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1. Salhia B, Rutka JT, Lingwood C, Nutikka A, Van Furth WR: The treatment of malignant meningioma with verotoxin. Neoplasia; 2002 Jul-Aug;4(4):304-11
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  • [Title] The treatment of malignant meningioma with verotoxin.
  • Malignant meningiomas (MMs) are aggressive intracranial neoplasms with a 75% 5-year recurrence rate.
  • To investigate the potential use of VT1 as a clinical agent for MM, we initially tested 16 meningiomas for Gb(3) expression.
  • Nine of 11 MMs (82%), but only one of five benign meningiomas (20%), were positive for Gb(3).
  • An orthotopic xenograft model was used to test the efficacy of VT1 treatment for MM.
  • We first demonstrated that Gb(3) was highly expressed by the MM cell line, IOMM-Lee, and that this cell line was highly sensitive to VT1 treatment in vitro.
  • VT1 treatment of MM is effective in our orthotopic xenograft model, and warrants further exploration as a potential treatment for these highly anaplastic and aggressive neoplasms.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Meningeal Neoplasms / drug therapy. Meningioma / drug therapy. Shiga Toxin 1 / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Division / drug effects. Drug Screening Assays, Antitumor. Female. Humans. Male. Mice. Mice, Nude. Middle Aged. Neovascularization, Pathologic / drug therapy. Trihexosylceramides / analysis. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • [Cites] Biochim Biophys Acta. 1999 Oct 8;1455(2-3):375-86 [10571026.001]
  • [Cites] Blood. 1999 Oct 15;94(8):2901-10 [10515895.001]
  • [Cites] Biosci Rep. 1999 Oct;19(5):345-54 [10763802.001]
  • [Cites] Acta Neurochir (Wien). 2000;142(5):493-505 [10898356.001]
  • [Cites] Brain Res. 2000 Nov 10;883(1):87-97 [11063991.001]
  • [Cites] J Neuropathol Exp Neurol. 2000 Oct;59(10):872-9 [11079777.001]
  • [Cites] J Neurooncol. 2000 Jun;48(2):151-60 [11083080.001]
  • [Cites] Steroids. 2000 Oct-Nov;65(10-11):795-800 [11108890.001]
  • [Cites] Neurol India. 2000 Dec;48(4):338-42 [11146597.001]
  • [Cites] J Neurooncol. 2000 Aug;49(1):27-39 [11131984.001]
  • [Cites] J Neurooncol. 2000 Sep;49(2):165-70 [11206012.001]
  • [Cites] Int J Cancer. 2001 May 15;92(4):551-4 [11304690.001]
  • [Cites] Microbes Infect. 2001 May;3(6):493-507 [11377211.001]
  • [Cites] Crit Rev Oncol Hematol. 2001 Jul-Aug;39(1-2):99-106 [11418306.001]
  • [Cites] Br J Haematol. 2001 Jun;113(4):891-7 [11442480.001]
  • [Cites] Acta Neuropathol. 2002 Jan;103(1):1-10 [11837741.001]
  • [Cites] Surg Neurol. 1986 Mar;25(3):233-42 [3945904.001]
  • [Cites] Neurosurgery. 1990 Sep;27(3):389-95; discussion 396 [2234331.001]
  • [Cites] Eur J Cancer. 1993;29A(15):2118-25 [8297651.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Jul 18;92(15):6996-7000 [7624357.001]
  • [Cites] J Pathol. 1996 Apr;178(4):442-6 [8691324.001]
  • [Cites] Trends Microbiol. 1996 Apr;4(4):147-53 [8728608.001]
  • [Cites] Blood. 1997 Oct 1;90(7):2757-67 [9326243.001]
  • [Cites] Oncol Res. 1997;9(10):553-63 [9507533.001]
  • [Cites] Acta Neurochir (Wien). 1998;140(4):333-40 [9689324.001]
  • [Cites] J Neurooncol. 1998 Nov;40(2):137-50 [9892096.001]
  • [Cites] Oncol Res. 1999;11(1):33-9 [10451029.001]
  • [Cites] J Neurosurg. 2000 Feb;92(2):306-14 [10659019.001]
  • (PMID = 12082546.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Shiga Toxin 1; 0 / Trihexosylceramides; 71965-57-6 / globotriaosylceramide
  • [Other-IDs] NLM/ PMC1531702
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2. Kondraganti S, Gondi CS, Gujrati M, McCutcheon I, Dinh DH, Rao JS, Olivero WC: Restoration of tissue factor pathway inhibitor inhibits invasion and tumor growth in vitro and in vivo in a malignant meningioma cell line. Int J Oncol; 2006 Jul;29(1):25-32
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  • [Title] Restoration of tissue factor pathway inhibitor inhibits invasion and tumor growth in vitro and in vivo in a malignant meningioma cell line.
  • Tissue factor pathway inhibitor 2 (TFPI-2) is a 32-kDa extracellular matrix-associated kunitz-type serine proteinase inhibitor.
  • Previous studies have shown high expression of TFPI-2 by benign tumors and low or absent expression in highly malignant tumors.
  • Malignant meningiomas constitute 10-15% of all meningiomas and our previous studies revealed loss of expression of TFPI-2 in malignant gliomas.
  • To investigate the role of TFPI-2 in the invasiveness of malignant meningiomas, we stably transfected the human meningioma cell line, IOMM-Lee, with a vector capable of expressing a transcript complementary to the full length of TFPI-2 mRNA in a sense orientation.
  • Our data substantiate our previous observation that TFPI-2 plays an important role in tumor progression and has potential in anti-cancer therapy.

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  • [Cites] Arch Biochem Biophys. 1995 Feb 20;317(1):311-4 [7872799.001]
  • [Cites] Cancer Res. 1993 Sep 15;53(18):4143-7 [8395977.001]
  • [Cites] J Biochem. 1994 Nov;116(5):939-42 [7896752.001]
  • [Cites] Arch Biochem Biophys. 1995 May 10;319(1):55-62 [7539605.001]
  • [Cites] Eur J Biochem. 1996 Jan 15;235(1-2):310-6 [8631347.001]
  • [Cites] Cancer. 1996 May 1;77(9):1877-83 [8646688.001]
  • [Cites] Genomics. 1996 Jul 1;35(1):267-8 [8661135.001]
  • [Cites] Oncology (Williston Park). 1996 May;10(5):747-56; discussion 756-9 [8738830.001]
  • [Cites] Science. 1997 Feb 21;275(5303):1132-6 [9027315.001]
  • [Cites] Cell. 1997 Feb 7;88(3):355-65 [9039262.001]
  • [Cites] Clin Exp Metastasis. 1997 Jul;15(4):440-6 [9219733.001]
  • [Cites] Trends Biochem Sci. 1997 Aug;22(8):299-306 [9270303.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 1998 Jan;18(1):40-6 [9445254.001]
  • [Cites] Blood. 1998 Apr 15;91(8):2698-703 [9531578.001]
  • [Cites] Placenta. 1998 Mar-Apr;19(2-3):217-23 [9548189.001]
  • [Cites] Int J Cancer. 1998 May 29;76(5):749-56 [9610735.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9064-6 [9689032.001]
  • [Cites] Semin Thromb Hemost. 1998;24(3):207-10 [9701449.001]
  • [Cites] Cancer Res. 1998 Oct 1;58(19):4461-7 [9766679.001]
  • [Cites] Oncogene. 1998 Dec 24;17(25):3247-59 [9916987.001]
  • [Cites] Cell Death Differ. 1999 Jul;6(7):673-82 [10453078.001]
  • [Cites] Arch Biochem Biophys. 1999 Oct 1;370(1):112-8 [10496984.001]
  • [Cites] J Neurosurg. 1995 Jan;82(1):17-27 [7815129.001]
  • [Cites] J Invest Dermatol. 1995 Mar;104(3):379-83 [7861006.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Apr 12;91(8):3353-7 [8159751.001]
  • [Cites] Int J Oncol. 2001 Jan;18(1):127-31 [11115549.001]
  • [Cites] Clin Cancer Res. 2001 Mar;7(3):570-6 [11297250.001]
  • [Cites] J Biol Chem. 2001 Apr 13;276(15):12241-8 [11278667.001]
  • [Cites] Clin Exp Metastasis. 2000;18(3):239-44 [11315097.001]
  • [Cites] Int J Oncol. 2001 Sep;19(3):591-7 [11494041.001]
  • [Cites] Gynecol Oncol. 2001 Nov;83(2):325-33 [11606093.001]
  • [Cites] Oncogene. 2001 Oct 18;20(47):6938-45 [11687973.001]
  • [Cites] Cancer Res. 2002 Apr 1;62(7):2184-91 [11929842.001]
  • [Cites] Nature. 1970 Aug 15;227(5259):680-5 [5432063.001]
  • [Cites] Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 [388439.001]
  • [Cites] Cancer Res. 1990 Dec 15;50(24):7758-64 [2253219.001]
  • [Cites] J Biochem. 1990 Oct;108(4):537-43 [1963430.001]
  • [Cites] Cancer Res. 1992 Sep 15;52(18):5046-53 [1387587.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Dec 15;89(24):11832-6 [1465406.001]
  • (PMID = 16773181.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS47699; United States / NCI NIH HHS / CA / R01 CA075557; United States / NCI NIH HHS / CA / CA75557; United States / NCI NIH HHS / CA / CA116708; United States / NCI NIH HHS / CA / CA95058; United States / NCI NIH HHS / CA / R01 CA116708; United States / NINDS NIH HHS / NS / R01 NS047699; United States / NCI NIH HHS / CA / R01 CA095058; United States / NCI NIH HHS / CA / R01 CA092393; United States / NCI NIH HHS / CA / CA92393
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Glycoproteins; 0 / Laminin; 0 / Lipoproteins; 0 / Proteoglycans; 0 / bcl-2-Associated X Protein; 0 / lipoprotein-associated coagulation inhibitor; 0 / tissue-factor-pathway inhibitor 2; 119978-18-6 / matrigel; 9007-34-5 / Collagen; 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ NIHMS9141; NLM/ PMC1479607
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3. Haase D, Schmidl S, Ewald C, Kalff R, Huebner C, Firsching R, Keilhoff G, Evert M, Paulus W, Gutmann DH, Lal A, Mawrin C: Fatty acid synthase as a novel target for meningioma therapy. Neuro Oncol; 2010 Aug;12(8):844-54
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  • [Title] Fatty acid synthase as a novel target for meningioma therapy.
  • Similar to other hormone receptor-positive tumor types, meningiomas are progesterone receptor- and estrogen receptor-immunoreactive brain tumors.
  • To define the role of FAS in human meningioma growth control, we first analyzed the FAS expression using a tissue microarray containing 38 meningiomas and showed increased FAS expression in 70% of atypical WHO grade II and anaplastic WHO grade III meningiomas compared with 10% of benign WHO grade I tumors.
  • We next confirmed this finding by real-time PCR and Western blotting.
  • Second, we demonstrated that treatment with the FAS inhibitor, cerulenin (Cer), significantly decreased meningioma cell survival in vitro.
  • Third, we showed that Cer treatment reduced FAS expression by modulating Akt phosphorylation (activation).
  • Fourth, we demonstrated that Cer treatment of mice bearing meningioma xenografts resulted in significantly reduced tumor volumes associated with increased meningioma cell death.
  • Collectively, our data suggest that the increased FAS expression in human meningiomas represents a novel therapeutic target for the treatment of unresectable or malignant meningioma.
  • [MeSH-major] Cerulenin / pharmacology. Fatty Acid Synthases / metabolism. Fatty Acid Synthesis Inhibitors / pharmacology. Meningeal Neoplasms / enzymology. Meningioma / enzymology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Cell Survival / drug effects. DNA Fragmentation / drug effects. Enzyme-Linked Immunosorbent Assay. Female. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Mice. Mice, SCID. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Tissue Array Analysis. Xenograft Model Antitumor Assays

