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6. Weingart J, Grossman SA, Carson KA, Fisher JD, Delaney SM, Rosenblum ML, Olivi A, Judy K, Tatter SB, Dolan ME: Phase I trial of polifeprosan 20 with carmustine implant plus continuous infusion of intravenous O6-benzylguanine in adults with recurrent malignant glioma: new approaches to brain tumor therapy CNS consortium trial. J Clin Oncol; 2007 Feb 1;25(4):399-404
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  • [Title] Phase I trial of polifeprosan 20 with carmustine implant plus continuous infusion of intravenous O6-benzylguanine in adults with recurrent malignant glioma: new approaches to brain tumor therapy CNS consortium trial.
  • PURPOSE: This phase I trial was designed to (1) establish the dose of O6-benzylguanine (O6-BG) administered intravenously as a continuous infusion that suppresses O6-alkylguanine-DNA alkyltransferase (AGT) levels in brain tumors, (2) evaluate the safety of extending continuous-infusion O6-BG at the optimal dose with intracranially implanted carmustine wafers, and (3) measure the pharmacokinetics of O6-BG and its metabolite.
  • Tumor samples were evaluated for AGT levels.
  • Future trials are required to determine if the inhibition of tumor AGT levels results in increased efficacy.

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  • [Cites] Clin Cancer Res. 2000 Aug;6(8):3025-31 [10955780.001]
  • [Cites] J Clin Oncol. 1998 Nov;16(11):3570-5 [9817277.001]
  • [Cites] J Clin Oncol. 2005 Oct 1;23(28):7178-87 [16192602.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):997-1003 [15758010.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] Cancer Res. 2000 Nov 15;60(22):6307-10 [11103789.001]
  • [Cites] J Clin Oncol. 2002 May 1;20(9):2277-83 [11980998.001]
  • [Cites] Neuro Oncol. 2003 Apr;5(2):79-88 [12672279.001]
  • [Cites] J Clin Oncol. 2003 May 1;21(9):1845-9 [12721262.001]
  • [Cites] Neuro Oncol. 2004 Jan;6(1):28-32 [14769137.001]
  • [Cites] Clin Cancer Res. 2004 Mar 15;10(6):1871-4 [15041700.001]
  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jul;87(14):5368-72 [2164681.001]
  • [Cites] Cancer Commun. 1990;2(11):371-7 [2242301.001]
  • [Cites] J Neurosurg. 1991 Mar;74(3):441-6 [1993909.001]
  • [Cites] Cancer Res. 1991 Jul 1;51(13):3367-72 [1647266.001]
  • [Cites] J Neurosurg. 1992 Apr;76(4):640-7 [1545259.001]
  • [Cites] Cancer Chemother Pharmacol. 1993;32(6):471-6 [8258196.001]
  • [Cites] Cancer Res. 1994 Oct 1;54(19):5123-30 [7923129.001]
  • [Cites] Lancet. 1995 Apr 22;345(8956):1008-12 [7723496.001]
  • [Cites] Prog Nucleic Acid Res Mol Biol. 1995;51:167-223 [7659775.001]
  • [Cites] Cancer Res. 1996 Feb 15;56(4):783-8 [8631014.001]
  • [Cites] Br J Cancer. 1996 Oct;74(7):1030-6 [8855970.001]
  • [Cites] Neurosurgery. 1997 Jul;41(1):44-8; discussion 48-9 [9218294.001]
  • [Cites] J Clin Oncol. 1998 May;16(5):1803-10 [9586894.001]
  • [Cites] J Clin Oncol. 2000 Oct 15;18(20):3522-8 [11032594.001]
  • (PMID = 17264335.001).
  • [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 / P30 CA14599; United States / NCI NIH HHS / CA / P30 CA014599; United States / NCI NIH HHS / CA / U01 CA062475; United States / NCRR NIH HHS / RR / M01 RR000055; United States / NCI NIH HHS / CA / U01 CA069852-12; United States / NCRR NIH HHS / RR / M01 RR000055-400764; United States / NCI NIH HHS / CA / CA69852; United States / NCRR NIH HHS / RR / RR000055-400764; United States / NCI NIH HHS / CA / CA069852-12; United States / NCI NIH HHS / CA / P30 CA014599-289015; United States / NCI NIH HHS / CA / CA62475; United States / NCI NIH HHS / CA / U01 CA069852; United States / NCI NIH HHS / CA / CA014599-289015
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / carmustine with prolifeprosan 20; 19916-73-5 / O(6)-benzylguanine; 5Z93L87A1R / Guanine; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase; U68WG3173Y / Carmustine
  • [Other-IDs] NLM/ NIHMS66419; NLM/ PMC2556256
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7. Ali Y, Rahme R, Moussa R, Abadjian G, Menassa-Moussa L, Samaha E: Multifocal meningeal melanocytoma: a new pathological entity or the result of leptomeningeal seeding? J Neurosurg; 2009 Sep;111(3):488-91
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  • Meningeal melanocytoma is a rare benign CNS tumor derived from the leptomeningeal melanocytes.
  • [MeSH-major] Cerebellar Neoplasms / pathology. Cerebellopontine Angle. Melanocytes / pathology. Melanoma / pathology. Meningeal Neoplasms / pathology. Neoplasm Seeding. Spinal Cord Neoplasms / pathology
  • [MeSH-minor] Adult. Humans. Magnetic Resonance Imaging. Male

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  • (PMID = 19361258.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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8. Armstrong GT, Liu Q, Yasui Y, Huang S, Ness KK, Leisenring W, Hudson MM, Donaldson SS, King AA, Stovall M, Krull KR, Robison LL, Packer RJ: Long-term outcomes among adult survivors of childhood central nervous system malignancies in the Childhood Cancer Survivor Study. J Natl Cancer Inst; 2009 Jul 1;101(13):946-58
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  • [Title] Long-term outcomes among adult survivors of childhood central nervous system malignancies in the Childhood Cancer Survivor Study.
  • BACKGROUND: Adult survivors of childhood central nervous system (CNS) malignancies are at high risk for long-term morbidity and late mortality.
  • However, patterns of late mortality, the long-term risks of subsequent neoplasms and debilitating medical conditions, and sociodemographic outcomes have not been comprehensively characterized for individual diagnostic and treatment groups.
  • METHODS: We collected information on treatment, mortality, chronic medical conditions, and neurocognitive functioning of adult 5-year survivors of CNS malignancies diagnosed between 1970 and 1986 within the Childhood Cancer Survivor Study.
  • Using competing risk framework, we calculated cumulative mortality according to cause of death and cumulative incidence of subsequent neoplasms according to exposure and dose of cranial radiation therapy (RT).
  • Neurocognitive impairment and socioeconomic outcomes were assessed with respect to dose of CNS radiotherapy to specific brain regions.
  • Patients who received cranial RT of 50 Gy or more (n = 813) had a cumulative incidence of a subsequent neoplasm within the CNS of 7.1% (95% CI = 4.5% to 9.6%) at 25 years from diagnosis compared with 1.0% (95% CI = 0% to 2.3%) for patients who had no RT.
  • Neurocognitive impairment was high and proportional to radiation dose for specific tumor types.
  • CONCLUSIONS: Survivors of childhood CNS malignancies are at high risk for late mortality and for developing subsequent neoplasms and chronic medical conditions.

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  • [Cites] BMJ. 1994 Jul 16;309(6948):162-6 [8044095.001]
  • [Cites] J Natl Cancer Inst. 2008 Oct 1;100(19):1368-79 [18812549.001]
  • [Cites] J Natl Cancer Inst. 2001 Apr 18;93(8):618-29 [11309438.001]
  • [Cites] J Clin Oncol. 2001 Jul 1;19(13):3163-72 [11432882.001]
  • [Cites] Med Pediatr Oncol. 2002 Apr;38(4):229-39 [11920786.001]
  • [Cites] J Neurol. 2002 Aug;249(8):955-60 [12195437.001]
  • [Cites] Cancer. 2003 Feb 1;97(3):663-73 [12548609.001]
  • [Cites] Cancer. 2003 Feb 15;97(4):1115-26 [12569614.001]
  • [Cites] J Neurooncol. 2003 Jul;63(3):279-87 [12892234.001]
  • [Cites] J Clin Oncol. 2003 Sep 1;21(17):3255-61 [12947060.001]
  • [Cites] JAMA. 2003 Sep 24;290(12):1583-92 [14506117.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Oct;88(10):4731-9 [14557448.001]
  • [Cites] Pediatr Hematol Oncol. 2003 Dec;20(8):617-25 [14578032.001]
  • [Cites] Neuropsychology. 2003 Oct;17(4):548-55 [14599268.001]
  • [Cites] Curr Opin Neurol. 2003 Dec;16(6):677-83 [14624076.001]
  • [Cites] J Clin Oncol. 2004 Mar 15;22(6):999-1006 [15020603.001]
  • [Cites] Ann Fam Med. 2004 Jan-Feb;2(1):61-70 [15053285.001]
  • [Cites] Cancer. 2004 May 15;100(10):2246-52 [15139071.001]
  • [Cites] J Clin Epidemiol. 2004 Sep;57(9):933-44 [15504636.001]
  • [Cites] Am J Epidemiol. 1986 Jan;123(1):174-84 [3509965.001]
  • [Cites] Am J Clin Oncol. 1985 Dec;8(6):472-6 [3936349.001]
  • [Cites] Arch Dis Child. 1990 Dec;65(12):1356-63 [2270944.001]
  • [Cites] J Clin Oncol. 1991 Apr;9(4):592-9 [2066756.001]
  • [Cites] J Clin Oncol. 1992 Sep;10(9):1397-406 [1517782.001]
  • [Cites] Cancer. 2008 Oct 15;113(8):2188-97 [18792068.001]
  • [Cites] Int J Epidemiol. 1998 Feb;27(1):91-5 [9563700.001]
  • [Cites] J Clin Oncol. 1998 May;16(5):1723-8 [9586884.001]
  • [Cites] Ann Neurol. 1998 Sep;44(3):313-6 [9749596.001]
  • [Cites] Med Pediatr Oncol. 1998 Dec;31(6):506-11 [9835903.001]
  • [Cites] Stat Med. 1999 Mar 30;18(6):695-706 [10204198.001]
  • [Cites] J Neurooncol. 1999 Jan;41(1):47-53 [10222422.001]
  • [Cites] Br J Cancer. 2004 Nov 29;91(11):1905-10 [15534607.001]
  • [Cites] J Clin Oncol. 2004 Dec 15;22(24):4979-90 [15576413.001]
  • [Cites] Pediatr Blood Cancer. 2005 Aug;45(2):155-61 [15880357.001]
  • [Cites] Pediatr Blood Cancer. 2006 May 1;46(5):637-44 [16421901.001]
  • [Cites] Pediatr Blood Cancer. 2006 Jul;47(1):83-8 [16317732.001]
  • [Cites] J Clin Oncol. 2006 Jun 1;24(16):2536-43 [16735706.001]
  • [Cites] Radiat Res. 2006 Jul;166(1 Pt 2):141-57 [16808603.001]
  • [Cites] Haematologica. 2006 Aug;91(8):1084-91 [16870549.001]
  • [Cites] N Engl J Med. 2006 Oct 12;355(15):1572-82 [17035650.001]
  • [Cites] Eur J Cancer. 2007 Jan;43(2):351-62 [17141498.001]
  • [Cites] Pediatr Blood Cancer. 2007 Apr;48(4):460-7 [16767717.001]
  • [Cites] J Clin Oncol. 2007 Apr 20;25(12):1532-8 [17442996.001]
  • [Cites] Pediatr Blood Cancer. 2007 Jul;49(1):47-51 [16755550.001]
  • [Cites] Blood. 2008 Apr 15;111(8):4014-21 [18258798.001]
  • [Cites] Cancer. 2008 May 1;112(9):2071-9 [18327823.001]
  • [Cites] Pediatr Blood Cancer. 2008 Aug;51(2):245-50 [18386785.001]
  • [Cites] J Clin Oncol. 2008 Sep 20;26(27):4401-9 [18802152.001]
  • [CommentIn] J Natl Cancer Inst. 2009 Jul 1;101(13):908-10 [19549957.001]
  • [CommentIn] J Natl Cancer Inst. 2009 Jul 1;101(13):909 [19549959.001]
  • (PMID = 19535780.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U24-CA55727
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2704230
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9. Strojnik T, Røsland GV, Sakariassen PO, Kavalar R, Lah T: Neural stem cell markers, nestin and musashi proteins, in the progression of human glioma: correlation of nestin with prognosis of patient survival. Surg Neurol; 2007 Aug;68(2):133-43; discussion 143-4
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  • BACKGROUND: The IF protein nestin and the RNA-binding protein musashi are expressed by neural progenitor cells during CNS development.
  • Their expression in glial tumors was evaluated by immunohistochemistry, and the histopathological scores correlated with levels of cysteine cathepsins that are known prognostic markers in several tumors.
  • METHODS: The levels of nestin, musashi, and cathepsins B and L were assessed by immunohistochemical analysis of biopsies from 87 patients with primary CNS tumors.
  • To confirm the immunohistochemical data, nestin expression was analyzed by real-time PCR in 12 brain tumor biopsies.
  • The total IHC score for nestin was significantly higher in high- than in low-grade tumors (P < .0001).
  • IHC staining of nestin in a xenograft model showed that its expression is localized mainly in the invasive tumor cells at the tumor periphery.
  • The presented data links the invasive glioma cells to CNS precursor cells, indicating that the most malignant cells in the gliomas may well be closely related to the glioma stem cells.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Glioma / metabolism. Glioma / pathology. Intermediate Filament Proteins / metabolism. Nerve Tissue Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Animals. Cathepsin B / metabolism. Cathepsin L. Cathepsins / metabolism. Child. Child, Preschool. Cysteine Endopeptidases / metabolism. Female. Humans. Male. Middle Aged. Nestin. RNA, Messenger / metabolism. RNA-Binding Proteins / metabolism. Rats. Survival Rate

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  • (PMID = 17537489.001).
  • [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; 0 / Intermediate Filament Proteins; 0 / MSI1 protein, human; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, rat; 0 / Nestin; 0 / RNA, Messenger; 0 / RNA-Binding Proteins; EC 3.4.- / Cathepsins; EC 3.4.22.- / Cysteine Endopeptidases; EC 3.4.22.1 / Cathepsin B; EC 3.4.22.15 / CTSL1 protein, human; EC 3.4.22.15 / Cathepsin L; EC 3.4.22.15 / Ctsl protein, rat
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10. Honda S, Toda K, Tozuka Y, Yasuzawa S, Iwabuchi K, Tomooka Y: Migration and differentiation of neural cell lines transplanted into mouse brains. Neurosci Res; 2007 Oct;59(2):124-35
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  • In the past few years, the plasticity of the regional specification of the CNS has been widely debated on the results from in utero transplantation.
  • These lines were established from a cerebellum of an adult p53-deficient mouse.
  • Our results showed that transplanted cells migrated into various regions of the CNS and supported the independent distribution.
  • [MeSH-minor] Animals. Animals, Newborn. Biomarkers / metabolism. Blood Vessels / embryology. Cell Line. Cell Lineage / physiology. Cell Shape / physiology. Cell Survival / physiology. Clone Cells / cytology. Clone Cells / metabolism. Clone Cells / transplantation. Female. Male. Mice. Mice, Knockout. Nerve Tissue Proteins / metabolism. Neurites / ultrastructure. Organ Culture Techniques. Sex Characteristics. Time Factors. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 17651850.001).
  • [ISSN] 0168-0102
  • [Journal-full-title] Neuroscience research
  • [ISO-abbreviation] Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Nerve Tissue Proteins; 0 / Tumor Suppressor Protein p53
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16. Kim B, Myung JK, Seo JH, Park CK, Paek SH, Kim DG, Jung HW, Park SH: The clinicopathologic values of the molecules associated with the main pathogenesis of the glioblastoma. J Neurol Sci; 2010 Jul 15;294(1-2):112-8
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  • Glioblastoma (GBM) is a malignant CNS neoplasm.
  • Stratified by age, resectability and tumor size <5 cm were favorable survival factors in young (40<yrs) and old age groups (> or =40 yrs), respectively.
  • Furthermore, the patients with supratentorial tumor lived longer than the patients with infratentorial tumor (p<0.05).
  • [MeSH-major] Brain Neoplasms / metabolism. Glioblastoma / metabolism
  • [MeSH-minor] Adult. Age Factors. Brain / metabolism. Brain / surgery. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Infratentorial Neoplasms / diagnosis. Infratentorial Neoplasms / metabolism. Infratentorial Neoplasms / mortality. Infratentorial Neoplasms / pathology. Male. PTEN Phosphohydrolase / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Prognosis. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Epidermal Growth Factor / metabolism. Supratentorial Neoplasms / diagnosis. Supratentorial Neoplasms / metabolism. Supratentorial Neoplasms / mortality. Supratentorial Neoplasms / pathology. Survival Analysis. Tumor Suppressor Protein p53 / metabolism


17. Lotrich FE, Ferrell RE, Rabinovitz M, Pollock BG: Labile anger during interferon alfa treatment is associated with a polymorphism in tumor necrosis factor alpha. Clin Neuropharmacol; 2010 Jul;33(4):191-7
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  • [Title] Labile anger during interferon alfa treatment is associated with a polymorphism in tumor necrosis factor alpha.
  • Evidence also indicates a central nervous system role for tumor necrosis factor alpha (TNF-alpha), whose expression may be increased by interferon alfa.

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  • [Cites] J Neuropsychiatry Clin Neurosci. 1991 Spring;3(2):S44-51 [1821222.001]
  • [Cites] Arch Gen Psychiatry. 1997 Dec;54(12):1081-8 [9400343.001]
  • [Cites] Acta Psychiatr Scand. 1998 Apr;97(4):309-13 [9570493.001]
  • [Cites] Psychiatry Res. 1998 Jun 15;79(2):163-73 [9705054.001]
  • [Cites] N Engl J Med. 1998 Nov 19;339(21):1485-92 [9819446.001]
  • [Cites] Brain Behav Immun. 1999 Jun;13(2):175-86 [10373280.001]
  • [Cites] Adv Exp Med Biol. 1999;461:117-27 [10442171.001]
  • [Cites] J Clin Psychiatry. 2005 Jan;66(1):41-8 [15669887.001]
  • [Cites] J Affect Disord. 2005 Feb;84(2-3):117-25 [15708408.001]
  • [Cites] World J Gastroenterol. 2005 Mar 28;11(12):1769-74 [15793861.001]
  • [Cites] J Clin Psychiatry. 2005 Aug;66(8):1050-7 [16086622.001]
  • [Cites] Eur Arch Psychiatry Clin Neurosci. 2005 Aug;255(4):215-22 [16133740.001]
  • [Cites] Neurol Res. 2005 Oct;27(7):679-84 [16197804.001]
  • [Cites] AIDS. 2005 Oct;19 Suppl 3:S174-8 [16251815.001]
  • [Cites] J Autoimmun. 2005 Sep;25(2):150-4 [16046099.001]
  • [Cites] Arch Gen Psychiatry. 2005 Dec;62(12):1377-84 [16330726.001]
  • [Cites] Obes Res. 2005 Dec;13(12):2122-31 [16421346.001]
  • [Cites] Curr Opin Psychiatry. 2006 Jan;19(1):1-8 [16612171.001]
  • [Cites] Nature. 2006 Apr 20;440(7087):1054-9 [16547515.001]
  • [Cites] J Affect Disord. 2006 May;92(1):19-33 [16635528.001]
  • [Cites] J Neurosci. 2006 May 24;26(21):5709-19 [16723527.001]
  • [Cites] J Hum Genet. 2006;51(8):677-85 [16865291.001]
  • [Cites] Psychosomatics. 2007 May-Jun;48(3):223-9 [17478591.001]
  • [Cites] Eur J Gastroenterol Hepatol. 2007 Aug;19(8):639-46 [17625432.001]
  • [Cites] J Psychosom Res. 2007 Aug;63(2):131-5 [17662748.001]
  • [Cites] Int Rev Neurobiol. 2007;82:247-63 [17678965.001]
  • [Cites] Biol Psychiatry. 2007 Sep 1;62(5):536-40 [17300755.001]
  • [Cites] N Engl J Med. 2002 Sep 26;347(13):975-82 [12324553.001]
  • [Cites] Mol Psychiatry. 2002;7(9):942-7 [12399946.001]
  • [Cites] Mol Psychiatry. 2002;7(9):1023-9 [12399958.001]
  • [Cites] Brain Behav Immun. 2002 Oct;16(5):569-74 [12401470.001]
  • [Cites] Brain Behav Immun. 2002 Dec;16(6):675-84 [12480498.001]
  • [Cites] Psychosomatics. 2003 Mar-Apr;44(2):104-12 [12618532.001]
  • [Cites] J Clin Psychiatry. 2003 Jun;64(6):708-14 [12823087.001]
  • [Cites] Biol Psychiatry. 2003 Jul 1;54(1):34-9 [12842306.001]
  • [Cites] Psychiatr Genet. 2003 Sep;13(3):179-81 [12960751.001]
  • [Cites] Psychiatry Res. 2004 Jan 30;125(1):65-8 [14967554.001]
  • [Cites] Eur J Immunogenet. 2004 Feb;31(1):15-9 [15009176.001]
  • [Cites] J Affect Disord. 2004 Mar;78(3):273-7 [15013254.001]
  • [Cites] Psychosomatics. 2004 Mar-Apr;45(2):176 [15016930.001]
  • [Cites] Hum Immunol. 2004 Apr;65(4):347-51 [15120189.001]
  • [Cites] Psychoneuroendocrinology. 2004 Oct;29(9):1119-28 [15219635.001]
  • [Cites] J Affect Disord. 2008 Apr;107(1-3):293-8 [17850879.001]
  • [Cites] Brain Behav Immun. 2008 May;22(4):573-89 [18191534.001]
  • [Cites] Psychopharmacology (Berl). 2008 May;197(4):629-35 [18274729.001]
  • [Cites] Arthritis Rheum. 2008 May;58(5):1258-63 [18438841.001]
  • [Cites] Neuropsychobiology. 2008;57(1-2):88-94 [18515978.001]
  • [Cites] Psychopharmacology (Berl). 2008 Aug;199(2):231-44 [18491079.001]
  • [Cites] Mol Psychiatry. 2008 Aug;13(8):800-12 [18504423.001]
  • [Cites] Compr Psychiatry. 2008 Sep-Oct;49(5):469-75 [18702932.001]
  • [Cites] Biol Psychiatry. 2008 Sep 15;64(6):476-83 [18514165.001]
  • [Cites] Neurobiol Dis. 2008 Oct;32(1):125-32 [18672064.001]
  • [Cites] HIV Med. 2008 Oct;9(8):677-80 [18631256.001]
  • [Cites] Neuropsychobiology. 2008;58(2):71-80 [18832862.001]
  • [Cites] Natl Med J India. 2008 May-Jun;21(3):120-2 [19004142.001]
  • [Cites] Psychiatry Clin Neurosci. 2006 Oct;60(5):611-5 [16958946.001]
  • [Cites] J Neurosci. 2006 Sep 20;26(38):9703-12 [16988041.001]
  • [Cites] Aliment Pharmacol Ther. 2006 Oct 15;24(8):1223-30 [17014581.001]
  • [Cites] Brain Behav Immun. 2006 Nov;20(6):507-14 [16938427.001]
  • [Cites] Brain Res. 2006 Nov 20;1120(1):64-73 [17022949.001]
  • [Cites] Neuropsychopharmacology. 2006 Dec;31(12):2619-26 [16823390.001]
  • [Cites] J Psychiatr Res. 2007 Apr-Jun;41(3-4):326-31 [16870211.001]
  • [Cites] J Psychosom Res. 2007 Feb;62(2):207-14 [17270579.001]
  • [Cites] J Am Acad Child Adolesc Psychiatry. 2007 Mar;46(3):309-22 [17314717.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2007 Mar;292(3):G779-84 [17170025.001]
  • [Cites] Eur Neuropsychopharmacol. 2007 May-Jun;17(6-7):410-6 [17187964.001]
  • [Cites] Brain Behav Immun. 2007 May;21(4):374-83 [17360153.001]
  • [Cites] Gastroenterology. 2007 Apr;132(4):1279-86 [17408646.001]
  • [Cites] Bipolar Disord. 2007 Sep;9(6):596-602 [17845274.001]
  • [Cites] J Viral Hepat. 2007 Nov;14(11):788-96 [17927615.001]
  • [Cites] Mol Psychiatry. 2007 Nov;12(11):988-1000 [17457312.001]
  • [Cites] Br J Dermatol. 2007 Dec;157(6):1275-7 [17916204.001]
  • [Cites] J Clin Gastroenterol. 2008 Jan;42(1):92-6 [18097297.001]
  • [Cites] Psychoneuroendocrinology. 2008 Jan;33(1):68-76 [17988804.001]
  • [Cites] Neurosci Lett. 2008 Jan 17;430(3):264-8 [18063307.001]
  • [Cites] Prog Neuropsychopharmacol Biol Psychiatry. 2008 Feb 15;32(2):445-50 [17976882.001]
  • [Cites] Mol Immunol. 2008 Mar;45(6):1682-92 [17996942.001]
  • [Cites] Parkinsonism Relat Disord. 2008 Dec;14(8):636-40 [18362084.001]
  • [Cites] Brain Res. 2009 Jan 9;1247:178-81 [18992723.001]
  • [Cites] Am J Gastroenterol. 2008 Dec;103(12):3132-41 [18853973.001]
  • [Cites] J Psychiatr Res. 2009 Jan;43(4):471-6 [18640689.001]
  • [Cites] Psychiatry Clin Neurosci. 2009 Feb;63(1):50-5 [19154212.001]
  • [Cites] Biol Psychiatry. 2009 Feb 15;65(4):344-8 [18801474.001]
  • [Cites] Respir Med. 2009 Mar;103(3):386-92 [19022640.001]
  • [Cites] J Physiol Pharmacol. 2008 Dec;59 Suppl 6:607-14 [19218687.001]
  • [Cites] J Neurosci. 2009 Apr 1;29(13):4200-9 [19339614.001]
  • [Cites] Emotion. 2009 Jun;9(3):385-96 [19485616.001]
  • [Cites] Brain Behav Immun. 2009 Nov;23(8):1109-16 [19615438.001]
  • [Cites] CNS Spectr. 2009 Aug;14(8):419-25 [19890236.001]
  • [Cites] Mol Psychiatry. 2009 Dec;14(12):1095-104 [18458677.001]
  • [Cites] Psychiatry Res. 2010 May 15;177(1-2):240-5 [20381876.001]
  • [Cites] Am J Med. 1999 Dec 27;107(6B):2S-9S [10653448.001]
  • [Cites] Cytokine. 2000 Feb;12(2):110-9 [10671295.001]
  • [Cites] J Am Acad Child Adolesc Psychiatry. 2000 Apr;39(4):469-76 [10761349.001]
  • [Cites] Science. 2000 Jul 28;289(5479):591-4 [10915615.001]
  • [Cites] Ann N Y Acad Sci. 2000;917:4-18 [11268367.001]
  • [Cites] Psychiatr Genet. 2000 Dec;10(4):195-8 [11324946.001]
  • [Cites] Genes Immun. 2001 Apr;2(2):105-9 [11393654.001]
  • [Cites] Lancet. 2001 Sep 22;358(9286):958-65 [11583749.001]
  • [Cites] J Viral Hepat. 2002 Mar;9(2):84-100 [11876790.001]
  • [Cites] Science. 2002 Mar 22;295(5563):2282-5 [11910117.001]
  • [Cites] Eur J Neurosci. 2002 Mar;15(6):1061-76 [11918665.001]
  • [Cites] Neuropsychopharmacology. 2002 May;26(5):643-52 [11927189.001]
  • [Cites] Hum Mol Genet. 2002 May 15;11(11):1281-9 [12019209.001]
  • [Cites] Genes Immun. 2004 Aug;5(5):315-29 [14973548.001]
  • [Cites] Psychiatry Clin Neurosci. 2004 Oct;58(5):480-6 [15482578.001]
  • (PMID = 20661026.001).
  • [ISSN] 1537-162X
  • [Journal-full-title] Clinical neuropharmacology
  • [ISO-abbreviation] Clin Neuropharmacol
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / K23 MH074012; United States / NIMH NIH HHS / MH / MH074012-05; United States / NIMH NIH HHS / MH / K23 MH074012-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon-alpha; 0 / Recombinant Proteins; 0 / SLC6A4 protein, human; 0 / Serotonin Plasma Membrane Transport Proteins; 0 / Tumor Necrosis Factor-alpha; 76543-88-9 / interferon alfa-2a; 99210-65-8 / interferon alfa-2b
  • [Other-IDs] NLM/ NIHMS203707; NLM/ PMC2911643
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18. Roy S, Josephson SA, Fridlyand J, Karch J, Kadoch C, Karrim J, Damon L, Treseler P, Kunwar S, Shuman MA, Jones T, Becker CH, Schulman H, Rubenstein JL: Protein biomarker identification in the CSF of patients with CNS lymphoma. J Clin Oncol; 2008 Jan 1;26(1):96-105
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  • [Title] Protein biomarker identification in the CSF of patients with CNS lymphoma.
  • PURPOSE: Elucidation of the CSF proteome may yield insights into the pathogenesis of CNS disease.
  • We tested the hypothesis that individual CSF proteins distinguish CNS lymphoma from benign focal brain lesions.
  • METHODS: We used a liquid chromatography/mass spectrometry-based method to differentially quantify and identify several hundred CSF proteins in CNS lymphoma and control patients.
  • ATIII RNA transcripts were identified within CNS lymphomas, and ATIII protein was localized selectively to tumor neovasculature.
  • We propose that the discovery of CSF protein biomarkers will facilitate early and noninvasive diagnosis in patients with lesions not amenable to brain biopsy, as well as provide improved surrogates of prognosis and treatment response in CNS lymphoma and brain metastasis.
  • [MeSH-major] Biomarkers, Tumor / cerebrospinal fluid. Brain Neoplasms / cerebrospinal fluid. Lymphoma / cerebrospinal fluid. Neoplasm Proteins / cerebrospinal fluid
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antithrombin III / genetics. Antithrombin III / metabolism. Case-Control Studies. Chromatography, Liquid. Diagnosis, Differential. Enzyme-Linked Immunosorbent Assay. Female. Humans. Immunoblotting. Immunoenzyme Techniques. Leukemia, Myeloid / cerebrospinal fluid. Leukemia, Myeloid / pathology. Lymphoma, B-Cell / cerebrospinal fluid. Lymphoma, B-Cell / pathology. Lymphoma, B-Cell, Marginal Zone / cerebrospinal fluid. Lymphoma, B-Cell, Marginal Zone / pathology. Lymphoma, Large B-Cell, Diffuse / cerebrospinal fluid. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Non-Hodgkin / cerebrospinal fluid. Lymphoma, Non-Hodgkin / pathology. Male. Middle Aged. Proteomics. Sensitivity and Specificity. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Survival Rate

