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1. Scherer K, Johnston J, Panda M: Dural based mass: malignant or benign. J Radiol Case Rep; 2009;3(11):1-12

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In March 2007, a 68 year old female was diagnosed with colonic adenocarcinoma metastatic to the lungs and a frontoparietal parafalcine lesion suspected to be a meningioma was also noted.
  • For 14 months, she received chemotherapy with poor response.
  • In June 2008, she developed multiple focal neurologic deficits.
  • Enlargement of the parafalcine brain lesion was noted on head computerized tomography and magnetic resonance imaging.
  • All 3 modality findings confirmed a meningioma.
  • Embolization of the middle meningeal artery with craniotomy for excision of the suspected meningioma was performed.
  • Pathology indicated metastatic adenocarcinoma with colonic primary without evidence of meningioma.
  • Meningiomas are the most common dural based lesions; however, a variety of dural lesions mimic meningiomas.
  • Dural metastatic tumors mimicking meningiomas is an uncommon phenomenon, particularly when the primary location is the colon.
  • This paper additionally discusses the differentiation of benign dural based tumors like meningiomas from malignant findings.
  • Multiple adjunct studies can differentiate meningiomas from metastatic tumor.
  • The definitive diagnosis is based on histopathology.

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  • [Cites] Hum Pathol. 2002 Dec;33(12):1211-26 [12514791.001]
  • [Cites] AJNR Am J Neuroradiol. 2003 Feb;24(2):225-33 [12591638.001]
  • [Cites] Neurol Med Chir (Tokyo). 2004 Jun;44(6):317-20 [15253548.001]
  • [Cites] Acta Cytol. 1981 Sep-Oct;25(5):461-79 [7025541.001]
  • [Cites] Acta Cytol. 1981 Nov-Dec;25(6):599-610 [6947665.001]
  • [Cites] Neurosurgery. 1986 Nov;19(5):820-3 [3785633.001]
  • [Cites] J Neurosurg Sci. 1987 Jan-Mar;31(1):33-6 [3625287.001]
  • [Cites] Neuroradiology. 1993;35(4):272-3 [8492892.001]
  • [Cites] Neurol Med Chir (Tokyo). 1994 Feb;34(2):108-10 [7514757.001]
  • [Cites] Neurosurg Clin N Am. 1996 Jul;7(3):345-67 [8823768.001]
  • [Cites] Surg Neurol. 2002 Sep-Oct;58(3-4):241-5 [12480230.001]
  • [Cites] Otol Neurotol. 2002 Nov;23(6):975-9 [12438865.001]
  • [Cites] J Neurooncol. 2002 Jul;58(3):193-9 [12187955.001]
  • [Cites] Arch Pathol Lab Med. 2001 Jul;125(7):880-7 [11419971.001]
  • [Cites] Australas Radiol. 2005 Dec;49(6):497-500 [16351616.001]
  • [Cites] Clin Neurol Neurosurg. 1997 May;99(2):135-7 [9213059.001]
  • [Cites] Neurologist. 2006 Jan;12(1):48-52 [16547447.001]
  • [Cites] J Neurooncol. 2005 Oct;75(1):57-61 [16215816.001]
  • [Cites] Neurochirurgie. 1999 May;45(2):160-3 [10448659.001]
  • [Cites] J Neurosurg. 1998 Oct;89(4):552-8 [9761048.001]
  • (PMID = 22470624.001).
  • [ISSN] 1943-0922
  • [Journal-full-title] Journal of radiology case reports
  • [ISO-abbreviation] J Radiol Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3303278
  • [Keywords] NOTNLM ; Dural based mass / meningioma / metastatic dural based lesions
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2. Chamberlain MC, Glantz MJ: Cerebrospinal fluid-disseminated meningioma. Cancer; 2005 Apr 1;103(7):1427-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cerebrospinal fluid-disseminated meningioma.
  • BACKGROUND: Intracranial meningiomas are common and comprise 20% of all primary brain tumors.
  • Meningiomas infrequently metastasize; however, to the authors' knowledge there are limited data regarding the spread of disease through cerebrospinal fluid (CSF).
  • METHODS: Eight of 200 consecutive patients (4%) with meningiomas manifested CSF dissemination.
  • All patients had undergone prior surgery (range, one to five surgeries; median, two surgeries), radiotherapy (involved-field radiotherapy in seven patients and stereotactic radiotherapy in six patients), and chemotherapy (hydroxyurea in eight patients).
  • Multiple sites of metastases were seen in all patients and were both within the nervous system (subarachnoid or ventricular tumor: intracranial in eight patients, spinal cord in four patients) and extraneural (subcutaneous, cervical lymph nodes, orbit, or pulmonary in five patients).
  • Treatment utilized both systemic chemotherapy (temozolomide in four patients, irinotecan in three patients, hydroxyurea in three patients, interferon-alpha in two patients, and doxorubicin plus ifosfamide in one patient) and intraventricular chemotherapy (liposomal cytosine arabinoside in seven patients, thiotepa in one patient, and busulfan in one patient).
  • RESULTS: Treatment-related toxicity was seen in eight patients, including chemical meningitis in eight patients (Grade 2), neutropenia in five patients (Grade 2 in four patients and Grade 3 in one patient), fatigue in one patient (Grade 2), and gastrointestinal toxicity in one patient (Grade 2).
  • The median survival was 5.5 months, and 3 patients were alive with disease at the time of last follow-up.
  • CONCLUSIONS: The treatment of CSF-disseminated meningioma, although feasible and comparatively nontoxic, was associated with modest outcomes despite combined systemic and intraventricular chemotherapy.
  • [MeSH-major] Meningioma / secondary
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / therapeutic use. Brain Neoplasms / pathology. Brain Neoplasms / secondary. Central Nervous System Neoplasms / secondary. Cerebrospinal Fluid / cytology. Female. Humans. Lung Neoplasms / secondary. Lymphatic Metastasis. Male. Middle Aged. Skin Neoplasms / secondary. Spinal Cord Neoplasms / secondary

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  • [Copyright] Copyright 2005 American Cancer Society.
  • (PMID = 15690330.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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3. Plotkin SR, Halpin C, Blakeley JO, Slattery WH 3rd, Welling DB, Chang SM, Loeffler JS, Harris GJ, Sorensen AG, McKenna MJ, Barker FG 2nd: Suggested response criteria for phase II antitumor drug studies for neurofibromatosis type 2 related vestibular schwannoma. J Neurooncol; 2009 May;93(1):61-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Suggested response criteria for phase II antitumor drug studies for neurofibromatosis type 2 related vestibular schwannoma.
  • Neurofibromatosis type 2 (NF2) is a tumor suppressor gene syndrome characterized by multiple schwannomas, especially vestibular schwannomas (VS), and meningiomas.
  • Anticancer drug trials are now being explored, but there are no standardized endpoints in NF2.
  • We also identify research goals in NF2 to facilitate future trial conduct, such as identifying the expectations for time to tumor progression and time to measurable hearing loss in untreated NF2-related VS, and the relation of both endpoints to patient prognostic factors (such as age, baseline tumor volume, and measures of disease severity).
  • These data would facilitate future use of endpoints based on stability of tumor size and hearing, which might be more appropriate for testing certain drugs.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Clinical Trials, Phase II as Topic / standards. Neurofibromatosis 2 / complications. Neurofibromatosis 2 / drug therapy. Neuroma, Acoustic / drug therapy