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  • [Cites] J Histochem Cytochem. 2000 May;48(5):613-22 [10769045.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3450-4 [10716717.001]
  • [Cites] Clin Cancer Res. 2001 Jan;7(1):153-7 [11205903.001]
  • [Cites] Cancer Res. 2001 Feb 15;61(4):1493-9 [11245456.001]
  • [Cites] Am J Pathol. 2001 Aug;159(2):661-9 [11485924.001]
  • [Cites] Cancer. 2002 Mar 15;94(6):1626-35 [11920521.001]
  • [Cites] Exp Cell Res. 2003 Jan 15;282(2):132-7 [12531699.001]
  • [Cites] Histopathology. 2003 Sep;43(3):280-90 [12940781.001]
  • [Cites] Mol Cell Biol. 2003 Nov;23(21):7794-808 [14560023.001]
  • [Cites] Cancer Res. 2003 Nov 1;63(21):7330-7 [14612531.001]
  • [Cites] Oncol Rep. 2004 Aug;12(2):411-22 [15254710.001]
  • [Cites] Ann Neurol. 2004 Aug;56(2):295-8 [15293284.001]
  • [Cites] J Biol Chem. 2004 Aug 27;279(35):36608-15 [15220355.001]
  • [Cites] J Biochem. 1989 May;105(5):751-5 [2666407.001]
  • [Cites] Cancer. 1989 Dec 1;64(11):2243-9 [2804914.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jul 5;91(14):6379-83 [8022791.001]
  • [Cites] Cancer Res. 1996 Mar 15;56(6):1189-93 [8640795.001]
  • [Cites] Int J Gynecol Pathol. 1997 Jan;16(1):45-51 [8986532.001]
  • [Cites] Neurology. 1997 Jul;49(1):267-70 [9222206.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Dec 23;94(26):14719-24 [9405679.001]
  • [Cites] Anticancer Res. 1997 Nov-Dec;17(6D):4589-93 [9494573.001]
  • [Cites] Am J Physiol. 1999 Aug;277(2 Pt 1):L381-90 [10444533.001]
  • [Cites] Lab Invest. 2005 Jan;85(1):99-108 [15543204.001]
  • [Cites] Oncogene. 2005 Jan 6;24(1):39-46 [15489885.001]
  • [Cites] J Neurooncol. 2004 Nov;70(2):183-202 [15674477.001]
  • [Cites] J Pathol. 2005 Jun;206(2):214-9 [15880754.001]
  • [Cites] Clin Cancer Res. 2005 Jun 1;11(11):4074-82 [15930342.001]
  • [Cites] Oncogene. 2005 May 19;24(22):3574-82 [15806173.001]
  • [Cites] Cancer Res. 2005 Jun 15;65(12):5070-5 [15958550.001]
  • [Cites] Clin Neuropathol. 2005 Jul-Aug;24(4):175-83 [16033134.001]
  • [Cites] Lab Invest. 2005 Sep;85(9):1163-71 [15965488.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):5977-80 [16778164.001]
  • [Cites] Br J Cancer. 2006 Oct 9;95(7):869-78 [16969344.001]
  • [Cites] Cancer Res. 2007 Jan 15;67(2):735-45 [17234785.001]
  • [Cites] Acta Neuropathol. 2007 Aug;114(2):97-109 [17618441.001]
  • [Cites] Nat Rev Cancer. 2007 Oct;7(10):763-77 [17882277.001]
  • [Cites] Biomed Pharmacother. 2007 Oct;61(9):578-87 [17904792.001]
  • [Cites] Cancer Res. 2008 Jan 1;68(1):314-22 [18172325.001]
  • [Cites] J Neuropathol Exp Neurol. 2000 Oct;59(10):872-9 [11079777.001]
  • (PMID = 20511185.001).
  • [ISSN] 1523-5866
  • [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
  • [Chemical-registry-number] 0 / Fatty Acid Synthesis Inhibitors; 0 / RNA, Messenger; 17397-89-6 / Cerulenin; EC 2.3.1.85 / Fatty Acid Synthases
  • [Other-IDs] NLM/ PMC2940685
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4. Chen YY, Tiang XY, Li Z, Luo BN, Huang Q: Sporadic meningioangiomatosis-associated atypical meningioma mimicking parenchymal invasion of brain: a case report and review of the literature. Diagn Pathol; 2010;5:39
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  • [Title] Sporadic meningioangiomatosis-associated atypical meningioma mimicking parenchymal invasion of brain: a case report and review of the literature.
  • In extremely rare condition, meningioma may occur together with meningioangiomatosis, and only 19 cases have been described in English literature until now.
  • We now report a case of meningioangiomatosis-associated meningioma with atypical and clear cell variant.
  • He had no stigmata of neurofibromatosis type 2.
  • Microscopically, parts of lesions were atypical and clear cell meningioma corresponding to WHO grade II.
  • Neoplastic cells in atypical meningioma area were immunoreactive to epithelial membrane antigen (EMA) with high MIB-1 index of up to 20%.
  • The diagnosis of atypical meningioma associated with sporadic meningioangiomatosis was made.
  • To our knowledge, this is the first case of a meningioangiomatosis-associated meningioma with atypical and clear cell variant component to be described.
  • The patient had been followed-up for 11 months without adjuvant radiotherapy or chemotherapy.
  • Meningioangiomatosis-associated meningioma is more likely to occur in younger patients and histologically to mimic parenchymal invasion of brain.
  • We suggest that postoperative radiotherapy or chemotherapy should be given careful consideration to avoid over-treatment due to erroneously interpret as malignant meningioma.
  • [MeSH-major] Brain Neoplasms / diagnosis. Central Nervous System Vascular Malformations / diagnosis. Cerebral Cortex / pathology. Meningeal Neoplasms / diagnosis. Meningioma / diagnosis
  • [MeSH-minor] Adult. Biopsy. Diagnosis, Differential. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Neoplasm Invasiveness. Treatment Outcome

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  • [Cites] J Neurosurg. 2000 Apr;92(4):706-10 [10761664.001]
  • [Cites] Acta Cytol. 2009 Jan-Feb;53(1):93-7 [19248561.001]
  • [Cites] Pediatr Dev Pathol. 2001 Nov-Dec;4(6):568-72 [11826364.001]
  • [Cites] Neuropathol Appl Neurobiol. 2002 Feb;28(1):48-56 [11849563.001]
  • [Cites] Nervenarzt. 2002 Oct;73(10):990-4 [12376888.001]
  • [Cites] Neuropathol Appl Neurobiol. 2003 Apr;29(2):170-4 [12662324.001]
  • [Cites] Brain Pathol. 2003 Oct;13(4):643-5 [14655769.001]
  • [Cites] Am J Clin Pathol. 1974 Oct;62(4):481-7 [4212953.001]
  • [Cites] J Neurosurg. 1982 Jan;56(1):154-7 [7054414.001]
  • [Cites] Acta Neuropathol. 1987;73(4):361-4 [3618128.001]
  • [Cites] J Neurosurg. 1990 Nov;73(5):715-9 [2213161.001]
  • [Cites] Pathol Res Pract. 1992 Feb;188(1-2):145-7 [1594484.001]
  • [Cites] J Neurosurg. 1993 Feb;78(2):287-9 [8421212.001]
  • [Cites] J Neuropathol Exp Neurol. 1997 May;56(5):485-9 [9143261.001]
  • [Cites] Am J Surg Pathol. 1999 Aug;23(8):872-5 [10435554.001]
  • [Cites] Brain Pathol. 2005 Jan;15(1):55-65 [15779237.001]
  • [Cites] Childs Nerv Syst. 2006 Jan;22(1):78-83 [16389566.001]
  • [Cites] Surg Neurol. 2006 Jun;65(6):595-603 [16720184.001]
  • [Cites] Am J Surg Pathol. 2002 Jan;26(1):125-9 [11756780.001]
  • (PMID = 20565869.001).
  • [ISSN] 1746-1596
  • [Journal-full-title] Diagnostic pathology
  • [ISO-abbreviation] Diagn Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2904739
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5. Ware ML, Larson DA, Sneed PK, Wara WW, McDermott MW: Surgical resection and permanent brachytherapy for recurrent atypical and malignant meningioma. Neurosurgery; 2004 Jan;54(1):55-63; discussion 63-4
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  • [Title] Surgical resection and permanent brachytherapy for recurrent atypical and malignant meningioma.
  • OBJECTIVE: Recurrent atypical and malignant meningiomas are difficult to treat successfully.
  • Chemotherapy to date has been unsuccessful, and radiosurgery is limited to smaller tumors.
  • The addition of brachytherapy at the time of operation is an option.
  • Here, we report the results of our series of patients with recurrent malignant meningioma treated with resection and brachytherapy with permanent low-dose (125)I.
  • METHODS: The charts of patients in our database with recurrent atypical and malignant meningiomas treated by surgical resection and permanent (125)I brachytherapy at the University of California, San Francisco, between 1988 and 2002 were selected for this study.
  • Univariate analysis between Kaplan-Meier curves was based on the log-rank statistic, with a significance level set at a value of P </= 0.05.
  • RESULTS: Seventeen patients had recurrent malignant meningioma, and four had recurrent atypical meningioma.
  • The median number of sources implanted after surgical resection was 30 (range, 4-112 sources), with a median total activity of 20 mCi (range, 3.3-85.9 mCi).
  • The median time to progression after brachytherapy was 11.6 months for patients with malignant meningioma and 10.4 months for the combined group.
  • There was a trend toward longer disease-free survival time in patients after gross total resection versus subtotal resection and in patients with tumors located at the convexity and parasagittally versus at the cranial base.
  • The median overall survival after diagnosis was 9.4 years for patients with atypical meningioma, 6.6 years for those with malignant meningioma, and 8.0 years for all patients combined.
  • Survival from the time of resection and implantation of (125)I was 1.6 years for patients with atypical meningioma, 2.4 years for patients with malignant meningioma, and 2.4 years for the combined group.
  • CONCLUSION: The options for patients with recurrent atypical or malignant meningiomas are limited.
  • Our results suggest that for tumors not suitable for radiosurgery, resection followed by permanent brachytherapy should be considered as a potential salvage treatment.
  • However, this approach results in a relatively high complication rate in these heavily treated patients and requires meticulous surgical technique and medical therapies to assist with wound healing after surgery.
  • [MeSH-major] Brachytherapy. Meningeal Neoplasms / radiotherapy. Meningeal Neoplasms / surgery. Meningioma / radiotherapy. Meningioma / surgery. Neoplasm Recurrence, Local / radiotherapy. Neoplasm Recurrence, Local / surgery
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged. Retrospective Studies. Salvage Therapy. Survival Rate. Treatment Outcome