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  • [Cites] J Clin Oncol. 1999 Feb;17(2):554-60 [10080599.001]
  • [Cites] Bioinformatics. 2004 Dec 12;20(18):3575-82 [15284095.001]
  • [Cites] J Clin Oncol. 2005 Aug 1;23(22):5034-43 [15955902.001]
  • [Cites] Hematol Oncol Clin North Am. 2005 Aug;19(4):705-17, vii [16083831.001]
  • [Cites] Mol Cell Proteomics. 2005 Sep;4(9):1341-9 [15970584.001]
  • [Cites] Dis Markers. 2006;22(1-2):3-26 [16410649.001]
  • [Cites] Blood. 2006 May 1;107(9):3716-23 [16418334.001]
  • [Cites] J Biol Chem. 2006 Dec 8;281(49):37302-10 [17040907.001]
  • [Cites] Expert Rev Mol Med. 2006;8(31):1-19 [17156576.001]
  • [Cites] Cancer Cell. 2007 Jan;11(1):83-95 [17222792.001]
  • [Cites] Anal Chem. 2003 Sep 15;75(18):4818-26 [14674459.001]
  • [Cites] J Clin Oncol. 2003 Jan 15;21(2):266-72 [12525518.001]
  • [Cites] Am J Pathol. 2002 Dec;161(6):2053-63 [12466122.001]
  • [Cites] Lancet. 2002 Feb 16;359(9306):572-7 [11867112.001]
  • [Cites] Curr Opin Neurol. 2000 Dec;13(6):641-8 [11148663.001]
  • [Cites] J Clin Oncol. 1998 Mar;16(3):864-71 [9508167.001]
  • [Cites] Clin Chem. 1993 Apr;39(4):561-77 [8472349.001]
  • [Cites] Br J Haematol. 2004 Jul;126(2):202-8 [15238140.001]
  • [Cites] Clin Cancer Res. 2004 May 1;10(9):2922-7 [15131026.001]
  • [Cites] Bioinformatics. 2004 Mar 22;20(5):777-85 [14751995.001]
  • [Cites] J Neurosurg. 2007 Jan;106(1):72-5 [17236490.001]
  • [CommentIn] J Clin Oncol. 2009 May 1;27(13):2302-3; author reply 2303-4 [19332721.001]
  • (PMID = 18056677.001).
  • [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 / K23 CA100291
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 9000-94-6 / Antithrombin III
  • [Other-IDs] NLM/ NIHMS612770; NLM/ PMC4134101
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19. Kim SH, Cheong JW, Park KH, Kim TS, Yang WI: Comparison of ataxia-telangiectasia mutated protein expression in diffuse large B-cell lymphomas of primary central nervous system and non-central nervous system origin. Arch Pathol Lab Med; 2007 Mar;131(3):457-67
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  • [Title] Comparison of ataxia-telangiectasia mutated protein expression in diffuse large B-cell lymphomas of primary central nervous system and non-central nervous system origin.
  • In primary central nervous system diffuse large B-cell lymphomas (PCNS DLBCLs), the pathogenetic role of ATM mutation has not been investigated.
  • OBJECTIVE: To investigate ATM protein expression in PCNS DLBCLs, in comparison with that in non-central nervous system (non-CNS) DLBCLs and to study the relationship of ATM protein loss with several clinicopathologic parameters.
  • DESIGN: This study included 42 cases of PCNS DLBCL and 33 cases of non-CNS DLBCL from immunocompetent patients.
  • RESULTS: The loss of ATM expression was statistically more frequent in PCNS DLBCLs (21/42 cases [50.0%]) than in non-CNS DLBCLs (0/33 cases [0.0%]; P < .001).
  • CONCLUSIONS: Our results suggest that the ATM protein is more strongly correlated with PCNS DLBCL lymphomagenesis than with non-CNS DLBCLs, especially in germinal center B-cell-like subtypes demonstrating low Ki-67 labeling indexes and low Bcl-2 expression.
  • [MeSH-major] Cell Cycle Proteins / metabolism. Central Nervous System Neoplasms / metabolism. DNA-Binding Proteins / metabolism. Lymphoma, B-Cell / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Protein-Serine-Threonine Kinases / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Ataxia Telangiectasia Mutated Proteins. Child. Child, Preschool. Epstein-Barr Virus Infections / diagnosis. Female. Humans. In Situ Hybridization. Male. Middle Aged. Prognosis. RNA, Messenger / analysis. RNA-Binding Proteins / genetics. Ribosomal Proteins / genetics

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  • (PMID = 17516749.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / RNA-Binding Proteins; 0 / Ribosomal Proteins; 0 / Tumor Suppressor Proteins; 135844-68-7 / RPL22 protein, human; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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20. Veselska R, Hermanova M, Loja T, Chlapek P, Zambo I, Vesely K, Zitterbart K, Sterba J: Nestin expression in osteosarcomas and derivation of nestin/CD133 positive osteosarcoma cell lines. BMC Cancer; 2008;8:300
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  • BACKGROUND: Nestin was originally identified as a class VI intermediate filament protein that is expressed in stem cells and progenitor cells in the mammalian CNS during development.
  • This protein is replaced in the adult organism by other intermediate filament proteins; however, nestin may be re-expressed under certain pathological conditions such as ischemia, inflammation, brain injury, and neoplastic transformation.
  • Nestin has been detected in many kinds of tumors, especially in tumors derived from the CNS.
  • Co-expression of nestin and the CD133 surface molecule is considered to be a marker for cancer stem cells in neurogenic tumors.
  • METHODS: Using immunodetection methods, we examined nestin in tumor tissue samples from 18 patients with osteosarcomas.
  • We also successfully established permanent cell lines from the tumor tissue of 4 patients and immunodetection of nestin and CD133 was performed on these cell lines.
  • RESULTS: Nestin-positive tumor cells were immunohistochemically detected in all of the examined osteosarcomas, but the proportion of these cells that were positively stained as well as the intensity of staining varied.
  • Nestin-positive cells were rarely observed in 2 tumor samples, and the remaining 16 tumor samples showed various nestin expression patterns ranging from very sporadic occurrence to an overwhelming proportion of cells with strong positive staining.
  • Three of the established osteosarcoma cell lines were demonstrated to be nestin-positive, and only one cell line showed no expression of nestin; this finding corresponds with the rare occurrence of nestin-positive cells in the respective tumor sample.
  • CONCLUSION: Our results represent the first evidence of nestin expression in osteosarcomas and suggest the possible occurrence of cells with a stem-like phenotype in these tumors.
  • [MeSH-minor] Adolescent. Adult. Cell Line, Tumor. Child. Female. Fluorescent Antibody Technique. Humans. Immunohistochemistry. Male. Middle Aged. Nestin

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  • [Cites] Histopathology. 2006 Apr;48(5):536-45 [16623779.001]
  • [Cites] J Neurosci. 1985 Dec;5(12):3310-28 [4078630.001]
  • [Cites] Acta Neuropathol. 2006 May;111(5):475-82 [16598485.001]
  • [Cites] Neurosci Lett. 2006 May 29;400(1-2):80-5 [16529857.001]
  • [Cites] J Pathol. 2006 Jul;209(3):287-97 [16770755.001]
  • [Cites] J Neuropathol Exp Neurol. 2006 Oct;65(10):1004-11 [17021405.001]
  • [Cites] Indian J Med Res. 2006 Sep;124(3):269-80 [17085830.001]
  • [Cites] Mol Cancer. 2006;5:67 [17140455.001]
  • [Cites] Cell Res. 2006 Dec;16(12):909-15 [17088899.001]
  • [Cites] Mod Pathol. 2007 Jan;20(1):102-7 [17143262.001]
  • [Cites] Cell Res. 2007 Jan;17(1):3-14 [17179981.001]
  • [Cites] Hepatobiliary Pancreat Dis Int. 2007 Feb;6(1):92-7 [17287174.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Apr 20;355(4):855-9 [17307142.001]
  • [Cites] Mol Cancer. 2007;6:26 [17407576.001]
  • [Cites] Mod Pathol. 2007 Jul;20(7):734-41 [17464317.001]
  • [Cites] J Clin Pathol. 2008 Apr;61(4):467-73 [17873113.001]
  • [Cites] Exp Neurol. 1999 Dec;160(2):348-60 [10619552.001]
  • [Cites] Am J Pathol. 2001 Mar;158(3):817-23 [11238030.001]
  • [Cites] Stem Cells. 2001;19(5):419-24 [11553850.001]
  • [Cites] J Histochem Cytochem. 2002 Feb;50(2):147-58 [11799134.001]
  • [Cites] Exp Neurol. 2002 Mar;174(1):89-95 [11869037.001]
  • [Cites] APMIS. 2002 Jun;110(6):499-507 [12193211.001]
  • [Cites] Int J Oncol. 2002 Oct;21(4):775-85 [12239616.001]
  • [Cites] Neurosci Res. 2002 Oct;44(2):207-12 [12354635.001]
  • [Cites] Cell. 1990 Feb 23;60(4):585-95 [1689217.001]
  • [Cites] Cancer Res. 1992 Oct 1;52(19):5334-41 [1382841.001]
  • [Cites] J Cell Sci. 1992 Oct;103 ( Pt 2):589-97 [1478958.001]
  • [Cites] Cancer Res. 1994 Jan 15;54(2):354-6 [8275467.001]
  • [Cites] Neuron. 1994 Jan;12(1):11-24 [8292356.001]
  • [Cites] Neuron. 1994 Nov;13(5):1071-82 [7946346.001]
  • [Cites] Brain Res Dev Brain Res. 1995 Jan 14;84(1):109-29 [7720210.001]
  • [Cites] Lab Invest. 1996 Jan;74(1):188-98 [8569181.001]
  • [Cites] Pediatr Pathol Lab Med. 1997 Nov-Dec;17(6):913-25 [9353831.001]
  • [Cites] Pediatr Res. 1998 Mar;43(3):386-92 [9505279.001]
  • [Cites] Curr Opin Cell Biol. 2004 Dec;16(6):708-12 [15530785.001]
  • [Cites] Lab Invest. 2004 Dec;84(12):1581-92 [15502861.001]
  • [Cites] J Clin Pathol. 2005 Feb;58(2):222-3 [15677549.001]
  • [Cites] J Neurooncol. 2005 Aug;74(1):1-8 [16078101.001]
  • [Cites] Cell Prolif. 2005 Dec;38(6):423-33 [16300654.001]
  • [Cites] Folia Histochem Cytobiol. 2005;43(4):175-81 [16382880.001]
  • [Cites] Histopathology. 2006 Mar;48(4):424-30 [16487364.001]
  • [Cites] BMC Cancer. 2006;6:32 [16457706.001]
  • [Cites] Am J Surg Pathol. 2003 Jul;27(7):1008-12 [12826895.001]
  • [Cites] Exp Mol Med. 2004 Feb 29;36(1):52-6 [15031671.001]
  • [Cites] J Biol Chem. 2004 Jul 2;279(27):27994-9 [15117961.001]
  • [Cites] Mod Pathol. 2006 May;19(5):659-68 [16528378.001]
  • (PMID = 18925963.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; 0 / Peptides
  • [Other-IDs] NLM/ PMC2588620
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21. Sundaram C, Uppin SG, Uppin MS, Rekha JS, Panigrahi MK, Purohit AK, Rammurti S: A clinicopathological and immunohistochemical study of central nervous system hemangiopericytomas. J Clin Neurosci; 2010 Apr;17(4):469-72
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  • [Title] A clinicopathological and immunohistochemical study of central nervous system hemangiopericytomas.
  • Hemangiopericytomas (HPC) of the central nervous system (CNS) are uncommon dural-based tumors that mimic meningiomas clinically and radiologically.
  • Because there are few reports about these tumors from India, we aimed to study the clinico-pathological and immunohistochemical features of CNS HPC.
  • During 2000 to 2008 all 23 patients diagnosed with HPC of CNS at our Institution were reviewed in the study (11 males and 12 females, mean age of 46 years).
  • There were 14 patients with grade II and nine with grade III tumors.
  • Immunohistochemistry with antibodies to epithelial membrane antigen (EMA), vimentin, S-100, CD34 and Ki-67 was done on routinely processed, paraffin-embedded sections of 20 tumors.
  • The mean Ki-67 labeling index was 4.25% in grade II tumors and 7.8% in grade III tumors.
  • [MeSH-major] Central Nervous System Neoplasms / pathology. Hemangiopericytoma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor / analysis. Child. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Meningeal Neoplasms / pathology. Meningioma / pathology. Middle Aged. Tomography, X-Ray Computed. Young Adult

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  • [Copyright] (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20167500.001).
  • [ISSN] 1532-2653
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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22. Kieran MW, Walker D, Frappaz D, Prados M: Brain tumors: from childhood through adolescence into adulthood. J Clin Oncol; 2010 Nov 10;28(32):4783-9
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  • [Title] Brain tumors: from childhood through adolescence into adulthood.
  • Clinical care is currently divided into adult or pediatric care; adolescent patients require specific expertise that most clinical practices do not have.
  • When illness coincides with the adolescent transition, the health system is severely challenged.
  • Health systems historically have varied widely in the age they choose for allocating an individual to the adult model of health care.
  • Tumors of the CNS complicate the difficult adjustments required in adolescents and young adults by virtue of their morbidity, complex treatment, and prognosis.
  • Some brain tumors are unique to children, some occur predominantly in adults, and others peak in adolescence.
  • Delays in the diagnosis of brain tumors can occur at any age but are particularly common in adolescence because of difficulties of accessing health systems, the difficulties of discriminating pathologic from typical adolescent behavioral characteristics, and changing endocrine function.
  • This article will discuss the changing brain tumor profile of children, adolescents, and adults, with a focus on our limited understanding of the adolescent/young adult transition period.
  • [MeSH-major] Brain Neoplasms / diagnosis
  • [MeSH-minor] Adolescent. Adolescent Medicine. Adult. Brain / growth & development. Child. Continuity of Patient Care. Glioma / diagnosis. Glioma / therapy. Humans. Medulloblastoma / diagnosis. Medulloblastoma / therapy. Neoplasms, Germ Cell and Embryonal / diagnosis. Neoplasms, Germ Cell and Embryonal / therapy

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  • (PMID = 20458039.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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23. Smith JR, Falkenhagen KM, Coupland SE, Chipps TJ, Rosenbaum JT, Braziel RM: Malignant B cells from patients with primary central nervous system lymphoma express stromal cell-derived factor-1. Am J Clin Pathol; 2007 Apr;127(4):633-41
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  • [Title] Malignant B cells from patients with primary central nervous system lymphoma express stromal cell-derived factor-1.
  • Although the pathogenesis of primary central nervous system lymphoma (PCNSL) remains unclear, it is hypothesized that specific chemokine-chemokine receptor interactions may attract malignant B lymphocytes into the CNS.
  • Tumor cells also stained positively for CXCR4.
  • [MeSH-major] B-Lymphocytes / metabolism. Brain Neoplasms / metabolism. Chemokines, CXC / biosynthesis. Lymphoma, B-Cell / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chemokine CCL20. Chemokine CXCL12. Chemokines, CC / biosynthesis. Female. Humans. Immunohistochemistry. Macrophage Inflammatory Proteins / biosynthesis. Male. Middle Aged. Receptors, CXCR4 / biosynthesis

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  • (PMID = 17369141.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY014909
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCL20 protein, human; 0 / CXCL12 protein, human; 0 / Chemokine CCL20; 0 / Chemokine CXCL12; 0 / Chemokines, CC; 0 / Chemokines, CXC; 0 / Macrophage Inflammatory Proteins; 0 / Receptors, CXCR4
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4. Navas M, Pascual JM, Fraga J, Pedrosa M, Shakur S, Carrasco R, Martínez P, Manzanares R, de Sola RG: Intracranial intermediate-grade meningeal melanocytoma with increased cellular proliferative index: an illustrative case associated with a nevus of Ota. J Neurooncol; 2009 Oct;95(1):105-115
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  • Solitary primary melanocytic tumors of the central nervous system (CNS) represent a spectrum of lesions ranging from well-differentiated melanocytoma to melanoma.
  • Only a minority of melanocytic tumors correspond to lesions of intermediate-grade malignancy, whose biological behavior and outcome remain undetermined.
  • The MIB-1/Ki-67 labeling index may have potential prognostic value in helping the clinician to predict an aggressive clinical behavior and/or malignant progression for primary melanocytic neoplasms of the CNS.
  • [MeSH-major] Melanoma / pathology. Meningeal Neoplasms / pathology. Nevus of Ota / pathology
  • [MeSH-minor] Adult. Humans. Male. Nevus, Pigmented / surgery. Radiography. Tomography Scanners, X-Ray Computed

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  • [Cites] Surg Neurol. 2003 Mar;59(3):200-10 [12681556.001]
  • [Cites] J Neurosurg. 2004 Sep;101(3):528-31 [15352613.001]
  • [Cites] J Neuroradiol. 2005 Jan;32(1):59-62 [15798616.001]
  • [Cites] Am J Surg Pathol. 1999 Jul;23(7):745-54 [10403296.001]
  • [Cites] Tumori. 1980 Jun 30;66(3):405-8 [7445117.001]
  • [Cites] Mt Sinai J Med. 1974 Nov-Dec;41(6):774-91 [4610369.001]
  • [Cites] J Neurosurg. 2002 Mar;96(3):619-23 [11883852.001]
  • [Cites] Dermatology. 1992;185(2):146-50 [1421629.001]
  • [Cites] Magn Reson Med. 1995 Jun;33(6):818-26 [7651119.001]
  • [Cites] Neurochirurgie. 2001 May;47(2-3 Pt 1):133-6 [11404684.001]
  • [Cites] Brain Tumor Pathol. 2003;20(1):21-5 [14604228.001]
  • [Cites] Strahlenther Onkol. 2002 Jun;178(6):336-42 [12122790.001]
  • [Cites] Cancer. 1983 Jun 15;51(12):2304-10 [6850510.001]
  • [Cites] Arch Neurobiol (Madr). 1989 Mar-Apr;52(2):93-9 [2667490.001]
  • [Cites] Neurosurgery. 2005 Jun;56(6):E1376; discussion E1376 [15918956.001]
  • [Cites] Neurosurgery. 1999 Nov;45(5):1216-21 [10549940.001]
  • [Cites] J Neurosurg. 1987 Jan;66(1):50-7 [3783260.001]
  • [Cites] J Neurooncol. 2003 Sep;64(3):259-63 [14558602.001]
  • [Cites] Oncol Rep. 2008 Jun;19(6):1367-72 [18497938.001]
  • [Cites] Acta Neurochir (Wien). 2005 Mar;147(3):313-5; discussion 315 [15618991.001]
  • [Cites] Neurosurgery. 2005 Aug;57(2):E369; discussion E369 [16094139.001]
  • [Cites] Clin Radiol. 2006 Mar;61(3):294-8 [16488214.001]
  • [Cites] J Neurosurg Spine. 2007 May;6(5):451-4 [17542513.001]
  • [Cites] Neurosurgery. 1992 Nov;31(5):945-8 [1436422.001]
  • [Cites] Childs Nerv Syst. 2006 Jun;22(6):556-61 [16491422.001]
  • [Cites] Klin Monbl Augenheilkd. 1992 Jun;200(6):665-70 [1507791.001]
  • [Cites] J Neurosurg. 1992 Apr;76(4):705-9 [1545267.001]
  • [Cites] Arch Pathol Lab Med. 1995 Jun;119(6):542-6 [7605172.001]
  • [Cites] Cancer. 1972 Nov;30(5):1286-94 [4343293.001]
  • [Cites] J Neurosurg. 2001 Oct;95(2 Suppl):225-31 [11599841.001]
  • [Cites] NMR Biomed. 1996 Apr;9(2):65-71 [8887370.001]
  • [Cites] Neurology. 1993 Feb;43(2):381-6 [8437707.001]
  • [Cites] Childs Nerv Syst. 2009 Apr;25(4):407-10 [19139906.001]
  • (PMID = 19449182.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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25. Bavaresco L, Bernardi A, Braganhol E, Wink MR, Battastini AM: Dexamethasone inhibits proliferation and stimulates ecto-5'-nucleotidase/CD73 activity in C6 rat glioma cell line. J Neurooncol; 2007 Aug;84(1):1-8
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  • Malignant gliomas are the most common and devastating primary tumors of the adult central nervous system.
  • Dexamethasone, a synthetic glucocorticoid, is commonly co-administered to control edema in the management of brain tumors during chemotherapy and radiotherapy.
  • [MeSH-major] 5'-Nucleotidase / metabolism. Anti-Inflammatory Agents / pharmacology. Brain Neoplasms / enzymology. Dexamethasone / pharmacology. Glioma / enzymology
  • [MeSH-minor] Adenosine Monophosphate / metabolism. Animals. Cell Death / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Protein Kinase C / metabolism. Purines / metabolism. Rats. Signal Transduction / drug effects. Time Factors

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  • [Cites] Anticancer Res. 1996 Mar-Apr;16(2):805-9 [8687132.001]
  • [Cites] Anal Biochem. 1986 Sep;157(2):375-80 [2946250.001]
  • [Cites] Am J Reprod Immunol. 2005 Mar;53(3):144-52 [15727569.001]
  • [Cites] Vascul Pharmacol. 2005 Mar;42(4):153-62 [15820441.001]
  • [Cites] J Cell Physiol. 2001 Jan;186(1):19-23 [11147810.001]
  • [Cites] J Neurooncol. 2001 Jan;51(2):105-10 [11386406.001]
  • [Cites] Science. 1968 Jul 26;161(3839):370-1 [4873531.001]
  • [Cites] Drug Metab Dispos. 2006 Jun;34(6):1063-9 [16531474.001]
  • [Cites] Pharmacol Rev. 1998 Sep;50(3):413-92 [9755289.001]
  • [Cites] Pharmacol Ther. 2003 Oct;100(1):31-48 [14550503.001]
  • [Cites] Neurology. 1997 Jun;48(6):1704-9 [9191791.001]
  • [Cites] Purinergic Signal. 2006 Jun;2(2):409-30 [18404480.001]
  • [Cites] Anticancer Res. 1994 Jul-Aug;14(4A):1585-8 [7979189.001]
  • [Cites] J Steroid Biochem Mol Biol. 2004 Dec;92(5):375-82 [15698542.001]
  • [Cites] Eur J Pharmacol. 1992 Oct 1;227(2):113-22 [1426027.001]
  • [Cites] Br J Pharmacol. 1997 Jan;120(2):273-81 [9117120.001]
  • [Cites] J Pharmacol Toxicol Methods. 2005 Sep-Oct;52(2):234-43 [16125621.001]
  • [Cites] Genes Dev. 1995 Jul 1;9(13):1608-21 [7628695.001]
  • [Cites] Neuroscience. 2000;96(2):417-25 [10683582.001]
  • [Cites] Cell Tissue Res. 2002 Dec;310(3):257-70 [12457224.001]
  • [Cites] Blood. 2003 Dec 15;102(13):4472-8 [12947007.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2001 Jan;280(1):R25-32 [11124130.001]
  • [Cites] Oncogene. 1998 Sep 24;17(12):1567-75 [9794234.001]
  • [Cites] Trends Pharmacol Sci. 2006 Mar;27(3):166-76 [16487603.001]
  • [Cites] Apoptosis. 1999 Jun;4(3):197-211 [14634282.001]
  • [Cites] Melanoma Res. 2006 Jun;16(3):213-22 [16718268.001]
  • [Cites] BMC Cancer. 2006 Sep 23;6:226 [16995949.001]
  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] Trends Pharmacol Sci. 2006 Apr;27(4):211-7 [16530853.001]
  • [Cites] Nucleic Acids Res. 1992 Feb 25;20(4):825-9 [1531873.001]
  • [Cites] Cancer Lett. 2003 Aug 20;198(2):211-8 [12957360.001]
  • [Cites] Biochem J. 1992 Jul 15;285 ( Pt 2):345-65 [1637327.001]
  • (PMID = 17453149.001).
  • [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 / Anti-Inflammatory Agents; 0 / Purines; 415SHH325A / Adenosine Monophosphate; 7S5I7G3JQL / Dexamethasone; EC 2.7.11.13 / Protein Kinase C; EC 3.1.3.5 / 5'-Nucleotidase
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26. Manitt C, Wang D, Kennedy TE, Howland DR: Positioned to inhibit: netrin-1 and netrin receptor expression after spinal cord injury. J Neurosci Res; 2006 Dec;84(8):1808-20
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  • Netrin-1 regulates axon extension during embryonic development and is expressed by neurons and myelinating oligodendrocytes in the adult CNS.
  • To investigate the potential role of netrin-1 after spinal cord injury, we examined the expression of netrin-1 and netrin receptors after sagittal myelotomy in adult rats.
  • [MeSH-major] Gene Expression Regulation / physiology. Nerve Growth Factors / metabolism. Receptors, Cell Surface / metabolism. Spinal Cord Injuries / metabolism. Spinal Cord Injuries / physiopathology. Tumor Suppressor Proteins / metabolism

