[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 25 of about 25
1. Scherer K, Johnston J, Panda M: Dural based mass: malignant or benign. J Radiol Case Rep; 2009;3(11):1-12

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dural based mass: malignant or benign.
  • 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.
  • Cerebral angiogram demonstrated a parafalcine mass supplied by the middle meningeal artery.
  • Embolization of the middle meningeal artery with craniotomy for excision of the suspected meningioma was performed.
  • 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.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


2. Norden AD, Raizer JJ, Abrey LE, Lamborn KR, Lassman AB, Chang SM, Yung WK, Gilbert MR, Fine HA, Mehta M, Deangelis LM, Cloughesy TF, Robins HI, Aldape K, Dancey J, Prados MD, Lieberman F, Wen PY: Phase II trials of erlotinib or gefitinib in patients with recurrent meningioma. J Neurooncol; 2010 Jan;96(2):211-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • There are no established treatments for recurrent meningioma when surgical and radiation options are exhausted.
  • The epidermal growth factor receptor (EGFR) is often over-expressed in meningiomas and may promote tumor growth.
  • Patients with recurrent histologically confirmed meningiomas with no more than 2 previous chemotherapy regimens were treated with gefitinib 500 mg/day or erlotinib 150 mg/day until tumor progression or unacceptable toxicity.
  • Eight patients (32%) had benign tumors, 9 (36%) atypical, and 8 (32%) malignant.
  • For benign tumors, the 6-month progression-free survival (PFS6) was 25%, 12-month PFS (PFS12) 13%, 6-month overall survival (OS6) 63%, and 12-month OS (OS12) 50%.
  • For atypical and malignant tumors, PFS6 was 29%, PFS12 18%, OS6 71%, and OS12 65%.
  • Although treatment was well-tolerated, neither gefitinib nor erlotinib appear to have significant activity against recurrent meningioma.

  • Genetic Alliance. consumer health - Meningioma.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Surg Gynecol Obstet. 1993 Nov;177(5):488-96 [8211601.001]
  • [Cites] Neurosurg Focus. 2007;23(4):E12 [17961036.001]
  • [Cites] J Neurooncol. 1995 Oct;26(1):45-51 [8583244.001]
  • [Cites] J Neurosurg. 1997 Aug;87(2):315-23 [9254099.001]
  • [Cites] Neuropathol Appl Neurobiol. 1998 Dec;24(6):441-52 [9888154.001]
  • [Cites] J Neurooncol. 2004 Nov;70(2):183-202 [15674477.001]
  • [Cites] Br J Neurosurg. 2004 Oct;18(5):495-9 [15799152.001]
  • [Cites] Neurosurgery. 2005 Sep;57(3):538-50; discussion 538-50 [16145534.001]
  • [Cites] Lancet. 2005 Oct 29-Nov 4;366(9496):1527-37 [16257339.001]
  • [Cites] J Clin Oncol. 2009 Mar 10;27(8):1268-74 [19204207.001]
  • [Cites] Neuro Oncol. 2009 Dec;11(6):853-60 [19293394.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Mar;61(3):215-25; discussion 226-9 [11895036.001]
  • [Cites] J Clin Oncol. 2004 Jan 1;22(1):133-42 [14638850.001]
  • [Cites] Neurology. 2004 Apr 13;62(7):1210-2 [15079029.001]
  • [Cites] J Neuropathol Exp Neurol. 2004 Apr;63(4):275-86 [15099018.001]
  • [Cites] Acta Neuropathol. 2004 Aug;108(2):135-42 [15148612.001]
  • [Cites] Curr Treat Options Oncol. 2004 Dec;5(6):499-509 [15509483.001]
  • [Cites] Cancer Res. 1987 Apr 15;47(8):2172-6 [3493842.001]
  • [Cites] Cancer. 1990 Jul 1;66(1):152-5 [2354402.001]
  • [Cites] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840.001]
  • [Cites] J Neuropathol Exp Neurol. 2005 Dec;64(12):1029-36 [16319713.001]
  • [Cites] J Neurooncol. 2006 Jul;78(3):271-6 [16628476.001]
  • [Cites] Br J Cancer. 2007 Apr 10;96(7):1047-51 [17353924.001]
  • [Cites] Hum Pathol. 1994 Feb;25(2):146-53 [8119714.001]
  • (PMID = 19562255.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA062407; United States / NCRR NIH HHS / RR / M01 RR000079; United States / NCATS NIH HHS / TR / UL1 TR000005; United States / NCI NIH HHS / CA / U01 CA062421-06; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCRR NIH HHS / RR / M01-RR0865; United States / NCI NIH HHS / CA / U01 CA62399; United States / NCRR NIH HHS / RR / M01 RR003186; United States / NCRR NIH HHS / RR / M01 RR000056; United States / NCRR NIH HHS / RR / M01-RR00079; United States / NCI NIH HHS / CA / U01CA62407-08; United States / NCI NIH HHS / CA / CA16672; United States / NCRR NIH HHS / RR / M01 RR000865; United States / NCI NIH HHS / CA / 5-U01CA62399-09; United States / NCI NIH HHS / CA / CA062421-06; United States / NCI NIH HHS / CA / U01 CA062399; United States / NCRR NIH HHS / RR / M01-RR00056; United States / NCI NIH HHS / CA / U01 CA062405; United States / NCI NIH HHS / CA / U01 CA062412; United States / NCI NIH HHS / CA / U01CA62421-08; United States / NCI NIH HHS / CA / CA62422; United States / NCI NIH HHS / CA / U01 CA062421; United States / NCI NIH HHS / CA / U01CA62405; United States / NCRR NIH HHS / RR / M01 RR03186; United States / NCI NIH HHS / CA / U01 CA062422; United States / NCI NIH HHS / CA / CA62399; United States / NCI NIH HHS / CA / CA62412
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; S65743JHBS / gefitinib
  • [Other-IDs] NLM/ NIHMS511532; NLM/ PMC3786190
  •  go-up   go-down


