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1. Lesser GJ: Chemotherapy of low-grade gliomas. Semin Radiat Oncol; 2001 Apr;11(2):138-44
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  • 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).
  • 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.
  • [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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2. Goodman JH, Yang W, Barth RF, Gao Z, Boesel CP, Staubus AE, Gupta N, Gahbauer RA, Adams DM, Gibson CR, Ferketich AK, Moeschberger ML, Soloway AH, Carpenter DE, Albertson BJ, Bauer WF, Zhang MZ, Wang CC: Boron neutron capture therapy of brain tumors: biodistribution, pharmacokinetics, and radiation dosimetry sodium borocaptate in patients with gliomas. Neurosurgery; 2000 Sep;47(3):608-21; discussion 621-2
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  • OBJECTIVE: The purpose of this study was to obtain tumor and normal brain tissue biodistribution data and pharmacokinetic profiles for sodium borocaptate (Na2B12H11SH) (BSH), a drug that has been used clinically in Europe and Japan for boron neutron capture therapy of brain tumors.
  • The study was performed with a group of 25 patients who had preoperative diagnoses of either glioblastoma multiforme (GBM) or anaplastic astrocytoma (AA) and were candidates for debulking surgery.
  • Multiple samples of tumor tissue, brain tissue around the tumors, and normal brain tissue were obtained at either 3 to 7 or 13 to 15 hours after infusion.
  • For a boron dose of 50 mg/kg body weight, the maximum (mean +/- standard deviation) solid tumor boron values at 3 to 7 hours after infusion were 17.1+/-5.8 and 17.3+/-10.1 microg/g for GBMs and AAs, respectively, and the mean tumor value averaged across all samples was 11.9 microg/g for both GBMs and AAs.
  • In contrast, the mean normal brain tissue values, averaged across all samples, were 4.6+/-5.1 and 5.5+/-3.9 microg/g and the tumor/normal brain tissue ratios were3.8 and 3.2 for patients with GBMs and AAs, respectively.
  • The large standard deviations indicated significant heterogeneity in uptake in both tumor and normal brain tissue.
  • Regions histopathologically classified either as a mixture of tumor and normal brain tissue or as infiltrating tumor exhibited slightly lower boron concentrations than those designated as solid tumor.
  • CONCLUSION: When tumor, blood, and normal tissue boron concentrations were taken into account, the most favorable tumor uptake data were obtained with a boron dose of 25 mg/kg body weight, 3 to 7 hours after termination of the infusion.
  • Although blood boron levels were high, normal brain tissue boron levels were almost always lower than tumor levels.
  • However, tumor boron concentrations were less than those necessary for boron neutron capture therapy, and there was significant intratumoral and interpatient variability in the uptake of BSH, which would make estimation of the radiation dose delivered to the tumor very difficult.
  • However, combining BSH with boronophenylalanine, the other compound that has been used clinically, and optimizing their delivery could increase tumor boron uptake and potentially improve the efficacy of boron neutron capture therapy.
  • [MeSH-major] Astrocytoma / radiotherapy. Borohydrides / pharmacokinetics. Boron Neutron Capture Therapy. Brain Neoplasms / radiotherapy. Glioblastoma / radiotherapy. Sulfhydryl Compounds / pharmacokinetics
  • [MeSH-minor] Adult. Aged. Biological Availability. Brain / metabolism. Brain / radiation effects. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Phantoms, Imaging. Radiometry. Radiotherapy, Adjuvant. Tissue Distribution. Treatment Outcome

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  • (PMID = 10981748.001).
  • [ISSN] 0148-396X
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Borohydrides; 0 / Sulfhydryl Compounds; 12294-22-3 / mercaptoundecahydrododecaborate
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3. Yuan Q, Matsumoto K, Nakabeppu Y, Iwaki T: A comparative immunohistochemistry of O6-methylguanine-DNA methyltransferase and p53 in diffusely infiltrating astrocytomas. Neuropathology; 2003 Sep;23(3):203-9
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  • [Title] A comparative immunohistochemistry of O6-methylguanine-DNA methyltransferase and p53 in diffusely infiltrating astrocytomas.
  • The DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) removes mutagenic adducts from the O6 position of guanine, thereby protecting the genome against guanine : cytosine to adenine : thymine transition and, meanwhile, conferring tumor resistance to many anti-cancer alkylating agents commonly used in the treatment of malignant gliomas.