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  • (PMID = 16998900.001).
  • [ISSN] 0360-4012
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Nerve Growth Factors; 0 / Receptors, Cell Surface; 0 / Tumor Suppressor Proteins; 0 / netrin receptors; 158651-98-0 / netrin-1
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27. 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).
  • We conclude that alterations of Protein 4.1 family members are common in ependymal tumors and that specific alterations are associated with distinct clinicopathologic subsets.
  • [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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28. Kabashi S, Muçaj S, Ahmetgjekaj I, Gashi S, Fazliu I, Dreshaj S, Shala N: Radiological imaging detection of tumors localized in fossa cranii posterior. Med Arh; 2008;62(5-6):271-4
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  • [Title] Radiological imaging detection of tumors localized in fossa cranii posterior.
  • Intracranial tumors are characterized by a variety imaging aspects and their detection is always a challenge.
  • Clinical application of Magnetic Resonance Imaging (MRI) and Computerized Tomography has provided an earlier detection and treatment of many CNS pathologies.
  • The aim of this study is to estimate the role of CT and MRI in the determination of posterior fossa tumors.
  • RESULTS: During period 2000-2005 in UCCK-Prishtina, 368 patients were diagnosed with intracranial tumors.
  • Fifty-nine of them were found to have tumor localized in fossa crani posterior (FCP) without any significant difference between genders (50.8% female vs. 49.2% male, chi2 test=0.02 p=0.896).
  • The average age of patients with FCP tumors was 33.1 (SD +/- 22.5, rank 1-70).
  • Tumor types that more often were found in young's individuals were: Astrocytomas with a peak incidence in teenagers (average age was 12-year-old SD +/- 7.5, rank 3-23), next was Medulloblastomas (average age was 11-years-old, SD +/- 2.9, rank 6-16 years) and ependymomas (average age was 6.8-years-old, SD +/- 4.6, rank 1-12).
  • Patients with osseous tumors are characterized by older age than median (61.0, SD +/- 4.2, rank 58-64), then metastases (53.0, SD +/- 5.3, rank 45-60) and meningiomas (50.8, SD +/- 7.7, rank 38-63).
  • CONCLUSION: Comparing with other countries, for some types of FCP tumors, lower morbidity is shown in Kosova, with mean incidence 0.41/100,000.
  • The most frequent tumors in children were medulloblastomas, brainstem gliomas, astrocytomas and ependymomas whereas meningiomas and metastasis were most often found in adults.
  • For FCP tumors detection, MRI had 100% sensitivity, specificity and predictive positive value, whereas brain CT was characterized by 95% sensitivity, 90.4 % specificity and 91% predictive positive value.
  • [MeSH-major] Infratentorial Neoplasms / diagnosis. Magnetic Resonance Imaging. Tomography, X-Ray Computed
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Infant. Male. Middle Aged. Young Adult

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  • (PMID = 19469268.001).
  • [Journal-full-title] Medicinski arhiv
  • [ISO-abbreviation] Med Arh
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Bosnia and Herzegovina
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29. Leães CG, Meurer RT, Coutinho LB, Ferreira NP, Pereira-Lima JF, da Costa Oliveira M: Immunohistochemical expression of aromatase and estrogen, androgen and progesterone receptors in normal and neoplastic human meningeal cells. Neuropathology; 2010 Feb 1;30(1):44-9
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  • Evidence suggests that sex hormones may play a role in the tumorigenesis of meningiomas, and studies have demonstrated the expression of hormone receptors in these tumors.
  • Aromatase expression has been detected in several normal tissues, including neurons in the CNS, and tumor tissues.
  • Behavior pattern differences observed between aromatase expression, present in normal tissues and absent in meningiomas, and estrogen and androgen hormone receptors, absent in normal tissues and present in meningiomas, suggest that there is heterogeneity in modulation by sex steroids in the development of these tumors.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Arachnoid Cysts / enzymology. Arachnoid Cysts / metabolism. Brazil. Cross-Sectional Studies. Female. Humans. Immunohistochemistry. Male. Middle Aged. Odds Ratio. Sex Characteristics. Young Adult

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  • (PMID = 19703265.001).
  • [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 / Receptors, Androgen; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; EC 1.14.14.1 / Aromatase
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30. Lepore AC, Neuhuber B, Connors TM, Han SS, Liu Y, Daniels MP, Rao MS, Fischer I: Long-term fate of neural precursor cells following transplantation into developing and adult CNS. Neuroscience; 2006 Sep 29;142(1):287-304
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  • [Title] Long-term fate of neural precursor cells following transplantation into developing and adult CNS.
  • Successful strategies for transplantation of neural precursor cells for replacement of lost or dysfunctional CNS cells require long-term survival of grafted cells and integration with the host system, potentially for the life of the recipient.
  • Few studies have examined the long-term properties of transplanted neural precursor cells in the CNS, particularly in non-neurogenic regions of the adult.
  • The aim of the present study was to extensively characterize the fate of defined populations of neural precursor cells following transplantation into the developing and adult CNS (brain and spinal cord) for up to 15 months, including integration of graft-derived neurons with the host.
  • We found that in both developing and adult CNS grafted cells showed long-term survival, morphological maturation, extensive distribution and differentiation into all mature CNS cell types (neurons, astrocytes and oligodendrocytes).
  • Graft-derived neurons also formed synapses, as identified by electron microscopy, suggesting that transplanted neural precursor cells integrated with adult CNS.
  • We did not detect tumor formation, cells did not localize to unwanted locations and no pronounced immune response was present at the graft sites.
  • The long-term stability of neuronal-restricted precursors and glial-restricted precursors and the lack of adverse effects suggest that transplantation of lineage-restricted neural precursor cells can serve as an effective and safe replacement therapy for CNS injury and degeneration.
  • [MeSH-major] Cell Differentiation / physiology. Central Nervous System / physiology. Neurons / physiology. Stem Cell Transplantation / methods. Stem Cells / physiology

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  • [RepublishedFrom] Neuroscience. 2006 May 12;139(2):513-30 [16458439.001]
  • (PMID = 17120358.001).
  • [ISSN] 0306-4522
  • [Journal-full-title] Neuroscience
  • [ISO-abbreviation] Neuroscience
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS 37515; United States / NINDS NIH HHS / NS / NS24707
  • [Publication-type] Comparative Study; Corrected and Republished Article; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gangliosides; 0 / Immunosuppressive Agents; 0 / Nerve Tissue Proteins; 0 / Neural Cell Adhesion Molecules; 0 / ganglioside A2B5
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31. Harter PN, Bunz B, Dietz K, Hoffmann K, Meyermann R, Mittelbronn M: Spatio-temporal deleted in colorectal cancer (DCC) and netrin-1 expression in human foetal brain development. Neuropathol Appl Neurobiol; 2010 Dec;36(7):623-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AIMS: Deleted in colorectal cancer (DCC) and its ligand netrin-1 are known as axonal guidance factors, being involved in angiogenesis, migration and survival of precursor cells in the embryonic mammalian central nervous system (CNS).
  • So far, little is known about the distribution of those molecules in human CNS development.
  • Together with the data from animal experiments, our findings might indicate also an important role for DCC and netrin-1 in human foetal CNS development.
  • [MeSH-major] Brain / embryology. Brain Chemistry / physiology. Nerve Growth Factors / biosynthesis. Receptors, Cell Surface / biosynthesis. Tumor Suppressor Proteins / biosynthesis
  • [MeSH-minor] Adult. Brain Stem / metabolism. Cerebellum / metabolism. Cerebral Cortex / metabolism. Choroid Plexus / metabolism. Ependyma / cytology. Ependyma / metabolism. Female. Fetal Development. Fetus / metabolism. Fluorescent Antibody Technique. Humans. Immunohistochemistry. Pregnancy

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  • [Copyright] © 2010 The Authors. Neuropathology and Applied Neurobiology © 2010 British Neuropathological Society.
  • (PMID = 20609112.001).
  • [ISSN] 1365-2990
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DCC protein, human; 0 / Nerve Growth Factors; 0 / Receptors, Cell Surface; 0 / Tumor Suppressor Proteins; 158651-98-0 / netrin-1
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32. Kushner YB, Brimo F, Schwartzman K, Auger M: A rare case of pulmonary cryptococcal inflammatory myofibroblastic tumor diagnosed by fine needle aspiration cytology. Diagn Cytopathol; 2010 Jun;38(6):447-51
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  • [Title] A rare case of pulmonary cryptococcal inflammatory myofibroblastic tumor diagnosed by fine needle aspiration cytology.
  • In a recent outbreak in British Columbia (BC), Canada, Cryptococcus gattii, a rare species of Cryptococcus, was noted to affect primarily immunocompetent hosts and cause limited pulmonary or CNS disease.
  • We herein report a rare case of a pulmonary inflammatory myofibroblastic tumor caused by a Cryptococcus infection, presumed to be of the gattii species, in a 20-year-old immunocompetent college student from Vancouver, BC who presented with a large lung mass.
  • Cryptococcal inflammatory myofibroblastic tumors have been reported, but neither in the lung nor in the setting of an immunocompetent host.
  • [MeSH-minor] Antifungal Agents / therapeutic use. Biopsy, Fine-Needle. Cryptococcus gattii. Female. Fluconazole / therapeutic use. Humans. Young Adult

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19937947.001).
  • [ISSN] 1097-0339
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 8VZV102JFY / Fluconazole
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33. Ahmed S: The culture of neural stem cells. J Cell Biochem; 2009 Jan 1;106(1):1-6
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  • Neural stem cells (NSCs) are present during embryonic development and in certain regions of the adult central nervous system (CNS).
  • Mobilizing adult NSCs to promote repair of injured or diseased CNS is a promising approach.
  • Since NSCs may give rise to brain tumor, they represent in vitro models for anti-cancer drug screening.
  • Important future directions that are highlighted in this review are; identification of markers for NSCs, the use of NSCs in high-throughput screens and the modelling of the central nervous development.
  • There is no doubt that the study of NSCs is crucial if we are to tackle the diseases of the CNS such as Parkinson's and Alzheimer's.
  • [MeSH-minor] Animals. Cells, Cultured. Central Nervous System / cytology. Humans. Models, Biological

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  • [Copyright] 2008 Wiley-Liss, Inc.
  • (PMID = 19021147.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 80
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34. Gerber DE, Grossman SA, Batchelor T, Ye X: Calculated versus measured creatinine clearance for dosing methotrexate in the treatment of primary central nervous system lymphoma. Cancer Chemother Pharmacol; 2007 May;59(6):817-23
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  • [Title] Calculated versus measured creatinine clearance for dosing methotrexate in the treatment of primary central nervous system lymphoma.
  • BACKGROUND: High-dose methotrexate (HDMTX) (>or=3 g/m2), the cornerstone of therapy for primary CNS lymphoma (PCNSL), is commonly dosed using a measured 24 h creatinine clearance (CrCl) every 2-4 weeks.
  • METHODS: A retrospective analysis was performed on data from all 287 treatment cycles from the 25 patients with PCNSL who participated in a multi-center phase II clinical trial of HDMTX conducted by the New Approaches to Brain Tumor Therapy (NABTT) CNS Consortium.
  • [MeSH-major] Central Nervous System Neoplasms / drug therapy. Creatinine / pharmacokinetics. Kidney Function Tests / methods. Lymphoma / drug therapy. Lymphoma / urine. Methotrexate / administration & dosage
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Metabolic Clearance Rate. Middle Aged. Retrospective Studies


35. Kimura N, Yamamoto Y, Kameyama R, Hatakeyama T, Kawai N, Nishiyama Y: Diagnostic value of kinetic analysis using dynamic 18F-FDG-PET in patients with malignant primary brain tumor. Nucl Med Commun; 2009 Aug;30(8):602-9
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  • [Title] Diagnostic value of kinetic analysis using dynamic 18F-FDG-PET in patients with malignant primary brain tumor.
  • OBJECTIVE: The purpose of this study was to evaluate the efficacy of quantitative imaging of glucose metabolism with positron emission tomography (PET) using kinetic analysis for differentiating between high-grade glioma and central nervous system (CNS) lymphoma.
  • METHODS: Dynamic fluorine-18-fluorodeoxyglucose (18F-FDG)-PET scans obtained in 20 patients with high-grade glioma (World Health Organization grade III, five lesions; grade IV, 15 lesions) and in 12 patients with CNS lymphoma (16 lesions) were retrospectively reviewed.
  • Fourteen CNS lymphoma lesions showed an increase of K1, 16 of k3, two of k4, and 14 of CMR(Glc).
  • Both k3 and CMR(Glc) values (mean+/-SD) of CNS lymphoma (0.096+/-0.046 and 77.4+/-37.7, respectively) were significantly higher than those of the normal gray matter (0.059+/-0.015 and 41.3+/-9.3, respectively; P<0.007 and P<0.002, respectively).
  • The k3 value of CNS lymphoma was significantly higher than that of grade III (0.058+/-0.022) and grade IV (0.065+/-0.024) gliomas (P<0.03 and P<0.04, respectively).
  • The CMR(Glc) value of CNS lymphoma was significantly higher than that of grade III (33.8+/-7.8) and grade IV (41.5+/-23.1) gliomas (P<0.001 and P<0.004, respectively).
  • The value of k2 of CNS lymphoma was significantly lower than that of grade IV glioma (P<0.05).
  • CONCLUSION: The direct measurement of the regional rate constants by kinetic analysis might be useful for the delineation of CNS lymphoma and for differential diagnosis of high-grade glioma and CNS lymphoma.
  • [MeSH-major] Brain Neoplasms / metabolism. Brain Neoplasms / radionuclide imaging. Fluorodeoxyglucose F18. Glucose / metabolism
  • [MeSH-minor] Adult. Aged. Diagnosis, Differential. Female. Glioma / metabolism. Glioma / radionuclide imaging. Humans. Kinetics. Lymphoma / metabolism. Lymphoma / radionuclide imaging. Magnetic Resonance Imaging. Male. Middle Aged. Positron-Emission Tomography. Retrospective Studies

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  • (PMID = 19521265.001).
  • [ISSN] 1473-5628
  • [Journal-full-title] Nuclear medicine communications
  • [ISO-abbreviation] Nucl Med Commun
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18; IY9XDZ35W2 / Glucose
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36. Xiong NX, Zhao HY, Zhang FC, He ZQ: Negative correlation of Nogo-A with the malignancy of oligodendroglial tumor. Neurosci Bull; 2007 Jan;23(1):41-5
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  • [Title] Negative correlation of Nogo-A with the malignancy of oligodendroglial tumor.
  • OBJECTIVE: Nogo-A is an axon regeneration inhibitor, and its function in central nervous system (CNS) is still unknown.
  • The present study is to explore the relationship between the expression of Nogo-A and the malignancy of oligodendroglial tumors in patients.
  • METHODS: Tumor tissue samples with different malignancy grade were obtained from the hospitals.
  • The samples used for detection had been diagnosed as oligodendroglial tumors (oligodendroglioma or anaplastic oligodendroglioma).
  • The correlation test between the Nogo-A expression and the morphological changes (the percentages of atypical cells and mitotic cells in the tumors) related to the malignancy of tumor tissues was performed.
  • RESULTS: There was significant negative correlation between the Nogo-A expression and the morphological change of tumor tissues according to immunohistochemistry.
  • CONCLUSION: Nogo-A expression was negatively correlated with the malignancy grade of oligodendroglial tumors.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Brain Neoplasms / diagnosis. Brain Neoplasms / metabolism. Myelin Proteins / metabolism. Oligodendroglioma / diagnosis. Oligodendroglioma / metabolism
  • [MeSH-minor] Adult. Down-Regulation / physiology. Female. Humans. Immunohistochemistry. Male. Middle Aged. Mitotic Index. Neoplasm Invasiveness / diagnosis. Nogo Proteins. Predictive Value of Tests

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  • [Cites] J Neurosci. 2002 May 1;22(9):3553-67 [11978832.001]
  • [Cites] J Neurosci. 2003 Jul 2;23 (13):5393-406 [12843238.001]
  • [Cites] Oncogene. 2001 Jul 5;20(30):3929-36 [11494121.001]
  • [Cites] J Mol Neurosci. 2005;25(1):1-6 [15781961.001]
  • [Cites] J Cell Physiol. 2003 Aug;196 (2):312-8 [12811824.001]
  • [Cites] Nature. 2000 Jan 27;403(6768):434-9 [10667796.001]
  • [Cites] J Biol Chem. 2003 May 23;278(21):19280-5 [12639960.001]
  • [Cites] Nature. 2000 Jan 27;403(6768):439-44 [10667797.001]
  • [Cites] Cancer Res. 1998 Jan 1;58(1):149-58 [9426071.001]
  • [Cites] J Neurochem. 2004 Sep;90(5):1156-62 [15312170.001]
  • [Cites] Oncogene. 2003 Mar 6;22(9):1390-9 [12618765.001]
  • [Cites] Oncogene. 2000 Nov 23;19(50):5736-46 [11126360.001]
  • [Cites] Biochem J. 2005 Oct 15;391(Pt 2):433-40 [16095439.001]
  • [Cites] Oncogene. 2004 Apr 15;23(17):2977-87 [15021917.001]
  • [Cites] Apoptosis. 2003 Jan;8(1):5-9 [12510146.001]
  • (PMID = 17592524.001).
  • [ISSN] 1673-7067
  • [Journal-full-title] Neuroscience bulletin
  • [ISO-abbreviation] Neurosci Bull
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Myelin Proteins; 0 / Nogo Proteins; 0 / RTN4 protein, human
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37. Kim DS, Na DG, Kim KH, Kim JH, Kim E, Yun BL, Chang KH: Distinguishing tumefactive demyelinating lesions from glioma or central nervous system lymphoma: added value of unenhanced CT compared with conventional contrast-enhanced MR imaging. Radiology; 2009 May;251(2):467-75
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  • [Title] Distinguishing tumefactive demyelinating lesions from glioma or central nervous system lymphoma: added value of unenhanced CT compared with conventional contrast-enhanced MR imaging.
  • PURPOSE: To determine retrospectively whether unenhanced computed tomographic (CT) images of the brain have added value in distinguishing tumefactive demyelinating lesions (TDLs) from primary glioma or central nervous system (CNS) lymphoma, compared with conventional contrast material-enhanced magnetic resonance (MR) images only.
  • Unenhanced CT and MR images in 15 patients with TDLs (seven women, eight men; mean age, 42 years; range, 27-57 years) and 48 patients with primary brain tumor (27 women, 21 men; mean age, 48 years; range, 19-70 years; 10 lymphomas, 38 gliomas) were retrospectively reviewed.
  • The diagnostic accuracy of MR imaging for differentiating TDLs from tumors was compared with that of MR imaging plus CT.
  • RESULTS: The following MR imaging features were found more frequently in patients with TDL than in those with brain tumor: incomplete rim enhancement, mixed T2-weighted iso- and hyperintensity of enhanced regions, absence of a mass effect, and absence of cortical involvement (all P values < .05).
  • CT hypoattenuation of MR enhanced regions was observed in 14 (93%) of 15 patients with TDL but in only two (4%) of 48 patients with tumor.
  • The CT attenuation of MR enhanced regions was significantly lower for patients with TDL than for those with tumor (P < .001).
  • CONCLUSION: Unenhanced CT plus MR imaging was more accurate for distinguishing TDLs from glioma or CNS lymphoma than contrast-enhanced MR imaging alone.
  • [MeSH-major] Brain Neoplasms / diagnosis. Demyelinating Diseases / diagnosis. Glioma / diagnosis. Image Enhancement / methods. Lymphoma / diagnosis. Magnetic Resonance Imaging / methods. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Adult. Contrast Media. Female. Humans. Male. Middle Aged. Reproducibility of Results. Sensitivity and Specificity. Young Adult


38. Kunwar S, Prados MD, Chang SM, Berger MS, Lang FF, Piepmeier JM, Sampson JH, Ram Z, Gutin PH, Gibbons RD, Aldape KD, Croteau DJ, Sherman JW, Puri RK, Cintredekin Besudotox Intraparenchymal Study Group: Direct intracerebral delivery of cintredekin besudotox (IL13-PE38QQR) in recurrent malignant glioma: a report by the Cintredekin Besudotox Intraparenchymal Study Group. J Clin Oncol; 2007 Mar 1;25(7):837-44
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  • PURPOSE: Glioblastoma multiforme (GBM) is a devastating brain tumor with a median survival of 6 months after recurrence.
  • PATIENTS AND METHODS: Three phase I clinical studies evaluated intracerebral CED of CB along with tumor resection.
  • All patients underwent tumor resection followed by a single intraparenchymal infusion (in addition to the intraparenchymal one following resection), with a portion of patients who had a preresection intratumoral infusion.
  • The maximum tolerated intraparenchymal concentration was 0.5 microg/mL and tumor necrosis was observed at this concentration.
  • CB- and procedure-related adverse events were primarily limited to the CNS.
  • [MeSH-major] Drug Delivery Systems / methods. Exotoxins / administration & dosage. Glioma / drug therapy. Immunotoxins / administration & dosage. Interleukin-13 / administration & dosage. Supratentorial Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Catheterization. Convection. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Tissue Distribution

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  • (PMID = 17327604.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Exotoxins; 0 / IL13-PE38QQR; 0 / Immunotoxins; 0 / Interleukin-13
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39. Gläsker S, Klingler JH, Müller K, Würtenberger C, Hader C, Zentner J, Neumann HP, Velthoven VV: Essentials and pitfalls in the treatment of CNS hemangioblastomas and von Hippel-Lindau disease. Cent Eur Neurosurg; 2010 May;71(2):80-7
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  • [Title] Essentials and pitfalls in the treatment of CNS hemangioblastomas and von Hippel-Lindau disease.
  • Hemangioblastomas are rare CNS tumors, which are mostly located in the posterior fossa or spinal cord and occasionally in spinal nerves.
  • They can occur sporadically or as a component tumor of von Hippel-Lindau (VHL) disease, an autosomal dominant tumor syndrome.
  • [MeSH-major] Cerebellar Neoplasms / pathology. Cerebellar Neoplasms / surgery. Hemangioblastoma / pathology. Hemangioblastoma / surgery. Neurosurgical Procedures / methods. Spinal Cord Neoplasms / pathology. Spinal Cord Neoplasms / surgery. von Hippel-Lindau Disease / pathology. von Hippel-Lindau Disease / surgery
  • [MeSH-minor] Adult. Humans. Magnetic Resonance Imaging. Male

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  • [Copyright] Copyright Georg Thieme Verlag KG Stuttgart . New York.
  • (PMID = 20229452.001).
  • [ISSN] 1868-4912
  • [Journal-full-title] Central European neurosurgery
  • [ISO-abbreviation] Cent Eur Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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40. Neder L, Scheithauer BW, Turel KE, Arnesen MA, Ketterling RP, Jin L, Moynihan TJ, Giannini C, Meyer FB: Desmoplastic small round cell tumor of the central nervous system: report of two cases and review of the literature. Virchows Arch; 2009 Apr;454(4):431-9
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  • [Title] Desmoplastic small round cell tumor of the central nervous system: report of two cases and review of the literature.
  • Desmoplastic small round cell tumor (DSRCT) is a malignant tumor often involving the abdominal and/or pelvic peritoneum.
  • Only one fully documented example has arisen in the central nervous system (CNS).
  • In conclusion, CNS DSRCT follows a similar aggressive course as do peritoneal examples.
  • Although rare, DSRCT warrants consideration in the differential diagnosis of "malignant small blue cell tumors" of the CNS.
  • [MeSH-major] Carcinoma, Small Cell / pathology. Cerebellar Neoplasms / pathology. Cerebellopontine Angle / pathology
  • [MeSH-minor] Adult. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Magnetic Resonance Imaging. Male. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • [Cites] Am J Surg Pathol. 1992 Oct;16(10):998-1006 [1384373.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Mar;61(3):215-25; discussion 226-9 [11895036.001]
  • [Cites] Am J Surg Pathol. 1998 Nov;22(11):1303-13 [9808123.001]
  • [Cites] Am J Surg Pathol. 1990 Jul;14(7):633-42 [2356923.001]
  • [Cites] J Clin Oncol. 1998 Sep;16(9):3028-36 [9738572.001]
  • [Cites] Diagn Mol Pathol. 1998 Feb;7(1):24-8 [9646031.001]
  • [Cites] Am J Surg Pathol. 1996 Jan;20(1):112-7 [8540602.001]
  • [Cites] Hum Pathol. 1997 Apr;28(4):502-9 [9104953.001]
  • [Cites] Cancer Cell. 2002 Dec;2(6):497-505 [12498718.001]
  • [Cites] Arch Pathol Lab Med. 2006 May;130(5):728-32 [16683894.001]
  • [Cites] Hum Pathol. 1992 Apr;23(4):454-64 [1563748.001]
  • [Cites] Arch Pathol Lab Med. 1989 Sep;113(9):1019-29 [2505732.001]
  • [Cites] Am J Surg Pathol. 2002 Jul;26(7):823-35 [12131150.001]
  • [Cites] Am J Surg Pathol. 1989 May;13(5):413-21 [2469334.001]
  • [Cites] Nature. 1990 Jul 12;346(6280):194-7 [2164159.001]
  • [Cites] Am J Surg Pathol. 1995 Jun;19(6):659-65 [7755152.001]
  • [Cites] Diagn Mol Pathol. 2005 Mar;14(1):23-8 [15714060.001]
  • [Cites] Am J Surg Pathol. 1999 Nov;23(11):1408-13 [10555010.001]
  • [Cites] Cancer Genet Cytogenet. 1993 Aug;69(1):17-21 [8374894.001]
  • [Cites] Exp Cell Res. 2001 Mar 10;264(1):74-99 [11237525.001]
  • [Cites] Acta Cytol. 1995 Mar-Apr;39(2):377-8 [7887076.001]
  • [Cites] J Surg Oncol. 1999 Aug;71(4):269-72 [10440769.001]
  • [Cites] J Neurosurg. 1996 Jul;85(1):56-65 [8683283.001]
  • [Cites] Acta Neuropathol. 2007 Aug;114(2):97-109 [17618441.001]
  • [Cites] Acta Cytol. 1993 Jan-Feb;37(1):77-82 [7679537.001]
  • [Cites] Semin Diagn Pathol. 1996 Aug;13(3):204-12 [8875710.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Feb 14;92(4):1028-32 [7862627.001]
  • [Cites] Am J Surg Pathol. 2004 May;28(5):644-50 [15105654.001]
  • [Cites] Virchows Arch. 1998 Feb;432(2):135-41 [9504858.001]
  • [Cites] Mod Pathol. 1999 Jul;12(7):729-34 [10430278.001]
  • [Cites] Ultrastruct Pathol. 2000 Sep-Oct;24(5):333-7 [11071572.001]
  • [Cites] Hum Pathol. 1999 Apr;30(4):430-5 [10208465.001]
  • [Cites] Pediatr Pathol. 1989;9(2):177-83 [2473463.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1991;418(3):207-14 [1900966.001]
  • [Cites] Cancer Res. 1994 Jun 1;54(11):2837-40 [8187063.001]
  • [Cites] Am J Surg Pathol. 1991 Jun;15(6):499-513 [1709557.001]
  • [Cites] Gynecol Oncol. 2000 Oct;79(1):124-8 [11006044.001]
  • [Cites] Arch Pathol Lab Med. 2002 Oct;126(10):1226-8 [12296765.001]
  • [Cites] Semin Cancer Biol. 2005 Jun;15(3):197-205 [15826834.001]
  • [Cites] Semin Diagn Pathol. 2003 Feb;20(1):25-45 [12693673.001]
  • [Cites] Pediatr Blood Cancer. 2008 Oct;51(4):545-8 [18561179.001]
  • (PMID = 19263077.001).
  • [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
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / EWS1-WT1 fusion protein, human; 0 / Oncogene Proteins, Fusion
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41. Küsters-Vandevelde HV, Klaasen A, Küsters B, Groenen PJ, van Engen-van Grunsven IA, van Dijk MR, Reifenberger G, Wesseling P, Blokx WA: Activating mutations of the GNAQ gene: a frequent event in primary melanocytic neoplasms of the central nervous system. Acta Neuropathol; 2010 Mar;119(3):317-23
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  • [Title] Activating mutations of the GNAQ gene: a frequent event in primary melanocytic neoplasms of the central nervous system.
  • Primary melanocytic neoplasms of the central nervous system (CNS) are uncommon neoplasms derived from melanocytes that normally can be found in the leptomeninges.
  • Characteristic genetic alterations in this group of neoplasms have not yet been identified.
  • Using direct sequencing, we investigated 19 primary melanocytic lesions of the CNS (12 melanocytomas, 3 intermediate-grade melanocytomas, and 4 melanomas) for hotspot oncogenic mutations commonly found in melanocytic tumors of the skin (BRAF, NRAS, and HRAS genes) and uvea (GNAQ gene).
  • Somatic mutations in the GNAQ gene at codon 209, resulting in constitutive activation of GNAQ, were detected in 7/19 (37%) tumors, including 6/12 melanocytomas, 0/3 intermediate-grade melanocytomas, and 1/4 melanomas.
  • These GNAQ-mutated tumors were predominantly located around the spinal cord (6/7).
  • One melanoma carried a BRAF point mutation that is frequently found in cutaneous melanomas (c.1799 T>A, p.V600E), raising the question whether this is a metastatic rather than a primary tumor.
  • We conclude that somatic mutations in the GNAQ gene at codon 209 are a frequent event in primary melanocytic neoplasms of the CNS.
  • This finding provides new insight in the pathogenesis of these lesions and suggests that GNAQ-dependent mitogen-activated kinase signaling is a promising therapeutic target in these tumors.
  • The prognostic and predictive value of GNAQ mutations in primary melanocytic lesions of the CNS needs to be determined in future studies.
  • [MeSH-major] Central Nervous System Neoplasms / genetics. Central Nervous System Neoplasms / pathology. GTP-Binding Protein alpha Subunits / genetics. Melanocytes / pathology. Melanoma / pathology. Mutation / genetics
  • [MeSH-minor] Adult. Aged. Codon / genetics. DNA, Neoplasm / genetics. DNA, Neoplasm / isolation & purification. Female. Genes, ras / genetics. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Proto-Oncogene Proteins B-raf / genetics. Retrospective Studies. Tissue Fixation