3. Tyagi D, Sharma BS, Gupta SK, Kaul D, Vasishta RK, Khosla VK: Expression of Bcl2 proto-oncogene in primary tumors of the central nervous system. Neurol India; 2002 Sep;50(3):290-4
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of Bcl2 proto-oncogene in primary tumors of the central nervous system.
  • The present study was addressed to find out the expression of Bcl2 proto-oncogene in tumor tissues derived from 25 patients with primary central nervous system tumors.
  • Brain parenchyma in 8 cases, with deeply located tumor, was also examined for Bcl2 expression which served as control.
  • Both benign and malignant tumors (confirmed by histopathological examination) expressed Bcl2 gene product.
  • Tumors exhibited 2-6 fold increase in Bcl2 expression as compared to the normal parenchyma adjacent to some of these tumors studied.
  • However, no correlation was found between the histopathological types of tumor, glial fibrillary acidic protein positivity and degree of Bcl2 expression.
  • Based on this study, we propose that the overexpression of Bcl2 gene product found in primary CNS tumors may be an important molecular event which is known to make the various types of tumor resistant to chemotherapy or radiotherapy.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Proto-Oncogene Proteins c-bcl-2 / biosynthesis
  • [MeSH-minor] Adenoma / metabolism. Adult. Child. Ependymoma / metabolism. Female. Glioblastoma / metabolism. Humans. Male. Meningeal Neoplasms / metabolism. Meningioma / metabolism. Middle Aged. Neurilemmoma / metabolism

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12391455.001).
  • [ISSN] 0028-3886
  • [Journal-full-title] Neurology India
  • [ISO-abbreviation] Neurol India
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2
  •  go-up   go-down


Advertisement
4. Kalamarides M, Hunter-Schaedle K, Blakeley J, Allen J, Babovic-Vuskanovic D, Belzberg A, Bollag G, Chen R, DiTomaso E, Golfinos J, Harris G, Jacob A, Kalpana G, Karajannis M, Korf B, Kurzrock R, Law M, McClatchey A, Packer R, Roehm P, Rubenstein A, Slattery W 3rd, Tonsgard JH, Welling DB, Widemann B, Yohay K: Consensus recommendations to accelerate clinical trials for neurofibromatosis type 2. Clin Cancer Res; 2009 Aug 15;15(16):5032-5039
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Consensus recommendations to accelerate clinical trials for neurofibromatosis type 2.
  • PURPOSE: Neurofibromatosis type 2 (NF2) is a rare autosomal dominant disorder associated primarily with bilateral schwannomas seen on the superior vestibular branches of the eighth cranial nerves.
  • Significant morbidity can result from surgical treatment of these tumors.
  • Meningiomas, ependymomas, and other benign central nervous system tumors are also common in NF2.
  • The lack of effective treatments for NF2 marks an unmet medical need.
  • RESULTS: Workshop participants reached a consensus that, based on current knowledge, the time is right to plan and implement NF2 clinical trials.
  • Obstacles impeding NF2 clinical trials and how to address them were discussed, as well as the candidate therapeutic pipeline for NF2.
  • [MeSH-major] Clinical Trials as Topic / methods. Consensus. Health Planning Guidelines. Neurofibromatosis 2 / therapy
  • [MeSH-minor] Animals. Auditory Brain Stem Implants. Cochlear Implants. Drug Evaluation, Preclinical / methods. Drug Evaluation, Preclinical / trends. Humans. Meningeal Neoplasms / therapy. Meningioma / therapy. Time Factors

  • Genetic Alliance. consumer health - Neurofibromatosis.
  • Genetic Alliance. consumer health - Neurofibromatosis type 2.
  • MedlinePlus Health Information. consumer health - Clinical Trials.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Oncol. 2002 Mar;20(3):475-82 [11836557.001]
  • [Cites] Curr Biol. 2006 Apr 4;16(7):702-9 [16581517.001]
  • [Cites] J Med Genet. 2007 Jul;44(7):424-8 [17307835.001]
  • [Cites] Hum Gene Ther. 2006 Jan;17(1):20-30 [16409122.001]
  • [Cites] Genes Dev. 2000 Jul 1;14(13):1617-30 [10887156.001]
  • [Cites] J Med Genet. 2008 Jun;45(6):332-9 [18285426.001]
  • [Cites] J Neurosurg. 2000 May;92(5):766-70 [10794289.001]
  • [Cites] Brain Pathol. 2008 Jan;18(1):62-70 [17924978.001]
  • [Cites] Laryngoscope. 2007 Jun;117(6):1069-72 [17545869.001]
  • [Cites] Nat Cell Biol. 2006 Jan;8(1):27-36 [16341207.001]
  • [Cites] Genes Dev. 2005 Oct 1;19(19):2265-77 [16204178.001]
  • [Cites] Neoplasia. 2002 Nov-Dec;4(6):501-9 [12407444.001]
  • [Cites] Oncogene. 2009 Feb 12;28(6):854-65 [19029950.001]
  • [Cites] J Med Genet. 1992 Dec;29(12 ):841-6 [1479598.001]
  • [Cites] Genes Dev. 1999 Apr 15;13(8):978-86 [10215625.001]
  • [Cites] Genes Dev. 2002 May 1;16(9):1060-5 [12000789.001]
  • [Cites] Otol Neurotol. 2005 Jul;26(4):733-40 [16015177.001]
  • [Cites] Otol Neurotol. 2008 Jan;29(1):58-68 [18199958.001]
  • [Cites] J Neuropathol Exp Neurol. 2001 Oct;60(10):994-1003 [11589430.001]
  • [Cites] Otol Neurotol. 2005 Jan;26(1):93-7 [15699726.001]
  • [Cites] J Neurosurg. 2002 Jun;96(6):1063-71 [12066908.001]
  • [Cites] Am J Hum Genet. 2002 Oct;71(4):715-23 [12235555.001]
  • [Cites] Neurology. 2002 Dec 10;59(11):1759-65 [12473765.001]
  • [Cites] Am J Otol. 1998 Sep;19(5):638-43 [9752973.001]
  • [Cites] J Neurooncol. 1996 Sep;29(3):197-205 [8858525.001]
  • [Cites] Neurosurgery. 2008 Jun;62(6):1314-9; discussion 1319-20 [18824998.001]
  • [Cites] Neurology. 2007 Feb 27;68(9):643-7 [17215493.001]
  • [Cites] Br J Cancer. 2007 Sep 3;97(5):577-81 [17726450.001]
  • [Cites] Stat Med. 1999 Aug 15;18(15):1905-42 [10532877.001]
  • [Cites] Am J Hum Genet. 2007 Apr;80(4):805-10 [17357086.001]
  • [Cites] Neurology. 2000 Jan 11;54(1):71-6 [10636128.001]
  • [Cites] Br J Neurosurg. 2005 Feb;19(1):5-12 [16147576.001]
  • [Cites] J Cell Biol. 2007 Jun 4;177(5):893-903 [17548515.001]
  • [Cites] Lancet Neurol. 2006 Dec;5(12):1045-54 [17110285.001]
  • (PMID = 19671848.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDCD NIH HHS / DC / K08 DC009288
  • [Publication-type] Consensus Development Conference; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Number-of-references] 36
  • [Other-IDs] NLM/ NIHMS707923; NLM/ PMC4513640
  •  go-up   go-down