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  • (PMID = 14683541.001).
  • [ISSN] 0148-396X
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
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6. Falavigna A, Santos JA, Chimelli L, Ferraz FA, Bonatelli Ad Ade P: Anaplastic meningioma: case report. Arq Neuropsiquiatr; 2001 Dec;59(4):939-43
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  • [Title] Anaplastic meningioma: case report.
  • Intracranial meningiomas continue to challenge our best clinical efforts to eliminate them once discovered and deemed appropriate for treatment.
  • Malignant meningiomas constitute 10% to 15% of all meningiomas and limited information exists regarding adjuvant treatment.
  • Traditional chemotherapy has proven ineffective; thus, new chemotherapeutic agents and new methods of delivery should be developed.
  • Immunotherapy may be considered for patients with malignant meningiomas when all others previous treatment have failed.
  • We report a case of anaplastic papillary meningioma.
  • A computerized tomography and magnetic resonance image demonstrated a large left temporo-occipital mass with diffuse contrast enhancement and extensive surrounding edema.
  • The treatment was complemented by external whole brain radiation.
  • [MeSH-major] Meningeal Neoplasms / therapy. Meningioma / therapy

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  • (PMID = 11733842.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Brazil
  • [Number-of-references] 28
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7. Puduvalli VK, Li JT, Chen L, McCutcheon IE: Induction of apoptosis in primary meningioma cultures by fenretinide. Cancer Res; 2005 Feb 15;65(4):1547-53
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  • [Title] Induction of apoptosis in primary meningioma cultures by fenretinide.
  • Due to its ease of administration, long-term tolerability, and low incidence of long-term side effects, we explored its potential as a therapeutic agent against meningiomas by examining its efficacy in vitro against such cells in primary culture.
  • Cells, cultured from freshly resected benign, atypical, or malignant meningiomas, were exposed to fenretinide (10 mumol/L).
  • Treatment effects were assessed using flow cytometry, Western blot analysis, semiquantitative reverse transcription-PCR for retinoid receptor expression, and changes in insulin-like growth factor-I (IGF-I)-induced proliferation.
  • Fenretinide induced apoptosis in the three grades of meningioma primary cells tested, as shown by the appearance of a sub-G(1) fraction in flow cytometric analysis and by the detection of poly-adenosyl ribonucleotidyl phosphorylase cleavage indicating caspase activation.
  • Fenretinide treatment also increased levels of the death receptor DR5 and caused mitochondrial membrane depolarization.
  • IGF-I-induced proliferation in the meningioma cells was abolished by fenretinide.
  • We conclude that fenretinide induces apoptosis in all three histologic subtypes of meningioma and exerts diverse cellular effects, including DR5 up-regulation, modulation of retinoid receptor levels, and inhibition of IGF-I-induced proliferation.
  • These results provide preliminary evidence that fenretinide has activity against meningiomas and suggest that further studies are warranted to explore its potential as a therapeutic agent against meningiomas.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Fenretinide / pharmacology. Meningioma / drug therapy
  • [MeSH-minor] Humans. Insulin-Like Growth Factor I / antagonists & inhibitors. Insulin-Like Growth Factor I / pharmacology. Membrane Potentials / drug effects. Mitochondria / drug effects. Mitochondria / physiology. Polyribonucleotide Nucleotidyltransferase / metabolism. Receptors, Retinoic Acid / biosynthesis. Receptors, TNF-Related Apoptosis-Inducing Ligand. Receptors, Tumor Necrosis Factor / biosynthesis. Retinoid X Receptor alpha / biosynthesis. Up-Regulation / drug effects

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  • (PMID = 15735044.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Retinoic Acid; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Retinoid X Receptor alpha; 0 / TNFRSF10B protein, human; 0 / retinoic acid receptor alpha; 0 / retinoic acid receptor gamma; 187EJ7QEXL / Fenretinide; 67763-96-6 / Insulin-Like Growth Factor I; EC 2.7.7.8 / Polyribonucleotide Nucleotidyltransferase
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8. Gogineni VR, Kargiotis O, Klopfenstein JD, Gujrati M, Dinh DH, Rao JS: RNAi-mediated downregulation of radiation-induced MMP-9 leads to apoptosis via activation of ERK and Akt in IOMM-Lee cells. Int J Oncol; 2009 Jan;34(1):209-18
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  • Patients afflicted with meningiomas are most often treated with radiation therapy followed by surgical resection.
  • However, resistance to radiation treatment has been well documented among different cancers of the brain.
  • In this study, we demonstrate that the malignant meningioma cells (IOMM-Lee cells) overexpress MMP-9 at both the mRNA and protein levels after radiation treatment.
  • Treatment with U0126 and transfection with dominant negative ERK plasmid resulted in the decreased phosphorylation of ERK and Akt.
  • Ectopic expression of HA myr-Akt was found to be associated with an increase in pERK, and treatment with LY294002 was shown to block the phosphorylation of Akt and ERK with the restoration of c-JUN.

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  • [Cites] Oncogene. 2006 Nov 9;25(53):7009-18 [16732316.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8511-9 [16951163.001]
  • [Cites] Mol Cancer Ther. 2007 Mar;6(3):789-801 [17363476.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4956-64 [17510426.001]
  • [Cites] Am J Physiol Cell Physiol. 2007 Sep;293(3):C1171-80 [17634416.001]
  • [Cites] Int J Cancer. 2007 Nov 15;121(10):2307-16 [17657740.001]
  • [Cites] Surg Neurol. 2007 Dec;68(6):610-3; discussion 613-4 [17765959.001]
  • [Cites] J Biol Chem. 2008 Jan 18;283(3):1545-52 [17991734.001]
  • [Cites] Int J Oncol. 2008 Mar;32(3):557-64 [18292932.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2003 Jul 15;56(4):1161-9 [12829155.001]
  • [Cites] Oncogene. 2003 Sep 4;22(38):5967-75 [12955075.001]
  • [Cites] Cancer Gene Ther. 2003 Nov;10(11):823-32 [14605668.001]
  • [Cites] Biol Chem. 2004 Jan;385(1):75-86 [14977049.001]
  • [Cites] J Neurooncol. 2004 Mar-Apr;67(1-2):147-57 [15072462.001]
  • [Cites] Anticancer Res. 2004 Mar-Apr;24(2B):967-72 [15161051.001]
  • [Cites] Neurotoxicology. 2004 Dec;25(6):915-24 [15474610.001]
  • [Cites] Surg Neurol. 1986 Mar;25(3):233-42 [3945904.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Jan 1;46(1):57-61 [10656373.001]
  • [Cites] Ann Surg. 2000 May;231(5):644-54 [10767785.001]
  • [Cites] J Neurooncol. 2000 May;48(1):51-5 [11026697.001]
  • [Cites] Int J Cancer. 2000 Dec 1;88(5):766-71 [11072246.001]
  • [Cites] J Neurooncol. 2000 Jun;48(2):151-60 [11083080.001]
  • [Cites] Cancer Res. 2001 Mar 15;61(6):2744-50 [11289157.001]
  • [Cites] J Neurosurg. 2001 Jun;94(6):978-84 [11409528.001]
  • [Cites] Adv Exp Med Biol. 2000;486:355-9 [11783515.001]
  • [Cites] J Biol Chem. 2002 Feb 15;277(7):4932-44 [11733515.001]
  • [Cites] Clin Cancer Res. 2002 Apr;8(4):1223-7 [11948136.001]
  • [Cites] Biochem J. 2002 Jul 1;365(Pt 1):31-40 [12071839.001]
  • [Cites] Oncogene. 2002 Aug 15;21(36):5601-8 [12165859.001]
  • [Cites] Anal Biochem. 1987 Apr;162(1):156-9 [2440339.001]
  • [Cites] Neurosurgery. 1987 Apr;20(4):525-8 [3587542.001]
  • [Cites] BMC Cancer. 2002 Dec 3;2:34 [12464160.001]
  • [Cites] J Neurosurg. 1994 Feb;80(2):195-201 [8283256.001]
  • [Cites] Med Phys. 1995 Nov;22(11 Pt 2):1889-97 [8587542.001]
  • [Cites] Pflugers Arch. 1998 Mar;435(4):546-54 [9446703.001]
  • [Cites] J Surg Res. 1999 Jun 15;84(2):162-7 [10357914.001]
  • [Cites] J Appl Toxicol. 2005 Sep-Oct;25(5):374-82 [16013042.001]
  • [Cites] J Neurooncol. 2005 Sep;74(2):99-103 [16193379.001]
  • [Cites] J Immunol. 2006 Jun 1;176(11):6785-93 [16709838.001]
  • [Cites] J Neurooncol. 2006 Mar;77(1):73-7 [16292489.001]
  • [Cites] J Pharmacol Exp Ther. 2006 Dec;319(3):991-7 [16801453.001]
  • (PMID = 19082492.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS061835; United States / NINDS NIH HHS / NS / R01 NS057529; United States / NCI NIH HHS / CA / R01 CA075557; United States / NCI NIH HHS / CA / R01 CA116708-03; United States / NCI NIH HHS / CA / R01 CA095058-04; United States / NINDS NIH HHS / NS / R01 NS057529-02; United States / NINDS NIH HHS / NS / R01 NS061835-01; United States / NCI NIH HHS / CA / CA 75557; United States / NCI NIH HHS / CA / CA116708-03; United States / NCI NIH HHS / CA / CA075557-10; United States / NCI NIH HHS / CA / CA 92393; United States / NINDS NIH HHS / NS / NS061835-01; United States / NCI NIH HHS / CA / CA 95058; United States / NCI NIH HHS / CA / R01 CA116708; United States / NINDS NIH HHS / NS / R01 NS047699; United States / NINDS NIH HHS / NS / NS057529-02; United States / NCI NIH HHS / CA / CA092393-04; United States / NCI NIH HHS / CA / R01 CA095058; United States / NCI NIH HHS / CA / R01 CA092393; United States / NCI NIH HHS / CA / CA 116708; United States / NCI NIH HHS / CA / R01 CA092393-04; United States / NINDS NIH HHS / NS / R01 NS047699-04A2; United States / NINDS NIH HHS / NS / NS047699-04A2; United States / NCI NIH HHS / CA / CA095058-04; United States / NCI NIH HHS / CA / R01 CA075557-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Drug Combinations; 0 / Enzyme Inhibitors; 0 / FAS protein, human; 0 / Laminin; 0 / Matrix Metalloproteinase Inhibitors; 0 / Proteoglycans; 0 / RNA, Small Interfering; 119978-18-6 / matrigel; 9007-34-5 / Collagen; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ NIHMS71812; NLM/ PMC2605673
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9. Kunishio K, Kobayashi K, Kagawa M, Makabe T, Matsumoto A, Matsumoto Y: [A case of malignant meningioma treated by individual adjuvant chemotherapy based on the mRNA expression of drug-resistance gene]. Gan To Kagaku Ryoho; 2007 Feb;34(2):265-8
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  • [Title] [A case of malignant meningioma treated by individual adjuvant chemotherapy based on the mRNA expression of drug-resistance gene].
  • We report a case with malignant meningioma in which new preliminary treatment trial was performed by chemotherapy using anti-cancer drugs selected on the basis of multidrug resistance gene mRNA expression, such as MDR1, MGMT, MRP1, MRP2, MXR1, and DNA topoisomerase II alpha, from RT-PCR assay.
  • A 43-year-old female had been operated for parasagittal anaplastic meningioma three times because of recurrences. partial removal of tumor was performed at the 3rd operation.
  • RT-PCR assay of this tissue revealed overexpression of MDR1, MRP1, MRP2 and MGMT mRNA, but no ABCG 2 expression was observed.
  • Preliminary individual adjuvant chemotherapy based on mRNA expression of drug-resistance gene is available for the treatment of recurrent malignant meningioma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance, Multiple / genetics. Drug Resistance, Neoplasm / genetics. Meningeal Neoplasms / drug therapy. Meningioma / drug therapy
  • [MeSH-minor] Adult. Combined Modality Therapy. DNA Modification Methylases. DNA Repair Enzymes. Drug Administration Schedule. Female. Humans. Hydroxyurea / administration & dosage. Membrane Transport Proteins / biosynthesis. Mitoxantrone / administration & dosage. Multidrug Resistance-Associated Proteins / biosynthesis. P-Glycoprotein / biosynthesis. P-Glycoprotein / genetics. RNA, Messenger / biosynthesis. Tumor Suppressor Protein p14ARF / biosynthesis. Tumor Suppressor Proteins