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  • [Cites] J Clin Oncol. 2009 May 1;27(13):2290-1 [19349541.001]
  • [Cites] Br J Cancer. 2009 Sep 1;101(5):813-5 [19654573.001]
  • [Cites] PLoS One. 2009;4(8):e6833 [19718445.001]
  • [Cites] Nature. 1999 Dec 2;402(6761):496-501 [10591209.001]
  • [Cites] Annu Rev Biochem. 2000;69:795-827 [10966476.001]
  • [Cites] Clin Cancer Res. 2002 Nov;8(11):3468-74 [12429636.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5761-6 [14522897.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2257-317 [14671650.001]
  • [Cites] J Invest Dermatol. 2003 Nov;121(5):1160-2 [14708620.001]
  • [Cites] Int J Cancer. 2004 Sep 20;111(5):705-10 [15252839.001]
  • [Cites] Nat Genet. 2004 Sep;36(9):961-8 [15322542.001]
  • [Cites] Nat Genet. 2004 Sep;36(9):935-6 [15340429.001]
  • [Cites] Neurosurgery. 1981 Jan;8(1):26-30 [7207769.001]
  • [Cites] J Invest Dermatol. 1984 Mar;82(3):235-8 [6699426.001]
  • [Cites] J Neurosurg. 1987 Jun;66(6):948 [3572529.001]
  • [Cites] Annu Rev Biochem. 1987;56:779-827 [3304147.001]
  • [Cites] Cancer. 1988 May 1;61(9):1926-34 [3355984.001]
  • [Cites] J Am Acad Dermatol. 1991 May;24(5 Pt 1):747-55 [1869648.001]
  • [Cites] Neurology. 1993 Feb;43(2):381-6 [8437707.001]
  • [Cites] Science. 1993 Dec 17;262(5141):1895-901 [8266082.001]
  • [Cites] Neurosurgery. 1994 Mar;34(3):533-7; discussion 637 [8190231.001]
  • [Cites] Pathologica. 1997 Apr;89(2):168-74 [9411364.001]
  • [Cites] Am J Surg Pathol. 1999 Jul;23(7):745-54 [10403296.001]
  • [Cites] Acta Neurochir (Wien). 2005 Mar;147(3):313-5; discussion 315 [15618991.001]
  • [Cites] Melanoma Res. 2006 Apr;16(2):97-103 [16567964.001]
  • [Cites] Melanoma Res. 2006 Aug;16(4):267-73 [16845322.001]
  • [Cites] Cell Oncol. 2007;29(1):19-24 [17429138.001]
  • [Cites] Hum Mutat. 2007 Jun;28(6):578-88 [17295241.001]
  • [Cites] Curr Opin Oncol. 2008 Mar;20(2):183-9 [18300768.001]
  • [Cites] J Neurosurg Spine. 2008 Jul;9(1):48-54 [18590410.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2008 Dec;49(12):5230-4 [18719078.001]
  • [Cites] Nature. 2009 Jan 29;457(7229):599-602 [19078957.001]
  • (PMID = 19936769.001).
  • [ISSN] 1432-0533
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Codon; 0 / DNA, Neoplasm; 0 / GNAQ protein, human; 0 / GTP-Binding Protein alpha Subunits; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
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42. Souglakos J, Vamvakas L, Apostolaki S, Perraki M, Saridaki Z, Kazakou I, Pallis A, Kouroussis C, Androulakis N, Kalbakis K, Millaki G, Mavroudis D, Georgoulias V: Central nervous system relapse in patients with breast cancer is associated with advanced stages, with the presence of circulating occult tumor cells and with the HER2/neu status. Breast Cancer Res; 2006;8(4):R36
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  • [Title] Central nervous system relapse in patients with breast cancer is associated with advanced stages, with the presence of circulating occult tumor cells and with the HER2/neu status.
  • INTRODUCTION: To evaluate the incidence of central nervous system (CNS) involvement in patients with breast cancer treated with a taxane-based chemotherapy regimen and to determine predictive factors for CNS relapse.
  • METHODS: The medical files of patients with early breast cancer (n = 253) or advanced stage breast cancer (n = 239) as well of those with other solid tumors (n = 336) treated with or without a taxane-based chemotherapy regimen during a 42-month period were reviewed.
  • HER2/neu overexpression was identified by immunohistochemistry, whereas cytokeratin 19 (CK-19) mRNA-positive circulating tumor cells (CTCs) in the peripheral blood were identified by real-time PCR.
  • RESULTS: The incidence of CNS relapse was similar in patients suffering from breast cancer or other solid tumors (10.4% and 11.4%, respectively; P = 0.517).
  • The incidence of CNS relapse was significantly higher in breast cancer patients with advanced disease (P = 0.041), visceral disease and bone disease (P = 0.036), in those who were treated with a taxane-containing regimen (P = 0.024), in those with HER2/neu-overexpressing tumors (P = 0.022) and, finally, in those with detectable CK-19 mRNA-positive CTCs (P = 0.008).
  • Multivariate analysis revealed that the stage of disease (odds ratio, 0.23; 95% confidence interval, 0.007-0.23; P = 0.0001), the HER2/neu status (odds ratio, 29.4; 95% confidence interval, 7.51-101.21; P = 0.0001) and the presence of CK-19 mRNA-positive CTCs (odds ratio, 8.31; 95% confidence interval, 3.97-12.84; P = 0.001) were independent predictive factors for CNS relapse.
  • CONCLUSION: CNS relapses are common among breast cancer patients treated with a taxane-based chemotherapy regimen, patients with HER2/neu-positive tumor and patients with CK-19 mRNA-positive CTCs.
  • [MeSH-major] Breast Neoplasms / pathology. Breast Neoplasms / physiopathology. Central Nervous System Neoplasms / physiopathology. Neoplastic Cells, Circulating
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / therapeutic use. Female. Humans. Keratin-19. Middle Aged. Neoplasm Staging. Predictive Value of Tests. RNA, Messenger. Receptor, ErbB-2 / biosynthesis. Taxoids / therapeutic use


43. Brandt-Bohne U, Keene DR, White FA, Koch M: MEGF9: a novel transmembrane protein with a strong and developmentally regulated expression in the nervous system. Biochem J; 2007 Jan 15;401(2):447-57
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  • [Title] MEGF9: a novel transmembrane protein with a strong and developmentally regulated expression in the nervous system.
  • MEGF9 [multiple EGF (epidermal growth factor)-like-domains 9], a novel transmembrane protein with multiple EGF-like repeats, is predominantly expressed in the developing and adult CNS (central nervous system) and PNS (peripheral nervous system).
  • [MeSH-major] Central Nervous System / metabolism. Gene Expression Regulation, Developmental. Membrane Proteins / biosynthesis. Nerve Tissue Proteins / biosynthesis. Peripheral Nervous System / metabolism
  • [MeSH-minor] Amino Acid Sequence. Animals. Epidermal Growth Factor / genetics. Humans. Keratinocytes / metabolism. Mice. Molecular Sequence Data. Protein Processing, Post-Translational. Protein Structure, Tertiary. Rats. Sequence Alignment. Skin / cytology. Tongue / cytology. Tumor Cells, Cultured

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • [Cites] J Biol Chem. 1991 May 25;266(15):9678-86 [2033060.001]
  • [Cites] Pediatr Res. 2005 May;57(5 Pt 2):104R-109R [15817497.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 May 1;90(9):4037-41 [8483919.001]
  • [Cites] Hum Mutat. 1999;14(5):394-400 [10533065.001]
  • [Cites] J Biol Chem. 1999 Nov 5;274(45):31751-4 [10542193.001]
  • [Cites] J Neurosci. 1999 Nov 15;19(22):9900-12 [10559399.001]
  • [Cites] J Cell Biol. 2000 Oct 16;151(2):221-34 [11038171.001]
  • [Cites] J Comp Neurol. 2001 Feb 19;430(4):485-500 [11169482.001]
  • [Cites] Arch Oral Biol. 2001 Aug;46(8):745-57 [11389866.001]
  • [Cites] Circ Res. 2002 Mar 22;90(5):506-8 [11909813.001]
  • [Cites] Hum Mol Genet. 2002 Sep 1;11(18):2113-8 [12189163.001]
  • [Cites] J Biol Chem. 2003 May 2;278(18):15457-60 [12556455.001]
  • [Cites] Matrix Biol. 1994 Aug;14(4):275-81 [7827749.001]
  • [Cites] Mol Biol Cell. 2003 Jul;14(7):2665-76 [12857855.001]
  • [Cites] Neuron. 2003 Sep 25;40(1):113-27 [14527437.001]
  • [Cites] DNA Res. 2003 Aug 31;10(4):167-80 [14621295.001]
  • [Cites] Cell Prolif. 2004 Apr;37(2):161-75 [15030550.001]
  • [Cites] Annu Rev Biochem. 2004;73:491-537 [15189151.001]
  • [Cites] Int J Biochem Cell Biol. 2004 Oct;36(10):1861-7 [15203098.001]
  • [Cites] Nature. 1970 Aug 15;227(5259):680-5 [5432063.001]
  • [Cites] FEBS Lett. 1988 Apr 11;231(1):1-4 [3282918.001]
  • [Cites] Adv Protein Chem. 1988;39:1-50 [3149870.001]
  • [Cites] FEBS Lett. 1989 Jul 17;251(1-2):1-7 [2666164.001]
  • [Cites] Annu Rev Physiol. 1995;57:607-34 [7778880.001]
  • [Cites] Genomics. 1996 Feb 15;32(1):54-64 [8786121.001]
  • [Cites] J Lipid Res. 1996 Feb;37(2):368-81 [9026534.001]
  • [Cites] Genomics. 1998 Jul 1;51(1):27-34 [9693030.001]
  • [Cites] Dev Biol. 2005 Feb 15;278(2):381-95 [15680358.001]
  • [Cites] Mol Psychiatry. 2005 Mar;10(3):251-7 [15583703.001]
  • [Cites] Glia. 1991;4(1):11-24 [1828781.001]
  • (PMID = 16981854.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Databank-accession-numbers] RefSeq/ NM/ 172694/ XM/ 3769095
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS049136
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MEGF9 protein, human; 0 / MEGF9 protein, mouse; 0 / Membrane Proteins; 0 / Nerve Tissue Proteins; 62229-50-9 / Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC1820795
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44. Raney B, Anderson J, Breneman J, Donaldson SS, Huh W, Maurer H, Michalski J, Qualman S, Ullrich F, Wharam M, Meyer W, Soft-Tissue Sarcoma Committee of the Children's Oncology Group, Arcadia, California, USA: Results in patients with cranial parameningeal sarcoma and metastases (Stage 4) treated on Intergroup Rhabdomyosarcoma Study Group (IRSG) Protocols II-IV, 1978-1997: report from the Children's Oncology Group. Pediatr Blood Cancer; 2008 Jul;51(1):17-22
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  • Treatment included vincristine, actinomycin D, and cyclophosphamide (VAC) chemotherapy and radiotherapy to the primary tumor and up to five metastatic sites/tissues.
  • Sites of first progression/relapse were distant (55%), local (12%), CNS extension (8%), mixed (6%), and uncertain (18%).
  • Factors indicating likelihood of 10-year FFS included tumor arising in "better" versus "worse" sites (FFS 46% vs. 18%, P = 0.02) and embryonal versus other histology (FFS 37% vs. 19%, P = 0.06).

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18266224.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-98543; United States / NCI NIH HHS / CA / CA-24507; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / CA-72989; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA-29511
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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45. Cooper PB, Auerbach A, Aguilera NS, Adair C, Moores L, Geyer D, Rushing EJ: Rare primary CNS anaplastic large cell lymphoma in an immunocompetent adult: a clinical-pathologic case report and review case of the literature. Clin Neuropathol; 2006 Sep-Oct;25(5):232-6
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  • [Title] Rare primary CNS anaplastic large cell lymphoma in an immunocompetent adult: a clinical-pathologic case report and review case of the literature.
  • OBJECTIVE AND IMPORTANCE: Isolated anaplastic large cell lymphoma (ALCL) presenting in the primary central nervous system is distinctly uncommon.
  • The authors describe a case that clinically and radiographically simulated a primary glial neoplasm.
  • There appeared to be a clear demarcation between white matter and tumor with no obvious necrosis.
  • CONCLUSION: Reported in less than 20 patients, primary ALCL in an immunocompetent patient is rarely found intracranially; however, its ability to mimic glial neoplasms as well as other pathologies underlines its importance.
  • [MeSH-major] Brain Neoplasms / pathology. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Biomarkers, Tumor / analysis. Combined Modality Therapy. Diagnosis, Differential. Glioma / pathology. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Radiotherapy. Seizures / etiology


46. Selkirk SM, Morrow J, Barone TA, Hoffer A, Lock J, DeChant A, Mangla S, Plunkett RJ, Miller RH: Elevation of osteopontin levels in brain tumor cells reduces burden and promotes survival through the inhibition of cell dispersal. J Neurooncol; 2008 Feb;86(3):285-96
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  • [Title] Elevation of osteopontin levels in brain tumor cells reduces burden and promotes survival through the inhibition of cell dispersal.
  • Osteopontin (OPN) is a pleotrophic molecule that has been associated with multiple disorders of the central nervous system (CNS).
  • Its roles in CNS malignancy are unclear but suggest that higher levels of OPN expression correlate with increased tumor grade and increased migratory capacity of tumor cells.
  • Implantation of tumor cells expressing high levels of OPN into adult Fischer rats and nude rats resulted in morphologically distinct tumors and prolonged host survival relative to controls.
  • We propose that local produced, high level OPN expression limits the malignant character of glioma cells and that the downstream mechanisms involved represent pathways that may have therapeutic value in the treatment of human CNS malignancy.

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  • [Cites] J Biol Chem. 1999 Dec 17;274(51):36328-34 [10593924.001]
  • [Cites] Cancer Res. 2006 Oct 15;66(20):10024-31 [17047065.001]
  • [Cites] Exp Cell Res. 2000 Aug 1;258(2):342-51 [10896785.001]
  • [Cites] J Biol Chem. 2000 Aug 11;275(32):24565-74 [10835423.001]
  • [Cites] Int J Exp Pathol. 2000 Dec;81(6):373-90 [11298186.001]
  • [Cites] J Biol Chem. 2001 Jul 27;276(30):28261-7 [11375993.001]
  • [Cites] Science. 2001 Nov 23;294(5547):1731-5 [11721059.001]
  • [Cites] J Biol Chem. 2001 Dec 7;276(49):46024-30 [11590166.001]
  • [Cites] Biochim Biophys Acta. 2001 Dec 28;1552(2):61-85 [11825687.001]
  • [Cites] QJM. 2002 Jan;95(1):3-13 [11834767.001]
  • [Cites] Cancer Res. 2002 Sep 15;62(18):5336-43 [12235004.001]
  • [Cites] Cancer Res. 2002 Nov 1;62(21):6318-22 [12414663.001]
  • [Cites] Oncogene. 2003 Feb 27;22(8):1198-205 [12606946.001]
  • [Cites] J Neuroimmunol. 2003 Mar;136(1-2):125-9 [12620651.001]
  • [Cites] J Biol Chem. 2003 Aug 1;278(31):28593-606 [12771144.001]
  • [Cites] Mol Cancer Res. 2003 Sep;1(11):810-9 [14517343.001]
  • [Cites] J Biol Chem. 2004 Mar 19;279(12):11051-64 [14704150.001]
  • [Cites] J Neuroimmunol. 2004 Oct;155(1-2):155-60 [15342207.001]
  • [Cites] Cell. 1979 Apr;16(4):885-93 [88265.001]
  • [Cites] J Biol Chem. 1987 Feb 25;262(6):2900-7 [3469201.001]
  • [Cites] J Biol Chem. 1987 Jul 15;262(20):9702-8 [3597437.001]
  • [Cites] J Exp Med. 1989 Jul 1;170(1):145-61 [2787378.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Jan 1;89(1):426-30 [1729712.001]
  • [Cites] Am J Pathol. 1994 Sep;145(3):610-23 [8080043.001]
  • [Cites] Biochem J. 1994 Oct 1;303 ( Pt 1):255-62 [7945249.001]
  • [Cites] Lab Invest. 1995 Jan;72(1):55-63 [7837791.001]
  • [Cites] J Clin Invest. 1995 Feb;95(2):713-24 [7532190.001]
  • [Cites] Lung Cancer. 1996 Nov;15(3):311-23 [8959677.001]
  • [Cites] J Biol Chem. 1997 Apr 11;272(15):10110-6 [9092556.001]
  • [Cites] Arch Pathol Lab Med. 1997 Jun;121(6):578-84 [9199622.001]
  • [Cites] Clin Cancer Res. 1997 Apr;3(4):605-11 [9815727.001]
  • [Cites] Cancer Res. 1999 Jan 1;59(1):219-26 [9892210.001]
  • [Cites] J Cell Biochem Suppl. 1998;30-31:92-102 [9893260.001]
  • [Cites] J Biol Chem. 2005 May 13;280(19):19381-92 [15757900.001]
  • [Cites] Trends Cell Biol. 2006 Feb;16(2):79-87 [16406521.001]
  • [Cites] Cancer Res. 2006 Jul 1;66(13):6638-48 [16818637.001]
  • [Cites] Bioessays. 2006 Sep;28(9):923-34 [16937364.001]
  • [Cites] Ann N Y Acad Sci. 1999;890:204-22 [10668427.001]
  • (PMID = 17928956.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA10373602; United States / NINDS NIH HHS / NS / R01 NS036674; United States / NINDS NIH HHS / NS / NS030800-14; United States / NINDS NIH HHS / NS / R01 NS030800; United States / NINDS NIH HHS / NS / NS-3080011; United States / NINDS NIH HHS / NS / R37 NS036674; United States / NINDS NIH HHS / NS / R01 NS030800-14; United States / NINDS NIH HHS / NS / NS-36674-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD31; 106441-73-0 / Osteopontin; 147336-22-9 / Green Fluorescent Proteins; G34N38R2N1 / Bromodeoxyuridine
  • [Other-IDs] NLM/ NIHMS196650; NLM/ PMC2911624
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47. Kuchelmeister K, Nestler U, Siekmann R, Schachenmayr W: Liponeurocytoma of the left lateral ventricle--case report and review of the literature. Clin Neuropathol; 2006 Mar-Apr;25(2):86-94
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  • In this location, liponeurocytomas are very exceptional, whereas it is the typical site for classic central neurocytomas.
  • Thus, cerebellar liponeurocytoma is the most frequent neuroepithelial CNS tumor with adipose-like cells followed by ependymomas with a lipid component and supratentorial intraventricular liponeurocytoma.
  • Adipose-like cells in neurocytomas may originate by lipidization of tumor cells, metaplastic transformation of neuroectodermal cells into fat cells or by true adipocytic differentiation.
  • The present case showed also focal glial differentiation with GFAP-positivity of some tumor cells as often seen in cerebellar liponeurocytomas but much rarer in central neurocytomas.
  • Future WHO tumor classification should consider that liponeurocytomas are not restricted to the cerebellum.
  • [MeSH-major] Cerebral Ventricle Neoplasms / pathology. Lipoma / pathology. Neurocytoma / pathology
  • [MeSH-minor] Adult. Cerebellar Neoplasms / pathology. Diagnosis, Differential. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry. Male

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  • (PMID = 16550742.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein
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48. Lush ME, Li Y, Kwon CH, Chen J, Parada LF: Neurofibromin is required for barrel formation in the mouse somatosensory cortex. J Neurosci; 2008 Feb 13;28(7):1580-7
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  • The rodent barrel cortex is a useful system to study the role of genes and neuronal activity in the patterning of the nervous system.
  • Neurofibromin is a tumor suppressor protein that has Ras GTPase activity, thus attenuating the MAPK (mitogen-activated protein kinase) and and PI-3 kinase (phosphatidylinositol 3-kinase) pathways, and is mutated in humans with the condition neurofibromatosis type 1 (NF1).
  • Neurofibromin is widely expressed in the developing and adult nervous system, and a common feature of NF1 is deficits in intellectual development.
  • Thus, NF1 may have important roles in normal CNS development and function.
  • To explore roles for neurofibromin in the development of the CNS, we took advantage of a mouse conditional allele.

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  • [Cites] Nat Neurosci. 2000 Jul;3(7):661-9 [10862698.001]
  • [Cites] Nature. 2000 Feb 24;403(6772):895-8 [10706287.001]
  • [Cites] Genesis. 2000 Nov-Dec;28(3-4):147-55 [11105057.001]
  • [Cites] Am J Med Genet. 2000 Summer;97(2):119-27 [11180219.001]
  • [Cites] Nat Neurosci. 2001 Mar;4(3):282-8 [11224545.001]
  • [Cites] Cell. 2001 Feb 23;104(4):593-604 [11239415.001]
  • [Cites] Exp Cell Res. 2001 Mar 10;264(1):19-28 [11237520.001]
  • [Cites] Genet Med. 1999 May-Jun;1(4):136-40 [11258348.001]
  • [Cites] Genes Dev. 2001 Apr 1;15(7):859-76 [11297510.001]
  • [Cites] Trends Neurosci. 2001 Oct;24(10):589-95 [11576673.001]
  • [Cites] Genesis. 2001 Oct;31(2):85-94 [11668683.001]
  • [Cites] Nat Neurosci. 2002 Feb;5(2):95-6 [11788835.001]
  • [Cites] Nature. 2002 Jan 31;415(6871):526-30 [11793011.001]
  • [Cites] Trends Mol Med. 2003 Jan;9(1):19-23 [12524206.001]
  • [Cites] Neuron. 2003 Mar 6;37(5):751-64 [12628166.001]
  • [Cites] Am J Med Genet B Neuropsychiatr Genet. 2004 Nov 15;131B(1):43-7 [15389774.001]
  • [Cites] J Neurosci. 2005 Apr 13;25(15):3774-86 [15829629.001]
  • [Cites] Cancer Cell. 2005 Aug;8(2):119-30 [16098465.001]
  • [Cites] Development. 2005 Dec;132(24):5577-88 [16314489.001]
  • [Cites] J Neurosci. 2006 Feb 1;26(5):1355-65 [16452659.001]
  • [Cites] Genesis. 2006 Mar;44(3):130-5 [16496331.001]
  • [Cites] J Neurosci. 2006 Mar 8;26(10):2692-703 [16525048.001]
  • [Cites] J Neurosci. 2006 Apr 19;26(16):4338-49 [16624954.001]
  • [Cites] J Neurosci. 2006 May 17;26(20):5393-401 [16707791.001]
  • [Cites] Neuron. 2007 Oct 25;56(2):339-55 [17964250.001]
  • [Cites] Neurology. 2003 Dec 23;61(12):1799-801 [14694053.001]
  • [Cites] Brain Res. 1970 Jan 20;17(2):205-42 [4904874.001]
  • [Cites] Proc Natl Acad Sci U S A. 1975 Jun;72(6):2165-9 [1056021.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Apr;77(4):2333-7 [6246540.001]
  • [Cites] Cell. 1990 Jul 13;62(1):187-92 [1694727.001]
  • [Cites] Cell. 1990 Jul 13;62(1):193-201 [2114220.001]
  • [Cites] Science. 1990 Jul 13;249(4965):181-6 [2134734.001]
  • [Cites] Science. 1991 Jun 14;252(5012):1556-60 [2047863.001]
  • [Cites] Nat Genet. 1994 Jul;7(3):353-61 [7920653.001]
  • [Cites] Genes Dev. 1994 May 1;8(9):1019-29 [7926784.001]
  • [Cites] Cell. 1995 Sep 8;82(5):733-42 [7671302.001]
  • [Cites] Science. 1996 Mar 29;271(5257):1864-7 [8596955.001]
  • [Cites] Neuron. 1996 Feb;16(2):297-307 [8789945.001]
  • [Cites] Science. 1997 May 2;276(5313):791-4 [9115203.001]
  • [Cites] Science. 1997 May 2;276(5313):795-8 [9115204.001]
  • [Cites] Neuron. 1998 Apr;20(4):683-91 [9581761.001]
  • [Cites] Neuron. 1998 May;20(5):895-904 [9620694.001]
  • [Cites] Nat Genet. 1998 Jul;19(3):289-91 [9662407.001]
  • [Cites] Hum Mol Genet. 1998 Aug;7(8):1261-8 [9668168.001]
  • [Cites] J Neurosci. 1998 Dec 15;18(24):10420-8 [9852579.001]
  • [Cites] Nat Genet. 1999 Jan;21(1):70-1 [9916792.001]
  • [Cites] Am J Med Genet. 1999 Dec 15;88(6):729-32 [10581497.001]
  • [Cites] Nature. 2000 Aug 17;406(6797):726-31 [10963597.001]
  • (PMID = 18272679.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS034296-09; United States / NINDS NIH HHS / NS / NS34296; United States / NINDS NIH HHS / NS / R37 NS033199-11; United States / NINDS NIH HHS / NS / R01 NS034296; United States / NINDS NIH HHS / NS / NS033199-11; United States / NINDS NIH HHS / NS / R37NS33199; United States / NINDS NIH HHS / NS / R37 NS033199; United States / NINDS NIH HHS / NS / R01 NS034296-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neurofibromin 1
  • [Other-IDs] NLM/ NIHMS149013; NLM/ PMC2760344
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49. Ogata M, Satou T, Kawano R, Takakura S, Goto K, Ikewaki J, Kohno K, Ikebe T, Ando T, Miyazaki Y, Ohtsuka E, Saburi Y, Saikawa T, Kadota J: Correlations of HHV-6 viral load and plasma IL-6 concentration with HHV-6 encephalitis in allogeneic stem cell transplant recipients. Bone Marrow Transplant; 2010 Jan;45(1):129-36
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  • Among 111 enrolled subjects, 12 patients developed central nervous system (CNS) dysfunction.
  • CNS dysfunction in four patients was found to have no association with HHV-6.
  • The remaining eight patients displayed HHV-6 encephalitis (n=3), limbic encephalitis (HHV-6 DNA in cerebrospinal fluid was not examined; n=3) or CNS dysfunction because of an unidentified cause (n=2).
  • Real-time PCR showed CNS dysfunction in the latter eight patients, which developed concomitant with the appearance of high plasma levels of HHV-6 DNA (> or =10(4) copies/ml).
  • Overall, eight of the 24 patients with high-level HHV-6 DNA developed CNS dysfunction, whereas no patients developed CNS dysfunction potentially associated with HHV-6 infection if peak HHV-6 DNA was <10(4) copies/ml.
  • We next analyzed plasma concentrations of IL-6, IL-10 and tumor necrosis factor-alpha among patients who displayed high-level plasma HHV-6 DNA and found elevated IL-6 concentrations preceding HHV-6 infection in patients who developed CNS dysfunction. (Mean+/-s.d.: 865.7+/-1036.3 pg/ml in patients with CNS dysfunction; 56.5+/-192.9 pg/ml in others; P=0.01).
  • [MeSH-minor] Adolescent. Adult. Child. DNA, Viral / blood. Female. Humans. Interleukin-10 / blood. Male. Middle Aged. Tumor Necrosis Factor-alpha / blood. Viral Load

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  • (PMID = 19465942.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10
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50. Jayadev S, Yun B, Nguyen H, Yokoo H, Morrison RS, Garden GA: The glial response to CNS HIV infection includes p53 activation and increased expression of p53 target genes. J Neuroimmune Pharmacol; 2007 Dec;2(4):359-70
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  • [Title] The glial response to CNS HIV infection includes p53 activation and increased expression of p53 target genes.
  • We have also shown that microglia from p53-deficient mice fail to induce neurotoxicity in response to the HIV coat protein gp120 in a coculture system, supporting the hypothesis that p53 plays a pathogenic role in the chronic neuroinflammatory component of HIV-associated neurodegeneration.
  • [MeSH-major] AIDS Dementia Complex / genetics. AIDS Dementia Complex / metabolism. Central Nervous System Infections / metabolism. Gene Expression Regulation, Viral / physiology. Neuroglia / metabolism. Neuroglia / virology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adult. Astrocytes / metabolism. Astrocytes / pathology. Astrocytes / virology. Female. Gene Targeting. HeLa Cells. Humans. Male. Microglia / metabolism. Microglia / pathology. Microglia / virology. Middle Aged. Oligodendroglia / metabolism. Oligodendroglia / pathology. Oligodendroglia / virology. Signal Transduction / genetics. Signal Transduction / physiology