5. Spalice A, Ruggieri M, Grosso S, Verrotti A, Polizzi A, Magro G, Caltabiano R, Pavone P, Del Balzo F, Platania N, Iannetti P: Dysembryoplastic neuroepithelial tumors: a prospective clinicopathologic and outcome study of 13 children. Pediatr Neurol; 2010 Dec;43(6):395-402
MedlinePlus Health Information. consumer health - Seizures.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dysembryoplastic neuroepithelial tumors: a prospective clinicopathologic and outcome study of 13 children.
  • Dysembryoplastic neuroepithelial tumors (DNETs) are benign intracortical masses that are typically observed in children and young adults and are classified as glioneuronal tumors (WHO grade I).
  • In 11/13 cases, the seizures were resistant to drug therapy, and all the children had surgery consisting of extended lesionectomy coupled with neuronavigation.
  • Pathology examination revealed cortical dysplasia (n = 8), glial nodules (n = 11), calcification (n = 4), cellular atypia (n = 3), endothelial proliferation (n = 1), perivascular inflammation (n = 3), and meningeal involvement (n = 6).
  • This first prospective study with follow-up monitoring of a childhood population with DNETs confirms, on a long-term basis, that the coupled strategy of extended lesionectomy and neuronavigation has good outcome for long-term seizure control.
  • [MeSH-major] Brain Neoplasms / pathology. Cerebral Cortex / pathology. Neoplasms, Neuroepithelial / pathology. Seizures / pathology
  • [MeSH-minor] Adolescent. Child. Electroencephalography. Female. Humans. Male. Prospective Studies. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21093729.001).
  • [ISSN] 1873-5150
  • [Journal-full-title] Pediatric neurology
  • [ISO-abbreviation] Pediatr. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


6. 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
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • It is secreted by all vascular cells and plays a role in tumor invasion and metastasis, presumably by plasmin-mediated matrix remodeling.
  • Previous studies have shown high expression of TFPI-2 by benign tumors and low or absent expression in highly malignant tumors.
  • 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.
  • Finally, TFPI-2 overexpression inhibited intracranial tumor formation in nude mice.
  • Our data substantiate our previous observation that TFPI-2 plays an important role in tumor progression and has potential in anti-cancer therapy.

  • Genetic Alliance. consumer health - Meningioma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


7. Mori Y, Kondo T, Iwakoshi T, Kida Y, Kobayashi T, Yoshimoto M, Hasegawa T: Malignant lymphoma arising in the cerebral parenchyma adjacent to a parasagittal meningioma. Neurol Med Chir (Tokyo); 2006 Aug;46(8):398-400
MedlinePlus Health Information. consumer health - Lymphoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • She gradually developed motor weakness in the left hand.
  • Magnetic resonance (MR) imaging disclosed a newly developed well-enhanced area in the cerebral parenchyma adjacent to the stable original meningioma.
  • Two separate tumors were identified with quite different histological features.
  • The extra-axial tumor was identified as benign transitional meningioma and the intra-axial tumor as diffuse large cell type malignant lymphoma.
  • The original site of the lymphoma remained free from relapse, but another lesion developed in the right frontal lobe 3 months later and chemotherapy was performed.
  • However, development of new different tumors is possible, although thought to be rare.
  • [MeSH-major] Brain Neoplasms / complications. Brain Neoplasms / pathology. Lymphoma / complications. Lymphoma / pathology. Meningeal Neoplasms / complications. Meningeal Neoplasms / pathology. Meningioma / complications. Meningioma / pathology

  • Genetic Alliance. consumer health - Meningioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16936461.001).
  • [ISSN] 0470-8105
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


8. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fatty acid synthase as a novel target for meningioma therapy.
  • High levels of fatty acid synthase (FAS) expression have been reported in hormone receptor-positive tumors, including prostate, breast, and ovarian cancers, and its inhibition reduces tumor growth in vitro and in vivo.
  • 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

  • Genetic Alliance. consumer health - Meningioma.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


9. Sioka C, Kyritsis AP: Chemotherapy, hormonal therapy, and immunotherapy for recurrent meningiomas. J Neurooncol; 2009 Mar;92(1):1-6
MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemotherapy, hormonal therapy, and immunotherapy for recurrent meningiomas.
  • Meningioma is a common intracranial tumor, originating from the meninges of the skull or spinal canal.
  • Most meningiomas are benign tumors, however atypical or anaplastic tumors can be found in 6% of cases.
  • Patients with asymptomatic small benign meningiomas can be followed without therapy, but in symptomatic patients complete surgical resection should be performed.
  • For recurrent previously resected tumors re-resection is recommended followed by radiotherapy in selected cases.
  • Antiprogesterone treatment can also be considered in recurrent benign meningiomas.
  • Immunotherapy with interferon-alpha and chemotherapy should be reserved for all cases of recurrent meningiomas (benign, atypical, and malignant) when all the standard therapies have failed or contraindicated.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Immunotherapy / methods. Meningeal Neoplasms / therapy. Meningioma / therapy. Neoplasm Recurrence, Local / therapy
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Clinical Trials as Topic. Humans