  • To examine the potential immunostaining pattern of MGMT expression and to evaluate the possible relationship between p53 and MGMT regulation, we assessed MGMT and p53 accumulation on 35 cases of diffusely infiltrating astrocytomas.
  • The percentage of labeled tumor cells was lower in high-grade astrocytomas than in low-grade astrocytomas (P < 0.05).
  • Additionally, p53-immunopositive tumor cells were usually immunonegative to MGMT.
  • Thus, it is suggested that MGMT expression is reduced during malignant transformation of diffusely infiltrating astrocytomas, and that mutant p53 protein might be associated with down regulation of the MGMT expression.
  • [MeSH-major] Astrocytoma / metabolism. Central Nervous System Neoplasms / metabolism. O(6)-Methylguanine-DNA Methyltransferase / biosynthesis. O(6)-Methylguanine-DNA Methyltransferase / genetics. Tumor Suppressor Protein p53 / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Cell Nucleus / metabolism. Child. Child, Preschool. Cytoplasm / metabolism. Down-Regulation. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Infant. Ki-67 Antigen / metabolism. Male. Middle Aged

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  • (PMID = 14570288.001).
  • [ISSN] 0919-6544
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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4. Yoshino A, Katayama Y, Yokoyama T, Watanabe T, Ogino A, Ota T, Komine C, Fukushima T, Kusama K: Therapeutic implications of interferon regulatory factor (IRF)-1 and IRF-2 in diffusely infiltrating astrocytomas (DIA): response to interferon (IFN)-beta in glioblastoma cells and prognostic value for DIA. J Neurooncol; 2005 Sep;74(3):249-60
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  • [Title] Therapeutic implications of interferon regulatory factor (IRF)-1 and IRF-2 in diffusely infiltrating astrocytomas (DIA): response to interferon (IFN)-beta in glioblastoma cells and prognostic value for DIA.
  • Furthermore, we attempted to determine whether or not IRF-1 and IRF-2 act as additional prognostic indicators in diffusely infiltrating astrocytomas (DIA).
  • Furthermore, we assessed the expression of type I IFN receptor, IRF-1, and IRF-2 using immunohistochemical techniques in 63 DIA (15 of WHO grade II, 18 of grade III, and 30 of grade IV), and analyzed their impact on prognosis.
  • [MeSH-major] Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Interferon Regulatory Factor-1 / metabolism. Interferon Regulatory Factor-2 / metabolism. Interferon-beta / pharmacology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Apoptosis / physiology. Blotting, Western. Caspases / drug effects. Caspases / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Enzyme Activation / physiology. Female. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Receptors, Interferon / metabolism

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  • [Cites] Acta Neurochir (Wien). 1994;127(1-2):55-9 [7942182.001]
  • [Cites] J Biol Chem. 1998 Jan 2;273(1):194-9 [9417064.001]
  • [Cites] Cancer Chemother Pharmacol. 2000;45(3):199-206 [10663637.001]
  • [Cites] Science. 1993 Feb 12;259(5097):971-4 [8438157.001]
  • [Cites] Nature. 1991 Jun 6;351(6326):453-6 [2046748.001]
  • [Cites] Cell. 1998 Sep 18;94(6):739-50 [9753321.001]
  • [Cites] J Biol Chem. 1992 Mar 15;267(8):5017-20 [1371992.001]
  • [Cites] Cancer Res. 2003 Jan 15;63(2):513-21 [12543810.001]