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  • [Cites] Neuroscience. 2001;103(1):203-18 [11311801.001]
  • [Cites] Am J Pathol. 1996 Sep;149(3):1027-53 [8780406.001]
  • [Cites] Neuron. 1996 Mar;16(3):675-86 [8785064.001]
  • [Cites] Cancer Lett. 2004 Jan 20;203(2):199-207 [14732228.001]
  • [Cites] N Engl J Med. 1995 Apr 6;332(14):934-40 [7877652.001]
  • [Cites] J Neurosci Res. 1997 Dec 1;50(5):798-808 [9418967.001]
  • [Cites] Neurology. 2003 Jan 28;60(2):307-14 [12552050.001]
  • [Cites] Dev Biol. 2006 May 15;293(2):358-69 [16581057.001]
  • [Cites] Brain Pathol. 1999 Apr;9(2):209-17 [10219738.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Jun 10;331(3):851-8 [15865941.001]
  • [Cites] FASEB J. 2004 Jul;18(10):1141-3 [15155568.001]
  • [Cites] AIDS. 2000 Sep 8;14(13):1949-54 [10997399.001]
  • [Cites] Neurology. 1993 Nov;43(11):2230-7 [8232935.001]
  • [Cites] J Leukoc Biol. 1994 Sep;56(3):389-98 [8083614.001]
  • [Cites] Ann Neurol. 2001 Jun;49(6):745-52 [11409426.001]
  • [Cites] Am J Pathol. 2005 Sep;167(3):695-704 [16127150.001]
  • [Cites] Curr Opin Neurol. 2001 Jun;14(3):375-9 [11371763.001]
  • [Cites] Brain Res Mol Brain Res. 1999 Jul 23;71(1):78-86 [10407189.001]
  • [Cites] J Alzheimers Dis. 2001 Feb;3(1):31-40 [12214070.001]
  • [Cites] Adv Neuroimmunol. 1995;5(3):335-58 [8748077.001]
  • [Cites] Semin Neurol. 1999;19(2):113-27 [10718533.001]
  • [Cites] Science. 1990 Dec 14;250(4987):1593-6 [2148832.001]
  • [Cites] Exp Neurol. 2006 Oct;201(2):349-58 [16814281.001]
  • [Cites] Nature. 2006 Feb 23;439(7079):988-92 [16372019.001]
  • [Cites] Glia. 1993 Jan;7(1):102-10 [8423057.001]
  • [Cites] Nature. 2001 Apr 19;410(6831):988-94 [11309629.001]
  • [Cites] J Cell Physiol. 2002 Jul;192(1):1-15 [12115731.001]
  • [Cites] Cell Death Differ. 2005 Aug;12 Suppl 1:855-8 [15846379.001]
  • [Cites] J Biol Chem. 2000 May 26;275(21):16202-12 [10821866.001]
  • [Cites] J Cell Physiol. 1999 Nov;181(2):231-9 [10497302.001]
  • [Cites] Neurobiol Aging. 2005 Mar;26(3):349-54 [15639313.001]
  • [Cites] J Neurosci. 2003 Sep 24;23(25):8682-91 [14507967.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jun 6;97(12 ):6763-8 [10823891.001]
  • [Cites] J Neural Transm Suppl. 1999;57:87-97 [10666670.001]
  • [Cites] J Neurotrauma. 2004 Jun;21(6):754-74 [15253803.001]
  • [Cites] Biochem Biophys Res Commun. 1992 Feb 14;182(3):1201-7 [1540165.001]
  • [Cites] Am J Pathol. 1995 May;146(5):1121-30 [7747806.001]
  • [Cites] J Acquir Immune Defic Syndr Hum Retrovirol. 1996 Jan 1;11(1):39-44 [8528731.001]
  • [Cites] Nature. 1997 May 15;387(6630):299-303 [9153396.001]
  • [Cites] Eur Arch Psychiatry Clin Neurosci. 2001 Aug;251(4):159-69 [11697580.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Apr 1;90(7):2769-73 [8464887.001]
  • [Cites] Neurochem Res. 2003 Jan;28(1):15-27 [12587660.001]
  • [Cites] Science. 2004 Feb 13;303(5660):1010-4 [14963330.001]
  • [Cites] Brain Pathol. 1991 Apr;1(3):143-52 [1669703.001]
  • [Cites] J Neurosci. 1995 Nov;15(11):7712-26 [7472522.001]
  • [Cites] Neuropathol Appl Neurobiol. 1999 Apr;25(2):123-33 [10216000.001]
  • [Cites] Toxicol Lett. 2003 Apr 4;139(2-3):199-206 [12628755.001]
  • [Cites] Nature. 1997 May 15;387(6630):296-9 [9153395.001]
  • [Cites] Arch Neurol. 2002 Dec;59(12):1930-6 [12470182.001]
  • [Cites] Lab Invest. 1998 Apr;78(4):401-11 [9564885.001]
  • [Cites] Development. 2004 Mar;131(6):1211-20 [14960496.001]
  • [Cites] Biochem Biophys Res Commun. 1997 Mar 17;232(2):418-21 [9125193.001]
  • [Cites] Ann Neurol. 1992 Sep;32(3):321-9 [1416802.001]
  • [Cites] Brain Pathol. 2003 Apr;13(2):195-210 [12744473.001]
  • [Cites] Am J Pathol. 2004 May;164(5):1717-25 [15111318.001]
  • [Cites] Ann Neurol. 1993 Jul;34(1):65-70 [8517682.001]
  • [Cites] Science. 1996 Jul 5;273(5271):59-63 [8658196.001]
  • [Cites] Nat Neurosci. 2001 Jul;4(7):702-10 [11426226.001]
  • [Cites] Ann Neurol. 1995 Nov;38(5):755-62 [7486867.001]
  • [Cites] Mod Pathol. 2000 Oct;13(10):1115-20 [11048806.001]
  • [Cites] Ann Neurol. 1991 Jun;29(6):651-7 [1909852.001]
  • [Cites] Cell Mol Life Sci. 2004 Apr;61(7-8):822-42 [15095006.001]
  • [Cites] J Neurovirol. 2000 May;6 Suppl 1:S38-43 [10871764.001]
  • [Cites] Oncogene. 1999 Nov 1;18(45):6145-57 [10557106.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jul 6;96(14):8212-6 [10393974.001]
  • [Cites] Science. 2006 Jun 16;312(5780):1650-3 [16728594.001]
  • [Cites] Science. 2000 Apr 21;288(5465):440-2 [10798979.001]
  • [Cites] Neurobiol Dis. 2000 Dec;7(6 Pt B):613-22 [11114260.001]
  • [Cites] J Neurovirol. 2004;10 Suppl 1:97-101 [14982746.001]
  • [Cites] Prog Neurobiol. 2004 Feb;72(2):111-27 [15063528.001]
  • [Cites] Glia. 2002 Nov;40(2):240-51 [12379911.001]
  • [Cites] Nature. 2000 Nov 16;408(6810):307-10 [11099028.001]
  • [Cites] Oncogene. 2001 Mar 8;20(10):1212-9 [11313865.001]
  • [Cites] Ann Neurol. 1997 Dec;42(6):963-72 [9403489.001]
  • [Cites] Neurology. 1992 Aug;42(8):1472-6 [1641138.001]
  • [Cites] Ann Neurol. 2003 Nov;54(5):605-14 [14595650.001]
  • [Cites] J Clin Invest. 1996 Nov 1;98(9):1979-90 [8903316.001]
  • (PMID = 18040854.001).
  • [ISSN] 1557-1904
  • [Journal-full-title] Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology
  • [ISO-abbreviation] J Neuroimmune Pharmacol
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS35533; United States / NICHD NIH HHS / HD / P30-HD02774; United States / NIA NIH HHS / AG / T32-AG000268; United States / NINDS NIH HHS / NS / NS45528; United States / NIMH NIH HHS / MH / U01 MH083545; United States / NIMH NIH HHS / MH / N01MH32002
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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51. Sultan I, Qaddoumi I, Rodríguez-Galindo C, Nassan AA, Ghandour K, Al-Hussaini M: Age, stage, and radiotherapy, but not primary tumor site, affects the outcome of patients with malignant rhabdoid tumors. Pediatr Blood Cancer; 2010 Jan;54(1):35-40
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  • [Title] Age, stage, and radiotherapy, but not primary tumor site, affects the outcome of patients with malignant rhabdoid tumors.
  • BACKGROUND: Malignant rhabdoid tumors (MRTs) are aggressive and often fatal; the Surveillance, Epidemiology, and End Results (SEER) database offers an opportunity to study this rare malignancy.
  • RESULTS: For the 229 patients included in our data, who were diagnosed from 1986 to 2005, primary tumors were located in the central nervous system (CNS) (35%), kidneys (20%), and extra-renal non-cranial sites (ERNC-MRTs) (45%).
  • Most patients with renal and CNS tumors were less than 18 years old (87% and 96%, respectively) while more than half of the patients with ERNC-MRTs (61%) were adults.
  • Among staged tumors, 23% were localized, 34% regional, and 43% distant.
  • Renal tumors had significantly more metastatic disease (47%; P = 0.006) than ERNC-MRTs.
  • Univariate and multivariate analyses showed that age at diagnosis (2-18 years), localized stage of tumors, and use of radiotherapy were significantly associated with improved survival.
  • Adults had a better outcome than young children (<2 years old) but a poorer outcome than older children (2-18 years old); tumor stage, but not radiotherapy use, affected outcome in adults.
  • CONCLUSION: Our population-based study indicates that age at diagnosis, tumor stage, and use of radiotherapy favorably impact survival rates of patients with MRTs.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / radiotherapy. Kidney Neoplasms / pathology. Kidney Neoplasms / radiotherapy. Rhabdoid Tumor / pathology. Rhabdoid Tumor / radiotherapy
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Male. Middle Aged. Neoplasm Staging. Prognosis. SEER Program. Survival Rate. Treatment Outcome. Young Adult


52. Kounin GK, Romansky KV, Traykov LD, Shotekov PM, Stoilova DZ: Primary spinal melanoma with bilateral papilledema. Clin Neurol Neurosurg; 2005 Oct;107(6):525-7
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  • A diagnosis of primary CNS melanoma was made after dermatological and ophthalmological consultations, ruled out a metastatic lesion.
  • Primary leptomeningeal melanoma is an extremely rare spinal tumor.
  • [MeSH-major] Melanoma / diagnosis. Papilledema / etiology. Spinal Cord Neoplasms / diagnosis
  • [MeSH-minor] Adult. Cerebrospinal Fluid / cytology. Cervical Vertebrae / pathology. Diagnosis, Differential. Erythrocyte Count. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Neoplasm Invasiveness. Spinal Cord / pathology. Spinal Cord Compression / diagnosis. Spinal Cord Compression / surgery. Tomography, X-Ray Computed

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  • (PMID = 16202828.001).
  • [ISSN] 0303-8467
  • [Journal-full-title] Clinical neurology and neurosurgery
  • [ISO-abbreviation] Clin Neurol Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports
  • [Publication-country] Netherlands
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53. Vasudevan V, Cheung MC, Yang R, Zhuge Y, Fischer AC, Koniaris LG, Sola JE: Pediatric solid tumors and second malignancies: characteristics and survival outcomes. J Surg Res; 2010 May 15;160(2):184-9
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  • [Title] Pediatric solid tumors and second malignancies: characteristics and survival outcomes.
  • BACKGROUND: To examine the incidence, characteristics, and outcomes for second malignancies following the diagnosis of a primary solid tumor in pediatric patients.
  • Mean age at diagnosis of the primary tumor was 7.7 y.
  • The most common primary malignancies were CNS tumors (22.5%), followed by soft tissue sarcoma (15.8%), retinoblastoma (14.1%), and bone tumors (13%).
  • Hematologic malignancies (35.5%) were the most common second malignancies noted in the cohort, followed by bone tumors (18%) and soft tissue sarcomas (15%).
  • Hematologic malignancies had a shorter latency (3.1 y) compared with solid second tumors (11.6 y).
  • For most tumor categories, development of a secondary malignancy was associated with lower 5- and 10-y survival than expected.
  • CONCLUSIONS: CNS tumors, retinoblastoma, and soft tissue sarcomas in children are the most common solid primary tumors, with an increased risk of a second malignancy.
  • Leukemia is the most common second malignancy seen in pediatric solid tumors.
  • [MeSH-major] Neoplasms / mortality. Neoplasms, Second Primary / mortality. SEER Program
  • [MeSH-minor] Adolescent. Bone Neoplasms / mortality. Central Nervous System Neoplasms / mortality. Child. Child, Preschool. Female. Follow-Up Studies. Hematologic Neoplasms / mortality. Humans. Incidence. Male. Retinoblastoma / mortality. Sarcoma / mortality. Soft Tissue Neoplasms / mortality. Survival Analysis. Young Adult

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 19765728.001).
  • [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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54. Scalabrino G, Galimberti D, Mutti E, Scalabrini D, Veber D, De Riz M, Bamonti F, Capello E, Mancardi GL, Scarpini E: Loss of epidermal growth factor regulation by cobalamin in multiple sclerosis. Brain Res; 2010 May 28;1333:64-71
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  • We investigated whether the physiological regulation of cerebrospinal fluid (CSF) levels of tumor necrosis factor (TNF)-alpha, epidermal growth factor (EGF), and nerve growth factor (NGF) by cobalamin (Cbl) that is observed in rat and human central nervous system (CNS) is retained in the CSF of patients with multiple sclerosis (MS).
  • (b) the decrease in EGF levels in the CSF may be one factor impeding CNS remyelination in MS; and (c) the PP clinical course may have different pathogenetic mechanism(s) also on the basis of the molecules investigated in this study.
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged. Radioimmunoassay / methods. Retrospective Studies. Statistics, Nonparametric. Tumor Necrosis Factor-alpha / cerebrospinal fluid

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  • [Copyright] 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20347721.001).
  • [ISSN] 1872-6240
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 12001-76-2 / Vitamin B Complex; 62229-50-9 / Epidermal Growth Factor; P6YC3EG204 / Vitamin B 12
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55. Madanat-Harjuoja LM, Malila N, Lähteenmäki PM, Boice JD Jr, Gissler M, Dyba T: Preterm delivery among female survivors of childhood, adolescent and young adulthood cancer. Int J Cancer; 2010 Oct 1;127(7):1669-79
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  • Site-specific analyses indicated that survivors of germ cell tumors and central nervous system (CNS) tumors were at increased risk of preterm delivery, although numbers were small.
  • In childhood survivors, kidney tumors formed the main cause of preterm delivery.
  • Pediatric, adolescent and young adult cancer survivors are at risk for preterm delivery.
  • Heightened surveillance is recommended especially for Wilms', germ cell and CNS tumor survivors.

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  • [Cites] Int J Epidemiol. 2008 Oct;37(5):1109-20 [18577529.001]
  • [Cites] BMJ. 2008;337:a2312 [18957469.001]
  • [Cites] Int J Cancer. 2008 Dec 15;123(12):2891-8 [18798259.001]
  • [Cites] J Clin Oncol. 2009 Jan 20;27(3):334-43 [19075285.001]
  • [Cites] Fertil Steril. 2009 Feb;91(2):325-30 [18384780.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2004 Oct 1;60(2):542-52 [15380591.001]
  • [Cites] JAMA. 1987 Jan 9;257(2):216-9 [3025465.001]
  • [Cites] Med Pediatr Oncol. 1988;16(4):233-40 [2843733.001]
  • [Cites] Int J Cancer. 1989 Mar 15;43(3):399-402 [2538400.001]
  • [Cites] Cancer. 1989 Dec 1;64(11):2335-9 [2804924.001]
  • [Cites] Duodecim. 1989;105(18):1540-6 [2680445.001]
  • [Cites] Acta Oncol. 1994;33(4):365-9 [8018367.001]
  • [Cites] Am J Hum Genet. 1998 Jan;62(1):45-52 [9443870.001]
  • [Cites] Cancer. 1999 Aug 15;86(4):697-709 [10440699.001]
  • [Cites] Radiother Oncol. 2004 Nov;73(2):119-31 [15542158.001]
  • [Cites] J Natl Cancer Inst. 2006 Oct 18;98(20):1453-61 [17047194.001]
  • [Cites] Pediatr Blood Cancer. 2007 Jul;49(1):47-51 [16755550.001]
  • [Cites] Paediatr Perinat Epidemiol. 2007 Sep;21(5):441-7 [17697074.001]
  • [Cites] J Matern Fetal Neonatal Med. 2007 Oct;20(10):719-23 [17763272.001]
  • [Cites] Obstet Gynecol. 2007 Oct;110(4):849-54 [17906019.001]
  • [Cites] Cancer. 2007 Nov 15;110(10):2313-20 [17896787.001]
  • [Cites] BJOG. 2008 Jan;115(1):38-43 [18053102.001]
  • [Cites] Hum Reprod. 2008 Jan;23(1):178-86 [18024486.001]
  • [Cites] Health Psychol. 2008 Jan;27(1):43-51 [18230013.001]
  • [Cites] Arch Pediatr Adolesc Med. 2009 Oct;163(10):879-86 [19805705.001]
  • [Cites] Eur J Cancer. 2009 Apr;45(6):992-1005 [19231160.001]
  • [Cites] J Clin Oncol. 2009 May 10;27(14):2319-27 [19364957.001]
  • [Cites] Br J Obstet Gynaecol. 1999 Dec;106(12):1265-72 [10609720.001]
  • [Cites] Epidemiology. 2000 Mar;11(2):161-6 [11021613.001]
  • [Cites] Med Pediatr Oncol. 2002 Apr;38(4):229-39 [11920786.001]
  • [Cites] J Clin Oncol. 2002 May 15;20(10):2506-13 [12011129.001]
  • [Cites] Am J Obstet Gynecol. 2002 Oct;187(4):1070-80 [12389007.001]
  • [Cites] Med Inform Internet Med. 2002 Mar;27(1):33-8 [12509121.001]
  • [Cites] Pediatrics. 2003 Jun;111(6 Pt 1):1253-61 [12777538.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2004 Apr 1;58(5):1364-8 [15050311.001]
  • [Cites] J Clin Oncol. 2008 Sep 10;26(26):4340-6 [18779621.001]
  • [Cites] J Epidemiol Community Health. 2009 Jun;63(6):420-5 [19211588.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2009 Aug;18(8):2239-47 [19661083.001]
  • (PMID = 20054856.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA104666; United States / NCI NIH HHS / CA / 1 R01 CA104666
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS180547; NLM/ PMC2919618
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56. Goos M, Lange P, Hanisch UK, Prinz M, Scheffel J, Bergmann R, Ebert S, Nau R: Fibronectin is elevated in the cerebrospinal fluid of patients suffering from bacterial meningitis and enhances inflammation caused by bacterial products in primary mouse microglial cell cultures. J Neurochem; 2007 Sep;102(6):2049-60
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  • Fibronectin, an extracellular matrix protein, is considered a potent stimulator of the innate immune system through TLR4.
  • For this reason, we hypothesized that these molecules may jointly stimulate the innate immune system and increase neuronal damage in bacterial meningitis.
  • In primary cultures of mouse microglial cells, co-administration of fibronectin at concentrations occurring in the CSF in bacterial meningitis (10 microg/mL) with defined TLR agonists [lipopolysaccharide (TLR4), the synthetic lipopeptide tripalmytoyl-cysteinyl-seryl-(lysyl)3-lysine (TLR2) and single-stranded unmethylated cytosine-guanosine oligodesoxynucleotide (TLR9)] led to an additive release of nitric oxide and tumor necrosis factor-alpha when compared with the release elicited by either compound alone.
  • In conclusion, the inflammatory reaction to bacterial compounds can be aggravated by endogenous fibronectin at elevated levels during bacterial CNS infections.
  • [MeSH-minor] Adult. Aged. Animals. Animals, Newborn. Cells, Cultured. Drug Synergism. Female. Humans. Immunity, Innate / immunology. Inflammation Mediators / pharmacology. Male. Mice. Mice, Inbred C57BL. Mice, Knockout. Middle Aged. Nerve Degeneration / immunology. Nerve Degeneration / microbiology. Nerve Degeneration / physiopathology. Nitric Oxide / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 17561936.001).
  • [ISSN] 0022-3042
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Fibronectins; 0 / Inflammation Mediators; 0 / Toll-Like Receptors; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide
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57. Alameda F, Lloreta J, Ariza A, Salido M, Espinet B, Baro T, Garcia-Fructoso G, Galito E, Munne A, Cruz Sanchez FF, Sole F, Serrano S: Primitive neuroectodermal tumor of the central nervous system with glial differentiation: a FISH study of an adult case. Clin Neuropathol; 2007 Jan-Feb;26(1):12-6
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  • [Title] Primitive neuroectodermal tumor of the central nervous system with glial differentiation: a FISH study of an adult case.
  • Primitive neuroectodermal tumors (PNETs) of the central nervous system (CNS), a rare occurrence in adults, may show glial differentiation and can be misinterpreted as pure astrocytic neoplasms.
  • Few fluorescence in situ hybridization (FISH) studies have been carried out on these tumors; isochromosome 17q was found to be the major chromosomal abnormality.
  • We present the case of an adult in which we performed a FISH study of both the glial and neuronal components.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Chromosomes, Human, Pair 17 / genetics. Neuroectodermal Tumors, Primitive / genetics. Neuroectodermal Tumors, Primitive / pathology. Trisomy / genetics
  • [MeSH-minor] Adult. Humans. In Situ Hybridization, Fluorescence. Male

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  • (PMID = 17290931.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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58. Gururangan S, Chi SN, Young Poussaint T, Onar-Thomas A, Gilbertson RJ, Vajapeyam S, Friedman HS, Packer RJ, Rood BN, Boyett JM, Kun LE: Lack of efficacy of bevacizumab plus irinotecan in children with recurrent malignant glioma and diffuse brainstem glioma: a Pediatric Brain Tumor Consortium study. J Clin Oncol; 2010 Jun 20;28(18):3069-75
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  • [Title] Lack of efficacy of bevacizumab plus irinotecan in children with recurrent malignant glioma and diffuse brainstem glioma: a Pediatric Brain Tumor Consortium study.
  • Toxicities related to BVZ included grade 1 to 3 fatigue in seven patients, grade 1 to 2 hypertension in seven patients, grade 1 CNS hemorrhage in four patients, and grade 4 CNS ischemia in two patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Brain Stem Neoplasms / drug therapy. Glioma / drug therapy. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adolescent. Adult. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Bevacizumab. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Child. Diffusion Magnetic Resonance Imaging. Humans. Phosphorylation. Survival Rate. Treatment Outcome. Vascular Endothelial Growth Factor Receptor-2 / metabolism. Young Adult

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  • [Cites] Clin Cancer Res. 2007 Feb 15;13(4):1253-9 [17317837.001]
  • [Cites] Cancer Cell. 2007 Jan;11(1):83-95 [17222792.001]
  • [Cites] Nat Rev Cancer. 2008 Apr;8(4):309-16 [18337733.001]
  • [Cites] Neuro Oncol. 2008 Aug;10(4):624-30 [18539884.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2008 Oct 1;72(2):383-9 [18793954.001]
  • [Cites] Pediatr Blood Cancer. 2008 Dec;51(6):806-11 [18802947.001]
  • [Cites] Clin Cancer Res. 2008 Oct 15;14(20):6371-5 [18927275.001]
  • [Cites] J Neurooncol. 2009 Feb;91(3):329-36 [18953493.001]
  • [Cites] J Clin Oncol. 2009 Feb 10;27(5):740-5 [19114704.001]
  • [Cites] J Clin Oncol. 2009 Oct 1;27(28):4733-40 [19720927.001]
  • [Cites] Cancer Res. 2000 Apr 1;60(7):1878-86 [10766175.001]
  • [Cites] Oncogene. 2000 Nov 20;19(49):5598-605 [11114740.001]
  • [Cites] Eur J Cancer. 2001 Nov;37(16):2064-72 [11597385.001]
  • [Cites] NMR Biomed. 2002 Feb;15(1):6-17 [11840548.001]
  • [Cites] J Neurooncol. 2002 Jul;58(3):237-53 [12187958.001]
  • [Cites] J Clin Oncol. 2002 Dec 15;20(24):4684-91 [12488414.001]
  • [Cites] J Clin Oncol. 2003 Sep 15;21(18):3542; author reply 3543 [12972536.001]
  • [Cites] N Engl J Med. 1971 Nov 18;285(21):1182-6 [4938153.001]
  • [Cites] J Natl Cancer Inst. 1990 Jan 3;82(1):4-6 [1688381.001]
  • [Cites] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840.001]
  • [Cites] Cancer. 1993 Jul 1;72(1):271-5 [8508417.001]
  • [Cites] J Clin Oncol. 1999 May;17(5):1516-25 [10334539.001]
  • [Cites] J Neurooncol. 1999 May;43(1):43-7 [10448870.001]
  • [Cites] Am J Health Syst Pharm. 2004 Nov 1;61(21 Suppl 5):S21-6 [15552623.001]
  • [Cites] J Natl Cancer Inst. 2005 Feb 2;97(3):172-87 [15687360.001]
  • [Cites] Neurol Res. 2005 Jun;27(4):371-7 [15949234.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2347-55 [15985545.001]
  • [Cites] Oncology. 2005;69 Suppl 3:25-33 [16301833.001]
  • [Cites] Cancer. 2006 Mar 15;106(6):1364-71 [16463390.001]
  • [Cites] Cancer Cell. 2007 Jan;11(1):69-82 [17222791.001]
  • [Cites] Cancer. 2007 Oct 1;110(7):1542-50 [17705175.001]
  • (PMID = 20479404.001).
  • [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 / NCRR NIH HHS / RR / M01 RR000188; United States / NCI NIH HHS / CA / U01 CA081457; United States / NCRR NIH HHS / RR / M01RR00188; United States / NCI NIH HHS / CA / U01CA81457
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0H43101T0J / irinotecan; 2S9ZZM9Q9V / Bevacizumab; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; XT3Z54Z28A / Camptothecin
  • [Other-IDs] NLM/ PMC2903337
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59. Sofo V, Salmeri FM, Di Bella P, Sessa E, D'Aleo G, Trimarchi G, Bramanti P: Short communication: impairment of membrane markers on peripheral blood mononuclear cells and imbalance of cytokine secretion in the pathogenesis of multiple sclerosis active phases. J Interferon Cytokine Res; 2005 Nov;25(11):661-5
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  • Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS).
  • In active disease, a transmigration of autoreactive T cells to myelin antigens recruited from the peripheral blood (PBMC) to the CNS occurs, and there these cells prolong their survival and contribute to the perpetuation of the inflammation.
  • The aim of this research is to study on PBMCs and in the serum of stable and active MS subjects (1) the behavior of the CD40/CD40L system and the consequent balance of Th1 and Th2 cytokines and (2) the apoptosis marker system CD95/CD95L and tumor necrosis factor (TNF)- binding receptors, TNFRI and TNFRII.
  • [MeSH-minor] Adult. Antigens, CD40 / biosynthesis. Antigens, CD95 / biosynthesis. Apoptosis. Cell Movement. Fas Ligand Protein. Female. Humans. Inflammation. Magnetic Resonance Imaging. Male. Membrane Glycoproteins / biosynthesis. Middle Aged. Myelin Sheath / chemistry. T-Lymphocytes / metabolism. Th1 Cells. Th2 Cells. Tumor Necrosis Factors / biosynthesis

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  • (PMID = 16318579.001).
  • [ISSN] 1079-9907
  • [Journal-full-title] Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
  • [ISO-abbreviation] J. Interferon Cytokine Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / Antigens, CD95; 0 / Cytokines; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Tumor Necrosis Factors
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60. Guan YG, Wang TH, Ni W, Li L, Lu YC, Gao ZY: [Distribution of Fas and FasL in the central nervous system of adult rhesus]. Sichuan Da Xue Xue Bao Yi Xue Ban; 2005 May;36(3):322-4
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  • [Title] [Distribution of Fas and FasL in the central nervous system of adult rhesus].
  • OBJECTIVE: To investigate the distribution of Fas and FasL in the CNS of adult rhesus.
  • CONCLUSION: The distribution profiles of Fas and FasL in various areas of CNS indicate that they may fill some roles in the immune and physical function of the aforesaid anatomic
  • [MeSH-major] Antigens, CD95 / metabolism. Brain Chemistry. Membrane Glycoproteins / metabolism. Tumor Necrosis Factors / metabolism