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurooncol. 2004 Jun;68(2):131-40 [15218949.001]
  • [Cites] J Neurosurg. 1997 May;86(5):840-4 [9126900.001]
  • [Cites] Cancer. 2007 Feb 1;109(3):588-97 [17177201.001]
  • [Cites] Neurosurgery. 1997 Feb;40(2):271-5 [9007858.001]
  • [Cites] J Clin Endocrinol Metab. 1992 Mar;74(3):543-7 [1346787.001]
  • [Cites] Rev Neurol. 1997 Dec;25(148):2002-5 [9528047.001]
  • [Cites] Clin Neuropathol. 2004 Jan-Feb;23(1):21-7 [14986930.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1992 Jun;55(6):486-90 [1619417.001]
  • [Cites] J Neurosurg. 2005 Sep;103(3):508-17 [16235684.001]
  • [Cites] Br J Neurosurg. 2004 Oct;18(5):495-9 [15799152.001]
  • [Cites] Clin Cancer Res. 2000 May;6(5):1865-74 [10815909.001]
  • [Cites] Eur J Cancer. 1991;27(11):1453-7 [1660295.001]
  • [Cites] J Clin Neurosci. 2008 Jun;15(6):721-2; author reply 722-3 [18406141.001]
  • [Cites] J Neurosurg. 1991 Jun;74(6):861-6 [2033444.001]
  • [Cites] J Neurosurg. 2007 Mar;106(3):455-62 [17367069.001]
  • [Cites] Neurosurgery. 1995 Feb;36(2):365-73; discussion 373-4 [7731518.001]
  • [Cites] Neurosurg Focus. 2007;23(4):E10 [17961034.001]
  • [Cites] J Neurooncol. 1993 Jan;15(1):75-7 [8455065.001]
  • [Cites] J Neurooncol. 2004 Jan;66(1-2):155-66 [15015781.001]
  • [Cites] J Neurooncol. 2002 Jan;56(2):133-42 [11995814.001]
  • [Cites] Gan To Kagaku Ryoho. 2007 Feb;34(2):265-8 [17301541.001]
  • [Cites] Neurochirurgie. 2004 Sep;50(4):461-7 [15547484.001]
  • [Cites] Neurology. 2007 Sep 4;69(10):969-73 [17785665.001]
  • [Cites] Cancer. 2005 Apr 1;103(7):1427-30 [15690330.001]
  • [Cites] Neurosurgery. 2006 Nov;59(5):1109-20; discussion 1120-1 [17143245.001]
  • [Cites] Eur J Cancer. 1991;27(4):416-9 [1828169.001]
  • [Cites] Skull Base. 2006 Aug;16(3):157-60 [17268588.001]
  • [Cites] J Neurooncol. 2000 Sep;49(2):165-70 [11206012.001]
  • [Cites] J Neurooncol. 1996 Sep;29(3):269-72 [8858533.001]
  • [Cites] J Neurosurg. 2000 Jul;93(1):132-5 [10883917.001]
  • [Cites] J Neurosurg. 2002 Aug;97(2):341-6 [12186462.001]
  • [Cites] J Neurooncol. 2005 Sep;74(2):157-65 [16193387.001]
  • [Cites] Cancer Invest. 2006 Dec;24(8):727-33 [17162554.001]
  • [Cites] J Neurooncol. 2006 Jul;78(3):271-6 [16628476.001]
  • [Cites] Hum Reprod. 1994 Jun;9 Suppl 1:202-7 [7962466.001]
  • [Cites] Clin Neurol Neurosurg. 2008 Jul;110(7):645-8 [18471956.001]
  • [Cites] Acta Neurol Scand. 1987 Jun;75(6):434-6 [2888257.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2007 Jun;15(2):187-92 [17525632.001]
  • [Cites] Lancet. 1995 Feb 4;345(8945):331 [7837901.001]
  • [Cites] Clin Cancer Res. 2001 Aug;7(8):2269-76 [11489801.001]
  • [Cites] J Neurooncol. 2004 Mar-Apr;67(1-2):221-6 [15072471.001]
  • [Cites] Neurosurgery. 2000 Mar;46(3):692-702; discussion 702-3 [10719866.001]
  • (PMID = 19023520.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal
  • [Number-of-references] 43
  •  go-up   go-down


10. McCall T, Binning M, Blumenthal DT, Jensen RL: Variations of disseminated choroid plexus papilloma: 2 case reports and a review of the literature. Surg Neurol; 2006 Jul;66(1):62-7; discussion 67-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Choroid plexus papillomas are typically considered benign lesions, but histology is not always predictive of their behavior.
  • These tumors can metastasize anywhere along the neuraxis and may be intraventricular, subarachnoid, or intraparenchymal.
  • Patient 2 also had a primary fourth ventricular tumor but with subsequent suprasellar and spinal drop metastases.
  • Patient 2 has been treated with several modalities, including radiation therapy and chemotherapy, with slowing of symptom progression.
  • There is no consensus on the most effective treatment for choroid plexus papilloma metastases; surgical resection, chemotherapy, and radiation therapy may all yield benefits.
  • [MeSH-major] Choroid Plexus / pathology. Choroid Plexus / surgery. Meningeal Neoplasms / diagnosis. Meningeal Neoplasms / therapy. Papilloma, Choroid Plexus / diagnosis. Papilloma, Choroid Plexus / therapy
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Arachnoid / pathology. Arachnoid / physiopathology. Arachnoid / surgery. Disease Progression. Female. Humans. Pia Mater / pathology. Pia Mater / physiopathology. Pia Mater / surgery. Subarachnoid Space / pathology. Subarachnoid Space / physiopathology. Subarachnoid Space / surgery. Treatment Outcome

  • Genetic Alliance. consumer health - Choroid Plexus Papilloma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16793445.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 34
  •  go-up   go-down


11. Chamberlain MC, Blumenthal DT: Intracranial meningiomas: diagnosis and treatment. Expert Rev Neurother; 2004 Jul;4(4):641-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intracranial meningiomas: diagnosis and treatment.
  • Meningiomas are extra-axial CNS tumors which have a female predominance and occur in middle-to-late adult life.
  • Most meningiomas (90%) are benign, 6% are atypical and a small proportion (2%) are malignant.
  • Most patients diagnosed with a meningioma undergo surgical resection to relieve neurological symptoms.
  • For most incompletely resected or recurrent tumors not previously irradiated, radiotherapy is administered.
  • Advocates of stereotactic radiotherapy have suggested this therapy in lieu of surgery particularly in poor surgical risk patients, patients with meningiomas in eloquent or surgically inaccessible locations and in patients of advanced age.
  • When the meningioma is unresectable or all other treatments (e.g., surgery and radiotherapy) have failed, hormonal chemotherapy may be considered.
  • [MeSH-major] Meningeal Neoplasms / diagnosis. Meningeal Neoplasms / therapy. Meningioma / diagnosis. Meningioma / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Female. Humans. Radiosurgery

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15853583.001).
  • [ISSN] 1744-8360
  • [Journal-full-title] Expert review of neurotherapeutics
  • [ISO-abbreviation] Expert Rev Neurother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 50
  •  go-up   go-down


12. Mason WP, Gentili F, Macdonald DR, Hariharan S, Cruz CR, Abrey LE: Stabilization of disease progression by hydroxyurea in patients with recurrent or unresectable meningioma. J Neurosurg; 2002 Aug;97(2):341-6
Hazardous Substances Data Bank. HYDROXYUREA .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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

  • Genetic Alliance. consumer health - Meningioma.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


13. 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
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intrinsic expression of drug resistance-associated factors in meningiomas.
  • Meningiomas, commonly benign tumors, rarely display aggressive behavior by recurrences and invasion.
  • 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.
  • 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.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