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  • [Cites] Neuro Oncol. 2007 Jan;9(1):29-38 [17108063.001]
  • [Cites] Neurol Med Chir (Tokyo). 2006 Dec;46(12):601-4 [17185887.001]
  • [Cites] Audiol Neurootol. 2007;12(1):1-12 [17033159.001]
  • [Cites] Cancer Cell. 2007 Jan;11(1):83-95 [17222792.001]
  • [Cites] Clin Cancer Res. 2007 Feb 1;13(3):972-6 [17277252.001]
  • [Cites] Neurosurgery. 2007 Mar;60(3):460-8; discussion 468-70 [17327790.001]
  • [Cites] Acta Neurochir (Wien). 2007 Mar;149(3):267-73; discussion 273 [17342379.001]
  • [Cites] J Am Acad Audiol. 2007 Feb;18(2):151-83 [17402301.001]
  • [Cites] Mol Cancer Ther. 2007 Apr;6(4):1180-5 [17431101.001]
  • [Cites] J Clin Oncol. 2007 May 1;25(13):1753-9 [17470865.001]
  • [Cites] J Clin Oncol. 2007 May 1;25(13):1760-4 [17470866.001]
  • [Cites] Ear Hear. 2007 Apr;28(2):187-95 [17496670.001]
  • [Cites] Pediatr Neurol. 2007 May;36(5):293-300 [17509460.001]
  • [Cites] BMC Cancer. 2007;7:106 [17587447.001]
  • [Cites] Int J Audiol. 2007 Aug;46(8):442-8 [17654086.001]
  • [Cites] N Engl J Med. 1998 Nov 12;339(20):1426-33 [9811917.001]
  • [Cites] Curr Opin Otolaryngol Head Neck Surg. 2007 Oct;15(5):341-6 [17823551.001]
  • [Cites] Pediatrics. 2007 Nov;120(5):1044-52 [17974742.001]
  • [Cites] Otol Neurotol. 2007 Dec;28(8):1083-90 [18043434.001]
  • [Cites] Am J Otol. 2000 Sep;21(5):722-8 [10993466.001]
  • [Cites] AJNR Am J Neuroradiol. 2000 Sep;21(8):1540-6 [11003293.001]
  • [Cites] Laryngoscope. 2000 Nov;110(11):1843-9 [11081597.001]
  • [Cites] Scand Audiol. 2000;29(4):266-75 [11195947.001]
  • [Cites] Radiother Oncol. 2001 Jul;60(1):45-8 [11410303.001]
  • [Cites] Clin Otolaryngol Allied Sci. 2001 Oct;26(5):388-93 [11678946.001]
  • [Cites] Otol Neurotol. 2001 Nov;22(6):917-21 [11698819.001]
  • [Cites] Laryngoscope. 2001 Nov;111(11 Pt 2 Suppl 98):1-21 [11802001.001]
  • [Cites] J Neurosurg. 2002 Feb;96(2):217-22 [11838793.001]
  • [Cites] J Neurosurg. 2002 Feb;96(2):223-8 [11838794.001]
  • [Cites] J Neurosurg. 2002 Apr;96(4):796-800 [11990824.001]
  • [Cites] Am J Hum Genet. 2002 Oct;71(4):715-23 [12235555.001]
  • [Cites] Int J Audiol. 2002 Dec;41(8):535-44 [12477174.001]
  • [Cites] Laryngoscope. 2003 Mar;113(3):420-6 [12616190.001]
  • [Cites] Int J Audiol. 2003 Apr;42(3):152-60 [12705780.001]
  • [Cites] Ann Otol Rhinol Laryngol. 2003 May;112(5):395-7 [12784975.001]
  • [Cites] Otol Neurotol. 2003 May;24(3):465-8 [12806300.001]
  • [Cites] Laryngoscope. 2003 Aug;113(8):1332-43 [12897555.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 2003 Sep;74(9):1288-93 [12933938.001]
  • [Cites] J Neurosurg. 2003 Sep;99(3):480-3 [12959433.001]
  • [Cites] Gerontologist. 2003 Oct;43(5):661-8 [14570962.001]
  • [Cites] Eur Arch Otorhinolaryngol. 2003 Oct;260(9):487-9 [12736745.001]
  • [Cites] Ann Otol Rhinol Laryngol. 2003 Nov;112(11):979-86 [14653368.001]
  • [Cites] Virchows Arch. 2003 Dec;443(6):768-73 [14508685.001]
  • [Cites] J Otolaryngol. 2003 Oct;32(5):323-7 [14974864.001]
  • [Cites] Otol Neurotol. 2004 Mar;25(2):150-4 [15021775.001]
  • [Cites] Laryngoscope. 2004 May;114(5):814-20 [15126736.001]
  • [Cites] Neurochirurgie. 2004 Jun;50(2-3 Pt 2):312-9 [15179284.001]
  • [Cites] Neurology. 2004 Aug 10;63(3):535-7 [15304589.001]
  • [Cites] Otol Neurotol. 2004 Sep;25(5):811-7 [15354016.001]
  • [Cites] Tech Rep SAM-TR. 1966 Jun;:1-12 [5296571.001]
  • [Cites] J Speech Hear Res. 1978 Sep;21(3):507-18 [713519.001]
  • [Cites] Neurosurgery. 1980 Aug;7(2):154-9 [6968414.001]
  • [Cites] Neurosurg Clin N Am. 1999 Apr;10(2):305-15 [10099095.001]
  • [Cites] Neurol Med Chir (Tokyo). 1999 Feb;39(2):141-7; discussion 147-9 [10193147.001]
  • [Cites] J Speech Hear Disord. 1952 Sep;17(3):321-37 [13053556.001]
  • [Cites] Cancer. 2005 Jan 15;103(2):339-48 [15578712.001]
  • [Cites] Otol Neurotol. 2005 Jan;26(1):93-7 [15699726.001]
  • [Cites] Otol Neurotol. 2005 Jan;26(1):98-101 [15699727.001]
  • [Cites] Laryngoscope. 2005 Mar;115(3):450-4 [15744156.001]
  • [Cites] Otol Neurotol. 2005 Mar;26(2):188-95 [15793403.001]
  • [Cites] Otol Neurotol. 2005 May;26(3):512-5 [15891658.001]
  • [Cites] Otol Neurotol. 2005 Jul;26(4):733-40 [16015177.001]
  • [Cites] J Clin Oncol. 2005 Aug 1;23(22):5094-8 [15983399.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2005 Sep 1;63(1):75-81 [16111574.001]
  • [Cites] J Neurosurg. 2005 Jul;103(1):59-63 [16121974.001]
  • [Cites] J Clin Oncol. 2005 Oct 1;23(28):7199-206 [16192604.001]
  • [Cites] J Med Genet. 2005 Dec;42(12):903-6 [15831594.001]
  • [Cites] Otol Neurotol. 2006 Jan;27(1):110-6 [16371857.001]
  • [Cites] Cochrane Database Syst Rev. 2006;(1):CD003998 [16437471.001]
  • [Cites] Otol Neurotol. 2006 Feb;27(2):197-208 [16436990.001]
  • [Cites] Neuro Oncol. 2006 Jan;8(1):38-46 [16443946.001]
  • [Cites] Neurosurgery. 2006 Feb;58(2):241-8; discussion 241-8 [16462477.001]
  • [Cites] J Neurosurg. 2006 Jan;104(1):157-62 [16509161.001]
  • [Cites] Clin Cancer Res. 2006 Apr 1;12(7 Pt 1):1966-9 [16609005.001]
  • [Cites] Otol Neurotol. 2006 Apr;27(3):403-9 [16639281.001]
  • [Cites] Eur Arch Otorhinolaryngol. 2006 Mar;263(3):267-70 [16025257.001]
  • [Cites] Neurosurgery. 2006 Jun;58(6):1119-28; discussion 1119-28 [16723891.001]
  • [Cites] Otol Neurotol. 2006 Jun;27(4):547-52 [16791048.001]
  • [Cites] Neurosurgery. 2006 Jul;59(1):67-76; discussion 67-76 [16823302.001]
  • [Cites] Otol Neurotol. 2006 Aug;27(5):705-12 [16868519.001]
  • [Cites] Lancet Oncol. 2006 Sep;7(9):741-6 [16945769.001]
  • [Cites] Ann Otol Rhinol Laryngol. 2006 Sep;115(9):694-8 [17044542.001]
  • [Cites] Neurology. 2006 Nov 28;67(10):1860-2 [17035676.001]
  • [Cites] Cancer. 1981 Jan 1;47(1):207-14 [7459811.001]
  • [Cites] Audiology. 1984;23(6):552-68 [6517748.001]
  • [Cites] Otolaryngol Head Neck Surg. 1985 Apr;93(2):146-7 [3921901.001]
  • [Cites] Arch Dermatol. 1987 Aug;123(8):1011-6 [3115189.001]
  • [Cites] Arch Otolaryngol Head Neck Surg. 1988 Jan;114(1):85-7 [3334825.001]
  • [Cites] Ann Otol Rhinol Laryngol. 1988 Jan-Feb;97(1):55-66 [3277525.001]
  • [Cites] Otolaryngol Head Neck Surg. 1988 Apr;98(4):273-82 [3132678.001]
  • [Cites] J Am Geriatr Soc. 1990 Jan;38(1):45-50 [2295767.001]
  • [Cites] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840.001]
  • [Cites] Otolaryngol Head Neck Surg. 1990 Dec;103(6):963-5 [2126130.001]
  • [Cites] Neurosurgery. 1991 May;28(5):646-50; discussion 650-1 [1876241.001]
  • [Cites] Neurosurgery. 1992 Nov;31(5):829-38; discussion 838-9 [1436407.001]
  • [Cites] J Med Genet. 1992 Dec;29(12):841-6 [1479598.001]
  • [Cites] Q J Med. 1992 Aug;84(304):603-18 [1484939.001]
  • [Cites] Acta Otolaryngol Suppl. 1991;487:91-8 [1843593.001]
  • [Cites] J Neuropathol Exp Neurol. 1993 Mar;52(2):106-13 [8440992.001]
  • [Cites] Ann Otol Rhinol Laryngol. 1993 Jul;102(7):518-20 [8333673.001]
  • [Cites] J Neurosurg. 1994 Mar;80(3):541-7 [8113868.001]
  • [Cites] Otolaryngol Head Neck Surg. 1995 Jul;113(1):5-14 [7603722.001]
  • [Cites] Neuroradiology. 1995 May;37(4):317-20 [7666970.001]
  • [Cites] Otolaryngol Head Neck Surg. 1995 Sep;113(3):176-8 [7675474.001]
  • [Cites] Otolaryngol Head Neck Surg. 1995 Sep;113(3):179-80 [7675475.001]
  • [Cites] J Clin Oncol. 1996 Mar;14(3):1018-26 [8622006.001]
  • [Cites] Ann Otol Rhinol Laryngol. 1996 Jun;105(6):415-22 [8638891.001]
  • [Cites] Laryngoscope. 1996 Jun;106(6):694-9 [8656953.001]
  • [Cites] Ir J Med Sci. 1996 Jul-Sep;165(3):151-2 [8824013.001]
  • [Cites] Neurosurgery. 1997 Apr;40(4):696-705; discussion 705-6 [9092842.001]
  • [Cites] AJNR Am J Neuroradiol. 1997 Feb;18(2):313-23 [9111669.001]
  • [Cites] J Neurosurg. 1997 Jul;87(1):60-6 [9202266.001]
  • [Cites] Am J Otol. 1997 Jul;18(4):421-6 [9233480.001]
  • [Cites] Am J Otol. 1997 Jul;18(4):427-35 [9233481.001]
  • [Cites] Surg Neurol. 1997 Oct;48(4):395-400 [9315139.001]
  • [Cites] Eur J Cancer. 1997 Dec;33(14):2326-32 [9616276.001]
  • [Cites] Biochim Biophys Acta. 2008 Jan;1785(1):32-54 [17980164.001]
  • [Cites] Otol Neurotol. 2008 Jan;29(1):50-7 [18199957.001]
  • [Cites] Brain. 2008 Mar;131(Pt 3):606-15 [17940085.001]
  • [Cites] J Clin Oncol. 2008 Mar 10;26(8):1346-54 [18285606.001]
  • [Cites] AJNR Am J Neuroradiol. 2008 Mar;29(3):419-24 [18272557.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 2008 Apr;79(4):431-6 [17673492.001]
  • [Cites] J Clin Oncol. 2008 Apr 20;26(12):1987-92 [18421050.001]
  • [Cites] Otolaryngol Head Neck Surg. 2008 May;138(5):667-71 [18439476.001]
  • [Cites] Lancet Oncol. 2008 May;9(5):453-61 [18452856.001]
  • [Cites] Neuro Oncol. 2008 Apr;10(2):162-70 [18356283.001]
  • [Cites] AJNR Am J Neuroradiol. 2008 May;29(5):906-10 [18296549.001]
  • [Cites] Clin Otolaryngol. 2008 Jun;33(3):255-9 [18559034.001]
  • [Cites] Acta Neurochir Suppl. 2008;101:169-73 [18642654.001]
  • [Cites] Neuro Oncol. 2008 Aug;10(4):631-42 [18559968.001]
  • [Cites] Nat Clin Pract Oncol. 2008 Aug;5(8):487-91 [18560388.001]
  • [Cites] Otol Neurotol. 2008 Aug;29(5):615-21 [18451751.001]
  • [Cites] Acta Oncol. 2008;47(6):1171-3 [18615326.001]
  • [Cites] Prog Neurol Surg. 2008;21:176-82 [18810217.001]
  • [Cites] Neurosurgery. 2008 Jun;62(6):1314-9; discussion 1319-20 [18824998.001]
  • [Cites] Nat Clin Pract Oncol. 2008 Nov;5(11):634-44 [18711427.001]
  • [Cites] Clin Otolaryngol. 2008 Oct;33(5):427-34 [18983375.001]
  • [Cites] Curr Opin Neurol. 2008 Dec;21(6):728-35 [18989120.001]
  • [Cites] Cancer. 2009 Jan 15;115(2):390-8 [19109818.001]
  • [Cites] Eur Arch Otorhinolaryngol. 2009 Jun;266(6):907-17 [19005632.001]
  • [Cites] J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437.001]
  • [Cites] Laryngoscope. 2000 Feb;110(2 Pt 1):250-5 [10680925.001]
  • [Cites] Otolaryngol Head Neck Surg. 2000 Apr;122(4):602-6 [10740189.001]
  • [Cites] Am J Otol. 2000 May;21(3):393-8 [10821554.001]
  • [Cites] Surg Neurol. 2000 Apr;53(4):383-89; discussion 389-90 [10825525.001]
  • [Cites] Rev Laryngol Otol Rhinol (Bord). 2000;121(1):21-6 [10865479.001]
  • [Cites] Lancet. 2000 Jul 29;356(9227):373-8 [10972369.001]
  • (PMID = 19430883.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 154
  • [Other-IDs] NLM/ NIHMS573252; NLM/ PMC4036446
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4. Evans DG: Neurofibromatosis type 2 (NF2): a clinical and molecular review. Orphanet J Rare Dis; 2009;4:16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neurofibromatosis type 2 (NF2): a clinical and molecular review.
  • Neurofibromatosis type 2 (NF2) is a tumour-prone disorder characterised by the development of multiple schwannomas and meningiomas.
  • The other main tumours are schwannomas of the other cranial, spinal and peripheral nerves; meningiomas both intracranial (including optic nerve meningiomas) and intraspinal, and some low-grade central nervous system malignancies (ependymomas).
  • Neurofibromatosis type 2 is a dominantly inherited tumour predisposition syndrome caused by mutations in the NF2 gene on chromosome 22.
  • Although truncating mutations (nonsense and frameshifts) are the most frequent germline event and cause the most severe disease, single and multiple exon deletions are common.
  • A strategy for detection of the latter is vital for a sensitive analysis.
  • Surgery remains the focus of current management although watchful waiting with careful surveillance and occasionally radiation treatment have a role.
  • Prognosis is adversely affected by early age at onset, a higher number of meningiomas and having a truncating mutation.
  • In the future, the development of tailored drug therapies aimed at the genetic level are likely to provide huge improvements for this devastating condition.


