULTS: The overall survival at 2 and 5 years was 39% and 22%, respectively, and maximum survival was more than 17 years for a patient with anaplastic astrocytoma and more than 5 years for a patient with glioblastoma.
  • CONCLUSION: Antineoplastons contributed to more than a 5-year survival in recurrent diffuse intrinsic glioblastomas and anaplastic astrocytomas of the brainstem in a small group of patients.
  • [MeSH-major] Benzeneacetamides / administration & dosage. Brain Stem Neoplasms / drug therapy. Glioma / drug therapy. Glutamine / analogs & derivatives. Neoplasm Recurrence, Local / drug therapy. Phenylacetates / administration & dosage. Piperidones / administration & dosage
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Combinations. Female. Follow-Up Studies. Humans. Injections, Intravenous. Magnetic Resonance Imaging. Male. Maximum Tolerated Dose. Neoplasm Staging. Risk Assessment. Survival Analysis. Treatment Outcome

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  • (PMID = 16484713.001).
  • [ISSN] 1534-7354
  • [Journal-full-title] Integrative cancer therapies
  • [ISO-abbreviation] Integr Cancer Ther
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzeneacetamides; 0 / Drug Combinations; 0 / Phenylacetates; 0 / Piperidones; 0RH81L854J / Glutamine; 104624-98-8 / antineoplaston AS 2-1; 91531-30-5 / antineoplaston A10
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28. Herrlinger U, Felsberg J, Küker W, Bornemann A, Plasswilm L, Knobbe CB, Strik H, Wick W, Meyermann R, Dichgans J, Bamberg M, Reifenberger G, Weller M: Gliomatosis cerebri: molecular pathology and clinical course. Ann Neurol; 2002 Oct;52(4):390-9
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  • Gliomatosis cerebri is a rare, diffusely growing neuroepithelial tumor characterized by extensive brain infiltration involving more than two cerebral lobes.
  • Among 13 patients with gliomatosis cerebri (median age, 46 years), biopsies showed features of diffuse astrocytoma (n = 4), oligoastrocytoma (n = 1), anaplastic astrocytoma (n = 5), anaplastic oligoastrocytoma (n = 1), or glioblastoma (n = 2).
  • Molecular genetic investigation showed TP53 mutations in three of seven tumors and both PTEN mutation and epidermal growth factor receptor overexpression in one tumor.
  • Four of six patients treated with procarbazine, carmustine, vincristine chemotherapy demonstrated partial remission (one patient), minor response (two patients), or stable disease (one patient).
  • Median survival time from diagnosis was 14 months (range, 4-91+ months).
  • We conclude that (1) the molecular genetic alterations in gliomatosis cerebri resemble those in diffuse astrocytomas;.
  • (2) the prognosis of gliomatosis cerebri is variable but for at least 50% of patients as poor as for glioblastoma; and (3) some patients respond to radiotherapy and/or procarbazine, carmustine, vincristine chemotherapy.
  • [MeSH-minor] Adult. Aged. Cause of Death. Combined Modality Therapy. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Female. Genetic Markers. Humans. Male. Middle Aged. PTEN Phosphohydrolase. Phosphoric Monoester Hydrolases / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins c-mdm2. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 12325066.001).
  • [ISSN] 0364-5134
  • [Journal-full-title] Annals of neurology
  • [ISO-abbreviation] Ann. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Genetic Markers; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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29. Komine C, Watanabe T, Katayama Y, Yoshino A, Yokoyama T, Fukushima T: Promoter hypermethylation of the DNA repair gene O6-methylguanine-DNA methyltransferase is an independent predictor of shortened progression free survival in patients with low-grade diffuse astrocytomas. Brain Pathol; 2003 Apr;13(2):176-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoter hypermethylation of the DNA repair gene O6-methylguanine-DNA methyltransferase is an independent predictor of shortened progression free survival in patients with low-grade diffuse astrocytomas.
  • In several human neoplasms including low-grade diffuse astrocytomas, promoter hypermethylation of MGMT has been shown to correlate with an increased frequency of p53 mutation.
  • The present findings indicate that aberrant methylation of the MGMT promoter independently augurs for an unfavorable clinical course in patients with low-grade diffuse astrocytomas.
  • Since the presence of MGMT methylation is expected to predict an increased sensitivity to alkylating chemotherapeutic agents, earlier chemotherapy could serve to improve an unfavorable natural history in tumors with MGMT methylation.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. DNA Methylation. Neoplasm Recurrence, Local / genetics. O(6)-Methylguanine-DNA Methyltransferase / genetics
  • [MeSH-minor] Adult. DNA Repair / genetics. Disease Progression. Disease-Free Survival. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Genes, p53 / genetics. Humans. Male. Predictive Value of Tests. Prognosis. Promoter Regions, Genetic. Survival Analysis

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  • (PMID = 12744471.001).
  • [ISSN] 1015-6305
  • [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] EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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30. Arai M, Kashihara K, Kaizaki Y, Taguchi M, Kitamura Y: [Gliomatosis cerebri: report of 3 cases and review of recent literatures]. No To Shinkei; 2003 Oct;55(10):890-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Gliomatosis cerebri is a rare tumor of the central nervous system characterized by widespread diffuse infiltration of the brain and spinal cord by neoplastic glial cells.
  • Case 1 showed transformation from type 1 gliomatosis cerebri to type 2.
  • After radiation therapy, the right cerebral cortex demonstrated hyperintensity on T1- and hypointensity on T2-weighted image.
  • These two cases did not demonstrate diffuse brain swelling or indistinctness of gray/white matter border on the first MR imaging.
  • Case 3 showed two histological components of oligodendroglioma in the corpus callosum and astrocytoma in the cingulate gyrus.
  • Case 3 improved in response to radiotherapy and chemotherapy using procarbazine/MCNU/vincristine (MVP).
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain / pathology. Diagnosis, Differential. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Procarbazine / administration & dosage. Vincristine / administration & dosage

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  • (PMID = 14635518.001).
  • [ISSN] 0006-8969
  • [Journal-full-title] Nō to shinkei = Brain and nerve
  • [ISO-abbreviation] No To Shinkei
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine
  • [Number-of-references] 11
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31. Watanabe T, Yoshino A, Katayama Y: [Genetic analysis and individualized therapy for diffuse glioma]. No Shinkei Geka; 2005 Jun;33(6):537-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Genetic analysis and individualized therapy for diffuse glioma].
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Brain Neoplasms / genetics. Glioma / drug therapy. Glioma / genetics
  • [MeSH-minor] Adult. Aged. Astrocytoma / drug therapy. Astrocytoma / genetics. Carboplatin / administration & dosage. Cell Cycle Proteins / genetics. Cyclin-Dependent Kinase Inhibitor p15. Cyclin-Dependent Kinases / genetics. Drug Administration Schedule. Etoposide / administration & dosage. Female. Genes, p53. Humans. Male. Middle Aged. Oligodendroglioma / drug therapy. Oligodendroglioma / genetics. Proteins / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 15952303.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / PSMF1 protein, human; 0 / Proteins; 0 / Tumor Suppressor Proteins; 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin; EC 2.7.11.22 / Cyclin-Dependent Kinases
  • [Number-of-references] 83
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