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  • (PMID = 15931857.001).
  • [ISSN] 1672-173X
  • [Journal-full-title] Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition
  • [ISO-abbreviation] Sichuan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Tumor Necrosis Factors
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61. Iwamoto FM, Lamborn KR, Robins HI, Mehta MP, Chang SM, Butowski NA, Deangelis LM, Abrey LE, Zhang WT, Prados MD, Fine HA: Phase II trial of pazopanib (GW786034), an oral multi-targeted angiogenesis inhibitor, for adults with recurrent glioblastoma (North American Brain Tumor Consortium Study 06-02). Neuro Oncol; 2010 Aug;12(8):855-61
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  • [Title] Phase II trial of pazopanib (GW786034), an oral multi-targeted angiogenesis inhibitor, for adults with recurrent glioblastoma (North American Brain Tumor Consortium Study 06-02).
  • Grade 3/4 toxicities included leukopenia (n = 1), lymphopenia (n = 2), thrombocytopenia (n = 1), ALT elevation (n = 3), AST elevation (n = 1), CNS hemorrhage (n = 1), fatigue (n = 1), and thrombotic/embolic events (n = 3); 8 patients required dose reduction.
  • Two patients had a partial radiographic response by standard bidimensional measurements, whereas 9 patients (6 at the 8-week point and 3 only within the first month of treatment) had decreased contrast enhancement, vasogenic edema, and mass effect but <50% reduction in tumor.
  • [MeSH-major] Angiogenesis Inhibitors / administration & dosage. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Neoplasm Recurrence, Local / drug therapy. Pyrimidines / administration & dosage. Sulfonamides / administration & dosage
  • [MeSH-minor] Administration, Oral. Adult. Aged. Disease Progression. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neovascularization, Pathologic / drug therapy. Treatment Outcome

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  • [Cites] J Clin Oncol. 1999 Aug;17(8):2572-8 [10561324.001]
  • [Cites] J Clin Oncol. 2009 Oct 1;27(28):4733-40 [19720927.001]
  • [Cites] Am J Pathol. 2003 Apr;162(4):1083-93 [12651601.001]
  • [Cites] Clin Cancer Res. 2003 Apr;9(4):1399-405 [12684411.001]
  • [Cites] J Clin Invest. 2003 May;111(9):1287-95 [12727920.001]
  • [Cites] J Neurosurg. 1977 Sep;47(3):329-35 [894339.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Oct;85(20):7748-52 [2845420.001]
  • [Cites] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840.001]
  • [Cites] Cancer Res. 1992 Jun 1;52(11):3213-9 [1317261.001]
  • [Cites] Nature. 1992 Oct 29;359(6398):845-8 [1279432.001]
  • [Cites] Science. 1998 Jan 23;279(5350):577-80 [9438854.001]
  • [Cites] Science. 2005 Jan 7;307(5706):58-62 [15637262.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] Cancer Res. 2005 Jul 1;65(13):5523-34 [15994924.001]
  • [Cites] Cancer Cell. 2006 Apr;9(4):287-300 [16616334.001]
  • [Cites] Cancer Cell. 2006 May;9(5):391-403 [16697959.001]
  • [Cites] Clin Cancer Res. 2006 Aug 15;12(16):4899-907 [16914578.001]
  • [Cites] N Engl J Med. 2007 Jan 11;356(2):115-24 [17215529.001]
  • [Cites] Cancer Cell. 2007 Jan;11(1):83-95 [17222792.001]
  • [Cites] Cell Oncol. 2007;29(5):399-408 [17726262.001]
  • [Cites] Neuro Oncol. 2008 Apr;10(2):162-70 [18356283.001]
  • [Cites] N Engl J Med. 2008 Jul 31;359(5):492-507 [18669428.001]
  • [Cites] J Clin Oncol. 2008 Oct 1;26(28):4659-65 [18824712.001]
  • [Cites] Curr Opin Investig Drugs. 2008 Dec;9(12):1324-35 [19037839.001]
  • [Cites] J Clin Oncol. 2009 Feb 10;27(5):740-5 [19114704.001]
  • [Cites] Cancer Cell. 2009 Mar 3;15(3):220-31 [19249680.001]
  • [Cites] PLoS One. 2009;4(4):e5123 [19352490.001]
  • [Cites] J Clin Oncol. 2009 May 20;27(15):2542-52 [19332720.001]
  • [Cites] J Clin Oncol. 2009 Jul 1;27(19):3126-32 [19451427.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2009 Sep 1;75(1):156-63 [19167838.001]
  • [Cites] Neoplasia. 2000 Jul-Aug;2(4):306-14 [11005565.001]
  • (PMID = 20200024.001).
  • [ISSN] 1523-5866
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00459381
  • [Grant] United States / NCI NIH HHS / CA / U01 CA062421-12; United States / NCRR NIH HHS / RR / M01-RR00079; United States / NCI NIH HHS / CA / 5-U01CA62399-09; United States / NCI NIH HHS / CA / U01CA62421-08; United States / NCI NIH HHS / CA / CA62422; United States / NCI NIH HHS / CA / U01 CA062421; United States / NCRR NIH HHS / RR / M01RR03186; United States / NCI NIH HHS / CA / CA62399
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Pyrimidines; 0 / Sulfonamides; 7RN5DR86CK / pazopanib
  • [Other-IDs] NLM/ PMC2940686
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62. Marchi N, Angelov L, Masaryk T, Fazio V, Granata T, Hernandez N, Hallene K, Diglaw T, Franic L, Najm I, Janigro D: Seizure-promoting effect of blood-brain barrier disruption. Epilepsia; 2007 Apr;48(4):732-42
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  • PURPOSE: It is generally accepted that blood-brain barrier (BBB) failure occurs as a result of CNS diseases, including epilepsy.
  • The contribution of tumor or chemotherapy to acute seizures was therefore excluded.
  • Acute vascular failure is sufficient to cause seizures in the absence of CNS pathologies or chemotherapy.

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  • [Cites] Epilepsy Res. 1999 Dec;37(3):223-32 [10584972.001]
  • [Cites] J Thorac Cardiovasc Surg. 2005 Nov;130(5):1278-86 [16256779.001]
  • [Cites] J Child Neurol. 2002 Mar;17(3):227-30 [12026242.001]
  • [Cites] World J Surg. 2002 Oct;26(10):1251-5 [12205550.001]
  • [Cites] J Neurosci. 2003 Mar 1;23(5):1949-55 [12629200.001]
  • [Cites] Epilepsia. 2003;44 Suppl 10:11-7 [14511389.001]
  • [Cites] Restor Neurol Neurosci. 2003;21(3-4):109-21 [14530574.001]
  • [Cites] Clin Chem Lab Med. 2003 Oct;41(10):1320-2 [14580159.001]
  • [Cites] Cell Mol Life Sci. 2004 Feb;61(3):369-85 [14770299.001]
  • [Cites] Clin Chim Acta. 2004 Apr;342(1-2):1-12 [15026262.001]
  • [Cites] Ann Thorac Surg. 2004 Jul;78(1):46-52; discussion 52-3 [15223400.001]
  • [Cites] J Neurosci. 2004 Sep 8;24(36):7829-36 [15356194.001]
  • [Cites] Life Sci. 1980 Jul 21;27(3):239-43 [6772908.001]
  • [Cites] AJR Am J Roentgenol. 1983 Oct;141(4):829-35 [6412531.001]
  • [Cites] Ann Neurol. 1983 Sep;14(3):316-24 [6195955.001]
  • [Cites] Ann Neurol. 1987 Jan;21(1):59-63 [3493728.001]
  • [Cites] Cancer Chemother Pharmacol. 1990;25(5):320-5 [2306791.001]
  • [Cites] J Clin Oncol. 1991 Sep;9(9):1580-90 [1875220.001]
  • [Cites] AJNR Am J Neuroradiol. 1991 Sep-Oct;12(5):885-90 [1950917.001]
  • [Cites] N Engl J Med. 1993 Oct 7;329(15):1057-64 [8371727.001]
  • [Cites] J Neurotrauma. 1993 Winter;10(4):415-30 [8145265.001]
  • [Cites] AJNR Am J Neuroradiol. 1994 Mar;15(3):581-90 [8197962.001]
  • [Cites] J Comput Assist Tomogr. 1994 Sep-Oct;18(5):731-6 [8089321.001]
  • [Cites] Glia. 1998 Apr;22(4):390-400 [9517571.001]
  • [Cites] Neurosurgery. 1998 May;42(5):1083-99; discussion 1099-100 [9588554.001]
  • [Cites] Epilepsy Res. 1998 Sep;32(1-2):275-85 [9761327.001]
  • [Cites] Brain. 1949 Sep;72(3):373-81, 3 pl [15409268.001]
  • [Cites] Rocz Akad Med Bialymst. 2004;49 Suppl 1:236-8 [15638435.001]
  • [Cites] Epilepsia. 2005 Jan;46(1):84-90 [15660772.001]
  • [Cites] J Clin Neurophysiol. 2005 Jan-Feb;22(1):1-9 [15689708.001]
  • [Cites] Ann Neurol. 2005 Mar;57(3):310-26 [15732097.001]
  • [Cites] J Neurophysiol. 2005 Aug;94(2):907-18 [15728766.001]
  • [Cites] Cancer. 2005 Aug 15;104(4):817-24 [15971200.001]
  • [Cites] Am J Hematol. 2005 Sep;80(1):35-7 [16138356.001]
  • [Cites] Brain Res. 2002 Jun 14;940(1-2):102-4 [12020881.001]
  • (PMID = 17319915.001).
  • [ISSN] 0013-9580
  • [Journal-full-title] Epilepsia
  • [ISO-abbreviation] Epilepsia
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS38195; United States / NINDS NIH HHS / NS / NS43284; United States / NINDS NIH HHS / NS / R01 NS046513; United States / NINDS NIH HHS / NS / NS46513; United States / NINDS NIH HHS / NS / R01 NS043284; United States / NHLBI NIH HHS / HL / HL51614; United States / NHLBI NIH HHS / HL / R01 HL051614; United States / NINDS NIH HHS / NS / NS049514; United States / NINDS NIH HHS / NS / R01 NS049514; United States / NINDS NIH HHS / NS / R01 NS038195
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers; 0 / S100 Proteins; 3OWL53L36A / Mannitol; YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ NIHMS608611; NLM/ PMC4135474
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63. Schuhmann MU, Zucht HD, Nassimi R, Heine G, Schneekloth CG, Stuerenburg HJ, Selle H: Peptide screening of cerebrospinal fluid in patients with glioblastoma multiforme. Eur J Surg Oncol; 2010 Feb;36(2):201-7
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  • CONCLUSION: The study showed that peptidomics technology is able to identify possible biomarkers of neoplastic CNS disease.
  • [MeSH-major] Biomarkers, Tumor / cerebrospinal fluid. Glioblastoma / cerebrospinal fluid. Peptides / cerebrospinal fluid. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Supratentorial Neoplasms / cerebrospinal fluid
  • [MeSH-minor] Adult. Aged. Albumins / cerebrospinal fluid. Chromatography, High Pressure Liquid. Female. Humans. Male. Middle Aged. Osteopontin / cerebrospinal fluid. Peptide Fragments. Prealbumin / cerebrospinal fluid. Proteomics / methods. alpha 1-Antichymotrypsin / cerebrospinal fluid

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19674866.001).
  • [ISSN] 1532-2157
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Albumins; 0 / Biomarkers, Tumor; 0 / Peptide Fragments; 0 / Peptides; 0 / Prealbumin; 0 / alpha 1-Antichymotrypsin; 106441-73-0 / Osteopontin
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64. Hoffman S, Propp JM, McCarthy BJ: Temporal trends in incidence of primary brain tumors in the United States, 1985-1999. Neuro Oncol; 2006 Jan;8(1):27-37
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  • [Title] Temporal trends in incidence of primary brain tumors in the United States, 1985-1999.
  • A number of reports have indicated an increasing incidence of primary brain tumors over the past few decades.
  • The purpose of this study was to describe incidence rate trends in a population-based series of newly diagnosed primary nonmalignant and malignant brain and other CNS tumors, contributing five additional years to previously published incidence trends.
  • Data for the years 1985 through 1999 from six collaborating state cancer registries of the Central Brain Tumor Registry of the United States were used to determine incidence trends in the broad age groups 0-19, 20-64, and >or=65 years, overall and for selected histologies.
  • Specific histologies that were increasing included anaplastic astrocytomas in individuals aged >or=65 years, microscopically confirmed gliomas in both adult age groups, and microscopically confirmed glioma, not otherwise specified (NOS), in children.
  • Increases that were not specific to any population subgroup were seen for oligodendrogliomas, ependymomas, meningiomas, and nerve sheath tumors.
  • Decreases were noted for astrocytoma, NOS, nonmicroscopically confirmed gliomas, and pituitary tumors.
  • However, increases in meningiomas and nerve sheath tumors deserve further attention.
  • [MeSH-major] Brain Neoplasms / epidemiology
  • [MeSH-minor] Adult. Aged. Child. Child, Preschool. Female. Humans. Incidence. Infant. Infant, Newborn. Male. Middle Aged. Registries

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  • [Cites] Neuroepidemiology. 2004 May-Jun;23(3):101-9 [15084778.001]
  • [Cites] Neuro Oncol. 2006 Jan;8(1):1-11 [16443943.001]
  • [Cites] N Engl J Med. 1985 Oct 3;313(14):859-64 [3897866.001]
  • [Cites] AJR Am J Roentgenol. 1986 Sep;147(3):453-5 [3488645.001]
  • [Cites] J Natl Cancer Inst. 1990 Oct 17;82(20):1621-4 [2213902.001]
  • [Cites] Am J Ind Med. 1991;19(4):421-31 [2035544.001]
  • [Cites] CMAJ. 1991 Dec 15;145(12):1583-91 [1742695.001]
  • [Cites] J Natl Cancer Inst. 1991 Nov 20;83(22):1679-81 [1749021.001]
  • [Cites] Cancer. 1992 Mar 1;69(5):1300-6 [1739929.001]
  • [Cites] J Natl Cancer Inst. 1992 Mar 18;84(6):442-5 [1538422.001]
  • [Cites] Neurosurgery. 1992 Jul;31(1):78-82 [1641113.001]
  • [Cites] Brain Pathol. 1993 Jul;3(3):255-68 [8293185.001]
  • [Cites] Br J Cancer. 1994 Nov;70(5):973-9 [7947107.001]
  • [Cites] Cancer. 1995 Jan 1;75(1 Suppl):330-7 [8001004.001]
  • [Cites] Ann Neurol. 1995 Jan;37(1):67-73 [7818260.001]
  • [Cites] Eur J Cancer. 1994;30A(10):1498-511 [7833109.001]
  • [Cites] IARC Sci Publ. 1994;(128):1-302 [7698823.001]
  • [Cites] Cancer. 1995 Nov 1;76(9):1634-42 [8635069.001]
  • [Cites] Cancer. 1996 Aug 1;78(3):532-41 [8697401.001]
  • [Cites] Paediatr Perinat Epidemiol. 1996 Jul;10(3):319-38 [8822774.001]
  • [Cites] Int J Epidemiol. 1995 Dec;24(6):1078-85 [8824847.001]
  • [Cites] Stat Med. 2000 Feb 15;19(3):335-51 [10649300.001]
  • [Cites] Cancer. 2000 May 15;88(10):2342-9 [10820357.001]
  • [Cites] N Engl J Med. 2001 Jan 11;344(2):79-86 [11150357.001]
  • [Cites] J Neuropathol Exp Neurol. 2001 Mar;60(3):248-62 [11245209.001]
  • [Cites] Neuro Oncol. 2001 Jul;3(3):141-51 [11465394.001]
  • [Cites] Neuro Oncol. 1999 Jan;1(1):14-25 [11554386.001]
  • [Cites] Brain Pathol. 2002 Apr;12(2):257-9 [11958379.001]
  • [Cites] Neurology. 2002 Apr 23;58(8):1304-6 [11971109.001]
  • [Cites] Cancer. 2002 Jul 1;95(1):193-202 [12115333.001]
  • [Cites] J Neurooncol. 2002 Oct;60(1):61-9 [12416547.001]
  • [Cites] J Neuropathol Exp Neurol. 2003 Feb;62(2):111-26 [12578221.001]
  • [Cites] Neuroepidemiology. 2003 Mar-Apr;22(2):124-9 [12629278.001]
  • [Cites] Int J Cancer. 2004 Jan 20;108(3):450-5 [14648713.001]
  • [Cites] Neuroepidemiology. 2004 Jan-Apr;23(1-2):85-93 [14739573.001]
  • [Cites] Am J Epidemiol. 2004 Feb 1;159(3):277-83 [14742288.001]
  • [Cites] Cancer. 1997 Apr 1;79(7):1381-93 [9083161.001]
  • [Cites] J Natl Cancer Inst. 1998 Sep 2;90(17):1269-77 [9731733.001]
  • [Cites] J Natl Cancer Inst. 1999 Apr 7;91(7):648-9 [10203289.001]
  • [Cites] AIDS. 1999 Jan 14;13(1):103-8 [10207551.001]
  • [Cites] Cancer. 1999 May 1;85(9):2077-90 [10223251.001]
  • [Cites] J Natl Cancer Inst. 1999 Jun 2;91(11):973-4 [10359552.001]
  • [Cites] J Natl Cancer Inst. 1999 Aug 18;91(16):1382-90 [10451443.001]
  • [Cites] Neurology. 1999 Sep 22;53(5):1141-3 [10496285.001]
  • [Cites] Cancer. 2004 Nov 15;101(10):2293-9 [15476282.001]
  • [Cites] Epidemiology. 2004 Nov;15(6):653-9 [15475713.001]
  • (PMID = 16443945.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1871920
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65. Nuttall RK, Silva C, Hader W, Bar-Or A, Patel KD, Edwards DR, Yong VW: Metalloproteinases are enriched in microglia compared with leukocytes and they regulate cytokine levels in activated microglia. Glia; 2007 Apr 01;55(5):516-26
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  • Microglia are resident immune cells within the central nervous system (CNS).
  • Also elevated in CNS injuries are proteases, including matrix metalloproteinases (MMPs) and A disintegrin and metalloproteinases (ADAMs).
  • The spectrum of metalloproteinase members expressed by microglia and by the systemic leukocytes that infiltrate the injured CNS is unknown, as are their functions.
  • Activation of microglia also resulted in increased levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-10 protein in the conditioned media of cells.
  • The results have implications for the regulation of neuroinflammation and its outcomes following CNS injuries.
  • [MeSH-minor] Adult. Cells, Cultured. Central Nervous System / injuries. Humans. Inflammation. Interleukin-10 / immunology. Interleukin-10 / metabolism. Interleukin-1beta / immunology. Interleukin-1beta / metabolism. Lipopolysaccharides / immunology. RNA / analysis. RNA, Messenger / analysis. Tumor Necrosis Factor-alpha / immunology. Tumor Necrosis Factor-alpha / metabolism. Up-Regulation / physiology

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17216595.001).
  • [ISSN] 0894-1491
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0100250
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-1beta; 0 / Lipopolysaccharides; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 63231-63-0 / RNA; EC 3.4.- / Metalloproteases; EC 3.4.24.- / ADAM Proteins
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66. Wadasadawala T, Trivedi S, Gupta T, Epari S, Jalali R: The diagnostic dilemma of primary central nervous system melanoma. J Clin Neurosci; 2010 Aug;17(8):1014-1017
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  • [Title] The diagnostic dilemma of primary central nervous system melanoma.
  • Melanomas are malignant neoplasms of melanocytes developing predominantly in the skin, but occasionally arising from eyes, mucous membranes, and the central nervous system (CNS).
  • The CNS can be affected by a spectrum of melanocytic lesions ranging from diffuse neurocutaneous melanosis, to a focal and benign neoplasm (melanocytoma), and to an overtly malignant tumor (melanoma).
  • Primary melanocytic lesions involving the CNS are typically concentrated in the perimedullary and high cervical region.
  • Primary CNS melanoma cannot be reliably distinguished from metastatic melanoma on neuroimaging and histopathological characteristics alone: its diagnosis is established only after exclusion of secondary metastatic disease from a cutaneous, mucosal or retinal primary.
  • We present two patients with primary CNS melanoma and discuss relevant issues, available treatment options, and expected outcomes.
  • Awareness of disease spectrum and clinico-biological differences may be used to guide therapeutic decision-making for a patient with a proven or suspected primary CNS melanoma.
  • [MeSH-major] Brain Neoplasms / pathology. Cerebellopontine Angle / pathology. Melanoma / pathology. Parietal Lobe / pathology
  • [MeSH-minor] Humans. Image Processing, Computer-Assisted. Magnetic Resonance Imaging. Male. Prognosis. Young Adult

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  • (PMID = 20627582.001).
  • [ISSN] 1532-2653
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
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67. Khatua S, Dhall G, O'Neil S, Jubran R, Villablanca JG, Marachelian A, Nastia A, Lavey R, Olch AJ, Gonzalez I, Gilles F, Nelson M, Panigrahy A, McComb G, Krieger M, Fan J, Sposto R, Finlay JL: Treatment of primary CNS germinomatous germ cell tumors with chemotherapy prior to reduced dose whole ventricular and local boost irradiation. Pediatr Blood Cancer; 2010 Jul 15;55(1):42-6
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  • [Title] Treatment of primary CNS germinomatous germ cell tumors with chemotherapy prior to reduced dose whole ventricular and local boost irradiation.
  • BACKGROUND: The purpose of this study was to evaluate a reduced irradiation dose strategy for newly diagnosed primary central nervous system (CNS) germinomas.
  • Initial tumor markers for beta-human chorionic gonadotrophin (HCGbeta) and alpha-fetoprotein (AFP) were evaluated in serum and lumbar cerebrospinal fluid (CSF).
  • RESULTS: Eighteen of 20 patients are without evidence of residual or recurrent tumor.
  • Both relapsing patients were subsequently determined to harbor malignant non-germinomatous germ cell tumor (NGGCT).
  • CONCLUSION: Chemotherapy followed by reduced dose whole ventricular and local boost irradiation appears to be effective in patients with localized pure CNS germinoma with evidence of preservation of neurocognitive function.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / therapy. Central Nervous System Neoplasms / therapy. Germinoma / therapy. Neoplasms, Germ Cell and Embryonal / therapy
  • [MeSH-minor] Adolescent. Adult. Carboplatin / adverse effects. Carboplatin / therapeutic use. Child. Child, Preschool. Chorionic Gonadotropin, beta Subunit, Human / blood. Combined Modality Therapy. Dose-Response Relationship, Radiation. Etoposide / adverse effects. Etoposide / therapeutic use. Female. Humans. Infant. Magnetic Resonance Imaging. Male. Retrospective Studies. Young Adult. alpha-Fetoproteins / analysis

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  • (PMID = 20222020.001).
  • [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 / Chorionic Gonadotropin, beta Subunit, Human; 0 / alpha-Fetoproteins; 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin
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68. Hosono A, Makimoto A, Kawai A, Takaue Y: Segregated graft-versus-tumor effect between CNS and non-CNS lesions of Ewing's sarcoma family of tumors. Bone Marrow Transplant; 2008 Jun;41(12):1067-8
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  • [Title] Segregated graft-versus-tumor effect between CNS and non-CNS lesions of Ewing's sarcoma family of tumors.
  • [MeSH-major] Central Nervous System Neoplasms / secondary. Graft vs Tumor Effect. Hematopoietic Stem Cell Transplantation / methods. Neoplasm Recurrence, Local / therapy. Sarcoma, Ewing / therapy
  • [MeSH-minor] Adult. Female. Humans. Siblings. Transplantation, Homologous

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  • (PMID = 18332914.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
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69. Voloschin AD, Betensky R, Wen PY, Hochberg F, Batchelor T: Topotecan as salvage therapy for relapsed or refractory primary central nervous system lymphoma. J Neurooncol; 2008 Jan;86(2):211-5
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  • [Title] Topotecan as salvage therapy for relapsed or refractory primary central nervous system lymphoma.
  • Treatment for patients with refractory or relapsed primary CNS lymphoma (PCNSL) remains unsatisfactory.
  • All 15 patients had measurable, contrast-enhancing tumor on cranial MRI at the time of relapse.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Lymphoma, Non-Hodgkin / drug therapy. Neoplasm Recurrence, Local / drug therapy. Salvage Therapy. Topotecan / therapeutic use
  • [MeSH-minor] Adult. Aged. Disease-Free Survival. Enzyme Inhibitors / therapeutic use. Female. Humans. Male. Middle Aged. Prospective Studies. Treatment Outcome


70. Nicoletti F, Arcella A, Iacovelli L, Battaglia G, Giangaspero F, Melchiorri D: Metabotropic glutamate receptors: new targets for the control of tumor growth? Trends Pharmacol Sci; 2007 May;28(5):206-13
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  • [Title] Metabotropic glutamate receptors: new targets for the control of tumor growth?
  • Cancer stem cells are currently a target for the treatment of malignant tumors.
  • Transformed neural stem-progenitor cells of the brain subventricular zone and the external granular layer of the cerebellum are the putative cells of origin of malignant gliomas and medulloblastomas, which are the most frequent malignant brain tumors in adults and children, respectively.
  • The proliferation of neural stem-progenitor cells is regulated by metabotropic glutamate (mGlu) receptors, which are G-protein-coupled receptors that are activated by glutamate, the major excitatory neurotransmitter of the CNS.
  • At least two receptor subtypes - mGlu(3) and mGlu(4) receptors - control the proliferation of brain tumor cells, whereas mGlu(1) receptors have been implicated in the development of melanomas.
  • We believe that individual mGlu receptor subtypes represent new potential targets for the treatment of several malignant tumors, including brain tumors.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Brain Neoplasms / drug therapy. Drug Delivery Systems. Receptors, Metabotropic Glutamate / drug effects
  • [MeSH-minor] Adult. Animals. Cell Proliferation. Child. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / physiopathology. Drug Resistance, Neoplasm. Gene Expression. Humans. Ligands. Melanoma / drug therapy. Melanoma / physiopathology. Neoplastic Stem Cells / drug effects. Skin Neoplasms / drug therapy. Skin Neoplasms / physiopathology

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  • (PMID = 17433452.001).
  • [ISSN] 0165-6147
  • [Journal-full-title] Trends in pharmacological sciences
  • [ISO-abbreviation] Trends Pharmacol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ligands; 0 / Receptors, Metabotropic Glutamate
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71. Mao XC, Su ZP, Yu WQ, Zheng WM, Zeng YJ: Familial and genetic researches on three Chinese families with von Hippel-Lindau disease. Neurol Res; 2009 Sep;31(7):743-7
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  • OBJECTIVE: Hemangioblastoma of the central nervous system (CNS) occur as sporadic tumors or as a part of von Hippel-Lindau (VHL) disease, an autosomal dominant hereditary tumor syndrome caused by germline mutation of the VHL tumor suppressor gene.
  • Twenty VHL disease patients in the three families have the most common manifestation of CNS hemangioblastoma.
  • The CNS hemangioblastoma is the early manifestation in VHL disease.
  • It is recommended that every patient with CNS hemangioblastoma should be screened for VHL gene mutation.
  • [MeSH-major] Genetic Predisposition to Disease. Mutation / genetics. Von Hippel-Lindau Tumor Suppressor Protein / genetics. von Hippel-Lindau Disease / genetics
  • [MeSH-minor] Adolescent. Adult. Asian Continental Ancestry Group / ethnology. Brain Neoplasms / etiology. Brain Neoplasms / genetics. DNA Mutational Analysis. Female. Genetic Testing. Genotype. Hemangioblastoma / etiology. Hemangioblastoma / genetics. Humans. Male. Middle Aged. Phenotype. Retrospective Studies. Severity of Illness Index. Young Adult

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  • (PMID = 19133167.001).
  • [ISSN] 0161-6412
  • [Journal-full-title] Neurological research
  • [ISO-abbreviation] Neurol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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72. 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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  • Multiple primary tumors in the central nervous system of different histological cell types are uncommon.
  • 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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73. Varghese M, Olstorn H, Berg-Johnsen J, Moe MC, Murrell W, Langmoen IA: Isolation of human multipotent neural progenitors from adult filum terminale. Stem Cells Dev; 2009 May;18(4):603-13
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  • [Title] Isolation of human multipotent neural progenitors from adult filum terminale.
  • Stem cells have been isolated from several CNS regions, including the spinal cord.
  • We show for the first time that progenitor cells exhibiting the hallmarks of stem cells can be isolated from adult human filum terminale (FTNPs).
  • Significantly, no tumor formation or aberrant cell morphology was seen in or adjacent to the graft area.
  • Thus, filum terminale provides a novel source of adult human neural progenitor cells that develop into functional neurons with possible clinical applications.
  • [MeSH-minor] Adult. Animals. Biopsy. Cell Differentiation / physiology. Cell Proliferation. Cells, Cultured. Child. Humans. Membrane Potentials / physiology. Middle Aged. Patch-Clamp Techniques. Rats. Stem Cell Transplantation. Young Adult