5. McDonnell JJ, Kalbko K, Keating JH, Sato AF, Faissler D: Multiple meningiomas in three dogs. J Am Anim Hosp Assoc; 2007 Jul-Aug;43(4):201-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multiple meningiomas in three dogs.
  • Three dogs with seizures were diagnosed with multiple intracranial meningiomas.
  • Treatment consisted of surgery and radiation (n=2) or chemotherapy (n=1).
  • In two dogs, the meningiomas had the same histological pattern, while in one dog the histological subtypes were different.
  • [MeSH-major] Dog Diseases / diagnosis. Meningeal Neoplasms / veterinary. Meningioma / veterinary. Seizures / veterinary

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  • (PMID = 17615400.001).
  • [ISSN] 1547-3317
  • [Journal-full-title] Journal of the American Animal Hospital Association
  • [ISO-abbreviation] J Am Anim Hosp Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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6. Moss J, DeCastro R, Patronas NJ, Taveira-DaSilva A: Meningiomas in lymphangioleiomyomatosis. JAMA; 2001 Oct 17;286(15):1879-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Meningiomas in lymphangioleiomyomatosis.
  • However, meningiomas have progesterone receptors, and progesterone is believed to be a mitogen for meningioma cells in culture.
  • OBJECTIVE: To determine the prevalence of meningiomas in women with LAM.
  • PATIENTS: Two hundred fifty women with sporadic LAM who were referred for screening by magnetic resonance imaging (MRI) and/or computed tomography (CT) of the brain.
  • MAIN OUTCOME MEASURES: Presence of meningiomas on MRI and/or CT scans.
  • RESULTS: Eight women with LAM (3 with and 5 without a diagnosis of TSC) had lesions on MRI scans compatible with meningiomas.
  • Multiple meningiomas were observed in 2 patients.
  • CONCLUSIONS: Women with LAM appear to have a high prevalence of meningiomas.
  • We recommend that patients with LAM be screened for meningiomas regardless of diagnosis of TSC.
  • In view of the lack of a documented effect of progesterone on progression of lung disease in LAM and the reported mitogenic response of meningiomas to progesterone, we recommend that the drug not be given to LAM patients with an MRI result consistent with diagnosis of meningioma.