  • [Cites] J Biol Chem. 1998 Oct 23;273(43):28378-83 [9774464.001]
  • [Cites] Oncogene. 1994 Nov;9(11):3313-20 [7936656.001]
  • [Cites] Nature. 1996 Aug 29;382(6594):816-8 [8752276.001]
  • [Cites] Cancer Res. 2000 Oct 15;60(20):5673-80 [11059759.001]
  • [Cites] J Cell Biol. 1999 Jan 25;144(2):281-92 [9922454.001]
  • [Cites] Science. 1998 Aug 28;281(5381):1312-6 [9721091.001]
  • [Cites] Cell. 1998 Aug 7;94(3):339-52 [9708736.001]
  • [Cites] Cancer Res. 2000 Dec 15;60(24):7133-41 [11156422.001]
  • [Cites] Science. 1998 Aug 28;281(5381):1309-12 [9721092.001]
  • [Cites] Annu Rev Cell Dev Biol. 1999;15:269-90 [10611963.001]
  • [Cites] Toxicol Lett. 1998 Dec 28;102-103:121-9 [10022243.001]
  • [Cites] J Neurooncol. 2003 Jan;61(2):171-6 [12622456.001]
  • [Cites] J Biol Chem. 1999 Feb 19;274(8):5053-60 [9988752.001]
  • [Cites] Cell. 1997 Nov 14;91(4):479-89 [9390557.001]
  • [Cites] Science. 1991 Jul 5;253(5015):49-53 [1905840.001]
  • [Cites] Trends Cell Biol. 1996 Jul;6(7):245-8 [15157443.001]
  • [Cites] Biochimie. 1998 Aug-Sep;80(8-9):641-50 [9865486.001]
  • [Cites] Eur Cytokine Netw. 1998 Dec;9(4):619-31 [9889406.001]
  • [Cites] Immunol Today. 1988 Dec;9(12):393-400 [2475121.001]
  • [Cites] Ann Oncol. 2000 Jun;11(6):707-14 [10942060.001]
  • [Cites] Oncogene. 1998 Dec 24;17(25):3237-45 [9916986.001]
  • [Cites] Cell. 1996 Oct 18;87(2):171 [8861900.001]
  • [Cites] Int J Cancer. 2000 Feb 1;85(3):416-23 [10652435.001]
  • [Cites] Nature. 1995 Aug 17;376(6541):596-9 [7637809.001]
  • [Cites] Ann Surg Oncol. 1999 Sep;6(6):604-8 [10493631.001]
  • [Cites] J Immunol Methods. 1983 Dec 16;65(1-2):55-63 [6606682.001]
  • [Cites] Cancer Res. 1996 May 15;56(10):2417-21 [8625321.001]
  • [Cites] J Biol Chem. 1999 Apr 23;274(17):11549-56 [10206961.001]
  • [Cites] Cell. 1997 Nov 14;91(4):443-6 [9390553.001]
  • [Cites] Cancer Res. 1993 Sep 15;53(18):4164-8 [8364909.001]
  • [Cites] Oncogene. 2000 Jul 13;19(30):3372-83 [10918594.001]
  • [Cites] Clin Chem. 1996 Jun;42(6 Pt 1):858-68 [8665676.001]
  • [Cites] Clin Cancer Res. 2001 Jun;7(6):1821-31 [11410525.001]
  • [Cites] Cell. 1998 Sep 18;94(6):695-8 [9753316.001]
  • [Cites] Mol Cell. 1998 Jun;1(7):949-57 [9651578.001]
  • [Cites] Cancer Invest. 1996;14(1):25-53 [8597888.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Apr 21;257(3):672-7 [10208842.001]
  • [Cites] Clin Cancer Res. 2001 May;7(5):1293-8 [11350897.001]
  • [Cites] Leukemia. 1997 Jul;11(7):933-9 [9204971.001]
  • [Cites] Trends Biochem Sci. 1995 May;20(5):198-202 [7610484.001]
  • [Cites] Ann Surg. 2001 May;233(5):623-9 [11323500.001]
  • [Cites] Cancer Res. 1998 Oct 1;58(19):4453-60 [9766678.001]
  • [Cites] J Biol Chem. 1997 Jun 27;272(26):16351-7 [9195941.001]
  • [Cites] Genes Dev. 1998 Jun 1;12(11):1551-70 [9620844.001]
  • [Cites] J Biol Chem. 2000 Mar 10;275(10):7337-42 [10702305.001]
  • [Cites] Biochem J. 1997 Aug 15;326 ( Pt 1):1-16 [9337844.001]
  • [Cites] J Interferon Cytokine Res. 2002 Jan;22(1):39-47 [11846974.001]
  • [Cites] J Natl Cancer Inst. 1996 Oct 16;88(20):1442-55 [8841019.001]
  • (PMID = 16187022.001).
  • [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] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon Regulatory Factor-1; 0 / Interferon Regulatory Factor-2; 0 / Receptors, Interferon; 77238-31-4 / Interferon-beta; EC 3.4.22.- / Caspases
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