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  • (PMID = 18652547.001).
  • [ISSN] 1557-8534
  • [Journal-full-title] Stem cells and development
  • [ISO-abbreviation] Stem Cells Dev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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74. Woessmann W, Seidemann K, Mann G, Zimmermann M, Burkhardt B, Oschlies I, Ludwig WD, Klingebiel T, Graf N, Gruhn B, Juergens H, Niggli F, Parwaresch R, Gadner H, Riehm H, Schrappe M, Reiter A, BFM Group: The impact of the methotrexate administration schedule and dose in the treatment of children and adolescents with B-cell neoplasms: a report of the BFM Group Study NHL-BFM95. Blood; 2005 Feb 1;105(3):948-58
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  • [Title] The impact of the methotrexate administration schedule and dose in the treatment of children and adolescents with B-cell neoplasms: a report of the BFM Group Study NHL-BFM95.
  • In the Non-Hodgkin Lymphoma-Berlin-Frankfurt-Münster 95 (NHL-BFM95) study, we tested by randomization whether for patients with B-cell neoplasms methotrexate as intravenous infusion over 4 hours (MTX-4h) is not inferior to, but less toxic than, a 24-hour intravenous infusion (MTX-24h).
  • Second, we investigated against the historical control of study NHL-BFM90, whether for patients with moderate tumor mass MTX can be reduced from 5 g/m(2) to 1 g/m(2).
  • Patients received 2 5-day therapy courses in risk group R1 (resected), 4 in R2 (lactate dehydrogenase [LDH] < 500 U/L), 5 in R3 (LDH > 500 to < 1000 U/L) and 6 in R4 (LDH > 1000 U/L and/or central nervous system [CNS] disease).
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease-Free Survival. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Infant. Male. Survival Analysis. Time Factors

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  • (PMID = 15486066.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] YL5FZ2Y5U1 / Methotrexate
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75. Kim YJ, Kim YS, Kim MS, Ryu JC: The inhibitory mechanism of methylmercury on differentiation of human neuroblastoma cells. Toxicology; 2007 May 5;234(1-2):1-9
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  • Methylmercury (MeHg) is a ubiquitous environmental toxicant and shows neurotoxicity to central nerve system (CNS) or neuronal cells.
  • It has been known that MeHg has more influence to developing or differentiating CNS/neuronal cells than adult or differentiated CNS/neuronal cells.
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Cell Survival / drug effects. Comet Assay. DNA Damage. Dose-Response Relationship, Drug. Drug Synergism. Flavonoids / pharmacology. Flow Cytometry. Humans. Indoles / pharmacology. Interphase / drug effects. Maleimides / pharmacology. Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 3 / metabolism. Neuroblastoma / genetics. Neuroblastoma / metabolism. Neuroblastoma / pathology. Phosphorylation / drug effects. Protein Kinase C-alpha / antagonists & inhibitors. Protein Kinase C-alpha / metabolism. Time Factors. Tretinoin / pharmacology

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  • (PMID = 17350151.001).
  • [ISSN] 0300-483X
  • [Journal-full-title] Toxicology
  • [ISO-abbreviation] Toxicology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Flavonoids; 0 / Indoles; 0 / Maleimides; 0 / Methylmercury Compounds; 133052-90-1 / bisindolylmaleimide I; 5688UTC01R / Tretinoin; EC 2.7.11.13 / Protein Kinase C-alpha; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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76. Hurst LA, Bunning RA, Couraud PO, Romero IA, Weksler BB, Sharrack B, Woodroofe MN: Expression of ADAM-17, TIMP-3 and fractalkine in the human adult brain endothelial cell line, hCMEC/D3, following pro-inflammatory cytokine treatment. J Neuroimmunol; 2009 May 29;210(1-2):108-12
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  • [Title] Expression of ADAM-17, TIMP-3 and fractalkine in the human adult brain endothelial cell line, hCMEC/D3, following pro-inflammatory cytokine treatment.
  • ADAM-17 expression is localised to endothelial cells in the human central nervous system (CNS) and is increased in multiple sclerosis (MS) white matter, suggesting a role in MS pathogenesis.
  • Fractalkine shedding may regulate immune cell trafficking into the CNS, however, this does not appear to be directly controlled by ADAM-17 activity.
  • [MeSH-minor] Cell Line. Chemotaxis, Leukocyte / immunology. Encephalitis / immunology. Encephalitis / metabolism. Encephalitis / physiopathology. Gene Expression / drug effects. Gene Expression / physiology. Humans. RNA, Messenger / analysis. RNA, Messenger / drug effects. RNA, Messenger / metabolism. Tissue Inhibitor of Metalloproteinase-3 / genetics. Tissue Inhibitor of Metalloproteinase-3 / metabolism. Tumor Necrosis Factor-alpha / metabolism. Tumor Necrosis Factor-alpha / pharmacology. Up-Regulation / drug effects. Up-Regulation / immunology

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  • (PMID = 19324423.001).
  • [ISSN] 1872-8421
  • [Journal-full-title] Journal of neuroimmunology
  • [ISO-abbreviation] J. Neuroimmunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / CX3CL1 protein, human; 0 / Chemokine CX3CL1; 0 / Cytokines; 0 / RNA, Messenger; 0 / Tissue Inhibitor of Metalloproteinase-3; 0 / Tumor Necrosis Factor-alpha; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase
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77. Katz J, Keenan B, Snyder EY: Culture and manipulation of neural stem cells. Adv Exp Med Biol; 2010;671:13-22
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  • Both murine and human neural stem cells (NSCs) have been shown to migrate through the central nervous system (CNS) and infiltrate tumors and other pathological disease states of the brain.
  • Genetic modification of NSCs to produce cytotoxic or immunomodulatory agents in the vicinity of a primary tumor and/or satellite lesion or has proven instrumental to the reduction of tumor bulk in murine models.
  • Although the use of stem cells proves to be a volatile social topic, scientists have discovered that NSCs are present in the adult brain and continue to propagate and differentiate.
  • These cells may be isolated and cultured to produce clonal NSC lines that are capable of self renewal and differentiation when introduced into the CNS.
  • In this chapter, we describe protocols currently used in ourlab for the successful maintenance of NSCs in vitro advancing the role of neural stem cells in the treatment of brain tumors.

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  • (PMID = 20455492.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Prodrugs
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78. Yamanaka R, Morii K, Shinbo Y, Takeuchi S, Tamura T, Hondoh H, Takahashi H, Onda K, Takahashi H, Tanaka R: Modified ProMACE-MOPP hybrid regimen with moderate-dose methotrexate for patients with primary CNS lymphoma. Ann Hematol; 2005 Jul;84(7):447-55
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  • [Title] Modified ProMACE-MOPP hybrid regimen with moderate-dose methotrexate for patients with primary CNS lymphoma.
  • The object of this study was to assess the estimation of 2- and 5-year overall survival and tumor response and the frequency and severity of treatment morbidity with a modified ProMACE-MOPP hybrid protocol in patients with primary CNS lymphoma (PCNSL).
  • Eighteen patients were followed up with neuroimaging and neuropsychological assessments for evidence of CNS toxicity.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Central Nervous System Neoplasms / therapy. Cranial Irradiation. Lymphoma / therapy. Methotrexate / administration & dosage
  • [MeSH-minor] Adult. Aged. Cyclophosphamide / administration & dosage. Cyclophosphamide / toxicity. Disease-Free Survival. Doxorubicin / administration & dosage. Doxorubicin / toxicity. Etoposide / administration & dosage. Etoposide / toxicity. Female. Humans. Leukopenia / chemically induced. Male. Mechlorethamine / administration & dosage. Mechlorethamine / toxicity. Middle Aged. Pneumonia / etiology. Pneumonia / mortality. Prednisone / administration & dosage. Prednisone / toxicity. Procarbazine / administration & dosage. Procarbazine / toxicity. Retrospective Studies. Sepsis / etiology. Sepsis / mortality. Vincristine / administration & dosage. Vincristine / toxicity

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  • (PMID = 15747120.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 35S93Y190K / Procarbazine; 50D9XSG0VR / Mechlorethamine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ProMACE-MOPP protocol
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79. Propp JM, McCarthy BJ, Davis FG, Preston-Martin S: Descriptive epidemiology of vestibular schwannomas. Neuro Oncol; 2006 Jan;8(1):1-11
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  • Vestibular schwannomas, commonly termed acoustic neuromas, arise from the vestibular branch of the eighth cranial nerve (acoustic nerve) and are benign, slow-growing brain tumors that negatively impact patient quality of life.
  • They are thought to account for the majority of intracranial nerve sheath tumors.
  • To describe incidence rate patterns and trends of primary nerve sheath tumors of the brain/CNS and the subset of vestibular schwannomas in two population-based incidence registries, data were obtained from 11 Central Brain Tumor Registry of the United States (CBTRUS) collaborating state registries and the Los Angeles County Cancer Surveillance Program (LACCSP) (1975-1998).
  • Multiplicative Poisson regression models were used to compare trends in primary nerve sheath tumors of the brain/CNS overall and in subgroups, including vestibular schwannomas, controlling for age, gender, race, microscopic confirmation, and region.
  • The overall incidence of primary nerve sheath tumors of the brain/CNS was 1.1 per 100,000 person-years (CBTRUS, 1995-1999 and LACCSP, 1995-1998).
  • Moreover, the incidence of primary nerve sheath tumors of the brain/CNS overall (CBTRUS, 1985-1999 and LACCSP, 1975-1998) and of vestibular schwannomas (CBTRUS, 1992-1999 and LACCSP, 1992-1998) increased over time.
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Male. Middle Aged

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  • [Cites] Am J Epidemiol. 1992 Jun 15;135(12):1349-57 [1510081.001]
  • [Cites] J Natl Cancer Inst. 1992 Mar 18;84(6):442-5 [1538422.001]
  • [Cites] Ann Neurol. 1995 Jan;37(1):67-73 [7818260.001]
  • [Cites] Laryngoscope. 1999 May;109(5):736-40 [10334223.001]
  • [Cites] Stat Med. 2000 Feb 15;19(3):335-51 [10649300.001]
  • [Cites] Am J Otol. 2000 Sep;21(5):690-4 [10993460.001]
  • [Cites] N Engl J Med. 2001 Jan 11;344(2):79-86 [11150357.001]
  • [Cites] J Natl Cancer Inst. 2001 Feb 7;93(3):203-7 [11158188.001]
  • [Cites] Neuro Oncol. 2001 Jul;3(3):141-51 [11465394.001]
  • [Cites] Neurology. 2002 Apr 23;58(8):1304-6 [11971109.001]
  • [Cites] Neuroepidemiology. 2003 Mar-Apr;22(2):124-9 [12629278.001]
  • [Cites] Am J Epidemiol. 2004 Feb 1;159(3):277-83 [14742288.001]
  • [Cites] J Toxicol Environ Health B Crit Rev. 2004 Sep-Oct;7(5):351-84 [15371240.001]
  • [Cites] Epidemiology. 2004 Nov;15(6):653-9 [15475713.001]
  • [Cites] Health Care Financ Rev. 1984 Winter;6(2):1-29 [10310949.001]
  • [Cites] N Engl J Med. 1988 Oct 20;319(16):1033-9 [3173432.001]
  • [Cites] Br J Cancer. 1989 May;59(5):783-6 [2736213.001]
  • [Cites] Neuroepidemiology. 1989;8(6):283-95 [2586698.001]
  • [Cites] Cancer. 1992 Mar 1;69(5):1300-6 [1739929.001]
  • [Cites] Brain Pathol. 1993 Jul;3(3):255-68 [8293185.001]
  • (PMID = 16443943.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1871924
  •  go-up   go-down


80. Kamoshima Y, Sawamura Y, Ikeda J, Shirato H, Aoyama H: Late recurrence and salvage therapy of CNS germinomas. J Neurooncol; 2008 Nov;90(2):205-11
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  • [Title] Late recurrence and salvage therapy of CNS germinomas.
  • Central nervous system (CNS) germinoma is a curable tumor and its recurrence rate after initial therapy may be approximately 10% or higher.
  • All patients had been tumor-free for at least 6 months after the initial treatment.
  • Seventeen patients (68%) were salvaged and were tumor-free at the final observation.
  • At first recurrence, 11 patients were treated using radiation therapy with or without surgery and 7 out of the 11 patients died due to the recurrent tumor.
  • On the other hand, 13 patients who received salvage chemotherapy and radiotherapy were tumor-free at the last follow-up.
  • In conclusion, late recurrence is not a rare event in patients with CNS germinoma.
  • [MeSH-major] Central Nervous System Neoplasms / prevention & control. Germinoma / prevention & control. Salvage Therapy / methods
  • [MeSH-minor] Adolescent. Adult. Child. Female. Follow-Up Studies. Humans. Male. Remission Induction. Retrospective Studies. Secondary Prevention. Time Factors. Young Adult

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  • [Cites] J Clin Oncol. 2006 Dec 10;24(35):5503-11 [17158535.001]
  • [Cites] J Neurosurg. 1998 Jan;88(1):66-72 [9420074.001]
  • [Cites] Int J Urol. 2005 Sep;12(9):855-8 [16201988.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1995 Jul 15;32(4):943-9 [7607968.001]
  • [Cites] J Clin Oncol. 2002 Feb 1;20(3):857-65 [11821471.001]
  • [Cites] Pediatr Blood Cancer. 2004 Aug;43(2):126-33 [15236278.001]
  • [Cites] J Neurosurg. 1997 Aug;87(2):262-6 [9254091.001]
  • [Cites] Cancer. 2006 Nov 1;107(9):2228-36 [17019739.001]
  • [Cites] J Urol. 2005 Mar;173(3):824-9 [15711278.001]
  • [Cites] J Clin Oncol. 1998 Jan;16(1):204-9 [9440744.001]
  • [Cites] J Clin Oncol. 2004 May 15;22(10):1934-43 [15143087.001]
  • [Cites] J Clin Oncol. 1999 Aug;17(8):2585-92 [10561326.001]
  • [Cites] Cancer. 1994 Aug 1;74(3):940-4 [8039122.001]
  • [Cites] Radiology. 2001 Feb;218(2):452-6 [11161161.001]
  • [Cites] Childs Nerv Syst. 2007 Oct;23(10):1155-61 [17610071.001]
  • [Cites] Br J Neurosurg. 1999 Aug;13(4):376-81 [10616563.001]
  • [Cites] Br J Cancer. 2006 Mar 27;94(6):820-7 [16508636.001]
  • [Cites] Cancer. 2002 Aug 1;95(3):520-30 [12209744.001]
  • [Cites] Eur J Cancer. 1998 Jan;34(1):104-10 [9624246.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2004 Sep 1;60(1):214-7 [15337558.001]
  • [Cites] Urol Int. 2004;73(1):84-6 [15263799.001]
  • [Cites] J Clin Oncol. 1996 Nov;14(11):2908-15 [8918487.001]
  • [Cites] Neurosurgery. 1999 Dec;45(6):1292-7; discussion 1297-8 [10598695.001]
  • [Cites] Acta Oncol. 2006;45(4):476-83 [16760185.001]
  • [Cites] J Pediatr Hematol Oncol. 2006 Jan;28(1):36-9 [16394891.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1988 Aug;15(2):291-7 [3403312.001]
  • [Cites] J Neurooncol. 2001 Sep;54(3):311-6 [11767296.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Mar 15;46(5):1171-6 [10725628.001]
  • [Cites] J Clin Oncol. 1999 Mar;17(3):933-40 [10071287.001]
  • [Cites] Am J Clin Oncol. 2007 Apr;30(2):205-10 [17414472.001]
  • [Cites] J Neurooncol. 2007 May;83(1):71-9 [17245622.001]
  • (PMID = 18604473.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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81. Yan H, Parsons DW, Jin G, McLendon R, Rasheed BA, Yuan W, Kos I, Batinic-Haberle I, Jones S, Riggins GJ, Friedman H, Friedman A, Reardon D, Herndon J, Kinzler KW, Velculescu VE, Vogelstein B, Bigner DD: IDH1 and IDH2 mutations in gliomas. N Engl J Med; 2009 Feb 19;360(8):765-73
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  • BACKGROUND: A recent genomewide mutational analysis of glioblastomas (World Health Organization [WHO] grade IV glioma) revealed somatic mutations of the isocitrate dehydrogenase 1 gene (IDH1) in a fraction of such tumors, most frequently in tumors that were known to have evolved from lower-grade gliomas (secondary glioblastomas).
  • METHODS: We determined the sequence of the IDH1 gene and the related IDH2 gene in 445 central nervous system (CNS) tumors and 494 non-CNS tumors.
  • Tumors without mutations in IDH1 often had mutations affecting the analogous amino acid (R172) of the IDH2 gene.
  • Tumors with IDH1 or IDH2 mutations had distinctive genetic and clinical characteristics, and patients with such tumors had a better outcome than those with wild-type IDH genes.

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  • [Copyright] 2009 Massachusetts Medical Society
  • [Cites] Cancer Res. 1996 Jan 1;56(1):150-3 [8548755.001]
  • [Cites] Oncogene. 1996 Sep 5;13(5):983-94 [8806688.001]
  • [Cites] Am J Pathol. 1994 Nov;145(5):1175-90 [7977648.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):2965-9 [1557402.001]
  • [Cites] Science. 1997 Mar 28;275(5308):1943-7 [9072974.001]
  • [Cites] Biochemistry. 1997 Nov 4;36(44):13743-7 [9354646.001]
  • [Cites] Am J Pathol. 1999 Aug;155(2):375-86 [10433931.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] Science. 2006 Oct 13;314(5797):268-74 [16959974.001]
  • [Cites] Am J Pathol. 2007 May;170(5):1445-53 [17456751.001]
  • [Cites] Genes Dev. 2007 Nov 1;21(21):2683-710 [17974913.001]
  • [Cites] Free Radic Res. 2008 Jul;42(7):618-24 [18608518.001]
  • [Cites] N Engl J Med. 2008 Jul 31;359(5):492-507 [18669428.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1807-12 [18772396.001]
  • [Cites] Nature. 2008 Oct 23;455(7216):1061-8 [18772890.001]
  • [Cites] Cancer Res. 2008 Nov 1;68(21):8673-7 [18974108.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):3089-94 [14970324.001]
  • [Cites] J Biol Chem. 2004 Aug 6;279(32):33946-57 [15173171.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):6892-9 [15466178.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Oct;84(19):6899-903 [3477813.001]
  • [Cites] Nature. 1989 Dec 7;342(6250):705-8 [2531845.001]
  • [CommentIn] N Engl J Med. 2009 May 21;360(21):2248; author reply 2249 [19458374.001]
  • [CommentIn] N Engl J Med. 2009 May 21;360(21):2248-9; author reply 2249 [19469031.001]
  • [CommentIn] N Engl J Med. 2009 Feb 19;360(8):813-5 [19228626.001]
  • (PMID = 19228619.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA043460-27; United States / NCI NIH HHS / CA / CA57345; United States / NCI NIH HHS / CA / R01CA118822; United States / NCI NIH HHS / CA / R37 CA043460; United States / NCI NIH HHS / CA / R37 CA043460-27; United States / NCI NIH HHS / CA / P50 CA108786; United States / NINDS NIH HHS / NS / P50 NS020023; United States / NCI NIH HHS / CA / 2P30-CA-14236; United States / NCI NIH HHS / CA / 5P50-CA-108786; United States / NCI NIH HHS / CA / CA121113; United States / NCI NIH HHS / CA / CA062924-150012; United States / NCI NIH HHS / CA / R37 CA043460-26; United States / NCI NIH HHS / CA / 5R37-CA-11898; United States / NCI NIH HHS / CA / R37CA11898-34; United States / NCI NIH HHS / CA / R01 CA121113; United States / NCI NIH HHS / CA / R01 CA140316; United States / NCI NIH HHS / CA / CA43460; United States / NCI NIH HHS / CA / CA043460-26; United States / NCI NIH HHS / CA / R01 CA121113-04; United States / NINDS NIH HHS / NS / NS20023-21; United States / NCI NIH HHS / CA / CA057345-17; United States / NCI NIH HHS / CA / R37 CA057345-17; United States / NCI NIH HHS / CA / R37 CA057345; United States / NCI NIH HHS / CA / P30 CA014236; United States / NCI NIH HHS / CA / P50 CA062924-150012; United States / NCI NIH HHS / CA / R01 CA057345; United States / NCI NIH HHS / CA / R01 CA118822; United States / NINDS NIH HHS / NS / 5P50-NS-20023; United States / NCI NIH HHS / CA / R37 CA011898
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human
  • [Other-IDs] NLM/ NIHMS107443; NLM/ PMC2820383
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82. Klosky JL, Tyc VL, Lawford J, Ashford J, Lensing S, Buscemi J: Predictors of non-participation in a randomized intervention trial to reduce environmental tobacco smoke (ETS) exposure in pediatric cancer patients. Pediatr Blood Cancer; 2009 May;52(5):644-9
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  • Medical features that significantly associated with study non-participation included CNS tumor diagnosis (P = 0.030), no history of chemotherapy (P = 0.012), history of surgery prior to study recruitment (P = 0.036), and having future radiation therapy planned post study recruitment (P = 0.009).
  • Multivariable logistic regression modeling revealed that study non-participation was associated with the primary caregiver being a smoker (OR = 6.48, P = 0.002) or female (OR = 8.56, P = 0.023), and patient CNS tumor diagnosis (OR = 4.63, P = 0.021).
  • [MeSH-major] Neoplasms. Patient Participation. Pediatrics. Randomized Controlled Trials as Topic. Tobacco Smoke Pollution / adverse effects
  • [MeSH-minor] Adult. Child. Female. Humans. Male

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • [Cites] Pediatrics. 2001 Mar;107(3):540-2 [11230596.001]
  • [Cites] Am J Public Health. 2005 Apr;95(4):652-9 [15798126.001]
  • [Cites] Pediatrics. 2002 Nov;110(5):946-56 [12415035.001]
  • [Cites] Pediatrics. 2003 Jan;111(1):140-5 [12509567.001]
  • [Cites] J Pediatr Psychol. 2003 Dec;28(8):519-28 [14602842.001]
  • [Cites] J Child Health Care. 2004 Dec;8(4):288-300 [15507466.001]
  • [Cites] Thorax. 1982 Mar;37(3):175-80 [6285541.001]
  • [Cites] N Engl J Med. 1990 Aug 9;323(6):378-82 [2370889.001]
  • [Cites] N Engl J Med. 1991 Mar 21;324(12):808-15 [1997853.001]
  • [Cites] N Engl J Med. 1991 Nov 7;325(19):1330-6 [1922234.001]
  • [Cites] Hematol Oncol Clin North Am. 1993 Apr;7(2):401-15 [8468273.001]
  • [Cites] Curr Probl Pediatr. 1993 Mar;23(3):102-31 [8513680.001]
  • [Cites] Health Psychol. 1993 Nov;12(6):443-50 [8293727.001]
  • [Cites] Pediatrics. 1996 Apr;97(4):560-8 [8632946.001]
  • [Cites] Pediatrics. 1998 Feb;101(2):E8 [9445518.001]
  • [Cites] BMJ. 1999 May 29;318(7196):1456-9 [10346773.001]
  • [Cites] Thorax. 1999 Apr;54(4):357-66 [10092699.001]
  • [Cites] Chest. 2001 Nov;120(5):1709-22 [11713157.001]
  • (PMID = 19156856.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA085406; United States / NCI NIH HHS / CA / R01 CA085406-05
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tobacco Smoke Pollution
  • [Other-IDs] NLM/ NIHMS124032; NLM/ PMC2733242
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83. Gabrovski N, Poptodorov G, Velinov N, Gabrovski S: [Late metastases from breast cancer--report of two cases]. Khirurgiia (Sofiia); 2010;(1):62-6
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  • Due to complain of headache and nausea CT scan was performed showing a tumor lesion in the right frontal lobe.
  • Metastasis in CNS should be taken into consideration in patients treated for breast cancer no matter the time from the initial diagnosis when clinical symptoms appear.
  • [MeSH-major] Brain / pathology. Brain / surgery. Brain Neoplasms / secondary. Brain Neoplasms / surgery. Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / pathology
  • [MeSH-minor] Adult. Breast / pathology. Breast / surgery. Female. Follow-Up Studies. Humans. Mastectomy. Middle Aged


84. Schittenhelm J, Thiericke J, Nagel C, Meyermann R, Beschorner R: WT1 expression in normal and neoplastic cranial and peripheral nerves is independent of grade of malignancy. Cancer Biomark; 2010;7(2):73-7
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  • OBJECTIVE: Wilms' tumor protein (WT1) expression is usually absent in normal glial cells of the CNS but is highly upregulated in brain tumor cells and its expression correlates with tumor grade.
  • However, knowledge on WT1 expression in tumors of the peripheral nerve system (PNS) is limited.
  • METHODS: We analyze the immunohistochemical expression of WT1 in 101 samples consisting of 13 normal nerves, 10 neurofibromas, 69 schwannomas and 9 malignant peripheral nerve sheath tumors (MPNST).
  • Tumor samples included 14 specimen from patients with a proven neurocutaneous disorder (neurofibromatosis type 1 and 2) and 3 cases of schwannomatosis.
  • In 50 vestibular schwannomas tumor growth extension was correlated to WT1 expression.
  • In peripheral nerve sheath tumors, cytoplasmic WT1 protein is expressed in the cytoplasm of the neoplastic cells in all tumors, including MPNST, neurofibromas and schwannomas.
  • The WT1 expression is independent of tumor malignancy or tumor growth extension and is not associated with a neurocutaneous disorder.
  • CONCLUSION: WT1 expression in normal and neoplastic tissue differs in the peripheral and the central nervous system.
  • These findings may point to a different functional role of WT1 in the PNS and the CNS.
  • [MeSH-major] Cranial Nerve Neoplasms / metabolism. Cranial Nerves / metabolism. Nerve Sheath Neoplasms / metabolism. Peripheral Nerves / metabolism. WT1 Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Case-Control Studies. Child. Female. Humans. Male. Middle Aged. Neurilemmoma / metabolism. Neurofibroma / metabolism. Young Adult

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  • (PMID = 21178265.001).
  • [ISSN] 1875-8592
  • [Journal-full-title] Cancer biomarkers : section A of Disease markers
  • [ISO-abbreviation] Cancer Biomark
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / WT1 Proteins
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85. Olszanecka-Glinianowicz M, Zahorska-Markiewicz B, Kocełak P, Janowska J, Semik-Grabarczyk E, Wikarek T, Gruszka W, Dabrowski P: Is chronic inflammation a possible cause of obesity-related depression? Mediators Inflamm; 2009;2009:439107
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  • Adult obesity has been associated with depression, especially in women.
  • [MeSH-minor] Age Factors. Body Mass Index. Enzyme-Linked Immunosorbent Assay. Female. Humans. Interleukin-6 / blood. Leptin / blood. Middle Aged. Receptors, Tumor Necrosis Factor / blood. Sex Factors. Tumor Necrosis Factor-alpha / blood