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  • [CommentIn] JAMA. 2002 Mar 20;287(11):1397-8 [11903021.001]
  • (PMID = 11597290.001).
  • [ISSN] 0098-7484
  • [Journal-full-title] JAMA
  • [ISO-abbreviation] JAMA
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 4G7DS2Q64Y / Progesterone
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7. Zwerdling T, Dothage J: Meningiomas in children and adolescents. J Pediatr Hematol Oncol; 2002 Mar-Apr;24(3):199-204
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  • [Title] Meningiomas in children and adolescents.
  • PURPOSE: To review the diagnosis, treatment, and long-term outcome of children and adolescents with meningiomas diagnosed by a single institution and compare these findings with other published data.
  • PATIENTS AND METHODS: A 25-year retrospective analysis of 18 patients with meningioma diagnosed at Children's Hospital Medical Center, Cincinnati, Ohio was performed.
  • A literature review of published reports was undertaken to compare evaluation. treatment, and outcome for similar patients.
  • The most common symptoms were headache (5) and seizures (5), although most patients had multiple symptoms.
  • Comorbid diagnoses were common, including developmental delay, balanced chromosomal translocation, type I diabetes mellitus, neurofibromatosis, Klinefelter syndrome, and seizures.
  • Four patients had malignant meningiomas.
  • Two patients were treated with radiotherapy only, one had chemotherapy only, and two underwent both.
  • Long-term sequelae include seizures, diabetes insipidus, blindness, neuropsychologic abnormalities, and multiple surgical procedures.
  • CONCLUSIONS: Based on this study and a literature review, the roles of surgery, radiation, and chemotherapy remain unclear.
  • Long-term outcome for patients with meningiomas, especially as it relates to cognitive function, is rarely reported.
  • This group of patients has a high incidence of morbidity associated not only with treatment but also with preexisting diseases.
  • These data indicate the need for a national cooperative group study to better understand the evaluation, treatment, and outcome for children and adolescents who are treated for meningiomas.
  • [MeSH-major] Meningeal Neoplasms / pathology. Meningioma / pathology
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Combined Modality Therapy. Diabetes Insipidus, Neurogenic / etiology. Female. Humans. Infant. Male. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / therapy. Radiotherapy. Retrospective Studies. Seizures / etiology. Treatment Outcome

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  • (PMID = 11990306.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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8. Ragel BT, Couldwell WT, Wurster RD, Jensen RL: Chronic suppressive therapy with calcium channel antagonists for refractory meningiomas. Neurosurg Focus; 2007;23(4):E10
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  • [Title] Chronic suppressive therapy with calcium channel antagonists for refractory meningiomas.
  • In this article, the authors review the research supporting the use of calcium channel antagonists (CCAs) in the treatment of recurrent or unresectable meningiomas.
  • Calcium channel antagonists (for example, diltiazem and verapamil) are known to augment the effects of chemotherapy drugs (for example, vincristine) in multiple cancers.
  • The authors' initial work in this field was based on the then-emerging data that meningiomas are receptor positive for growth factor receptors (for example, platelet-derived growth factor [PDGF]), which are known to trigger calcium-dependent secondary messenger pathways.
  • In fact, they were able to show that CCAs block the growth stimulatory effects of multiple growth factors, including PDGF, in vitro and augment the growth inhibitory effects of hydroxyurea and RU486 (mifepristone).
  • In addition, diltiazem- and verapamil-treated meningiomas are less vascular and smaller, with decreased cell proliferation and increased apoptosis.
  • The use of CCAs is attractive as an adjunct treatment for unresectable or recurrent meningiomas because they are safe drugs with well-known side effect profiles that lend themselves to long-term chronic therapy.
  • [MeSH-major] Calcium Channel Blockers / therapeutic use. Meningeal Neoplasms / drug therapy. Meningioma / drug therapy
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Cell Proliferation / drug effects. Drug Therapy, Combination. Humans. Receptors, Growth Factor / drug effects

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  • (PMID = 17961034.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Calcium Channel Blockers; 0 / Receptors, Growth Factor
  • [Number-of-references] 3
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9. Batay F, Al-Mefty O: Growth dynamics of meningiomas in patients with multiple sclerosis treated with interferon: report of two cases. Acta Neurochir (Wien); 2002 Apr;144(4):365-8
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  • [Title] Growth dynamics of meningiomas in patients with multiple sclerosis treated with interferon: report of two cases.
  • BACKGROUND: Although multiple sclerosis (MS) is a common disease of the central nervous system, the association of intraparenchymal tumour has been rarely reported and the potential relationship between intracranial meningioma and MS has not been seriously analysed.
  • This report addresses the association of multiple sclerosis and intracranial meningioma and discusses the effect of interferon treatment on tumour progression.
  • CLINICAL PRESENTATION: We report two cases with multiple sclerosis, who developed meningioma four and twenty years after the diagnosis of MS was made.
  • Neither patient had a history of meningioma initially and both were being treated interferon when the meningioma was progressed.
  • FINDINGS: Histological examination of two cases revealed meningothelial meningioma.
  • CONCLUSIONS: We reported the association of multiple sclerosis and intracranial meningioma and observed the progression of the meningiomas during interferon treatment.
  • Although, we cannot exclude the coincidence between the two diseases we discussed suspicious relationship between the interferon treatment and the tumour progression.
  • [MeSH-major] Adjuvants, Immunologic / adverse effects. Adjuvants, Immunologic / therapeutic use. Interferon-beta / adverse effects. Interferon-beta / therapeutic use. Meningeal Neoplasms / pathology. Meningioma / pathology. Multiple Sclerosis / complications. Multiple Sclerosis / drug therapy
  • [MeSH-minor] Disease Progression. Female. Humans. Interferon beta-1a. Interferon beta-1b. Male. Middle Aged. Tomography, X-Ray Computed

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  • (PMID = 12021883.001).
  • [ISSN] 0001-6268
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 145155-23-3 / Interferon beta-1b; 77238-31-4 / Interferon-beta; XRO4566Q4R / Interferon beta-1a
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10. Lillehei KO, Donson AM, Kleinschmidt-DeMasters BK: Radiation-induced meningiomas: clinical, cytogenetic, and microarray features. Acta Neuropathol; 2008 Sep;116(3):289-301
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  • [Title] Radiation-induced meningiomas: clinical, cytogenetic, and microarray features.
  • Limited information exists about the clinical and biological features of radiation-induced meningiomas (RIMs), particularly those that follow high-dose therapeutic radiation.
  • Multiple RIMs were seen in six patients, with one patient developing his six RIMs sequentially over a 22-year interval.
  • Most RIMs could be managed surgically, either with a single extensive resection or additional resection(s).
  • Adjuvant stereotactic radiosurgery, external beam radiation, or chemotherapy were required in a minority (n = 6).
  • Most were WHO grade I meningiomas.
  • [MeSH-major] Meningeal Neoplasms / pathology. Meningioma / pathology. Neoplasms, Radiation-Induced / genetics. Neoplasms, Radiation-Induced / pathology
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Cytogenetics. Female. Gene Expression Profiling. Humans. In Situ Hybridization, Fluorescence. Infant. Karyotyping. Male. Middle Aged. Neoplasms / radiotherapy. Oligonucleotide Array Sequence Analysis. Time Factors

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  • (PMID = 18604545.001).
  • [ISSN] 1432-0533
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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11. Pozzati E, Zucchelli M, Schiavina M, Contini P, Foschini MP: Rapid growth and regression of intracranial meningiomas in lymphangioleiomyomatosis: case report. Surg Neurol; 2007 Dec;68(6):671-4; discussion 674-5
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  • [Title] Rapid growth and regression of intracranial meningiomas in lymphangioleiomyomatosis: case report.
  • It has been suggested that estrogens play a role in its evolution, and progesterone therapy is often provided in these cases.
  • CASE DESCRIPTION: We present a case of a postmenopausal woman with LAM treated with progesterone; subsequently, rapid growth of multiple intracranial meningiomas was observed.
  • CONCLUSIONS: This is a rare case of a non-pregnancy-related regression of meningiomas in a woman affected by LAM.
  • The significance of this association and the hormonal treatment of the disease are discussed.
  • [MeSH-major] Lymphangioleiomyomatosis / drug therapy. Meningeal Neoplasms / chemically induced. Meningioma / chemically induced. Progesterone / adverse effects. Progestins / adverse effects

