icroarray analysis of meningiomas in the past with different aims, microarray platforms and statistical approaches. The result of such a variety of approaches is no shared genes deregulated in all these studies. One possible reason for these results may be the existence of different molecular subgroups of meningioma. The intrinsic variation of aggressiveness and genetic alterations within benign meningioma highly impacts the statistical results of molecular studies on meningioma. Perez-Magan et al. compared previously reported gene expression profiles associated with meningioma progression and buy Neuromedin N detected a profile potentially associated with recurrence. The final candidate genes were extracted from 4 original tumors that recurred later out of a total of 44 meningiomas with microarray gene expression data. In this context, the use of molecular phenotypic criteria for the determination of meningioma subgroups would help in obtaining more robust gene expression profiles. The determination 17149874 of these profiles combined with other markers of molecular aggressiveness may also aid in determining 
the aggressiveness of surgical resection and the necessity of combined radiation therapy. The aim of this study was to determine the relationship between gene expression profiles and new metabolic subgroups of benign meningioma. We obtained molecular profiles in 40 benign and 14 atypical meningioma tissue samples by performing metabolic, cytogenetic and gene expression analysis. Based on recently published criteria for molecular classification, we detected benign meningioma molecular subgroups and explored differential gene expression between them. Cytogenetics Cytogenetic analyses were performed by short-term culture of the tumors. Fresh tumor samples were disaggregated with 2 mg/ mL of collagenase II. The cells were seeded in flasks using RPMI1640 medium supplemented with 20% fetal bovine serum, Lglutamine, and antibiotics. The cells were processed after 72 h of culture by a standard technique. Air dried slides were banded by trypsin-Giemsa. Karyotypic analyses were performed according to International System for Human Cytogenetics . Fluorescence In Situ Hybridization The samples of meningioma used for Florescence In-itu Hybridization analysis were studied by tissue microarrays. We removed four 0.6-mm cores from the corresponding areas on the paraffin block in each case, using the Beecher Instruments Manual Tissue ArrayerI. For the investigation of chromosome abnormalities by iFISH the probes LSI 22q12, LSI 1p36/LSI 1q25 and LSI t IGH/CCND1 were used. Hybridizations were performed according to the instructions that accompany the probe. Counterstaining of nuclei was carried out using 49,6-diamidino-2-phenylindole. The fluorescent signal was detected using a photomicroscope Axioplan 2 and Axiophot 2 equipped with a set of the appropriate filters. For each hybridization, green and orange signals were counted in the four regions of a total of 100200 non-overlapping nuclei. An interpretation of deletion or imbalance was made when.20% of the nuclei harbored these alterations. Cutoffs for deletions were 15225680 based on the frequencies of signals for the same probes in non-neoplastic brain controls and ranged from 14 to 21% for chromosome 1, from 16 to 22% for chromosome 14, and from 15 to 20% for monosomy 22. We considered deletion when appeared one or less signal for chromosome with respect to the signal of control and we considered normal with the probes used present