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  • (PMID = 17301541.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Membrane Transport Proteins; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p14ARF; 0 / Tumor Suppressor Proteins; 0 / multidrug resistance-associated protein 2; BZ114NVM5P / Mitoxantrone; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes; X6Q56QN5QC / Hydroxyurea
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10. Soares D, Char G, Crandon I, Shaw H: Malignant meningioma with extension into the neck. West Indian Med J; 2000 Mar;49(1):66-9
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  • [Title] Malignant meningioma with extension into the neck.
  • One per cent of all brain tumours and twenty per cent of meningiomas eventually develop an extracranial extension.
  • We report a case of malignant meningioma with extension into the neck of a 39-year-old male.
  • [MeSH-major] Head and Neck Neoplasms / diagnosis. Meningeal Neoplasms / drug therapy. Meningioma / diagnosis
  • [MeSH-minor] Adult. Brain / pathology. Fatal Outcome. Humans. Magnetic Resonance Imaging. Male. Prognosis. Tomography, X-Ray Computed

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  • (PMID = 10786459.001).
  • [ISSN] 0043-3144
  • [Journal-full-title] The West Indian medical journal
  • [ISO-abbreviation] West Indian Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] JAMAICA
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11. Regel JP, Schoch B, Sandalcioglu IE, Wieland R, Westermeier C, Stolke D, Wiedemayer H: Malignant meningioma as a second malignancy after therapy for acute lymphatic leukemia without cranial radiation. Childs Nerv Syst; 2006 Feb;22(2):172-5
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  • [Title] Malignant meningioma as a second malignancy after therapy for acute lymphatic leukemia without cranial radiation.
  • RATIONALE: Meningiomas in the pediatric age group are very rare tumors, comprising about 1-4.2% of all primary pediatric intracranial tumors.
  • CASE REPORT: We present a 17-year-old patient who suffered from an intraventricular malignant meningioma.
  • At the age of 2 years, acute lymphatic leukemia (common ALL [cALL]) was diagnosed and successfully treated with chemotherapy.
  • There was no cranial radiation therapy.
  • In December 2001, 13 years after diagnosis of cALL, he complained of headache, vomiting, and walking difficulties.
  • Histological diagnosis revealed a malignant papillary meningioma.
  • After removal of a recurrent meningioma 16 months later, he received local radiotherapy.
  • CONCLUSION: Pathogenetic mechanisms, treatment options, and prognosis of meningiomas and secondary malignancies of this age group are discussed.
  • [MeSH-major] Drug-Related Side Effects and Adverse Reactions. Meningeal Neoplasms / etiology. Meningioma / etiology. Neoplasms, Second Primary / etiology
  • [MeSH-minor] Adolescent. Drug Therapy / methods. Humans. Magnetic Resonance Imaging / methods. Male. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Tomography, X-Ray Computed / methods

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  • [Cites] Cancer. 2002 Dec 15;95(12):2562-70 [12467071.001]
  • [Cites] Pediatr Neurosurg. 2001 May;34(5):264-7 [11423779.001]
  • [Cites] J Clin Oncol. 1998 Mar;16(3):864-71 [9508167.001]
  • [Cites] Neurol Med Chir (Tokyo). 1996 Aug;36(8):598-601 [8831206.001]
  • [Cites] Childs Nerv Syst. 2000 Jul;16(7):406-16 [10958549.001]
  • [Cites] Childs Nerv Syst. 2001 Nov;17 (11):656-62 [11734983.001]
  • [Cites] Med Phys. 2001 Nov;28(11):2387-8 [11764047.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4257-64 [12036851.001]
  • [Cites] Prog Exp Tumor Res. 1987;30:247-54 [3628810.001]
  • [Cites] Am J Surg Pathol. 2001 Jul;25(7):964-9 [11420471.001]
  • (PMID = 16456690.001).
  • [ISSN] 0256-7040
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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12. Gupta V, Su YS, Samuelson CG, Liebes LF, Chamberlain MC, Hofman FM, Schönthal AH, Chen TC: Irinotecan: a potential new chemotherapeutic agent for atypical or malignant meningiomas. J Neurosurg; 2007 Mar;106(3):455-62
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  • [Title] Irinotecan: a potential new chemotherapeutic agent for atypical or malignant meningiomas.
  • OBJECT: There is currently no effective chemotherapy for meningiomas.
  • Although most meningiomas are treated surgically, atypical or malignant meningiomas and surgically inaccessible meningiomas may not be removed completely.
  • The authors have investigated the effects of the topoisomerase I inhibitor irinotecan (CPT-11) on primary meningioma cultures and a malignant meningioma cell line in vitro and in vivo.
  • METHODS: The effects of irinotecan on cellular proliferation in primary meningioma cultures and the IOMM-Lee malignant meningioma cell line were measured by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl tetrazolium bromide assay and flow cytometry.
  • Apoptosis following drug treatment was evaluated by the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling and the DNA laddering assays.
  • The effects of irinotecan in vivo on a meningioma model were determined with a subcutaneous murine tumor model using the IOMM-Lee cell line.
  • Irinotecan induced a dose-dependent antiproliferative effect with subsequent apoptosis in the primary meningioma cultures (at doses up to 100 microM) as well as in the IOMM-Lee human malignant meningioma cell line (at doses up to 20 microM) irinotecan.
  • In the animal model, irinotecan treatment led to a statistically significant decrease in tumor growth that was accompanied by a decrease in Bcl-2 and survivin levels and an increase in apoptotic cell death.
  • CONCLUSIONS: Irinotecan demonstrated growth-inhibitory effects in meningiomas both in vitro and in vivo.
  • Irinotecan was much more effective against the malignant meningioma cell line than against primary meningioma cultures.
  • Therefore, this drug may have an important therapeutic role in the treatment of atypical or malignant meningiomas and should be evaluated further for this purpose.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Camptothecin / analogs & derivatives. Meningioma / drug therapy. Meningioma / pathology. Soft Tissue Neoplasms / drug therapy. Soft Tissue Neoplasms / pathology. Subcutaneous Tissue

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  • (PMID = 17367069.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Proto-Oncogene Proteins c-bcl-2; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
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13. Travitzky M, Libson E, Nemirovsky I, Hadas I, Gabizon A: Doxil-induced regression of pleuro-pulmonary metastases in a patient with malignant meningioma. Anticancer Drugs; 2003 Mar;14(3):247-50
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  • [Title] Doxil-induced regression of pleuro-pulmonary metastases in a patient with malignant meningioma.
  • Metastatic meningioma is a rare disease, which has no effective chemotherapy.
  • We report on a treatment of this condition with Doxil, a liposomal doxorubicin formulation.
  • A 60-year-old woman with massive pleuro-pulmonary metastases from recurrent cranial meningioma was treated with Doxil (50-37.5 mg/m2) for 18 months with near-complete resolution of metastases and disappearance of pleural fluid.
  • Doxil was cleared very slowly in this patient with a monoexponential half-life of 108 h.
  • The patient remains in near-complete response for 6 months after treatment discontinuation.
  • This is the first report on an effective chemotherapy in a patient with typical metastatic meningioma.
  • The exact mechanism accounting for such an effective drug action is not clear, but may be related to a particularly high microvascular permeability to the liposome carriers in these metastatic lesions.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Doxorubicin / therapeutic use. Lung Neoplasms / drug therapy. Meningeal Neoplasms / drug therapy. Meningioma / drug therapy
  • [MeSH-minor] Female. Humans. Middle Aged. Pleural Effusion, Malignant

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  • [Copyright] Copyright 2003 Lippincott Williams & Wilkins
  • (PMID = 12634620.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 80168379AG / Doxorubicin
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14. 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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15. Hatta R, Nambu Y, Suzuki S, Tachi Y, Oikawa T, Nakagawa K, Tuchihara K, Tobe T, Osanai K, Toga H, Takahashi K, Ohya N: [A case of atypical pulmonary carcinoid accompanying skin metastasis]. Nihon Kokyuki Gakkai Zasshi; 2004 Apr;42(4):357-61
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  • A 73-year-old woman underwent cranial surgery in 1999 after receiving a diagnosis of suspected malignant meningioma.
  • She began complaining of headache 2 years postoperatively, and around the same time, she noticed a painful skin tumor.
  • EP therapy (etoposide + carboplatin) and CAV therapy (cyclophosphamide + doxorubicin + vincristin) were administered, but there was no clinical response.
  • The patient is currently doing well without chemotherapy and is being followed by the Outpatient Department.