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  • (PMID = 17586005.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Progestins; 4G7DS2Q64Y / Progesterone
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12. Mason WP, Gentili F, Macdonald DR, Hariharan S, Cruz CR, Abrey LE: Stabilization of disease progression by hydroxyurea in patients with recurrent or unresectable meningioma. J Neurosurg; 2002 Aug;97(2):341-6
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  • [Title] Stabilization of disease progression by hydroxyurea in patients with recurrent or unresectable meningioma.
  • OBJECT: The management of certain meningiomas of the skull base and those involving the dural venous sinuses remains a challenge.
  • In recent reports it has been suggested that hydroxyurea chemotherapy can cause regression of unresectable and recurrent meningiomas.
  • The authors report their experience in using hydroxyurea for the treatment of patients with recurrent or unresectable meningiomas.
  • METHODS: Hydroxyurea was administered at a dosage of approximately 20 mg/kg/day to 11 women and nine men (median age 59 years, range 31-75 years) with recurrent or unresectable intracranial meningiomas (12 basal, two parasagittal, and six multiple).
  • In 16 patients the meningiomas were benign, in three they had atypical features, and in one the meningioma was malignant.
  • Four patients with benign meningiomas had previously received radiotherapy (two were treated with conventional fractionated radiotherapy and two with stereotactic radiosurgery), three with atypical meningiomas received conventional fractionated radiotherapy, and the one with a malignant meningioma received conventional radiotherapy with additional stereotactic radiosurgery.
  • Tumor enlargement was documented in all patients on neuroimages obtained before initiation of hydroxyurea therapy.
  • All patients were evaluable for response to therapy.
  • In 12 patients with benign meningiomas, the disease had stabilized on neuroimages obtained posttreatment (median duration of treatment 122 weeks, range 8-151 weeks), and two of these showed clinical improvement.
  • One patient with a benign meningioma experienced a minor partial response that was noted after 39 weeks of treatment and was confirmed on neuroimaging and clinical evaluations.
  • In three others with benign meningiomas, progression was confirmed on neuroimages obtained after 41, 55, and 66 weeks, respectively: the 1-year freedom from progression rate was 0.93 (standard error 0.07) in patients with benign meningiomas.
  • In three patients with atypical meningiomas, the tumors had progressed on neuroimages obtained after 12, 19, and 45 weeks, respectively.
  • In the patient with a malignant meningioma, progression was confirmed on neuroimages obtained at 24 weeks.
  • Hydroxyurea has been reasonably well tolerated, although one patient discontinued therapy because of moderate myelosuppression.
  • CONCLUSIONS: Although tumor regression appears uncommon, these results indicate that hydroxyurea may arrest progression of unresectable or recurrent benign meningiomas.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Disease Progression. Hydroxyurea / therapeutic use. Meningeal Neoplasms / drug therapy. Meningeal Neoplasms / physiopathology. Meningioma / drug therapy. Meningioma / physiopathology. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / physiopathology
  • [MeSH-minor] Adult. Aged. Female. Humans. Karnofsky Performance Status. Male. Middle Aged. Remission Induction. Severity of Illness Index. Treatment Outcome

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  • (PMID = 12186462.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; X6Q56QN5QC / Hydroxyurea
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13. Ammoun S, Ristic N, Matthies C, Hilton DA, Hanemann CO: Targeting ERK1/2 activation and proliferation in human primary schwannoma cells with MEK1/2 inhibitor AZD6244. Neurobiol Dis; 2010 Jan;37(1):141-6
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  • Deficiency of the tumor suppressor merlin leads to the development of multiple tumors of the nervous system, such as schwannomas, meningiomas, and ependymomas.
  • Due to the benign character of these tumors, classical chemotherapy is ineffective.
  • Current therapies, surgery, and radiosurgery are local and quite invasive, thus new systemic treatments are required.
  • Here, we targeted MEK1/2 known as a convergence point for multiple cascades towards ERK1/2 activation and cell proliferation, using MEK1/2 inhibitor AZD6244 (ARRY-142886; Astra Zeneca).
  • Moreover, this drug was not toxic for either schwannoma or Schwann cells and has been reported to be safe with tolerable side effects.
  • Thus, AZD6244 can be considered as a drug candidate for schwannoma treatment.
  • [MeSH-major] Benzimidazoles / pharmacology. Enzyme Inhibitors / pharmacology. MAP Kinase Kinase 2 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Neurilemmoma / drug therapy. Neurilemmoma / physiopathology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Bromodeoxyuridine. Cell Proliferation / drug effects. Cells, Cultured. Humans. Immunoblotting. Immunohistochemistry. MAP Kinase Signaling System / drug effects. Phosphorylation. Platelet-Derived Growth Factor / metabolism. Schwann Cells / drug effects. Schwann Cells / physiology


14. Nayak L, Iwamoto FM: Primary brain tumors in the elderly. Curr Neurol Neurosci Rep; 2010 Jul;10(4):252-8
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  • Elderly patients with primary brain tumors also present unique challenges, such as the presence of multiple comorbidities and polypharmacy, decreased tolerance to chemotherapy, and an increased risk for radiation-induced neurotoxicity.
  • This review gives an overview of the treatment options for older patients with glioblastoma and other gliomas, primary central nervous system lymphomas (PCNSLs), and meningiomas.
  • Selected elderly glioblastoma patients with good performance status may benefit from aggressive treatment with surgical resection, radiotherapy, and possibly chemotherapy.
  • For older patients with PCNSLs, high-dose methotrexate-based chemotherapy should be the mainstay option; whole-brain radiation therapy should be avoided in chemosensitive tumors because of the high risk of irreversible and progressive neurotoxicity.
  • Meningiomas often may be followed up in elderly patients, as they usually are asymptomatic and have a slow growth rate.
  • Treatment for elderly patients with primary brain tumors should be individualized, and age alone should not preclude the use of more aggressive treatments.
  • [MeSH-minor] Aged. Aged, 80 and over. Diagnosis, Differential. Humans. Treatment Outcome

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  • [Cites] Neuroepidemiology. 2009;33(1):17-22 [19325245.001]
  • [Cites] Cancer. 2003 May 1;97(9):2262-6 [12712481.001]
  • [Cites] J Neurooncol. 2008 May;88(1):97-103 [18250965.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2008 Mar 15;70(4):987-92 [17967509.001]
  • [Cites] J Neurosurg. 2009 Jan;110(1):156-62 [18847342.001]
  • [Cites] J Clin Oncol. 2004 May 1;22(9):1583-8 [15051755.001]
  • [Cites] Cancer. 2009 Dec 1;115(23):5534-40 [19708033.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2001 Sep 1;51(1):100-7 [11516858.001]
  • [Cites] Cancer Res. 2001 Feb 1;61(3):1122-8 [11221842.001]
  • [Cites] J Clin Oncol. 2009 Feb 10;27(5):740-5 [19114704.001]
  • [Cites] Ann Neurol. 2008 Dec;64(6):628-34 [19107984.001]
  • [Cites] Cancer. 2003 Feb 1;97(3):657-62 [12548608.001]
  • [Cites] Neuro Oncol. 2002 Oct;4(4):278-99 [12356358.001]
  • [Cites] N Engl J Med. 2007 Apr 12;356(15):1527-35 [17429084.001]
  • [Cites] Cancer. 2009 Aug 15;115(16):3758-66 [19484785.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1992;23(1):9-17 [1572835.001]
  • [Cites] J Neurosurg. 1978 Sep;49(3):333-43 [355604.001]
  • [Cites] J Clin Oncol. 2009 Oct 1;27(28):4733-40 [19720927.001]
  • [Cites] Neuro Oncol. 2010 Feb;12(2):164-72 [20150383.001]
  • [Cites] Neuro Oncol. 2009 Apr;11(2):211-5 [18757775.001]
  • [Cites] Cancer. 2007 Sep 15;110(6):1338-44 [17647247.001]
  • [Cites] J Clin Oncol. 2006 Dec 20;24(36):5711-5 [17116938.001]
  • [Cites] Cancer. 2002 Oct 1;95(7):1504-10 [12237919.001]
  • [Cites] Neurosurgery. 2003 Jul;53(1):62-70; discussion 70-1 [12823874.001]
  • [Cites] J Clin Oncol. 2002 Dec 15;20(24):4643-8 [12488408.001]
  • [Cites] Acta Neurochir (Wien). 2003 Jan;145(1):5-10 [12545256.001]
  • [Cites] Cancer. 2004 May 15;100(10 ):2208-14 [15139066.001]
  • [Cites] Crit Rev Oncol Hematol. 2006 Dec;60(3):256-66 [17027278.001]
  • [Cites] J Neurooncol. 2009 Jan;91(1):95-100 [18758912.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1994 Jul 1;29(4):835-9 [8040031.001]
  • [Cites] J Clin Oncol. 2003 Jul 15;21(14):2726-31 [12860951.001]
  • [Cites] Arch Pathol Lab Med. 2005 May;129(5):624-31 [15859633.001]
  • [Cites] J Neurooncol. 2007 Nov;85(2):207-11 [17896079.001]
  • [Cites] Lancet. 2005 Sep 17-23;366(9490):985-90 [16168780.001]
  • [Cites] J Neurooncol. 2008 Aug;89(1):97-103 [18398569.001]
  • [Cites] Lancet. 2002 Mar 23;359(9311):1011-8 [11937180.001]
  • [Cites] Cancer. 1993 Apr 15;71(8):2585-97 [8453582.001]
  • [Cites] J Neurooncol. 1998 Aug;39(1):65-70 [9760071.001]
  • [Cites] J Clin Oncol. 2000 Sep;18(17):3144-50 [10963643.001]
  • [Cites] Neurology. 1997 May;48(5):1459-62 [9153494.001]
  • [Cites] Clin Cancer Res. 2004 Jan 1;10(1 Pt 1):228-33 [14734474.001]
  • [Cites] Neurosurgery. 2005 Nov;57(5):866-72; discussion 866-72 [16284557.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 2000 Jan;68(1):25-8 [10601396.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1979 Oct;5(10):1725-31 [231022.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10 ):987-96 [15758009.001]
  • [Cites] Neurology. 2009 Dec 15;73(24):2093-8 [19907009.001]
  • [Cites] Neurology. 2009 Apr 7;72(14):1217-22 [19349600.001]
  • (PMID = 20461477.001).
  • [ISSN] 1534-6293
  • [Journal-full-title] Current neurology and neuroscience reports
  • [ISO-abbreviation] Curr Neurol Neurosci Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 49
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15. Baird DT: Clinical uses of antiprogestogens. J Soc Gynecol Investig; 2000 Jan-Feb;7(1 Suppl):S49-52