14. Palmér L, Nordborg C, Steneryd K, Aman P, Kyllerman M: Large-cell medulloblastoma in Aicardi syndrome. Case report and literature review. Neuropediatrics; 2004 Oct;35(5):307-11
The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for large cell medulloblastoma .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • An eight-year-old girl with Aicardi syndrome (AIC) developed signs of increased intracranial pressure.
  • A clinical and radiological investigation revealed a tumor in the posterior fossa, which was resected.
  • The histopathological diagnosis was large-cell medulloblastoma.
  • Eight months later, she died of a local recurrence, despite treatment with chemotherapy and radiotherapy according to a PNET protocol.
  • In addition to the growth of a large-cell medulloblastoma at the location of the primary tumor and the meningeal spread of the tumor, the autopsy revealed major cortical and subcortical malformations of the brain.
  • Various benign (e.g., plexus papillomas) and malignant tumors (angiosarcoma, embryonic carcinoma, and hepatoblastoma) have been reported in connection with Aicardi syndrome.
  • A genetic analysis of AIC suggests that the mutation is localized on the distal part of the short arm of the X chromosome, an area that may be of importance for tumor development.
  • This is the first report of a primary malignant brain tumor -- large-cell medulloblastoma -- in a patient with Aicardi syndrome.
  • [MeSH-major] Agenesis of Corpus Callosum. Cerebellar Neoplasms / etiology. Choroid Diseases / complications. Medulloblastoma / etiology. Retinal Diseases / complications. Spasm / complications


15. Rockhill J, Mrugala M, Chamberlain MC: Intracranial meningiomas: an overview of diagnosis and treatment. Neurosurg Focus; 2007;23(4):E1

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intracranial meningiomas: an overview of diagnosis and treatment.
  • Meningiomas are extraaxial central nervous system tumors most often discovered in middle to late adult life, and are more often seen in women.
  • Ninety percent of meningiomas are benign, 6% are atypical, and 2% are malignant.
  • For the majority of incompletely resected or recurrent tumors not previously irradiated, radiotherapy is administered.
  • Radiotherapy may be administered as either conventional external-beam radiation therapy or stereotactically by linear accelerator, Leksell Gamma Knife, or Cyberknife radiosurgery.
  • Advocates of stereo-tactic radiotherapy have suggested this therapy in lieu of surgery particularly in high-risk patients, those with meningiomas in eloquent or surgically inaccessible locations, and elderly patients.
  • When the meningioma is unresectable or all other treatments (surgery and radiotherapy) have failed, hormonal therapy or chemotherapy may be considered.
  • [MeSH-major] Meningeal Neoplasms / diagnosis. Meningeal Neoplasms / therapy. Meningioma / diagnosis. Meningioma / therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17961033.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 62
  •  go-up   go-down


16. de Tella OI Jr, Agner C, Aguiar PH, Herculano MA, Prandini MN, Stavile JN: Aggressive management of orbital meningeal melanocytoma. Acta Neurochir (Wien); 2003 Dec;145(12):1121-6
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aggressive management of orbital meningeal melanocytoma.
  • OBJECTIVE: Meningeal melanocytoma generally occurs in the posterior fossa.
  • Computed tomography (CT) and Magnetic Resonance Imaging (MRI) of the brain showed an expansive intraconal mass lesion occupying the superior orbital compartment, the entire orbital apex, and the optic foramen.
  • Chemotherapy and irradiation followed the initial intervention.
  • A subfrontal tumor with massive edema was found on follow up CT scan.
  • INTERPRETATION: Meningeal melanocytomas are rare benign pigmented tumors of the central nervous system.
  • [MeSH-major] Meningeal Neoplasms / surgery. Nevus / surgery. Orbital Neoplasms / surgery
  • [MeSH-minor] Adult. Antigens, Neoplasm. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Chemotherapy, Adjuvant. Combined Modality Therapy. Craniotomy. Diagnosis, Differential. Follow-Up Studies. Humans. Male. Melanoma-Specific Antigens. Microsurgery. Neoplasm Proteins / analysis. Neoplasm Recurrence, Local / diagnosis. Orbit / pathology. Orbit / surgery. Postoperative Complications / diagnosis. Radiotherapy, Adjuvant. S100 Proteins / analysis. Tomography, X-Ray Computed

  • MedlinePlus Health Information. consumer health - Birthmarks.
  • MedlinePlus Health Information. consumer health - Moles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14663571.001).
  • [ISSN] 0001-6268
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Melanoma-Specific Antigens; 0 / Neoplasm Proteins; 0 / S100 Proteins
  •  go-up   go-down


17. Albert A, Cruz O, Montaner A, Vela A, Badosa J, Castañón M, Morales L: [Congenital solid tumors. A thirteen-year review]. Cir Pediatr; 2004 Jul;17(3):133-6
MedlinePlus Health Information. consumer health - Wilms Tumor.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Congenital solid tumors. A thirteen-year review].
  • [Transliterated title] Tumores sólidos congénitos. Revisión de 13 años.
  • Tumors diagnosed during the first month of life are infrequent: 0.5 to 2% of all childhood neoplasms.
  • This is an interesting group of tumors because their type, relative incidence, natural history and response to treatment differ from those seen in older children.
  • AIM: To contribute the experience of our institution in congenital tumors the last 13 years.
  • MATERIAL AND METHODS: The records of all neonates (< 31 days old) diagnosed with solid tumors since January 1990 to December 2002 have been retrospectively reviewed.
  • RESULTS: Twenty-seven neonates have been diagnosed with tumors in the last 13 years.
  • Neuroblastoma was the commonest tumor (10 cases, 37%), of which 4 were stage I, 4 stage IV-S and 2 stage III.
  • There were 8 teratomas (3 sacrocoxigeal, 1 retroperitoneal, 1 in the CNS, 1 orbitary and two oronasal), two hepatic tumors (1 hepatoblastoma, 1 hemangioendothelioma, two CNS tumors, two giant nevus (one on a hamartoma), and one each Wilms tumor, infantile fibrosarcoma and myofibroblastic tumor.
  • Treatment was surgical resection alone in 17 cases (68%) and surgery + chemotherapy in 8 (32%) (5 neuroblastomas, one CNS tumor, one Wilms tumor and one presacral teratoma who developed a yolk sac tumor); 3 patients died (11%): one at surgery, one of tumoural airway obstruction at birth and one with craniopharyngioma.
  • Among the 14 tumors that were initially not malignant, two can be locally agressive, one was an immature teratoma, the giant nevus with hamartoma developed in situ melanoma, the other nevus had meningeal melanosis with hydrocephalus, and one mature presacral teratoma developed a yolk sac tumor.
  • CONCLUSIONS: Diagnosis of congenital tumors is performed earlier in recent years due to the wide use of prenatal ultrasound.
  • Their natural history is more benign than in other age groups, except for CNS tumors and very large or obstructing tumors.
  • Complete surgical excision is the treatment of choice, most cases not need adjuvant chemotherapy.
  • We ought to pass this message on to our colleagues in prenatal diagnosis, so parents get reliable information.
  • [MeSH-major] Central Nervous System Neoplasms / congenital. Kidney Neoplasms / congenital. Liver Neoplasms / congenital. Neuroblastoma / congenital. Skin Neoplasms / congenital. Soft Tissue Neoplasms / congenital. Teratoma / congenital. Wilms Tumor / congenital
  • [MeSH-minor] Female. Follow-Up Studies. Humans. Infant, Newborn. Male. Neoplasm Recurrence, Local. Postoperative Complications. Pregnancy. Prenatal Diagnosis. Time Factors