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  • (PMID = 15114855.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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16. Payen JF, Faillot T, Audibert G, Vergnes MC, Bosson JL, Lestienne B, Bernard C, Bruder N: [Thromboprophylaxis in neurosurgery and head trauma]. Ann Fr Anesth Reanim; 2005 Aug;24(8):921-7
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  • The incidence of deep vein thrombosis (DVT) is between 20 and 35% using contrast venography, with a rate of symptomatic DVT between 2.3 and 6% in neurosurgery without any prophylaxis.
  • Specific risk factors in neurosurgery are: a motor deficit, a meningioma or malignant tumour, a large tumour, age over 60 years, surgery lasting more than 4 hours, a chemotherapy.
  • A postoperative prophylaxis with a LMWH does not seem to increase the risk of intracranial bleeding (grade C).

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  • (PMID = 16006086.001).
  • [ISSN] 0750-7658
  • [Journal-full-title] Annales françaises d'anesthèsie et de rèanimation
  • [ISO-abbreviation] Ann Fr Anesth Reanim
  • [Language] fre
  • [Publication-type] English Abstract; Guideline; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 34
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17. Nagai H, Yamasaki T, Yamamoto Y, Takada D, Miyazaki T, Sugimoto K, Matsumoto Y, Akiyama Y, Moritake K: [Evaluation of brain tumors by simultaneous dual isotope SPECT with 201Tl-chloride and 99mTc-MIBI]. No Shinkei Geka; 2004 Oct;32(10):1029-37
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  • Single photon emission computed tomography (SPECT) is useful for detecting brain tumors.
  • In this study, we evaluated the utility of simultaneous dual SPECT with 201Tl-Chloride (Tl) and 99mTc-MIBI (MIBI) for diagnosis of brain tumors.
  • We evaluated 20 cases, including 2 glioblastomas, 7 anaplastic astrocytomas, 2 oligodendrogliomas, 2 anaplastic ependymomas, 2 medulloblastomas, 2 meningiomas, 1 malignant meningioma, 1 pituitary adenoma, and 1 craniopharyngioma.
  • We discuss the difference in the mechanism of accumulation of two tracers and the significance of simultaneous dual SPECT using them for the differential diagnosis of pituitary tumors, regrowth of oligodendrogliomas, and multidrug resistance of chemotherapy.
  • Dual SPECT with Tl and MIBI appears to be useful for the diagnosis of brain tumor.
  • [MeSH-minor] Adenoma / radionuclide imaging. Adult. Aged. Child. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Pituitary Neoplasms / radionuclide imaging. Thallium. Tomography, Emission-Computed, Single-Photon / methods

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  • (PMID = 15529789.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0 / Thallium Radioisotopes; 7791-12-0 / thallium chloride; 971Z4W1S09 / Technetium Tc 99m Sestamibi; AD84R52XLF / Thallium
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18. Lah TT, Nanni I, Trinkaus M, Metellus P, Dussert C, De Ridder L, Rajcević U, Blejec A, Martin PM: Toward understanding recurrent meningioma: the potential role of lysosomal cysteine proteases and their inhibitors. J Neurosurg; 2010 May;112(5):940-50
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  • [Title] Toward understanding recurrent meningioma: the potential role of lysosomal cysteine proteases and their inhibitors.
  • OBJECT: The first aim of this study was to diagnose more aggressive and potentially recurrent meningiomas using an in vitro embryonic chick heart invasiveness assay in which lysosomal enzyme cathepsin B was used as the invasiveness marker.
  • The second aim was to confirm if cathepsin B and/or cathepsin L and their endogenous inhibitors were also prognostic parameters in the clinical study of 119 patients with meningioma.
  • METHODS: Primary meningioma cultured spheroids were "confronted" with embryonic chick heart spheroids in vitro, and cathepsin B was used as molecular marker to immunolabel the invasive tumor cells.
  • In vitro invasion assays of the malignant meningioma cells were used to assess the invasive potential related to the cysteine cathepsins.
  • As to the second aim, the possible association of cathepsin B along with selected molecular markers, cathepsin L, and endogenous cysteine protease inhibitors (stefins A and B and cystatin C) with meningioma malignancy was determined using enzyme-linked immunosorbent assays in tumor homogenates.
  • Univariate and multivariate analyses were used to compare these parameters with established biological markers of meningioma recurrence in 119 patients with meningiomas.
  • RESULTS: The more invasive tumors, which characteristically overgrew the normal tissue, were identified even within a group of histologically benign meningiomas.
  • Matrigel invasion of malignant meningioma cells was significantly altered by modulating cathepsin B activity and by stefin B silencing.
  • In the clinical samples of meningioma, the levels of cathepsins B and L, stefin B, and cystatin C were highest in the tumors of higher histological grades, whereas stefin A and progesterone receptor were the only markers that were significantly increased and decreased, respectively, in WHO Grade III lesions.
  • CONCLUSIONS: The data indicate that the cysteine cathepsins and their inhibitors are involved in a process related to early meningioma recurrence, regardless of their histological classification.
  • Of note, the known tumor invasiveness marker cathepsin B, measured in whole-tumor homogenates, was not prognostic, in contrast to its endogenous inhibitor stefin B, which was highly significant and the only independent prognostic factor to predict meningioma relapse in multivariate analysis and reported herein for the first time.
  • [MeSH-major] Brain Neoplasms / drug therapy. Brain Neoplasms / pathology. Cysteine Proteinase Inhibitors / pharmacology. Cysteine Proteinase Inhibitors / therapeutic use. Lysosomes / drug effects. Meningioma / drug therapy. Meningioma / pathology

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  • (PMID = 19747051.001).
  • [ISSN] 1933-0693
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CSTB protein, human; 0 / Cystatin A; 0 / Cysteine Proteinase Inhibitors; 88844-95-5 / Cystatin B; EC 3.4.22.1 / CTSB protein, human; EC 3.4.22.1 / Cathepsin B
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19. Gupta R, Suri V, Jain A, Sharma MC, Sarkar C, Singh MM, Joshi NP, Puri T, Julka PK: Anaplastic meningioma in an adolescent: a report of a rare case and brief review of literature. Childs Nerv Syst; 2009 Feb;25(2):241-5
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  • [Title] Anaplastic meningioma in an adolescent: a report of a rare case and brief review of literature.
  • OBJECTIVE: Anaplastic meningioma is an uncommon neoplasm in childhood and adolescence.
  • Due to the rarity, treatment options for anaplastic meningioma in this age group are not clearly outlined.
  • CASE: A 15-year-old boy presented with a left forehead swelling with a history of a left frontal tumor.
  • Radiological investigations revealed a dura-based tumor with a large extracranial and a smaller intracranial component.
  • Histopathological examination of the tumor showed features of an anaplastic meningioma.
  • The patient is currently receiving radiotherapy and chemotherapy.
  • However, he has developed scalp swellings while on radiotherapy.
  • CONCLUSION: Anaplastic meningioma is extremely rare in children.
  • Extensive sampling is required to recognize the meningothelial nature of the tumor and immunohistochemistry helps in making an accurate diagnosis in such cases.
  • Therapeutic interventions in such cases need to be closely monitored due to the aggressive behavior of this tumor.
  • [MeSH-major] Meningeal Neoplasms / diagnosis. Meningeal Neoplasms / therapy. Meningioma / diagnosis. Meningioma / therapy
  • [MeSH-minor] Adolescent. Combined Modality Therapy. Diagnosis, Differential. Humans. Immunohistochemistry. Male. Mucin-1 / analysis. Vimentin / analysis

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  • [Cites] J Neurosurg. 1997 May;86(5):840-4 [9126900.001]
  • [Cites] J Child Neurol. 2006 Jan;21(1):31-6 [16551450.001]
  • [Cites] Pediatr Neurosurg. 2005 Jan-Feb;41(1):1-7 [15886506.001]
  • [Cites] J Neurosurg. 2004 Feb;100(2 Suppl Pediatrics):179-82 [14758946.001]
  • [Cites] Acta Neuropathol. 2007 Aug;114(2):97-109 [17618441.001]
  • [Cites] Expert Rev Neurother. 2006 Oct;6(10):1447-64 [17078786.001]
  • [Cites] Childs Brain. 1980;7(1):43-56 [7428495.001]
  • [Cites] J Neurosurg. 1996 May;84(5):733-6 [8622144.001]
  • [Cites] Childs Nerv Syst. 1986;2(3):160-1 [3779674.001]
  • [Cites] J Neurooncol. 2005 Sep;74(2):157-65 [16193387.001]
  • [Cites] Neurol Med Chir (Tokyo). 1978;18(1 Pt 1):119-27 [77488.001]
  • (PMID = 18769931.001).
  • [ISSN] 1433-0350
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Mucin-1; 0 / Vimentin
  • [Number-of-references] 11
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20. Tews DS, Fleissner C, Tiziani B, Gaumann AK: Intrinsic expression of drug resistance-associated factors in meningiomas. Appl Immunohistochem Mol Morphol; 2001 Sep;9(3):242-9
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  • [Title] Intrinsic expression of drug resistance-associated factors in meningiomas.
  • Meningiomas, commonly benign tumors, rarely display aggressive behavior by recurrences and invasion.
  • In addition to surgery, irradiation is beneficial for recurrent, atypical, and malignant meningiomas.
  • The role of chemotherapy, however, remains controversial, although there is evidence that meningiomas respond well to adjuvant chemotherapy.
  • A major obstacle in chemotherapy remains drug resistance with reduced cellular drug accumulation through membrane efflux pumps, drug detoxification, and alterations in drug target specificity.
  • In 84 classic, atypical, and malignant meningiomas, the immunohistochemical expression profile of P-glycoprotein (P-gp), multidrug resistance-associated protein (MRP), lung resistance-related protein (LRP), metallothionein, and topoisomerase IIalpha were studied.
  • All types of meningiomas showed constant expression of P-gp, LRP, MRP, and topoisomerase IIalpha; metallothionein was found in 67% of the tumors, especially in atypical and malignant meningiomas.
  • P-gp, LRP, and topoisomerase IIalpha were strongly expressed by normal and neoplastic vessels, which may confer to impaired penetration of therapeutic agents through the blood-brain and blood-tumor barrier.
  • Neither recurrent nor previously irradiated meningiomas revealed any significant difference to primary tumors.
  • These intrinsic drug resistances indicate that successful chemotherapy may require additional inhibition of these factors to be a promising approach in the management of meningiomas.