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Compounds that inhibit the synthesis of progesterone, or antagonize progesterone action, have multiple effects including the induction of abortion, labor induction, contraception, and cervical ripening.
  • They also may be used in the treatment of endometriosis, fibromyomata, meningiomas, Cushing syndrome, and glaucoma.
  • Antiprogesterone compounds will play important roles in manipulating reproductive function for fertility control and in the treatment of hormone-dependent disease.
  • [MeSH-major] Hormone Antagonists / therapeutic use. Progestins / antagonists & inhibitors
  • [MeSH-minor] Abortion, Induced. Contraceptive Agents, Female. Female. Genital Diseases, Female / drug therapy. Humans. Labor, Induced. Pregnancy

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  • (PMID = 10732330.001).
  • [ISSN] 1071-5576
  • [Journal-full-title] Journal of the Society for Gynecologic Investigation
  • [ISO-abbreviation] J. Soc. Gynecol. Investig.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Contraceptive Agents, Female; 0 / Hormone Antagonists; 0 / Progestins
  • [Number-of-references] 37
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16. Rogers MP, Orav J, Black PM: The use of a simple Likert scale to measure quality of life in brain tumor patients. J Neurooncol; 2001 Nov;55(2):121-31
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  • The original scale, developed by Priestman, was modified to be more brain-tumor specific.
  • The patients had a variety of brain tumors ranging from meningiomas to high-grade gliomas.
  • The Total Score of the original scale and the Modified Total Score of the brain-specific version were explored in relationship to patient demographics and available clinical characteristics: age, gender, severity of tumor, location of tumor, survival rates, prior surgery, radiation, radiosurgery, and chemotherapy.
  • Patients with the worst prognosis in terms of tumor type were 5-6 points lower in quality of life than patients with intermediate or relatively good prognosis.
  • In a multiple regression model, adjusted for age, the overall score was related only to tumor severity and to gender, with women having significantly poorer functional status than men by 4 points.

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  • [Cites] Cancer. 1990 Jul 1;66(1):6-14 [2354409.001]
  • [Cites] J Neurooncol. 1997 Sep;34(3):263-78 [9258818.001]
  • [Cites] J Neurosci Nurs. 1998 Oct;30(5):322-5 [9816565.001]
  • [Cites] J Clin Oncol. 1992 Sep;10(9):1379-85 [1325539.001]
  • [Cites] Eur J Cancer. 1998 Nov;34(12):1902-9 [10023313.001]
  • [Cites] Ann Neurol. 1994 Jul;36(1):48-54 [8024261.001]
  • [Cites] J Neurooncol. 1992 Nov;14(3):243-53 [1460487.001]
  • [Cites] J Neurosurg. 1989 Jan;70(1):18-23 [2642546.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1992 May;55(5):372-6 [1602310.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1997 Apr 1;38(1):9-20 [9211998.001]
  • [Cites] Cancer. 1995 Mar 1;75(5):1151-61 [7850714.001]
  • [Cites] Br J Neurosurg. 1999 Oct;13(5):480-5 [10627779.001]
  • [Cites] J Neurosurg. 2000 Dec;93(6):917-26 [11117863.001]
  • [Cites] J Natl Cancer Inst. 1990 Mar 21;82(6):531-2 [2313727.001]
  • [Cites] Lancet. 1976 Apr 24;1(7965):899-900 [58161.001]
  • [Cites] Disabil Rehabil. 1996 Sep;18(9):460-8 [8877305.001]
  • [Cites] J Clin Oncol. 1994 Mar;12(3):608-16 [8120561.001]
  • [Cites] Radiother Oncol. 1996 Oct;41(1):55-9 [8961368.001]
  • [Cites] Brain. 1984 Mar;107 ( Pt 1):81-93 [6697163.001]
  • [Cites] Ann Neurol. 1990 Dec;28(6):818-22 [2178330.001]
  • (PMID = 11817703.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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17. McPherson CM, Brown J, Kim AW, DeMonte F: Regression of intracranial rosai-dorfman disease following corticosteroid therapy. Case report. J Neurosurg; 2006 May;104(5):840-4
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  • [Title] Regression of intracranial rosai-dorfman disease following corticosteroid therapy. Case report.
  • The treatment of CNS RDD as reported in the literature has primarily involved a surgical technique.
  • The authors report on the case of a 53-year-old man presenting with multiple skull base lesions mimicking meningiomas.
  • This report represents the first case of the resolution of intracranial RDD following corticosteroid therapy.
  • Corticosteroid agents should be considered an effective option in the treatment of CNS RDD.
  • [MeSH-minor] Brain Stem / pathology. Craniotomy. Diagnosis, Differential. Histiocytes / pathology. Humans. Lymphocytes / pathology. Magnetic Resonance Imaging. Male. Middle Aged. Neurologic Examination / drug effects. Postoperative Care. Recurrence. Skull Base / pathology


18. Epstein NE, Drexler S, Schneider J: Clear cell meningioma of the cauda equina in an adult: case report and literature review. J Spinal Disord Tech; 2005 Dec;18(6):539-43
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  • [Title] Clear cell meningioma of the cauda equina in an adult: case report and literature review.
  • In the pediatric population, clear cell meningiomas are more frequently intracranial than intraspinal in location.
  • Tumors recur in up to 40% of cases within 15 postoperative months and are often managed with repeated resection with or without radiation therapy.
  • The management strategy for adults with clear cell meningiomas involving the lumbar spinal canal (cauda equina) is less clearly defined.
  • Differential diagnoses included meningioma versus renal cell carcinoma.
  • Negative postoperative chest, abdominal, and pelvic computed tomography studies ruled out tumor of renal cell origin.
  • Consultations with multiple oncologists and radiation therapists recommended neither radiation nor chemotherapy following this initial surgery.
  • The high recurrence rate for clear cell meningiomas in children requires repeated tumor resection with or without secondary radiation therapy.
  • Following gross total resection of lumbar tumors in adults, reserving radiation therapy for secondary recurrences provides optimal management.
  • [MeSH-major] Cauda Equina / pathology. Cauda Equina / surgery. Meningioma / diagnosis. Meningioma / surgery. Peripheral Nervous System Neoplasms / diagnosis. Peripheral Nervous System Neoplasms / surgery
  • [MeSH-minor] Adult. Female. Humans. Paresis / diagnosis. Paresis / etiology. Treatment Outcome

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  • (PMID = 16306847.001).
  • [ISSN] 1536-0652
  • [Journal-full-title] Journal of spinal disorders & techniques
  • [ISO-abbreviation] J Spinal Disord Tech
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 10
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19. Kasuya H, Kikuchi K, Imamura T, Kawashima A, Aihara Y, Ochiai T, Yamaguchi K, Fukamachi K, Hori T, Shiseki M, Tozuka K: [Two cases of methicillin-resistant Staphylococcus aureus (MRSA) sepsis following craniotomy]. No Shinkei Geka; 2000 May;28(5):429-34
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  • In case 1, a petroclival meningioma was subtotally removed and lumbar drainage was inserted postoperatively to prevent cerebrospinal fluid leakage.
  • Two weeks after the procedure, the patient revealed continuous spiking fevers related to MRSA sepsis, which did not improve with vancomycin and arbekacin administration.
  • In case 2, seven days after surgery for multiple meningioma, the patient exhibited spiking fevers and swelling in the left leg.
  • [MeSH-major] Aminoglycosides. Craniotomy. Postoperative Complications. Sepsis / therapy. Staphylococcal Infections / therapy
  • [MeSH-minor] Adult. Aged. Alanine / administration & dosage. Alanine / analogs & derivatives. Ampicillin / administration & dosage. Anti-Bacterial Agents / administration & dosage. Dibekacin / administration & dosage. Dibekacin / analogs & derivatives. Drug Therapy, Combination / administration & dosage. Female. Humans. Male. Meningeal Neoplasms / surgery. Meningioma / surgery. Methicillin Resistance. Sulbactam / administration & dosage. Thienamycins / administration & dosage. Treatment Outcome. Vancomycin / administration & dosage

