iants, and represent over 39,000 well-characterized human genes was used for microarray analysis. The fragmentation of biotinylated cRNA derived from 300 ng of total RNA was used to hybridize to GeneChips. The hybridization cocktail was incubated overnight at 45uC while rotating in 
a hybridization oven. After 16 h of hybridization, the cocktail was removed and the arrays were washed and stained in an Affymetrix GeneChip Fluidics Station 450, according to the Affymetrix-recommended protocol. The distribution of fluorescent material on the array was obtained using GeneChip Scanner 3000 7G. GeneChip Operating Software supplied by Affymetrix was used to generate.CEL files and were analyzed and statistically filtered using software Partek Genomic Suite 6.4. Input files were normalized with the robust multi-chip average algorithm for gene array. To narrow the list of relevant genes, we applied a restrictive filtering algorithm using a combined criterion, which required both a fold change 17149874 absolute value of 2 or higher and a statistical significance of p,0.005 between subgroups. A BenjaminiHochberg step-up false discovery rate procedure was also used with a final maximum FDR value of 0.005. Subgroups of Benign Meningioma Cytogenetics and FISH analysis showed two clearly differentiated groups within the histopathological benign meningioma samples. These groups have been reported to have different metabolic behavior. According to these studies, classification of tumors in the benignB subgroup required the get Neuromedin N existence of chromosomal abnormalities detected either by FISH or by cytogenetics and/or levels of three out of four of the most representative metabolites within 2 standard deviations of the values for atypical meningioma reported. The benign tumors that did not fulfill these criteria were included in the benignA subgroup. The levels of choline, taurine, lactate and fatty acids were used to evaluate the degree of metabolic aggressiveness in the different subgroups. No other molecular correlation was detected with respect histological subtypes of 10712926 benign meningioma, tumor location or tumor size. The metabolic profile of these samples allowed the detection of a subgroup of benign meningioma with metabolic aggressiveness and metabolism closer to atypical tumors. The metabolic profile of metabolic aggressiveness includes higher levels of phospholipids precursors, by-products of energy metabolism and cell antioxidants. The meningioma subgroup benignA, containing 20 meningiomas, is defined by low metabolic aggressiveness and alterations in chromosome 22 as the only, if any, chromosomal anomaly. The meningioma subgroup benignB, which contained 20 meningiomas, includes tumors of histological grade I with additional chromosomal alterations. This meningioma subgroup exhibited higher metabolic aggressiveness than the subgroup benignA. In addition, metabolic levels in benignB meningioma were similar to those detected in atypical meningioma, suggesting increased clinical aggressiveness potential. Recurrence at 4 years was evaluated in a subset of 9 benignA, 11 benignB and 8 atypical meningioma patients for a preliminary assessment of potential clinical implications of these subgroups . The analyses from each contrast were compared for recurring functional themes. Real-time RT-PCR Validation The levels of expression of selected genes were quantified using real-time reverse transcription polymerase chain reaction analysis. Briefly, 300 ng total RNA was reverse