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  • (PMID = 11556752.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Neoplasm Proteins
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21. Tong-tong W, Li-juan B, Zhi L, Yang L, Bo-ning L, Quan H: Clear cell meningioma with anaplastic features: case report and review of literature. Pathol Res Pract; 2010 May 15;206(5):349-54
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  • [Title] Clear cell meningioma with anaplastic features: case report and review of literature.
  • Clear cell meningioma (CCM) is an uncommon variant of meningioma, corresponding to WHO grade II.
  • We present two cases of CCMs with anaplastic features in the intracranial and intraspinal region.
  • The first case is a 65-year-old male who gradually developed changes in behavior over a period of 1 year.
  • The second case is a 35-year-old female who presented with a 7-month history of posterior cervicothoracic pain and dysuria for 1 week.
  • On histological examination, both tumors partly exhibited unusual anaplastic appearances with nuclear pleomorphism, high mitotic activity and necrosis, distinct from classical CCMs.
  • Tumor cells were immunoreactive to epithelial membrane antigen (EMA) and vimentin, with a high MIB-1 index up to 40%.
  • The male patient was found to have developed local recurrence and lateral ventricle metastasis 3 months after surgery.
  • A diagnosis of CCM with anaplastic features was made (WHO grade III).
  • Based on its aggressive behavior, we recommend postoperative adjuvant radiotherapy or chemotherapy even if total excision of the tumor has been performed, and MRI scans every 3-6 months during the first period of follow-up.
  • [MeSH-major] Frontal Lobe / pathology. Meningeal Neoplasms / pathology. Meningioma / pathology

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  • [Copyright] (c) 2009. Published by Elsevier GmbH. All rights reserved.
  • (PMID = 19857933.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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22. Borgmann A, Zinn C, Hartmann R, Herold R, Kaatsch P, Escherich G, Möricke A, Henze G, von Stackelberg A, ALL-REZ BFM Study Group: Secondary malignant neoplasms after intensive treatment of relapsed acute lymphoblastic leukaemia in childhood. Eur J Cancer; 2008 Jan;44(2):257-68

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  • [Title] Secondary malignant neoplasms after intensive treatment of relapsed acute lymphoblastic leukaemia in childhood.
  • PURPOSE: To investigate the cumulative incidence of and the risk factors for developing second malignant neoplasms (SMN) in children and adolescents following treatment for relapse of acute lymphocytic leukaemia (ALL).
  • The treatment followed trial protocol in five consecutive multicentre trials of the ALL-REZ BFM Study Group between March 1983 and December 2001.
  • The incidence of SMN was analysed, correlated with clinical and therapeutic parameters, and compared to the age-specific incidence rates of cancers as cited in German cancer registries.
  • RESULTS: Out of the 1376 patients 21 were diagnosed with SMN including non-lymphoblastic leukaemia/myelodysplastic syndrome (n=6), osteo-/Ewing's-/fibroblastic sarcoma (n=4), B-cell ALL/lymphoma (n=2), thyroid carcinoma (n=2), basal cell carcinoma, adeno carcinoma, squamous cell carcinoma, meningioma, malignant histiocytosis, glioblastoma and anaplastic astrocytoma (n=1 each).
  • The overall cumulative risk of SMN at 15 years (median follow-up of 13.1 years) was 1.26%+/-0.38% (SE).
  • CONCLUSIONS: Despite repeated exposure to intense frontline and relapse treatment (including multiagent chemotherapy, cranial irradiation and stem cell transplantation in some patients) the cumulative incidence of SMN was unexpectedly low, though significantly higher than in the general age-matched population.
  • The association of SMN to SCT seemed to be a secondary effect at least partially mediated by exposure to high doses of VP16 and CY given for conditioning therapy.
  • [MeSH-major] Neoplasms, Second Primary / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Disease-Free Survival. Female. Germany / epidemiology. Humans. Incidence. Infant. Male. Multicenter Studies as Topic. Remission Induction. Risk Factors. Secondary Prevention

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  • (PMID = 17981026.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Investigator] Mertens R; Imbach P; Pongratz E; Rupprecht T; Henze G; Wickmann L; Otte J; Bode U; Eberl W; Pekrun A; Kirschstein M; Hofmann K; Frank R; Möbius D; Andler W; Niekrens C; Breu H; Suttorp M; Göbel U; Weinmann G; Sauerbrey A; Beck JF; Janka-Schaub G; Welte K; Kulozik A; Tautz C; Graf N; Fink FM; Zintl F; Hermann J; Rupprath G; Dupuis W; Rodehüser M; Schrappe M; Berthold F; Sternschulte W; Körholz D; Schmitt K; Selle B; Gutjahr P; Dürken M; Christiansen H; Rose M; Borkhardt A; Burdach S; Jürgens H; Scheurlen W; Eggers G; Geib R; Dickerhoff R; Bielack S; Rauh W; Niethammer D; Debatin KM; Gadner H; Dohrn B; Schlegel PG; Niggli F
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23. Turowski B, Zanella FE: Interventional neuroradiology of the head and neck. Neuroimaging Clin N Am; 2003 Aug;13(3):619-45
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  • Vascular interventions are important and helpful for treatment of various pathologies of the head and neck.
  • Interventional neuroradiology of the head and neck includes image-guided biopsies, vessel occlusion, and local chemotherapy.
  • Knowledge of anatomy, functional relationships between intra- and extracranial vessels, and pathology are the basis for therapeutic success.
  • Neuroradiologic imaging, especially CT and MR imaging, and appropriate analysis of angiographic findings help ensure indication for treatment and plan an intervention.
  • Examples of these interventions are: a hemangioma of the hard palate, a juvenile angiofibroma, a hemangiopericytoma, a malignant meningioma, a malignant fibrous histiocytoma, and a glomus tumor.
  • Effective treatment of vascular malformations, such as AV fistulas or angiomas, needs exact occlusion of the fistula or the angiomatous nidus, which is demonstrated in the case of an AV angioma of the base of the tongue.
  • Chemotherapy with local intra-arterial cisplatin combined with intravenous administration of sodium thiosulfate as antidote is indicated as an adjuvant modality in a multimodal regimen of oropharyngeal squamous cell carcinoma or as palliative treatment of recurrent and otherwise untreatable malignant tumors of the head and neck.
  • Palliative treatment of a bleeding oropharyngeal cancer is another example of interventional treatment.
  • Selective treatment, either occluding or pharmacologic, may be preoperative, palliative, or curative.
  • The objective is reduction of surgical risk, improvement of quality of life, or curative therapy of a lesion.
  • Thus, the interventional treatment should not be associated with morbidity or mortality.
  • The benefits, risks, and expected damages of neuroradiologic interventions must be balanced during the informed consent procedure with the patient.
  • [MeSH-major] Head and Neck Neoplasms / radiography. Head and Neck Neoplasms / therapy. Neuroradiography. Radiology, Interventional

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  • (PMID = 14631695.001).
  • [ISSN] 1052-5149
  • [Journal-full-title] Neuroimaging clinics of North America
  • [ISO-abbreviation] Neuroimaging Clin. N. Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 40
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24. Wen PY, Yung WK, Lamborn KR, Norden AD, Cloughesy TF, Abrey LE, Fine HA, Chang SM, Robins HI, Fink K, Deangelis LM, Mehta M, Di Tomaso E, Drappatz J, Kesari S, Ligon KL, Aldape K, Jain RK, Stiles CD, Egorin MJ, Prados MD: Phase II study of imatinib mesylate for recurrent meningiomas (North American Brain Tumor Consortium study 01-08). Neuro Oncol; 2009 Dec;11(6):853-60
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  • [Title] Phase II study of imatinib mesylate for recurrent meningiomas (North American Brain Tumor Consortium study 01-08).
  • Platelet-derived growth factor (PDGF) and its receptors (PDGFR) are frequently coexpressed in meningiomas, potentially contributing to their pathogenesis.
  • The North American Brain Tumor Consortium conducted a phase II study to evaluate the therapeutic potential of imatinib mesylate (Gleevec), a PDGFR inhibitor, in patients with recurrent meningiomas.
  • Patients were stratified into benign (WHO grade I) meningiomas or atypical (WHO grade II) and malignant (WHO grade III) meningiomas.
  • Patients requiring enzyme-inducing antiepileptic drugs were ineligible.
  • Twenty-three heavily pretreated patients were enrolled into the study (13 benign, 5 atypical, and 5 malignant meningiomas), of whom 22 were eligible.
  • Tissue was available only from a minority of patients, but in these specimens there was uniform distribution of PDGFR, the drug target.
  • For benign meningiomas, median PFS was 3 months (range, 1.1-34 months); 6M-PFS was 45%.
  • For atypical and malignant meningiomas, median PFS was 2 months (range, 0.7-3.7 months); 6M-PFS was 0%.
  • Single-agent imatinib was well tolerated but had no significant activity in recurrent meningiomas.