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  • (PMID = 10806626.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] JAPAN
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Anti-Bacterial Agents; 0 / Thienamycins; 2198-64-3 / N-benzoylalanine; 45ZFO9E525 / Dibekacin; 65DT0ML581 / sultamicillin; 6Q205EH1VU / Vancomycin; 7C782967RD / Ampicillin; G7V6SLI20L / habekacin; OF5P57N2ZX / Alanine; S4TF6I2330 / Sulbactam; W9769W09JF / panipenem
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20. Evans DG: Neurofibromatosis 2 [Bilateral acoustic neurofibromatosis, central neurofibromatosis, NF2, neurofibromatosis type II]. Genet Med; 2009 Sep;11(9):599-610
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  • [Title] Neurofibromatosis 2 [Bilateral acoustic neurofibromatosis, central neurofibromatosis, NF2, neurofibromatosis type II].
  • Meningiomas and ependymomas are other tumor features.
  • Although truncating mutations (nonsense and frameshifts) are the most frequent germline event and cause the most severe disease, single and multiple exon deletions are common.
  • A strategy for detection of the latter is vital for a sensitive analysis.
  • Surgery remains the focus of current management, although watchful waiting and occasionally radiation treatment have a role.
  • In the future, the development of tailored drug therapies aimed at the genetic level are likely to provide huge improvements for this devastating, life limiting condition.

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  • (PMID = 19652604.001).
  • [ISSN] 1530-0366
  • [Journal-full-title] Genetics in medicine : official journal of the American College of Medical Genetics
  • [ISO-abbreviation] Genet. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 85
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21. Stieber VW: Radiation therapy for visual pathway tumors. J Neuroophthalmol; 2008 Sep;28(3):222-30
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  • [Title] Radiation therapy for visual pathway tumors.
  • Most commonly, photons are delivered via multiple focused beams aimed at the tumor while sparing adjacent tissues.
  • The dose can be delivered in multiple treatments (radiation therapy) or in a single treatment (radiosurgery).
  • Children with visual pathway gliomas should be treated with chemotherapy alone, delaying the use of radiation therapy until progression.
  • Definitive radiation therapy of optic nerve sheath meningiomas results in stable vision in most patients.
  • Radiation therapy or radiosurgery for pituitary tumors can result in control of both tumor growth and hormone hypersecretion.
  • Postoperative radiation therapy or radiosurgery of craniopharyngiomas significantly improves local control rates compared with surgery alone.
  • Radiation therapy is highly effective for eradicating orbital pseudolymphoma and lymphoma.
  • The risk of complications from radiation treatment is dependent on the organ at risk, the cumulative dose it receives, and the dose delivered per fraction.
  • [MeSH-minor] Craniopharyngioma / complications. Craniopharyngioma / pathology. Craniopharyngioma / radiotherapy. Humans. Lymphoma / complications. Lymphoma / pathology. Lymphoma / radiotherapy. Meningioma / complications. Meningioma / pathology. Meningioma / radiotherapy. Pituitary Neoplasms / complications. Pituitary Neoplasms / pathology. Pituitary Neoplasms / radiotherapy. Pseudolymphoma / complications. Pseudolymphoma / pathology. Pseudolymphoma / radiotherapy. Radiation Dosage

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  • (PMID = 18769290.001).
  • [ISSN] 1536-5166
  • [Journal-full-title] Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society
  • [ISO-abbreviation] J Neuroophthalmol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 106
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22. Combes C, Redondo A, Rey A: [Contraception and neurology]. Ann Med Interne (Paris); 2002 Oct;153(6):363-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • There is however a formal contraindication for oral contraception, even with mini-dose contraceptives, for women with a history of cerebral venous thrombosis.
  • Contraception has no effect on epilepsy but oral contraceptives may be inhibited by inducing anti-seizure drugs.
  • Non-inducing drugs are preferable.
  • The course of certain brain tumors known to express estrogen or progesterone receptors (particularly meningiomas and hemangioblastomas) may worsen with oral contraception, which is formally contradicted except when search for hormone receptors is negative.
  • Oral contraception has no influence in other disease such as multiple sclerosis
  • [MeSH-minor] Adult. Age Factors. Brain / pathology. Drug Synergism. Epilepsy / drug therapy. Female. Hemangioblastoma / chemistry. Humans. Meningioma / chemistry. Receptors, Estrogen / analysis. Risk Factors. Sclerosis. Vasodilation

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  • (PMID = 12486383.001).
  • [ISSN] 0003-410X
  • [Journal-full-title] Annales de meĢdecine interne
  • [ISO-abbreviation] Ann Med Interne (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / Contraceptives, Oral, Hormonal; 0 / Receptors, Estrogen
  • [Number-of-references] 24
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23. Yonekawa Y: [Operative neurosurgery: personal view and historical backgrounds. (5) Meningioma]. No Shinkei Geka; 2009 Jan;37(1):71-90
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  • [Title] [Operative neurosurgery: personal view and historical backgrounds. (5) Meningioma].
  • The author reports his experience of 410 surgeries of meningiomas on 365 cases during the last 13.5 years, including 51 surgeries on recurrent meningiomas and 8 surgeries with the change of initial approach on the same meningiomas.
  • In the surgical management of meningiomas, following comments are to be emphasized: Appropriate approach and interruption of blood supply are of cardinal importance in surgical management of meningiomas.
  • For the latter purpose, preoperative embolization of feeding arteries is recommended especially in deep seated and large meningiomas more than 3 cm in diameter for carrying out their surgical extirpation fast and radically.
  • Olfactory groove meningiomas, planum sphenoidal meningiomas, tuberculum sellae meningiomas and sphenoid ridge meningiomas are managed with pterional approach.
  • The latter two meningiomas may necessitate selective extradural anterior clinoidectomy SEAC.
  • For the management of large midline meningiomas, combination with interhemispheric approach is necessary to manage pial supply appropriately for the preservation of circulation of the anterior cerebral artery ACA.
  • Extension of the former two meningiomas to the other side can be managed with falcal incision and/or drilling out of the crista galli without performing a bifrontal approach.
  • Reduction of exophthalmos due to sphenoid ridge meningiomas infiltrating Periorbita and extraocular muscles is hardly to be expected even after subtotal removal and extensive decompression of the orbita at the superior and lateral walls in combination with SEAC.
  • Meningiomas in the cavernous sinus should be observed as long as possible in case of no growth, as they remain the same in their size and extension mostly for a long time.
  • Appropriate approaches for meningiomas arising from the incisura tentorii would be either the amygdalohippocampectomy AHE approach namely transSylvian transsulcus circularis approach for their anterior localization or the supracerebellar transtentorial SCTT approach for the posterior localization in the sitting position.
  • Meningiomas of the falcotentorial junction are managed also with this approach but may necessitate combination of the suboccipital transtentorial approach large upper clivus meningiomas can be removed more effectively by paramedian or lateral suboccipital craniotomy via SCTT approach in the sitting position rather than the subtemporal transpetrosal approach.
  • Special mention is made to transvertebralis (dural) ring approach TVRA for the foramen magnum or lower clivus meningiomas, in which the vertebral artery can be mobilized without performing more extensive far lateral approach.
  • Difficulties of management of recurrent parasagittal meningiomas with the location corresponding to the gyrus paracentralis plus supplementary motor area are to be emphasized.
  • Difficulties of management of recurrent meningiomas represented by atypical or anaplastic meningiomas WHO grade II or III which can not be managed only by surgical removal is discussed by presenting some example cases.
  • Biological activity of meningiomas in different location can be quite different in multiple recurrent meningiomas.
  • Meningiomas intractable to irradiation and/or chemotherapy are another challenging topic, being beyond the scope of this paper.
  • [MeSH-major] Meningeal Neoplasms / surgery. Meningioma / surgery. Neurosurgical Procedures / methods
  • [MeSH-minor] Aged. Diagnostic Imaging. Embolization, Therapeutic. Female. Humans. Male. Middle Aged. Preoperative Care