  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15503950.001).
  • [ISSN] 0214-1221
  • [Journal-full-title] Cirugía pediátrica : organo oficial de la Sociedad Española de Cirugía Pediátrica
  • [ISO-abbreviation] Cir Pediatr
  • [Language] spa
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Spain
  •  go-up   go-down


18. Rao G, Klimo P Jr, Jensen RL, MacDonald JD, Couldwell WT: Surgical strategies for recurrent craniofacial meningiomas. Neurosurgery; 2006 May;58(5):874-80; discussion 874-80
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Recurrent cranial base meningiomas are among the most difficult tumors to treat surgically.
  • Although they are histologically benign, these tumors often invade through the cranial base into the infratemporal and pterygopalatine fossae.
  • We reviewed our experience with these tumors to describe the natural history of these lesions as well as provide a possible treatment paradigm.
  • Five patients were treated with transcranial approaches only, and two were treated with a combination of transcranial and transfacial approaches.
  • The original site of tumor was the sphenoid wing in four patients, the middle fossa in two patients, and the left frontal region in one patient.
  • The average interval between the most recent tumor resection and recurrence into the face was 9.9 years.
  • All but one patient had adjunctive therapy (including either radiation or chemotherapy) before recurrence into the face.
  • CONCLUSION: Meningiomas that recur into facial structures present a unique treatment challenge.
  • [MeSH-major] Facial Neoplasms / surgery. Meningeal Neoplasms / surgery. Meningioma / surgery. Neoplasm Recurrence, Local / surgery. Skull Base Neoplasms / surgery

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16639321.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


19. Norden AD, Drappatz J, Wen PY: Advances in meningioma therapy. Curr Neurol Neurosci Rep; 2009 May;9(3):231-40
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advances in meningioma therapy.
  • Meningiomas are the most common primary brain tumors in adults.
  • Most of them are benign (World Health Organization grade I), slow-growing lesions, but some are classified as atypical (WHO grade II) or malignant (WHO grade III).
  • Surgical resection is curative when complete removal of a benign meningioma is possible.
  • Incompletely resected tumors and high-grade lesions are frequently treated with fractionated radiotherapy or stereotactic radiosurgery.
  • High-grade meningiomas tend to recur following maximal treatment with surgery and radiation.
  • As the molecular pathogenesis of meningiomas is elucidated, targeted drug therapies may prove useful.
  • Angiogenesis inhibitors, agents that target fundamental cell signaling pathways, somatostatin analogues, and a variety of other molecular treatments appear promising.
  • [MeSH-major] Meningeal Neoplasms / therapy. Meningioma / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Cranial Irradiation. Humans. Radiosurgery / methods