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  • [Cites] Brain Tumor Pathol. 2001;18(1):1-5 [11517968.001]
  • [Cites] Blood. 2008 Apr 15;111(8):4022-8 [18256322.001]
  • [Cites] N Engl J Med. 2002 Aug 15;347(7):472-80 [12181401.001]
  • [Cites] J Neurosurg. 2001 Feb;94(2):293-300 [11213968.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1031-7 [11287972.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1038-42 [11287973.001]
  • [Cites] J Clin Neurosci. 2001 May;8 Suppl 1:49-53 [11386826.001]
  • [Cites] J Neurosurg. 2002 Aug;97(2):341-6 [12186462.001]
  • [Cites] J Chromatogr B Analyt Technol Biomed Life Sci. 2003 Jul 5;791(1-2):39-44 [12798163.001]
  • [Cites] Neurology. 2004 Apr 13;62(7):1210-2 [15079029.001]
  • [Cites] Acta Neuropathol. 2004 Aug;108(2):135-42 [15148612.001]
  • [Cites] J Neurosurg. 1985 Jan;62(1):18-24 [3964853.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1988 Aug;15(2):299-304 [3403313.001]
  • [Cites] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840.001]
  • [Cites] Int J Cancer. 1990 Jul 15;46(1):16-21 [2163990.001]
  • [Cites] J Clin Invest. 1990 Jul;86(1):131-40 [2164040.001]
  • [Cites] Int J Cancer. 1990 Nov 15;46(5):772-8 [1699901.001]
  • [Cites] J Biol Chem. 1991 Sep 5;266(25):16755-63 [1653246.001]
  • [Cites] Cancer Res. 1992 Jun 1;52(11):3213-9 [1317261.001]
  • [Cites] J Neurooncol. 1992 Jun;13(2):157-64 [1432033.001]
  • [Cites] J Neurooncol. 1993 Jan;15(1):75-7 [8455065.001]
  • [Cites] J Neurosurg. 1994 Sep;81(3):388-93 [8057146.001]
  • [Cites] Int J Cancer. 1995 Jan 17;60(2):168-73 [7829210.001]
  • [Cites] Cancer Res. 1996 Jan 1;56(1):100-4 [8548747.001]
  • [Cites] J Neurosurg. 1996 May;84(5):852-8; discussion 858-9 [8622161.001]
  • [Cites] J Neurooncol. 1996 Sep;29(3):197-205 [8858525.001]
  • [Cites] J Neurooncol. 1996 Sep;29(3):261-7 [8858532.001]
  • [Cites] Neurosurgery. 1997 Feb;40(2):271-5 [9007858.001]
  • [Cites] J Neurosurg. 1997 May;86(5):840-4 [9126900.001]
  • [Cites] J Neurosurg. 1997 Aug;87(2):315-23 [9254099.001]
  • [Cites] J Neurooncol. 1997 Dec;35(3):289-301 [9440026.001]
  • [Cites] J Neurosurg. 1998 May;88(5):938-9 [9576275.001]
  • [Cites] J Neurosurg. 1999 Jul;91(1):44-50 [10389879.001]
  • [Cites] Science. 2005 Jan 7;307(5706):58-62 [15637262.001]
  • [Cites] Br J Neurosurg. 2004 Oct;18(5):495-9 [15799152.001]
  • [Cites] Clin Pharmacokinet. 2005;44(9):879-94 [16122278.001]
  • [Cites] Ann Oncol. 2005 Oct;16(10):1702-8 [16033874.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9359-68 [16361636.001]
  • [Cites] J Neurooncol. 2006 Jul;78(3):271-6 [16628476.001]
  • [Cites] Br J Clin Pharmacol. 2006 Jul;62(1):97-112 [16842382.001]
  • [Cites] Clin Cancer Res. 2006 Aug 15;12(16):4899-907 [16914578.001]
  • [Cites] Neuro Oncol. 2007 Apr;9(2):145-60 [17293590.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3496-9 [17192396.001]
  • [Cites] Neurosurg Focus. 2007;23(4):E12 [17961036.001]
  • [Cites] PLoS Med. 2008 Jan 29;5(1):e24 [18232729.001]
  • [Cites] Neurosurgery. 2001 Nov;49(5):1029-37; discussion 1037-8 [11846894.001]
  • (PMID = 19293394.001).
  • [ISSN] 1523-5866
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA062407; United States / NCRR NIH HHS / RR / M01 RR000079; United States / NCRR NIH HHS / RR / M01 RR003186; United States / NCRR NIH HHS / RR / M01 RR000056; United States / NCRR NIH HHS / RR / M01 RR000865; United States / NCI NIH HHS / CA / U01 CA062399; United States / NCRR NIH HHS / RR / M01 RR000633; United States / NCI NIH HHS / CA / U01 CA062412; United States / NCI NIH HHS / CA / CA 62399; United States / NCI NIH HHS / CA / CA062421-07; United States / NCI NIH HHS / CA / U01 CA062421-07; United States / NCI NIH HHS / CA / U01 CA062421; United States / NCI NIH HHS / CA / U01 CA105663
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
  • [Other-IDs] NLM/ PMC2802405
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25. 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.
  • RESULTS: Patients ranged from ages 19 months to 17 years at diagnosis.
  • 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.
  • Sixteen patients remain alive and two patients, having had malignant tumors, are dead of disease.
  • 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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26. 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.
  • [Title] Dural based mass: malignant or benign.
  • 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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27. Delgado-López PD, Martín-Velasco V, Castilla-Díez JM, Fernández-Arconada O, Corrales-García EM, Galacho-Harnero A, Rodríguez-Salazar A, Pérez-Mies B: Metastatic meningioma to the eleventh dorsal vertebral body: total en bloc spondylectomy. Case report and review of the literature. Neurocirugia (Astur); 2006 Jun;17(3):240-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metastatic meningioma to the eleventh dorsal vertebral body: total en bloc spondylectomy. Case report and review of the literature.
  • INTRODUCTION: One in every thousand intracranial meningiomas metastatize extracranially.
  • To our knowledge, this is the first description of a total en bloc spondylectomy through a posterior approach for the treatment of an intraosseous metastatic meningioma to the eleventh dorsal vertebra.
  • CASE REPORT: In March 1996, a 37 year-old male underwent surgical resection for a left occipital intraventricular benign meningioma (WHO I).
  • By the end on 2003 he developed progressively invalidating dorsolumbar pain.
  • The pathological specimen was identified as adenocarcinoma and he initiated chemotherapy.
  • Advice from a second pathologist was seeked, who suggested the diagnosis of intraosseous meningioma.
  • In May 2004 the patient was admitted to our department and a new transpedicular biopsy confirmed the diagnosis.
  • In June 2004 he underwent T11 total en bloc spondylectomy (Tomita's procedure), fusion with bone and calcium substitute-filled stackable carbon-fiber cages, and T9 to L1 transpedicular screw fixation.
  • Definite pathology: benign meningioma (WHO I).
  • DISCUSSION: Distant metastases from intracranial meningiomas are rare entities, arising from benign lesions in, at least, 60% of cases.
  • Enam et al proposed a specific pathological score to differentiate benign, atypic and malignant meningiomas.
  • Such score correlates with the chance of metastatizing: more than 40% in malignant meningiomas compared to 3.8% of brain tumors overall.
  • [MeSH-major] Meningioma / pathology. Orthopedic Procedures / methods. Spinal Neoplasms / secondary. Spinal Neoplasms / surgery. Thoracic Vertebrae

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  • (PMID = 16855782.001).
  • [ISSN] 1130-1473
  • [Journal-full-title] Neurocirugía (Asturias, Spain)
  • [ISO-abbreviation] Neurocirugia (Astur)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Spain
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28. Föll JL, Oettel K, Horneff G, Kunze C, Herde J: [Eyelid swelling caused by a meningioma in an 8-year-old girl. Case report and review of the diagnosis and the treatment for meningiomas in childhood and adolescence]. Klin Monbl Augenheilkd; 2006 Sep;223(9):765-70
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  • [Title] [Eyelid swelling caused by a meningioma in an 8-year-old girl. Case report and review of the diagnosis and the treatment for meningiomas in childhood and adolescence].
  • [Transliterated title] Lidschwellung durch ein Meningeom bei einem 8-jährigen Mädchen: Fallbericht und Ubersicht über Meningeome im Kindes- und Jugendalter.
  • Orbital meningiomas are rare, particularly in childhood and adolescence.
  • CASE REPORT: We report the case of an 8-year-old girl with frontobasal meningioma, who was admitted to the hospital because of a one-sided upper eyelid swelling.
  • With the example of this case, the diagnosis, treatment and aftercare of meningiomas in childhood and adolescence will be discussed.
  • CONCLUSIONS: The treatment strategy of meningiomas in childhood requires a close interdisciplinary cooperation of ophthalmology, paediatric oncology, neurosurgery and radiotherapy.
  • Moreover, controlled investigations should yield information about the efficiency of modern irradiation techniques or adjuvant chemotherapy in the treatment of inoperable or malignant meningiomas.
  • [MeSH-major] Edema / diagnosis. Edema / etiology. Eyelid Neoplasms / complications. Eyelid Neoplasms / diagnosis. Meningioma / complications. Meningioma / diagnosis
  • [MeSH-minor] Adolescent. Child. Eyelid Diseases / complications. Eyelid Diseases / diagnosis. Female. Humans

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  • (PMID = 16986088.001).
  • [ISSN] 0023-2165
  • [Journal-full-title] Klinische Monatsblätter für Augenheilkunde
  • [ISO-abbreviation] Klin Monbl Augenheilkd
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 40
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29. Yamamoto T, Nakai K, Matsumura A: Boron neutron capture therapy for glioblastoma. Cancer Lett; 2008 Apr 18;262(2):143-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Boron neutron capture therapy for glioblastoma.
  • Boron neutron capture therapy (BNCT) theoretically allows the preferential destruction of tumor cells while sparing the normal tissue, even if the cells have microscopically spread to the surrounding normal brain.
  • Recent clinical studies of BNCT have focused on high-grade glioma and cutaneous melanoma; however, cerebral metastasis of melanoma, anaplastic meningioma, head and neck tumor, and lung and liver metastasis have been investigated as potential candidates for BNCT.
  • Improved tumor-targeting boron compounds and optimized administration methods, improved boron drug delivery systems, development of a hospital-based neutron source, and/or other combination modalities will enhance the therapeutic effectiveness of BNCT in the future.
  • [MeSH-major] Boron Neutron Capture Therapy. Brain Neoplasms / radiotherapy. Glioblastoma / radiotherapy
  • [MeSH-minor] Boron / therapeutic use. Clinical Trials as Topic. Forecasting. Humans. Photons / therapeutic use. Radiotherapy Dosage