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  • (PMID = 19175037.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 39
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24. Hanemann CO: Magic but treatable? Tumours due to loss of merlin. Brain; 2008 Mar;131(Pt 3):606-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Alterations in the NF2 gene coding for merlin cause all tumours that occur in patients suffering from neurofibromatosis type 2, all spontaneous schwannomas and the majority of meningiomas.
  • Thus merlin's tumours are quite frequent and also numerous when inherited as part of meurofibromatosis type 2.
  • Tumours caused by mutations in the NF2 gene are benign and thus do not respond to classical chemotherapy.
  • Surgery and radiosurgery are only local therapies and the patients frequently require multiple treatments.
  • This highlights the medical need to understand how merlin loss results in tumourigenesis and the need to find new systemic therapies.
  • This brings about the rather unique opportunity to both analyse the consequences of the gene defect and identify new therapeutic targets.
  • Existing therapeutic options, surgery and radiosurgery, including new data on the latter will be reviewed.
  • Finally, I will discuss how loss of merlin leads to tumourigenesis in order to understand the rationale for emerging new therapeutic targets.
  • [MeSH-minor] Adult. Diagnosis, Differential. Ependymoma / diagnosis. Ependymoma / genetics. Ependymoma / therapy. Humans. Meningioma / diagnosis. Meningioma / genetics. Meningioma / therapy. Middle Aged. Neurilemmoma / diagnosis. Neurilemmoma / genetics. Neurilemmoma / therapy

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  • (PMID = 17940085.001).
  • [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; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neurofibromin 2
  • [Number-of-references] 108
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25. Haroun RI, Clatterbuck RE, Gibbons MC, Burger PC, Parker R, Fruehauf JP, Brem H: Extreme drug resistance in primary brain tumors: in vitro analysis of 64 resection specimens. J Neurooncol; 2002 Jun;58(2):115-23
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  • [Title] Extreme drug resistance in primary brain tumors: in vitro analysis of 64 resection specimens.
  • Understanding chemoresistance profiles of brain tumors may aid in more educated selection of chemotherapeutic regimens for clinical trials and patient treatment.
  • Although the literature contains many reports of the application of drug resistance assays, little is known about extreme drug resistance (EDR) in primary brain tumors.
  • Brain tumor specimens were tested against 13 different chemotherapeutic agents using an extreme drug resistance assay.
  • A drug resistance profile (extreme, intermediate, or low) was determined based on statistical comparison to a historical database of tumor specimens tested against the same panel of chemotherapeutic agents.
  • Brain tumor specimens were classified histologically as Grade IV astrocytoma (glioblastoma multiforme, n = 35), Grade II/III astrocytoma (n = 11), oligodendroglioma (n = 6), meningioma (n = 9), hemangiopericytoma (n = 2), and ependymoma (n = 1).
  • A large percentage of glioblastomas displayed extreme drug resistance to paclitaxel (69%, n = 35), SN38 (75%, n = 28), and vincristine (38%, n = 29).
  • The majority of Grade II/III astrocytomas displayed extreme drug resistance to carboplatin (67%, n = 6), cisplatin (60%, n = 10), and paclitaxel (60%, n = 10).
  • In a similar fashion, oligodendrogliomas displayed extreme drug resistance to vincristine (60%, n = 5) and paclitaxel (50% n = 6).
  • Most meningiomas displayed extreme drug resistance to vincristine (75%, n = 8), dacarbazine (63%, n = 8), and 4-HC (50%, n = 8).
  • Through the continued analysis of brain tumor specimens and compilation of data from multiple institutions, chemoresistance profiles could assist in the development of rationale clinical trials and treatment regimens for patients with brain tumors.
  • [MeSH-major] Brain Neoplasms / drug therapy. Drug Resistance, Neoplasm
  • [MeSH-minor] Cell Division / drug effects. Humans

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  • [Cites] Cancer. 1997 Apr 1;79(7):1447-50 [9083168.001]
  • [Cites] J Clin Oncol. 1991 May;9(5):860-4 [1849986.001]
  • [Cites] Cancer. 1996 Mar 15;77(6):1020-5 [8635118.001]
  • [Cites] J Neurosurg. 1997 May;86(5):840-4 [9126900.001]
  • [Cites] Cancer Chemother Pharmacol. 1990;26(4):263-8 [2369790.001]
  • [Cites] Brain Pathol. 1993 Jul;3(3):255-68 [8293185.001]
  • [Cites] N Engl J Med. 1980 Dec 4;303(23):1323-9 [7001230.001]
  • [Cites] Br J Cancer. 1997;76(4):445-50 [9275020.001]
  • [Cites] Cancer Treat Rep. 1983 Feb;67(2):121-32 [6337710.001]
  • [Cites] Neurosurgery. 1997 Feb;40(2):271-5 [9007858.001]
  • [Cites] Cancer Treat Rep. 1984 Apr;68(4):611-3 [6713417.001]
  • [Cites] Cancer Treat Rev. 1998 Oct;24(5):307-16 [9861194.001]
  • [Cites] Adv Drug Deliv Rev. 1999 Apr 5;36(2-3):195-209 [10837716.001]
  • [Cites] Neurosurgery. 1999 Dec;45(6):1279-91; discussion 191 [10598694.001]
  • [Cites] J Natl Cancer Inst. 1990 Apr 4;82(7):582-8 [2313735.001]
  • [Cites] Neurosurgery. 1997 Jul;41(1):44-8; discussion 48-9 [9218294.001]
  • [Cites] J Clin Oncol. 1997 Dec;15(12):3427-32 [9396393.001]
  • [Cites] Cancer Res. 1985 Nov;45(11 Pt 1):5436-41 [4053017.001]
  • [Cites] J Clin Oncol. 1997 Sep;15(9):3121-8 [9294475.001]
  • [Cites] Cancer Res. 1993 Jan 15;53(2):329-33 [8417826.001]
  • [Cites] Leuk Res. 1986;10(4):445-9 [2421109.001]
  • [Cites] Neurosurg Rev. 1984;7(1):3-12 [6379510.001]
  • [Cites] Neurosurgery. 1993 Mar;32(3):365-70; discussion 371 [8455760.001]
  • [Cites] N Engl J Med. 2000 Nov 9;343(19):1350-4 [11070098.001]
  • [Cites] Lancet. 1991 Mar 23;337(8743):711-4 [1672185.001]
  • [Cites] J Neurooncol. 1994;20(2):111-20 [7807189.001]
  • [Cites] J Neurooncol. 1993 Jan;15(1):75-7 [8455065.001]
  • [Cites] J Natl Cancer Inst. 1990 Jan 17;82(2):96-101 [2403594.001]
  • [Cites] J Natl Cancer Inst. 1998 Oct 7;90(19):1473-9 [9776413.001]
  • [Cites] Cancer Chemother Rep. 1968 Dec;52(7):733-41 [5743710.001]
  • [Cites] Neurology. 1980 Sep;30(9):907-11 [6252514.001]
  • [Cites] J Neurosurg. 1978 Sep;49(3):333-43 [355604.001]
  • [Cites] J Neurooncol. 1992 Feb;12(2):187-91 [1560266.001]
  • [Cites] Anticancer Res. 1993 Sep-Oct;13(5C):1825-9 [8267387.001]
  • [Cites] N Engl J Med. 1966 May 26;274(21):1171-3 [5934954.001]
  • [Cites] Ann Neurol. 1988 Apr;23(4):360-4 [3382171.001]
  • [Cites] J Neurosurg. 1997 May;86(5):845-52 [9126901.001]
  • [Cites] J Neurosurg. 1992 May;76(5):741-5 [1564535.001]
  • [Cites] J Clin Oncol. 1995 Aug;13(8):2066-71 [7636549.001]
  • [Cites] Cancer Treat Rep. 1980 Feb-Mar;64(2-3):237-44 [7407756.001]
  • [Cites] Cancer Lett. 1988 Aug 30;41(3):323-32 [3165705.001]
  • [Cites] Cancer Lett. 1990 Dec 3;55(2):153-8 [2265415.001]
  • [Cites] Baillieres Clin Neurol. 1996 Jun;5(2):371-93 [8781278.001]
  • [Cites] J Neurooncol. 1996 Sep;29(3):269-72 [8858533.001]
  • [Cites] Cancer. 1973 Jul;32(1):38-43 [4716783.001]
  • [Cites] J Neurooncol. 1994;19(1):69-74 [7815106.001]
  • [Cites] N Engl J Med. 1978 Jun 15;298(24):1321-7 [77475.001]
  • [Cites] JAMA. 1972 Oct 30;222(5):549-52 [4343318.001]
  • [Cites] Cancer. 1993 Apr 15;71(8):2585-97 [8453582.001]
  • [Cites] Science. 1977 Jul 29;197(4302):461-3 [560061.001]
  • [Cites] Cancer. 1973 May;31(5):1164-9 [4705154.001]
  • [Cites] J Clin Oncol. 1996 Aug;14(8):2316-21 [8708723.001]
  • [Cites] Science. 1990 Mar 23;247(4949 Pt 1):1457-61 [2108497.001]
  • [Cites] J Clin Oncol. 1994 Oct;12(10):2013-21 [7931469.001]
  • [Cites] J Neurosurg. 1991 Mar;74(3):441-6 [1993909.001]
  • [Cites] Lancet. 1995 Apr 22;345(8956):1008-12 [7723496.001]
  • (PMID = 12164682.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-09574; United States / NCI NIH HHS / CA / U19 CA52857
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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