  • Genetic Alliance. consumer health - Meningioma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Zentralbl Neurochir. 2005 Feb;66(1):17-23 [15744624.001]
  • [Cites] Eur J Endocrinol. 2005 Jan;152(1):161-2 [15762200.001]
  • [Cites] J Biomed Opt. 2005 Nov-Dec;10(6):064026 [16409091.001]
  • [Cites] N Engl J Med. 2007 Dec 6;357(23):2411-2 [18057351.001]
  • [Cites] Neurosurgery. 2007 Nov;61(5):1048-59; discussion 1060-1 [18091281.001]
  • [Cites] J Clin Oncol. 2008 Jan 10;26(2):279-82 [18182668.001]
  • [Cites] Neuro Oncol. 2007 Oct;9(4):438-46 [17704362.001]
  • [Cites] J Neurooncol. 2008 Jul;88(3):251-9 [18365142.001]
  • [Cites] Cancer. 2007 Aug 1;110(3):471-6 [17580362.001]
  • [Cites] Cancer Res. 2006 May 15;66(10):5295-303 [16707455.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Aug;16(8):1655-61 [17684142.001]
  • [Cites] Nat Genet. 1994 Feb;6(2):180-4 [8162072.001]
  • [Cites] Neurosurgery. 2007 May;60(5):787-98; discussion 787-98 [17460514.001]
  • [Cites] Neurosurgery. 2005 Jul;57(1 Suppl):107-13; discussion 107-13 [15987576.001]
  • [Cites] Brain. 2008 Mar;131(Pt 3):606-15 [17940085.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1957 Feb;20(1):22-39 [13406590.001]
  • [Cites] Neurosurg Focus. 2007;23(4):E9 [17961046.001]
  • [Cites] Neurosurg Focus. 2007;23(4):E11 [17961035.001]
  • [Cites] Int J Cancer. 2009 Jan 15;124(2):346-51 [19003955.001]
  • [Cites] J Neurooncol. 1993 Jan;15(1):75-7 [8455065.001]
  • [Cites] J Neurooncol. 2004 Jan;66(1-2):155-66 [15015781.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2007 Jul 1;68(3):858-63 [17379447.001]
  • [Cites] J Neuropathol Exp Neurol. 2005 Dec;64(12):1029-36 [16319713.001]
  • [Cites] J Neurooncol. 2007 May;83(1):33-8 [17245625.001]
  • [Cites] Neoplasia. 2008 Nov;10(11):1204-12 [18953429.001]
  • [Cites] Cancer Genet Cytogenet. 2008 Nov;187(1):25-7 [18992637.001]
  • [Cites] Cancer Genet Cytogenet. 2008 Jul 15;184(2):87-93 [18617056.001]
  • [Cites] J Neuropathol Exp Neurol. 2000 Oct;59(10):872-9 [11079777.001]
  • [Cites] Neurosurgery. 1997 May;40(5):1016-26 [9149260.001]
  • [Cites] J Neurol. 2008 Jun;255(6):891-5 [18350353.001]
  • [Cites] Curr Med Chem. 2008;15(8):826-33 [18393851.001]
  • [Cites] Neurology. 2007 Sep 4;69(10):969-73 [17785665.001]
  • [Cites] Neurosurgery. 2000 Apr;46(4):938-47; discussion 947-8 [10764269.001]
  • [Cites] J Neurosurg. 2001 Mar;94(3):487-92 [11235955.001]
  • [Cites] N Engl J Med. 2008 May 8;358(19):2039-49 [18463380.001]
  • [Cites] Crit Rev Oncol Hematol. 2008 Aug;67(2):153-71 [18342535.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Oct;17 (10 ):2663-70 [18843008.001]
  • [Cites] J Clin Oncol. 2001 Aug 1;19(15):3547-53 [11481362.001]
  • [Cites] J Neurosurg. 2007 Jun;106(6):1034-40 [17564176.001]
  • [Cites] Hybridoma. 2001 Apr;20(2):131-6 [11394532.001]
  • [Cites] J Neurosurg. 1994 Feb;80(2):195-201 [8283256.001]
  • [Cites] Neurology. 2004 Apr 13;62(7):1210-2 [15079029.001]
  • [Cites] J Neurosurg. 1996 May;84(5):733-6 [8622144.001]
  • [Cites] Neurosurgery. 2008 Jun;62(6 Suppl 3):1115-21; discussion 1121-3 [18695533.001]
  • [Cites] Acta Neuropathol. 2007 Aug;114(2):147-56 [17594108.001]
  • [Cites] J Neurooncol. 2005 Jul;73(3):219-23 [15980972.001]
  • [Cites] J Natl Cancer Inst. 2008 Feb 20;100(4):270-6 [18270339.001]
  • [Cites] Neurosurgery. 2008 Mar;62(3 Suppl 1):102-3; discussion 103-4 [18424972.001]
  • [Cites] Eur J Endocrinol. 2002 May;146(5):707-16 [11980628.001]
  • [Cites] Neoplasia. 2008 Jun;10(6):604-12 [18516297.001]
  • [Cites] Neurosurgery. 2001 Nov;49(5):1029-37; discussion 1037-8 [11846894.001]
  • [Cites] J Neurooncol. 2006 Jul;78(3):271-6 [16628476.001]
  • [Cites] J Neurooncol. 1998 Apr;37(2):177-88 [9524097.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Jan 1;46(1):57-61 [10656373.001]
  • [Cites] Neurosurg Focus. 2007;23(4):E5 [17961042.001]
  • [Cites] Cancer Genet Cytogenet. 2008 May;183(1):14-20 [18474292.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2008 Aug 1;71(5):1388-93 [18294779.001]
  • [Cites] Neurosurgery. 2008 Jan;62(1):61-9; discussion 69-70 [18300892.001]
  • [Cites] Surg Neurol. 2003 Oct;60(4):298-305; discussion 305 [14505844.001]
  • [Cites] J Neurosurg. 2000 Dec;93 Suppl 3:62-7 [11143265.001]
  • [Cites] Cancer. 2008 Oct 15;113(8):2146-51 [18756531.001]
  • [Cites] Int J Cancer. 2005 Dec 20;117(6):996-1001 [15986431.001]
  • [Cites] Neurosurg Focus. 2008;24(5):E2 [18447741.001]
  • [Cites] Neurosurgery. 2007 Sep;61(3):495-503; discussion 503-4 [17881961.001]
  • [Cites] Cancer Res. 2008 Jan 1;68(1):314-22 [18172325.001]
  • [Cites] J Neuropathol Exp Neurol. 2004 Apr;63(4):275-86 [15099018.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 2008 May;79(5):574-80 [17766430.001]
  • [Cites] BMC Cancer. 2006 Jun 07;6:152 [16759391.001]
  • [Cites] Neurosurg Focus. 2007;23(4):E4 [17961041.001]
  • [Cites] BMC Genomics. 2007 Jan 12;8:16 [17222329.001]
  • [Cites] Neurology. 1975 Aug;25(8):705-12 [1171403.001]
  • [Cites] Surg Neurol. 1986 Nov;26(5):461-9 [3764651.001]
  • [Cites] Int J Cancer. 2007 Oct 1;121(7):1473-80 [17557299.001]
  • [Cites] Clin Cancer Res. 2001 Aug;7(8):2269-76 [11489801.001]
  • [Cites] Neurosurg Focus. 2003 May 15;14(5):e5 [15669816.001]
  • (PMID = 19348712.001).
  • [ISSN] 1534-6293
  • [Journal-full-title] Current neurology and neuroscience reports
  • [ISO-abbreviation] Curr Neurol Neurosci Rep
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 81
  •  go-up   go-down


20. Modha A, Gutin PH: Diagnosis and treatment of atypical and anaplastic meningiomas: a review. Neurosurgery; 2005 Sep;57(3):538-50; discussion 538-50
The Lens. Cited by Patents in .

  • [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.
  • We reviewed the current literature and attempted to integrate and summarize available information to determine a logical approach to these tumors.
  • Both tumors are rare and are often integrated with benign meningiomas when treatments are evaluated.
  • Malignant progression with accumulation of mutations in a benign meningioma can result in an atypical and/or anaplastic meningioma.
  • Both tumors are difficult to manage and have high recurrence and poor survival rates.
  • The extent of tumor resection and histological grade are the key determinants for recurrence.
  • 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

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


21. Lichtenbaum R, de Souza AA, Jafar JJ: Intratumoral hydrogen peroxide injection during meningioma resection. Neurosurgery; 2006 Oct;59(4 Suppl 2):ONS470-3; discussion ONS473
Hazardous Substances Data Bank. HYDROGEN PEROXIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Meningiomas, although histologically benign, pose a particular challenge to the neurosurgeon because of their extensive and exuberant vascularity.
  • We report a technique of meningioma resection that uses intratumoral hydrogen peroxide injection, reducing the potential for blood loss and shortening resection times.
  • METHODS: Seventy-five patients underwent resection of a meningioma using the direct intratumoral H2O2 injection technique.
  • RESULTS: The use of this technique greatly facilitated the removal of these tumors.
  • CONCLUSION: We demonstrate a previously unreported technique of meningioma resection that uses direct intratumoral hydrogen peroxide injection, potentially reducing blood loss, shortening resection times, and obviating the need for preoperative embolization.
  • [MeSH-major] Cerebral Hemorrhage / prevention & control. Hydrogen Peroxide / administration & dosage. Meningeal Neoplasms / drug therapy. Meningeal Neoplasms / surgery. Meningioma / drug therapy. Meningioma / surgery. Neurosurgical Procedures / adverse effects
  • [MeSH-minor] Combined Modality Therapy. Female. Hemostatics / administration & dosage. Humans. Injections, Intralesional. Male. Middle Aged. Treatment Outcome