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  • (PMID = 18313207.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] N9E3X5056Q / Boron
  • [Number-of-references] 77
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30. Modha A, Gutin PH: Diagnosis and treatment of atypical and anaplastic meningiomas: a review. Neurosurgery; 2005 Sep;57(3):538-50; discussion 538-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis and treatment of atypical and anaplastic meningiomas: a review.
  • Atypical and anaplastic meningiomas are uncommon tumors with a poorer prognosis than benign meningiomas.
  • Both tumors are rare and are often integrated with benign meningiomas when treatments are evaluated.
  • In addition, because there has not been one histopathological classification scheme for atypical and anaplastic meningiomas in the past, there are numerous inconsistencies in the literature.
  • Malignant progression with accumulation of mutations in a benign meningioma can result in an atypical and/or anaplastic meningioma.
  • Radiation therapy can be used as an adjunctive treatment after both total and subtotal resection.
  • In addition, the role of stereotactic radiosurgery is increasing, along with a possible role for brachytherapy.
  • A treatment algorithm is suggested.
  • [MeSH-major] Brain Neoplasms / therapy. Meningeal Neoplasms / therapy. Meningioma / therapy
  • [MeSH-minor] Algorithms. Anaplasia / diagnosis. Anaplasia / metabolism. Anaplasia / therapy. Disease Progression. Drug Therapy / methods. Humans. Immunohistochemistry / methods. Magnetic Resonance Imaging. Radiosurgery. Vascular Endothelial Growth Factor Receptor-2 / metabolism

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  • (PMID = 16145534.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  • [Number-of-references] 65
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31. Plotkin M, Amthauer H, Eisenacher J, Wurm R, Michel R, Wust P, Stockhammer F, Röttgen R, Gutberlet M, Ruf J, Felix R: Value of 123I-IMT SPECT for diagnosis of recurrent non-astrocytic intracranial tumours. Neuroradiology; 2005 Jan;47(1):18-26
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  • [Title] Value of 123I-IMT SPECT for diagnosis of recurrent non-astrocytic intracranial tumours.
  • The value of single-photon emission tomography (SPECT) using iodine-123-alpha-methyl-tyrosine (IMT) for the diagnosis of recurrent or residual gliomas is well established.
  • The study included 22 patients with suspected recurrent intracranial tumours of non-astrocytic origin (12 brain metastases, one supratentorial primitive neuroendocrine tumour (PNET), one rhabdoid tumour, two clivus chordomas, three ependymomas, two pituitary tumours, one anaplastic meningioma) who had previously been treated by surgery and/or radio/chemotherapy.
  • We concluded that the IMT-SPECT is a promising complementary imaging tool for the detection of recurrences of non-astrocytic intracranial tumours and their distinguishing from treatment-induced changes.
  • The limitation of the IMT-SPECT is its low sensitivity for the detection of small lesions.
  • [MeSH-major] Brain Neoplasms / diagnostic imaging. Iodine Radioisotopes. Methyltyrosines. Neoplasm Recurrence, Local / diagnostic imaging. Radiopharmaceuticals. Tomography, Emission-Computed, Single-Photon / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Chordoma / diagnostic imaging. Ependymoma / diagnostic imaging. False Negative Reactions. False Positive Reactions. Female. Follow-Up Studies. Glioma / diagnostic imaging. Humans. Magnetic Resonance Imaging. Male. Meningioma / diagnostic imaging. Middle Aged. Neuroendocrine Tumors / diagnostic imaging. Pituitary Neoplasms / diagnostic imaging. Retrospective Studies. Rhabdoid Tumor / diagnostic imaging. Sensitivity and Specificity. Supratentorial Neoplasms / diagnostic imaging

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  • [Cites] J Nucl Med. 2001 Apr;42(4):579-85 [11337545.001]
  • [Cites] Acta Radiol. 1989 Mar-Apr;30(2):121-8 [2493795.001]
  • [Cites] Ann Nucl Med. 2002 Nov;16(7):503-6 [12508845.001]
  • [Cites] J Neurooncol. 2004 Oct;70(1):49-58 [15527107.001]
  • [Cites] AJR Am J Roentgenol. 1994 Dec;163(6):1459-65 [7992747.001]
  • [Cites] Eur J Nucl Med. 1998 Feb;25(2):177-81 [9473267.001]
  • [Cites] J Nucl Med. 2000 Nov;41(11):1793-800 [11079485.001]
  • [Cites] Neuroimaging Clin N Am. 1999 Nov;9(4):801-19 [10517946.001]
  • [Cites] J Clin Oncol. 2002 Jan 15;20(2):396-404 [11786566.001]
  • [Cites] Eur J Nucl Med. 1999 Feb;26(2):144-51 [9933348.001]
  • [Cites] Semin Oncol. 1994 Apr;21(2):162-71 [8153662.001]
  • [Cites] Nuklearmedizin. 1995 Apr;34(2):71-5 [7761277.001]
  • [Cites] Semin Nucl Med. 2003 Apr;33(2):148-62 [12756647.001]
  • [Cites] AJNR Am J Neuroradiol. 1996 Feb;17 (2):345-53 [8938309.001]
  • [Cites] J Nucl Med. 1989 Jan;30(1):110-2 [2783455.001]
  • [Cites] J Nucl Med. 1998 Oct;39(10 ):1736-43 [9776279.001]
  • [Cites] J Nucl Med. 1998 Jan;39(1):23-7 [9443732.001]
  • [Cites] AJNR Am J Neuroradiol. 1993 May-Jun;14 (3):524-7 [8517335.001]
  • [Cites] Nucl Med Commun. 1996 Mar;17 (3):197-8 [8692485.001]
  • [Cites] J Nucl Med. 1997 Apr;38(4):517-22 [9098193.001]
  • [Cites] Radiology. 1993 Jan;186(1):37-44 [8416584.001]
  • [Cites] Acta Radiol. 1990 Sep;31(5):417-29 [2261284.001]
  • [Cites] Radiology. 2003 Jan;226(1):181-7 [12511688.001]
  • [Cites] Nuklearmedizin. 1997 Mar;36(2):36-41 [9148271.001]
  • [Cites] J Nucl Med. 2004 Mar;45(3):374-81 [15001676.001]
  • [Cites] J Comput Assist Tomogr. 1983 Dec;7(6):1062-6 [6415134.001]
  • [Cites] Neurosurgery. 1993 Jul;33(1):28-33 [8355844.001]
  • [Cites] AJR Am J Roentgenol. 1988 Jan;150(1):189-97 [3257119.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Aug 1;48(1):43-52 [10924970.001]
  • [Cites] Curr Opin Oncol. 1994 May;6(3):254-61 [8080854.001]
  • [Cites] J Nucl Med. 2004 Apr;45(4):579-86 [15073253.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 Nov 1;54(3):842-54 [12377338.001]
  • [Cites] Clin Cancer Res. 2000 Jun;6(6):2252-9 [10873075.001]
  • [Cites] J Nucl Med. 1998 May;39(5):778-85 [9591574.001]
  • [Cites] Nucl Med Commun. 1996 Jul;17 (7):609-15 [8843121.001]
  • [Cites] J Neurosurg. 2003 May;98 (5):1056-64 [12744366.001]
  • [Cites] Nuklearmedizin. 2002;41(4):191-6 [12224403.001]
  • [Cites] Ann Neurol. 1991 Apr;29(4):347-55 [1929205.001]
  • [Cites] J Nucl Med. 1990 Mar;31(3):281-6 [2155314.001]
  • (PMID = 15630586.001).
  • [ISSN] 0028-3940
  • [Journal-full-title] Neuroradiology
  • [ISO-abbreviation] Neuroradiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 0 / Methyltyrosines; 0 / Radiopharmaceuticals; A77N8J5H5T / 3-iodo-alpha-methyltyrosine
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32. Strassner C, Buhl R, Mehdorn HM: Recurrence of intracranial meningiomas: did better methods of diagnosis and surgical treatment change the outcome in the last 30 years? Neurol Res; 2009 Jun;31(5):478-82
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  • [Title] Recurrence of intracranial meningiomas: did better methods of diagnosis and surgical treatment change the outcome in the last 30 years?
  • OBJECTIVE: Meningiomas are benign intracranial tumors growing from the arachnoid cap cells.
  • METHODS: Between 1991 and 2002, 463 patients with an intracranial meningioma were operated in the Department of Neurosurgery, University of Kiel, Kiel, Germany.
  • We compared the outcome of these patients after operation and the different methods of radiation therapy and chemotherapy with the data from Buhl (1994), who analysed 661 patients with intracranial meningioma who were operated on in the Department of Neurosurgery, University of Essen, Essen, Germany, between 1968 and 1988, to find out whether better methods of diagnosis like magnetic resonance imaging scans, magnetic resonance spectroscopy, post-operative radiation therapy and chemotherapy have an influence on the recurrence and outcome after surgical treatment.
  • Both studies underlined the preponderance of female patients for intracranial meningiomas.
  • The intracranial localization of the meningiomas was similar to the distribution of the histological subtypes and the rate of recurrence; only the malignant meningiomas showed a higher grade of recurrence in the last study.
  • Indications for post-operative radiation therapy were given earlier in the last study owing to the experience from the primary study.
  • The outcome of the patients after surgical removal was improving in the last years; the 30 day post-operative mortality after a primary operation on an intracranial meningioma decreased from 12.1 to 3%.
  • After removal of a recurrent meningioma, the mortality declined from 20 to 12.5%.
  • CONCLUSION: In the last 30 years, nothing important changed at the time of appearance of meningiomas, concerning the gender distribution and localisation as well as histological subtypes.
  • With better operating modalities and additional treatment with radiation and gamma knife, the mortality decreased significantly from 12 to 3% and the outcome of the patients is still improving, so that even elderly patients with intracranial meningioma can undergo surgical treatment with minor risks.
  • [MeSH-major] Meningeal Neoplasms / diagnosis. Meningeal Neoplasms / therapy. Meningioma / diagnosis. Meningioma / therapy
  • [MeSH-minor] Combined Modality Therapy. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Radiosurgery. Time Factors. Treatment Outcome

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  • (PMID = 19500450.001).
  • [ISSN] 0161-6412
  • [Journal-full-title] Neurological research
  • [ISO-abbreviation] Neurol. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
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33. Puchner MJ, Hans VH, Harati A, Lohmann F, Glas M, Herrlinger U: Bevacizumab-induced regression of anaplastic meningioma. Ann Oncol; 2010 Dec;21(12):2445-6
Genetic Alliance. consumer health - Meningioma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bevacizumab-induced regression of anaplastic meningioma.

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  • (PMID = 21041375.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 2S9ZZM9Q9V / Bevacizumab
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