			Home About us Contact

Atypical Meningiomas (atypical + meningioma)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Cytologic features of meningiomas on crush preparations: A review

DIAGNOSTIC CYTOPATHOLOGY, Issue 4 2008
F.I.A.C., Momin T. Siddiqui M.D.
Abstract Meningiomas are rarely subjected to aspiration, however, since they may occur outside the central nervous system, it is important to recognize their cytologic features. The goal of this study was to examine the cytologic features of meningiomas in crush preparations and cytologic imprints prepared at the time of frozen section. A total of 97 cases of meningiomas evaluated intraoperatively by frozen section with concomitant crush preparation and cytologic imprint were reviewed to assess their cytologic features. The cytologic features of meningiomas identified in our study are cohesive syncitial clusters of cells with ill-defined boundaries. The nuclei are oval and may be eccentrically placed, along with small central nucleoli. The cytologic features may not reflect the histologic subtype. The psammomatous variant can however be easily recognized in touch preps/imprints. The presence of nuclear anaplasia, macronucleoli, mitotic activity, and sheet-like growth may suggest an atypical meningioma. In conclusion, the cytologic features identified would be helpful in diagnosis of meningiomas, especially in unusual locations. Diagn. Cytopathol. 2008;36:202,206. © 2008 Wiley-Liss, Inc. [source]

MIB-1 immunolabeling: A valuable marker in prediction of benign recurring meningiomas

NEUROPATHOLOGY, Issue 5 2007
Mahesha Vankalakunti
Histological analysis has limited value to predict biological behavior of meningiomas. We investigated the utility of cell proliferative indicator in the evaluation of histologically benign meningiomas. We selected 25 benign non-recurrent meningiomas, 15 benign recurrent meningiomas after complete surgical resection, 30 atypical meningiomas, and 15 anaplastic meningiomas out of 384 cases studied. MIB-1 Labeling Index was evaluated by two methods: Highest Labeling Index (HLI) and Random Labeling Index (RLI). There was no dependable histological parameter to predict recurrence among benign-looking meningiomas. HLI had significant difference when compared with RLI in all categories. The mean MIB-1 HLI values ± SD were 3.47 ± 2.0% for benign meningiomas, 5.08 ± 4.0% for atypical meningiomas and 11.66 ± 7.06% for anaplastic meningiomas. In comparison, the mean MIB-1 HLI of benign non-recurrent meningiomas were 2.66 ± 1.7% and with recurrence were 4.21 ± 2.78% (P = 0.0339). Using receiver operating characteristic, it was seen that neoplasm recurred with the MIB-1 HLI of > 2.6 having the sensitivity of 64.6% and specificity of 68% among benign (grade I) meningiomas. MIB-1 positive tumor cells were maximally aggregated at the periphery of excised specimen. MIB-1 HLI, integrated with standard histopathology can provide better information about the disease biological nature in benign meningiomas. [source]

Hypermethylation and Transcriptional Downregulation of the TIMP3 Gene is Associated with Allelic Loss on 22q12.3 and Malignancy in Meningiomas

BRAIN PATHOLOGY, Issue 3 2010
Dimitri Barski
Abstract The gene for the tissue inhibitor of metalloproteinase 3 (TIMP3) on 22q12.3 had been reported to be inactivated by promoter methylation in various types of cancers, with controversial findings in meningiomas. We performed direct sodium bisulfite sequencing in a series of 50 meningiomas, including 27 benign meningiomas [World Health Organization (WHO) grade I], 11 atypical meningiomas (WHO grade II) and 12 anaplastic meningiomas (WHO grade III), and found hypermethylation of TIMP3 in 67% of anaplastic meningiomas, but only 22% of atypical and 17% of benign meningiomas. Moreover, TIMP3 methylation scores were significantly inversely correlated with TIMP3 mRNA expression levels (P = 0.0123), and treatment of the meningioma cell line Ben-Men-1 with demethylating agents induced an increased TIMP3 mRNA expression. TIMP3 is located in the chromosomal band 22q12, the allelic loss of which occurs early in meningioma tumorigenesis and preferentially targets the NF2 tumor suppressor gene. In our tumor panel, all meningiomas with TIMP3 hypermethylation,except for a single case,exhibited allelic losses on 22q12.3. Thus, TIMP3 inactivation by methylation seems fairly exclusive to meningiomas with allelic losses on 22q12 but,in contrast to NF2 mutation,appears to be involved in meningioma progression as it is associated with a more aggressive, high-grade meningioma phenotype. [source]

Allelic Gain and Amplification on the Long Arm of Chromosome 17 in Anaplastic Meningiomas

BRAIN PATHOLOGY, Issue 2 2002
Rainer Büschges
Using comparative genomic hybridization (CGH) we have previously identified amplification at 17q21-qter as a common aberration in anaplastic meningiomas but not in atypical or benign meningiomas (19). To define the amplified genomic region, we analyzed 44 meningeal tumors, including 7 benign meningiomas of World Health Organization (WHO) grade I, 19 atypical meningiomas (WHO grade II) and 18 anaplastic meningiomas (WHO grade III) at 46 chromosome 17 loci (including 42 17q loci). In line with the CGH data we found evidence of increased numbers of alleles on 17q. The incidence rose with malignancy grade, culminating at 61% (11 of 18 cases) in the anaplastic meningioma group. The majority of cases showing increased allele numbers had, on average, low-level allelic gains (relative increase in allele dosage of 2- to 5-fold). Amplification of alleles (defined here as an average relative increase in allele dosage of more than 5 times) was detected in 2 anaplastic meningiomas. The amplification patterns in these tumors defined a number of common regions of amplification/increased allele copy number, the best defined include one between D17S790 and D17S1607 and one between D17S1160 and PS6K. Real-time PCR analysis of the PS6K candidate gene revealed no high-level amplification despite this affecting adjacent loci. Our findings are fundamental for the identification of the gene(s) in 17q22-q23 that is (are) the target(s) for increased copy number in anaplastic meningiomas and possibly other tumor types. [source]