  • Genetic Alliance. consumer health - Meningioma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17041519.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemostatics; BBX060AN9V / Hydrogen Peroxide
  •  go-up   go-down


22. 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
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • Although their behavior is usually benign, they tend to recur even after total removal, and their recurrence is dependent on different aspects.
  • 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.
  • Complete removal of the tumor was possible in 86.7% in both studies.
  • Indications for post-operative radiation therapy were given earlier in the last study owing to the experience from the primary study.
  • 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

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


23. 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
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The treatment of malignant meningioma with verotoxin.
  • Malignant meningiomas (MMs) are aggressive intracranial neoplasms with a 75% 5-year recurrence rate.
  • Verotoxin 1 (VT1) is an Escherichia coli toxin, which has recently been shown to have anti-neoplastic action by targeting the globotriosylceramide (Gb(3)) glycolipid on tumor cells and tumor neovasculature.
  • 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.
  • Factor-eight immunostaining of tumours harvested from VT1-treated animals revealed a marked reduction in the tumour microvascular density.
  • In addition, the tumors of VT1-treated animals displayed increased apoptosis by TUNEL analysis and showed a significant decrease in cell proliferation, as determined by MIB-5 immunostaining.
  • 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

  • Genetic Alliance. consumer health - Meningioma.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


24. Lamszus K, Lengler U, Schmidt NO, Stavrou D, Ergün S, Westphal M: Vascular endothelial growth factor, hepatocyte growth factor/scatter factor, basic fibroblast growth factor, and placenta growth factor in human meningiomas and their relation to angiogenesis and malignancy. Neurosurgery; 2000 Apr;46(4):938-47; discussion 947-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Angiogenesis is mediated by a number of different growth factors and appears vital for tumor growth.
  • The understanding of angiogenic mechanisms could offer new therapeutic perspectives; in this context, the role of four potentially angiogenic growth factors was analyzed in a large series of meningiomas of different grades.
  • METHODS: Vascular endothelial growth factor (VEGF), placenta growth factor, hepatocyte growth factor/scatter factor, and basic fibroblast growth factor were quantified in 69 tumors by enzyme-linked immunosorbent assay.
  • Microvessel density and proliferative activity were determined on paraffin sections, and clinical tumor invasiveness was rated.
  • RESULTS: Tumors included 40 benign (World Health Organization [WHO] Grade I), 21 atypical (WHO Grade II), and 8 anaplastic/malignant (WHO Grade III) meningiomas.
  • We found a correlation between meningioma grade and VEGF content (r = 0.37, P = 0.002), which was 2-fold higher in atypical than in benign meningiomas (P = 0.022) and 10-fold higher in malignant than in benign meningiomas (P = 0.025).
  • None of the other three factors investigated showed any association with tumor grade, microvessel density, or invasiveness, and VEGF also did not correlate with vascularity or invasiveness.
  • Nevertheless, the biological activity of VEGF and basic fibroblast growth factor in meningiomas suggests that both are potential targets for antiangiogenic therapy in meningiomas of all WHO grades.
  • [MeSH-major] Endothelial Growth Factors / metabolism. Fibroblast Growth Factor 2 / metabolism. Hepatocyte Growth Factor / metabolism. Lymphokines / metabolism. Meningeal Neoplasms / metabolism. Meningioma / metabolism. Pregnancy Proteins / metabolism
  • [MeSH-minor] Chemotaxis. Endothelium, Vascular / drug effects. Endothelium, Vascular / pathology. Endothelium, Vascular / physiopathology. Humans. Neoplasm Invasiveness. Neovascularization, Pathologic / chemically induced. Neovascularization, Pathologic / pathology. Tissue Extracts / pharmacology. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10764269.001).
  • [ISSN] 0148-396X
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Endothelial Growth Factors; 0 / Lymphokines; 0 / Pregnancy Proteins; 0 / Tissue Extracts; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 103107-01-3 / Fibroblast Growth Factor 2; 144589-93-5 / placenta growth factor; 67256-21-7 / Hepatocyte Growth Factor
  •  go-up   go-down


25. Mandat T, Roszkowski M, Barszcz S, Podgórski JK, Jurkiewicz E: [Neuroendoscopy in the treatment of third ventricular hydrocephalus accompanying tumors of the posterior part of the third ventricle in children]. Neurol Neurochir Pol; 2002 Jul-Aug;36(4):711-22
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Neuroendoscopy in the treatment of third ventricular hydrocephalus accompanying tumors of the posterior part of the third ventricle in children].
  • OBJECTIVE: The aim of the study was to evaluate the effectiveness of endoscopic third ventriculostomy (ETV) in non-communicating hydrocephalus secondary to tumour of the posterior part of the third ventricle tumours in children.
  • In 22 cases benign tectal mass (BTM) and 10 malignant neoplasms (including 9 germ cell tumours and 1 ependymoma) were diagnosed.
  • 8 patients with malignant neoplasms after initial chemotherapy underwent residual tumor excision (more than 3 months after ETVs) and in two of them the CFS meningeal tumor spreads were detected.
  • 3 of them were children with benign tectal masses and 3 with malignant tumours.
  • The reason of failure in 2 cases was associated with meningeal tumor dissemination, and in one with postoperative bleeding after surgical tumor excision (communicating hydrocephalus).
  • In 2 cases with benign tumours reasons of failures were not clear (patent stomies on PC MR-cine) and in 1 case late stomy occlusion on PC-MR flow study was diagnosed.
  • Five out of 6 patients underwent shunt placements and in 1 case with late ventriculostomy occlusion another endoscopic procedure (after 26 months) was successfully performed.
  • The PC MR flow study was a useful diagnostic tool in the stomy patency evaluation and in further treatment planning in cases of failures.
  • [MeSH-major] Cerebral Ventricle Neoplasms / complications. Cerebral Ventricle Neoplasms / surgery. Endoscopy. Hydrocephalus / etiology. Hydrocephalus / surgery. Third Ventricle. Ventriculostomy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Humans. Male. Treatment Outcome. Ventriculoperitoneal Shunt

  • Genetic Alliance. consumer health - Hydrocephalus.
  • MedlinePlus Health Information. consumer health - Endoscopy.
  • MedlinePlus Health Information. consumer health - Hydrocephalus.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12418136.001).
  • [ISSN] 0028-3843
  • [Journal-full-title] Neurologia i neurochirurgia polska
  • [ISO-abbreviation] Neurol. Neurochir. Pol.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  •  go-up   go-down






Advertisement