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  • [Cites] Neuropsychobiology. 1999 Nov;40(4):171-6 [10559698.001]
  • [Cites] Physiol Behav. 2007 Jul 24;91(4):449-58 [17543357.001]
  • [Cites] Arch Intern Med. 2000 May 22;160(10):1495-500 [10826464.001]
  • [Cites] Arch Intern Med. 2000 Jun 26;160(12):1761-8 [10871968.001]
  • [Cites] Am J Epidemiol. 2000 Jul 15;152(2):163-70 [10909953.001]
  • [Cites] Int J Obes Relat Metab Disord. 2000 Jun;24 Suppl 2:S80-5 [10997616.001]
  • [Cites] Int J Obes Relat Metab Disord. 2000 Nov;24(11):1392-5 [11126333.001]
  • [Cites] Diabetes Care. 2001 Jun;24(6):1069-78 [11375373.001]
  • [Cites] Int J Obes Relat Metab Disord. 2001 Jul;25(7):1047-56 [11443505.001]
  • [Cites] Pediatrics. 2002 Sep;110(3):497-504 [12205250.001]
  • [Cites] JAMA. 2002 Oct 9;288(14):1723-7 [12365955.001]
  • [Cites] Am J Cardiol. 2002 Dec 15;90(12):1279-83 [12480034.001]
  • [Cites] Diabetes Care. 2003 Mar;26(3):744-9 [12610032.001]
  • [Cites] Int J Obes Relat Metab Disord. 2003 Apr;27(4):514-21 [12664085.001]
  • [Cites] Brain Behav Immun. 2003 Aug;17(4):276-85 [12831830.001]
  • [Cites] Endocr Regul. 2003 Jun;37(2):51-68 [12932191.001]
  • [Cites] Am J Psychiatry. 2004 Feb;161(2):271-7 [14754776.001]
  • [Cites] Metabolism. 2004 Oct;53(10):1268-73 [15375781.001]
  • [Cites] Semin Vasc Med. 2004 May;4(2):161-5 [15478037.001]
  • [Cites] J Affect Disord. 1993 Oct-Nov;29(2-3):183-92 [8300977.001]
  • [Cites] N Engl J Med. 1996 Feb 1;334(5):292-5 [8532024.001]
  • [Cites] Obes Res. 2005 Feb;13(2):320-5 [15800290.001]
  • [Cites] Eur Cytokine Netw. 2006 Mar;17(1):4-12 [16613757.001]
  • [Cites] Endokrynol Pol. 2006 Sep-Oct;57(5):487-93 [17133313.001]
  • [Cites] Int J Immunopathol Pharmacol. 2007 Jan-Mar;20(1):145-54 [17346438.001]
  • [Cites] Aust N Z J Psychiatry. 2007 Mar;41(3):266-73 [17464708.001]
  • [Cites] Prog Neuropsychopharmacol Biol Psychiatry. 2007 Jun 30;31(5):1044-53 [17433516.001]
  • [Cites] Clin Cardiol. 2007 Jun;30(6):295-300 [17551966.001]
  • [Cites] Arch Intern Med. 2000 May 8;160(9):1261-8 [10809028.001]
  • (PMID = 19587822.001).
  • [ISSN] 1466-1861
  • [Journal-full-title] Mediators of inflammation
  • [ISO-abbreviation] Mediators Inflamm.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Leptin; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2705765
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86. Ifergan I, Kébir H, Bernard M, Wosik K, Dodelet-Devillers A, Cayrol R, Arbour N, Prat A: The blood-brain barrier induces differentiation of migrating monocytes into Th17-polarizing dendritic cells. Brain; 2008 Mar;131(Pt 3):785-99
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  • Trafficking of antigen-presenting cells into the CNS is essential for lymphocyte reactivation within the CNS compartment.
  • Our data support the notion that functional perivascular myeloid CNS dendritic cells arise as a consequence of migration of CD14+ monocytes across the human BBB, through the concerted actions of BBB-secreted transforming growth factor-beta and granulocyte-macrophage colony-stimulating factor.
  • [MeSH-minor] Adult. Antigen Presentation / immunology. Antigens, CD14 / analysis. CD4-Positive T-Lymphocytes / immunology. Cell Movement / immunology. Cells, Cultured. Chemokines / biosynthesis. Endothelium / immunology. Humans. Interferon-gamma / immunology. Interleukin-17 / biosynthesis. Lymphocyte Culture Test, Mixed. Middle Aged. Phagocytosis / immunology. Phenotype. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 18156156.001).
  • [ISSN] 1460-2156
  • [Journal-full-title] Brain : a journal of neurology
  • [ISO-abbreviation] Brain
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / Chemokines; 0 / Interleukin-17; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
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87. López M O: [Three-year survival of a patient with HIV and chagasic meningoencephalitis: case report]. Rev Chilena Infectol; 2010 Apr;27(2):160-4
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  • Central nervous system (CNS) evolvement (cerebral tumor or chagoma and diffuse meningoencephalitis) is similar to other opportunistic infections that present with cerebral expansive processes like toxoplasmosis or CNS primary lymphoma.
  • [MeSH-minor] Adult. Antiretroviral Therapy, Highly Active. Disease-Free Survival. Humans. Male. Nifurtimox / therapeutic use. Treatment Outcome. Trypanocidal Agents / therapeutic use

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  • (PMID = 20556321.001).
  • [ISSN] 0716-1018
  • [Journal-full-title] Revista chilena de infectología : órgano oficial de la Sociedad Chilena de Infectología
  • [ISO-abbreviation] Rev Chilena Infectol
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Chile
  • [Chemical-registry-number] 0 / Trypanocidal Agents; M84I3K7C2O / Nifurtimox
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88. Reardon DA, Zalutsky MR, Bigner DD: Antitenascin-C monoclonal antibody radioimmunotherapy for malignant glioma patients. Expert Rev Anticancer Ther; 2007 May;7(5):675-87
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  • Most of these tumors recur at or adjacent to the site of origin, which indicates that failure to eradicate local tumor growth is a major factor contributing to poor outcome.
  • Malignant gliomas selectively express several factors that are not present on normal CNS tissue.
  • Regional administration of radiolabeled monoclonal antibodies targeting tumor-specific antigens expressed by malignant gliomas offers an innovative therapeutic strategy that has recently demonstrated encouraging antitumor activity and acceptable toxicity in clinical trials at a number of centers.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Brain Neoplasms / radiotherapy. Glioma / radiotherapy. Radioimmunotherapy. Tenascin / immunology
  • [MeSH-minor] Administration, Topical. Adult. Humans

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  • (PMID = 17492931.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1-P50-CA108786-01; United States / NCI NIH HHS / CA / CA11898; United States / NCRR NIH HHS / RR / MO1 RR 30; United States / NINDS NIH HHS / NS / NS20023
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Tenascin
  • [Number-of-references] 97
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89. Kino T, Jaffe H, Amin ND, Chakrabarti M, Zheng YL, Chrousos GP, Pant HC: Cyclin-dependent kinase 5 modulates the transcriptional activity of the mineralocorticoid receptor and regulates expression of brain-derived neurotrophic factor. Mol Endocrinol; 2010 May;24(5):941-52
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  • Glucocorticoids, major end effectors of the stress response, play an essential role in the homeostasis of the central nervous system (CNS) and contribute to memory consolidation and emotional control through their intracellular receptors, the glucocorticoid and mineralocorticoid receptors.
  • Cyclin-dependent kinase 5 (CDK5), on the other hand, plays important roles in the morphogenesis and functions of the central nervous system, and its aberrant activation has been associated with development of neurodegenerative disorders.

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  • [Cites] J Neurochem. 1995 Jun;64(6):2681-90 [7760048.001]
  • [Cites] Science. 1995 Mar 17;267(5204):1658-62 [7886457.001]
  • [Cites] J Neurochem. 1995 Oct;65(4):1740-51 [7561872.001]
  • [Cites] Prog Cell Cycle Res. 1996;2:205-16 [9552397.001]
  • [Cites] Neuropharmacology. 1998 Apr-May;37(4-5):553-9 [9704996.001]
  • [Cites] J Biol Chem. 1998 Sep 11;273(37):24057-64 [9727024.001]
  • [Cites] J Biol Chem. 1998 Sep 18;273(38):24439-47 [9733735.001]
  • [Cites] Prog Nucleic Acid Res Mol Biol. 1998;61:1-23 [9752717.001]
  • [Cites] Endocr Rev. 1999 Jun;20(3):321-44 [10368774.001]
  • [Cites] Neurosci Res. 1999 May;34(1):21-9 [10413323.001]
  • [Cites] Nat Genet. 1999 Sep;23(1):99-103 [10471508.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 11;102(2):473-8 [15623560.001]
  • [Cites] Clin Biochem. 2005 May;38(5):401-9 [15820768.001]
  • [Cites] J Cell Biol. 2005 Jun 20;169(6):885-96 [15955845.001]
  • [Cites] Sci STKE. 2005 Oct 4;2005(304):pe48 [16204701.001]
  • [Cites] J Biol Chem. 2005 Dec 23;280(51):42067-77 [16249187.001]
  • [Cites] J Neurosci. 2006 Feb 15;26(7):1971-8 [16481429.001]
  • [Cites] Genes Dev. 2006 Jun 1;20(11):1405-28 [16751179.001]
  • [Cites] J Biosci. 2006 Sep;31(3):423-34 [17006024.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2007 Feb;3(2):168-79 [17237843.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4147-52 [17360491.001]
  • [Cites] Mol Endocrinol. 2007 Jul;21(7):1552-68 [17440046.001]
  • [Cites] Science. 2007 Sep 14;317(5844):1544-8 [17702911.001]
  • [Cites] J Proteome Res. 2007 Dec;6(12):4684-9 [17929885.001]
  • [Cites] Riv Biol. 2007 Sep-Dec;100(3):403-18 [18278739.001]
  • [Cites] Brain Res Bull. 2009 Mar 30;78(6):267-9 [19111910.001]
  • [Cites] Nat Med. 2009 Mar;15(3):331-7 [19198615.001]
  • [Cites] FASEB J. 2009 May;23(5):1572-83 [19141540.001]
  • [Cites] Steroids. 2010 Jan;75(1):1-12 [19818358.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 14;97(6):2910-5 [10706614.001]
  • [Cites] J Biol Chem. 2000 Jun 2;275(22):17166-72 [10748088.001]
  • [Cites] Nature. 2000 May 18;405(6784):360-4 [10830966.001]
  • [Cites] Prog Neurobiol. 2001 Jan;63(1):71-124 [11040419.001]
  • [Cites] EMBO Rep. 2000 Nov;1(5):447-51 [11258486.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Dec 19;92(26):12480-4 [8618925.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 1;93(20):11173-8 [8855328.001]
  • [Cites] Mol Cell Biol. 1996 Nov;16(11):6486-93 [8887677.001]
  • [Cites] J Neurosci Res. 1997 May 15;48(4):334-41 [9169859.001]
  • [Cites] J Biol Chem. 2001 Apr 27;276(17):14299-307 [11278286.001]
  • [Cites] Neuron. 2001 Apr;30(1):135-47 [11343650.001]
  • [Cites] Physiol Behav. 2001 Aug;73(5):811-25 [11566214.001]
  • [Cites] Nat Rev Mol Cell Biol. 2001 Oct;2(10):749-59 [11584302.001]
  • [Cites] J Biol Chem. 2002 Jan 25;277(4):2396-405 [11704662.001]
  • [Cites] Rev Neurosci. 2002;13(1):59-84 [12013026.001]
  • [Cites] J Mol Neurosci. 2002 Dec;19(3):267-73 [12540052.001]
  • [Cites] Trends Neurosci. 2003 Apr;26(4):171-3 [12689763.001]
  • [Cites] Nat Cell Biol. 2003 Aug;5(8):701-10 [12855954.001]
  • [Cites] Mol Cell Endocrinol. 2003 Aug 29;206(1-2):1-12 [12943985.001]
  • [Cites] Neuron. 2003 Oct 30;40(3):471-83 [14642273.001]
  • [Cites] Biochim Biophys Acta. 2004 Mar 11;1697(1-2):143-53 [15023357.001]
  • [Cites] Essays Biochem. 2004;40:137-55 [15242344.001]
  • [Cites] Science. 1989 Apr 14;244(4901):224-6 [2704997.001]
  • [Cites] J Biol Chem. 1993 Oct 5;268(28):20825-30 [8407912.001]
  • [Cites] Nature. 1994 Sep 29;371(6496):419-23 [8090221.001]
  • [Cites] Behav Brain Res. 1994 May 30;62(1):1-9 [7917027.001]
  • [Cites] Trends Neurosci. 1994 Nov;17(11):490-6 [7531892.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Sep 12;92(19):8856-60 [7568031.001]
  • (PMID = 20357208.001).
  • [ISSN] 1944-9917
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Brain-Derived Neurotrophic Factor; 0 / Purines; 0 / Receptors, Mineralocorticoid; 0 / roscovitine; 4964P6T9RB / Aldosterone; 7S5I7G3JQL / Dexamethasone; EC 2.7.11.22 / Cyclin-Dependent Kinase 5; W980KJ009P / Corticosterone
  • [Other-IDs] NLM/ PMC2870940
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90. Kocaoglu M, Ors F, Bulakbasi N, Onguru O, Ulutin C, Secer HI: Central neurocytoma: proton MR spectroscopy and diffusion weighted MR imaging findings. Magn Reson Imaging; 2009 Apr;27(3):434-40
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  • [Title] Central neurocytoma: proton MR spectroscopy and diffusion weighted MR imaging findings.
  • PURPOSE: To present proton magnetic resonance spectroscopy and diffusion-weighted imaging (DWI) findings of central neurocytoma (CN).
  • In addition to conventional magnetic resonance imaging features, we also assessed the metabolite ratios and tumor normalized apparent diffusion coefficient (NADC), which was calculated by dividing the tumor apparent diffusion coefficient (ADC) values by normal ADC.
  • RESULTS: The tumor choline/creatine ratios were 5.17+/-2.38, while N-acetyl aspartate/choline and N-acetyl aspartate/creatine ratios were 0.33+/-0.15 and 1.84+/-1.38, respectively.
  • On DWI, tumors had heterogeneous hyperintense appearances when compared with the contralateral parietal lobe white matter and tumor NADC values were 0.63+/-0.05.
  • Familiarity its physiologic features would help to presurgical diagnosis of ventricular and exraventricular CNs.
  • [MeSH-major] Brain Neoplasms / diagnosis. Brain Neoplasms / metabolism. Diffusion Magnetic Resonance Imaging / methods. Magnetic Resonance Spectroscopy / methods
  • [MeSH-minor] Adult. Female. Humans. Male. Protons. Reproducibility of Results. Sensitivity and Specificity. Young Adult

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  • (PMID = 18789624.001).
  • [ISSN] 1873-5894
  • [Journal-full-title] Magnetic resonance imaging
  • [ISO-abbreviation] Magn Reson Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protons
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91. 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.
  • These have been identified in several pediatric tumors including medulloblastoma, ependymomas, and malignant gliomas.
  • 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


92. Dalmau J, Bataller L: [Limbic encephalitis: the new cell membrane antigens and a proposal of clinical-immunological classification with therapeutic implications]. Neurologia; 2007 Oct;22(8):526-37
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  • RESULTS: 82 % of prospectively identified patients with non-viral limbic encephalitis at our institution had 526 antibodies against proteins of the CNS.
  • Patients with antibodies against these receptors are young women with benign-appearing cystic tumors of the ovary (mature or immature teratomas), who develop a severe and characteristic encephalitis that we report in detail.
  • Despite the severity of the disorder, patients often recover after treatment of the tumor and immunotherapy.
  • [MeSH-major] Antigens, Surface / immunology. Autoantigens / immunology. Demyelinating Autoimmune Diseases, CNS / immunology. Limbic Encephalitis / immunology. Membrane Proteins / immunology. Nerve Tissue Proteins / immunology
  • [MeSH-minor] Adolescent. Adult. Autoantibodies / immunology. Combined Modality Therapy. Female. Hippocampus / immunology. Humans. Immunotherapy. Models, Anatomic. Neuropil / immunology. Ovarian Neoplasms / complications. Ovarian Neoplasms / immunology. Potassium Channels / immunology. Receptors, N-Methyl-D-Aspartate / immunology. Retrospective Studies

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  • (PMID = 18000762.001).
  • [ISSN] 0213-4853
  • [Journal-full-title] Neurología (Barcelona, Spain)
  • [ISO-abbreviation] Neurologia
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antigens, Surface; 0 / Autoantibodies; 0 / Autoantigens; 0 / Membrane Proteins; 0 / Nerve Tissue Proteins; 0 / Potassium Channels; 0 / Receptors, N-Methyl-D-Aspartate
  • [Number-of-references] 55
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93. Chamberlain MC, Tsao-Wei D, Groshen S: Neoplastic meningitis-related encephalopathy. J Neurooncol; 2005 Apr;72(2):185-9
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  • Cohorts were matched with respect to age, primary tumor, performance status, absence of CSF compartmentalization and absence of neuroradiographic bulky CNS disease.
  • Primary tumor histology included the following: breast(10 patients); non-small cell lung cancer (8); non-Hodgkin's lymphoma (8); colorectal cancer (6); melanoma (4); small cell lung cancer (2); prostate cancer (2).
  • All patients received intraventricular chemotherapy and 16 patients received concurrent tumor-specific systemic chemotherapy.
  • [MeSH-major] Brain Neoplasms / mortality. Brain Neoplasms / secondary. Meningitis / mortality. Paraneoplastic Syndromes, Nervous System / mortality
  • [MeSH-minor] Adult. Aged. Confusion / etiology. Female. Humans. Male. Matched-Pair Analysis. Middle Aged. Retrospective Studies. Survival Analysis

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  • [Cites] Cancer. 1995 Jun 15;75(12):2919-31 [7773943.001]
  • [Cites] Neurology. 1996 Jun;46(6):1674-7 [8649568.001]
  • [Cites] Arch Neurol. 1996 Jul;53(7):626-32 [8929170.001]
  • [Cites] Neurology. 1990 Mar;40(3 Pt 1):435-8 [2314584.001]
  • [Cites] J Neurooncol. 2002 May;57(3):231-9 [12125986.001]
  • [Cites] Cancer. 2002 Sep 15;95(6):1311-6 [12216100.001]
  • [Cites] Ann Neurol. 1995 Jul;38(1):51-7 [7611725.001]
  • [Cites] J Clin Oncol. 1999 Oct;17(10):3110-6 [10506606.001]
  • [Cites] J Neurooncol. 1995;23 (3):233-8 [7673985.001]
  • [Cites] Clin Cancer Res. 1999 Nov;5(11):3394-402 [10589750.001]
  • [Cites] J Clin Oncol. 1993 Oct;11(10):1978-84 [7692000.001]
  • (PMID = 15926000.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


94. Grossman SA, Carson KA, Phuphanich S, Batchelor T, Peereboom D, Nabors LB, Lesser G, Hausheer F, Supko JG, New Approaches to Brain Tumor Therapy CNS Consortium: Phase I and pharmacokinetic study of karenitecin in patients with recurrent malignant gliomas. Neuro Oncol; 2008 Aug;10(4):608-16
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  • [Title] Phase I and pharmacokinetic study of karenitecin in patients with recurrent malignant gliomas.
  • Karenitecin is a highly lipophilic camptothecin analogue with a lactone ring that is relatively resistant to inactivating hydrolysis under physiologic conditions.
  • This phase I clinical trial was conducted to determine the maximum tolerated dose (MTD) of karenitecin in adults with recurrent malignant glioma (MG), to describe the effects of enzyme-inducing antiseizure drugs (EIASDs) on its pharmacokinetics, and to obtain preliminary evidence of activity.
  • Karenitecin was administered intravenously over 60 min daily for 5 consecutive days every 3 weeks to adults with recurrent MG who had no more than one prior chemotherapy regimen.
  • The continual reassessment method was used to escalate doses, beginning at 1.0 mg/m(2)/day, in patients stratified by EIASD use.
  • Treatment was continued until disease progression or treatment-related dose-limiting toxicity (DLT).
  • Plasma pharmacokinetics was determined for the first daily dose of karenitecin.
  • Thirty-two patients (median age, 52 years; median KPS score, 90) were accrued.
  • Seventy-eight percent had glioblastoma, and 22% had anaplastic glioma.
  • DLT was reversible neutropenia or thrombocytopenia.
  • The MTD was 2.0 mg/m(2) in daggerEIASD patients and 1.5 mg/m(2) in -EIASD patients.
  • The mean (+/-SD) total body clearance of karenitecin was 15.9 +/- 9.6 liters/h/m(2) in daggerEIASD patients and 10.2 +/- 3.5 liters/h/m(2) in -EIASD patients (p = 0.02).
  • No objective responses were observed in 11 patients treated at or above the MTD.
  • The total body clearance of karenitecin is significantly enhanced by the concurrent administration of EIASDs.
  • This schedule of karenitecin, a novel lipophilic camptothecin analogue, has little activity in recurrent MG.

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  • [Cites] Invest New Drugs. 2000 Aug;18(3):275-80 [10958598.001]
  • [Cites] Cancer Chemother Pharmacol. 2004 Jun;53(6):527-32 [14997342.001]
  • [Cites] J Med Chem. 2000 Oct 19;43(21):3970-80 [11052802.001]
  • [Cites] Pharm Res. 2000 Dec;17(12):1551-7 [11303967.001]
  • [Cites] Cancer Chemother Pharmacol. 2001 Jul;48(1):83-7 [11488529.001]
  • [Cites] Clin Cancer Res. 2001 Aug;7(8):2182-94 [11489791.001]
  • [Cites] Clin Cancer Res. 2002 Mar;8(3):641-61 [11895891.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 Jul 15;53(4):980-6 [12095566.001]
  • [Cites] Ann Oncol. 2003 Apr;14(4):603-14 [12649109.001]
  • [Cites] Oncology (Williston Park). 2003 May;17(5 Suppl 5):9-14 [12800600.001]
  • [Cites] Chem Pharm Bull (Tokyo). 1985 Apr;33(4):1620-32 [4042238.001]
  • [Cites] J Clin Oncol. 1994 Sep;12(9):1886-9 [8083712.001]
  • [Cites] J Pharm Sci. 1995 Apr;84(4):518-9 [7629749.001]
  • [Cites] Cancer Chemother Pharmacol. 1996;37(3):195-202 [8529278.001]
  • [Cites] Ann Oncol. 1996 Feb;7(2):205-7 [8777179.001]
  • [Cites] J Biopharm Stat. 1997 Mar;7(1):171-8 [9056596.001]
  • [Cites] Cancer Chemother Pharmacol. 1998;41(6):429-36 [9554585.001]
  • [Cites] Cancer Chemother Pharmacol. 1998;41(6):464-8 [9554590.001]
  • [Cites] Cancer. 1999 Mar 1;85(5):1160-5 [10091802.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] Clin Cancer Res. 2005 Apr 15;11(8):3009-16 [15837755.001]
  • [Cites] Lung Cancer. 2005 Jun;48(3):399-407 [15893009.001]
  • [Cites] Neuro Oncol. 2006 Apr;8(2):189-93 [16533878.001]
  • [Cites] Clin Cancer Res. 2003 Aug 1;9(8):2940-9 [12912940.001]
  • [Cites] Neuro Oncol. 2004 Jan;6(1):21-7 [14769136.001]
  • [Cites] Int J Cancer. 2000 Oct 15;88(2):260-6 [11004678.001]
  • (PMID = 18577560.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01-CA62475; United States / NCI NIH HHS / CA / U01 CA062475; United States / NCI NIH HHS / CA / P30-CA0516; United States / NCI NIH HHS / CA / U01-CA105689; United States / NCI NIH HHS / CA / U01 CA105689
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / Antineoplastic Agents; 24R60NVC41 / cositecan; XT3Z54Z28A / Camptothecin
  • [Other-IDs] NLM/ PMC2666235
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95. Osborne PB, Halliday GM, Cooper HM, Keast JR: Localization of immunoreactivity for deleted in colorectal cancer (DCC), the receptor for the guidance factor netrin-1, in ventral tier dopamine projection pathways in adult rodents. Neuroscience; 2005;131(3):671-81
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  • [Title] Localization of immunoreactivity for deleted in colorectal cancer (DCC), the receptor for the guidance factor netrin-1, in ventral tier dopamine projection pathways in adult rodents.
  • DCC (deleted in colorectal cancer)-the receptor of the netrin-1 neuronal guidance factor-is expressed and is active in the central nervous system (CNS) during development, but is down-regulated during maturation.
  • The substantia nigra contains the highest level of netrin-1 mRNA in the adult rodent brain, and corresponding mRNA for DCC has also been detected in this region but has not been localized to any particular neuron type.
  • In this study, an antibody raised against DCC was used to determine if the protein was expressed by adult dopamine neurons, and identify their distribution and projections.
  • The unique distribution of DCC-immunoreactivity in adult ventral midbrain dopamine neurons suggests that netrin-1/DCC signaling could function in plasticity and remodeling previously identified in dopamine projection pathways.
  • In particular, a recent report that DCC is regulated through the ubiquitin-proteosome system via Siah/Sina proteins, is consistent with a potential involvement in genetic and sporadic forms of Parkinson's disease.
  • [MeSH-major] Brain / cytology. Cell Adhesion Molecules / metabolism. Dopamine / metabolism. Gene Expression Regulation / physiology. Neural Pathways / metabolism. Neurons / metabolism. Tumor Suppressor Proteins / metabolism

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  • (PMID = 15730872.001).
  • [ISSN] 0306-4522
  • [Journal-full-title] Neuroscience
  • [ISO-abbreviation] Neuroscience
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calbindins; 0 / Cell Adhesion Molecules; 0 / Dcc protein, mouse; 0 / Nerve Growth Factors; 0 / Receptors, Cell Surface; 0 / Receptors, Opioid, mu; 0 / S100 Calcium Binding Protein G; 0 / Tumor Suppressor Proteins; 158651-98-0 / netrin-1; EC 1.14.16.2 / Tyrosine 3-Monooxygenase; VTD58H1Z2X / Dopamine
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96. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Ependymomas generally arise in the central nervous system (CNS), although rare primary extraneural ependymomas have been observed.
  • 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.
  • Electron microscopic studies revealed that tumor cells form micro rosettes, into which microvilli and cilia projected.
  • There is no evidence of local tumor recurrence or distant metastasis after 30 months follow up.
  • The present case adds yet another unique example to the already diverse spectrum of head and neck neoplasms encountered in surgical pathology.
  • [MeSH-major] Ependymoma / pathology. Head and Neck Neoplasms / pathology
  • [MeSH-minor] Adult. Glial Fibrillary Acidic Protein / analysis. Humans. Male. Mucin-1 / analysis. Vimentin / analysis


97. Gori S, Sidoni A, Colozza M, Ferri I, Mameli MG, Fenocchio D, Stocchi L, Foglietta J, Ludovini V, Minenza E, De Angelis V, Crinò L: EGFR, pMAPK, pAkt and PTEN status by immunohistochemistry: correlation with clinical outcome in HER2-positive metastatic breast cancer patients treated with trastuzumab. Ann Oncol; 2009 Apr;20(4):648-54
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  • BACKGROUND: In an attempt to identify markers of resistance to trastuzumab, we evaluated both the profiling of human epidermal growth factor receptor 2 (HER2)-positive tumor cells measuring the relative levels of EGFR, pMAPK, pAkt and PTEN and their correlations with clinical outcome in HER2-positive metastatic breast cancer patients treated with trastuzumab.
  • PATIENTS AND METHODS: Tumor tissues for this retrospective analysis were available from 45 out of 76 patients with metastatic breast cancer treated from April 1999 to March 2006 with trastuzumab-based therapy at our Institution.
  • Evaluations of EGFR, pMAPK, pAkt and PTEN status by immunohistochemistry (IHC) were carried out on all 45 tissue samples and their correlations with response to trastuzumab, incidence of central nervous system (CNS) metastases, time to progression (TTP), overall survival from diagnosis of breast cancer (OS1), from diagnosis of metastatic disease (OS2) and from the start of trastuzumab (OS3) were analyzed.
  • EGFR, pMAPK, pAkt and PTEN status by IHC were not significantly associated with response to trastuzumab, TTP, overall survival (OS1, OS2, OS3) and CNS metastases incidence.
  • It is likely that high expression of pMAPK (pMAPK-positive status) or pAkt (pAkt-positive status) could identify a subgroup of HER2-positive tumors with high activity of proliferation and survival pathways and with resistance to trastuzumab.
  • CONCLUSIONS: In HER2-positive metastatic breast cancers, EGFR, pMAPK, pAkt and PTEN status evaluated by IHC was not significantly associated with response to trastuzumab, TTP, OS and CNS metastases incidence.


98. 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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  • At surgery an intradural, extramedullary, firm, black neoplasm was encountered, which invaded the ventral dura and elevated and distorted the spinal cord.
  • 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.
  • Primary meningeal melanocytic tumors (PMMTs) are rare; fewer than 100 cases have been described.
  • PMMTs of the CNS consist of a spectrum of tumors ranging from well-differentiated melanocytoma to its overtly malignant counterpart, melanoma.
  • 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.
  • Radiotherapy is recommended for incomplete resection of IMGs and melanomas; the recurrence potential of low-grade melanocytomas is less clear and watchful waiting may be employed, since recurrent tumors may be treated surgically prior to radiation.
  • [MeSH-major] Meningioma / pathology. Paresis / etiology. Spinal Cord Neoplasms / pathology
  • [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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99. Raison CL, Borisov AS, Woolwine BJ, Massung B, Vogt G, Miller AH: Interferon-alpha effects on diurnal hypothalamic-pituitary-adrenal axis activity: relationship with proinflammatory cytokines and behavior. Mol Psychiatry; 2010 May;15(5):535-47
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