Disease relevance of Meningioma

• The NF2 protein, called schwannomin or merlin, is absent in virtually all schwannomas, and many meningiomas and ependymomas [1].
• In view of the lack of a documented effect of progesterone on progression of lung disease in LAM and the reported mitogenic response of meningiomas to progesterone, we recommend that the drug not be given to LAM patients with an MRI result consistent with diagnosis of meningioma [2].
• Significant elevation of VEGPF gene expression was observed in 81% (22/27) of the highly vascular and edema-associated CNS neoplasms (6/8 GBM, 8/8 capillary hemangioblastomas, 6/7 meningiomas, and 2/4 cerebral metastases) [3].
• TNF from both ddy mice and Japanese albino rabbits (sp act, 3-5 X 10(5) U/mg, respectively) was found to inhibit the migration of bovine capillary endothelial (BCE) cells stimulated by factors from tumor cells, such as the medium conditioned with mouse sarcoma 180 cells or human meningioma extract [4].
• Glioma induction has been previously reported after external beam radiation for leukaemia, pituitary adenoma, tinea capitus, and meningioma [5].

High impact information on Meningioma

• The involvement of calpain-dependent proteolysis of the tumor suppressor NF2 (merlin) in schwannomas and meningiomas [6].
• Biallelic NF2 gene inactivation is common in sporadic and in neurofibromatosis type 2 (NF2)-related meningiomas [7].
• However, meningiomas have progesterone receptors, and progesterone is believed to be a mitogen for meningioma cells in culture [2].
• We recommend that patients with LAM be screened for meningiomas regardless of diagnosis of TSC [2].
• Expression and localization of endothelin-1 and endothelin receptors in human meningiomas. Evidence for a role in tumoral growth [8].

Chemical compound and disease context of Meningioma

• Successful mifepristone treatment of recurrent, inoperable meningioma [9].
• Hydroxyurea for treatment of unresectable meningiomas [10].
• Treatment of meningioma with octreotide [11].
• Experiments to rescue virus from the T-antigen-positive meningioma cells were performed: fusion of cells pretreated with 8-azaguanine with cells premissive for SV40 led to a low percentage (0.01-0.05%) of V-antigen-positive nuclei in heterokaryon cultures [12].
• It appears that additional serum components are required for both estradiol-stimulated growth and for maximal proliferation of human meningioma cells under serum-free conditions [13].
• Metabolic differences between meningioma grades include changes in the levels of glutathione [14].

Biological context of Meningioma

• Schwannomas and meningiomas occur as multiple tumors in sufferers of neurofibromatosis 2 (NF2) and as solitary tumors in the general population due to the inactivation of a gene at chromosome 22q12 [15].
• 3. Reverse transcription (RT)-PCR and northern blot hybridization revealed expression of the gene encoding MGEA5 in several meningioma and additional human tissues [16].
• The longest open reading frame was found to be 2412 bp encoding an immunoreactive antigen termed meningioma expressed antigen 6 (MEA6) [17].
• We have studied the effects of insulin, epidermal growth factor (EGF), fibroblast growth factor (FGF), platelet-derived growth factor, and steroid hormones (estradiol, progesterone, and cortisol) on human meningioma cell proliferation and DNA synthesis in a serum-free culture system [13].
• Although loss of 10q was detected by comparative genomic hybridization and/or LOH analysis in 14 of the 34 meningiomas investigated (41%), none of these tumors showed evidence of PTEN mutations or homozygous gene deletions [18].

Anatomical context of Meningioma

• The type of constitutional NF2 mutation is an important determinant of the number of NF2-associated intracranial meningiomas, spinal tumors, and peripheral nerve tumors [19].
• In the immunoblot analysis, E-cadherin was detected at the main band of Mr 124,000 in all of the arachnoid villi, as well as syncytial and transitional types of meningiomas, but not in the fibroblastic type [20].
• The present experiments were performed to evaluate whether the absence of ER from the majority of human meningioma cytosols can be attributed to: occurrence of only a small number of ER-positive cells in an otherwise ER-negative tissue; resistance of nuclear receptors to extraction; or impairment of steroid binding [21].
• We have characterized the epidermal growth factor (EGF) receptor in human meningioma (biopsy) microsomes, cellularly derived microsomes, and intact meningioma cells in culture [22].
• Media conditioned by cells cultured from six meningiomas also contained latent TGF beta-like activity [23].

Gene context of Meningioma

• These findings thus suggest that VEGF may be a positive factor in tumor angiogenesis in both human gliomas and meningiomas [24].
• In addition, these findings highlight the utility of combining genomic, epigenetic, and expression data to identify clinically significant tumor biomarkers, and suggest that NDRG2 expression will be a useful and functionally relevant biomarker to predict aggressive behavior in patients with meningioma [25].
• CCK-A receptors were expressed rarely in tumors except in gastroenteropancreatic tumors (38%), meningiomas (30%), and some neuroblastomas (19%) [26].
• Meningioma transcript profiles reveal deregulated Notch signaling pathway [27].
• Logistic regression analysis showed GSTT1 null and CYP2D6 poor metabolizer were risk factors in astrocytoma (odds ratio = 2.67 P = 0.0005 and odds ratio = 4.17 P = 0.0043, respectively) and meningioma (odds ratio = 4.52, P = 0.0001 and odds ratio = 4.90, P = 0.0132, respectively) when corrected for the other variables [28].
• Meningiomas displayed different patterns of genetic alterations during progression according to their NF2 status: NF2-mutated meningiomas showed higher chromosome instability during progression than NF2-nonmutated meningiomas, which had very few imbalanced chromosome segments [29].

Analytical, diagnostic and therapeutic context of Meningioma

• Northern blot analysis of 70 sporadic meningiomas showed specific loss of expression in 8 tumors, suggesting inactivation of BAM22 [30].
• The study of PDGF autocrine loops and human meningioma has been slowed by the scarcity of meningioma cell culture model systems [31].
• In the control group of 25 fibroblastic meningiomas, 11 cases were identified to carry an NF2 mutation.These results support the concept of different molecular subgroups of meningiomas which overlap with histological variants [32].
• Immunoblotting and immunostaining analyses with this antibody show that the PDGF-beta receptor is constitutively phosphorylated at tyrosine 751 within multiple fresh surgical isolates of human meningioma [31].
• In this study we characterized the expression of Fas and Fas ligand in different types of meningiomas and examined the effect of Fas ligation on the death of meningioma cells in culture [33].

References