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Meningiomas are solid tumors of the Central Nervous System arising from arachnoid layer cells, which cover the brain and spinal cord. Meningiomas account for about 34% of primary intracranial tumors, with an annual incidence rate of 6.17 per 100,000 person-year, as reported in a recent population-based study (Yee G. 2009). Many small meningiomas go unnoticed during life and are found incidentally in up to 1.4% of people in autopsy series (Rohringer, Sutherland et al. 1989). In general, meningiomas display a broad range of histological patterns. The current World Health Organization (WHO) classification lists 16 different variants or subtypes, falling into 3 grade designations. The WHO classification of tumors of the nervous system distinguishes between grade I (benign), grade II (atypical) and grade III (anaplastic or malignant) meningiomas (Table 1, Fig. 1) (Perry, Louis et al. 2007). About 90% of all meningiomas are slowly growing benign tumors of WHO grade I. Atypical meningiomas constitute about 6-8% of cases, although using more current definitions, it has been reported in up to 20%. These WHO grade II meningiomas are histologically defined by increased mitotic activity (four or more mitoses per 10 high-power microscopic fields) and/or at least three of the following criteria: increased cellularity, high nucleus/cytoplasm ratio, prominent nucleoli, uninterrupted patternless or sheet-like growth and necrosis. Approximately 2-3% of all meningiomas show histological features of frank malignancy, including a high level of mitotic activity (20 or more mitosis per 10 high-power microscopic fields) and/or a histological appearance similar to sarcoma, carcinoma or melanoma (Perry, Louis et al. 2007). Tumor recurrence is the major clinical complication in meningiomas, occurring in 10-15% and 25-37% of patients undergoing curative surgery after 5and 10-year follow-up periods, respectively (Mirimanoff, Dosoretz et al. 1985; Maillo, Orfao et al. 2007). The most important factors that determine the recurrence of meningiomas are the extension of the tumor resection and the histologic grade (Riemenschneider, Perry et al. 2006; Louis, Ohgaki et al. 2007). Therefore, prediction of relapse occurrence in meningiomas during the first few years following diagnostic surgery still remains a major challenge.

Established tumor-derived cell lines are widely and routinely used as in vitro cancer models for various kinds of biomedical research. The easy management of these cell cultures, in contrast to the inherent difficulty in establishing and mantaining primary tumoral cultures, has contributed to the wide use of these inmortalized cell lines in order to characterize the biological significance of specific genomic aberrations identified in primary tumors. Therefore, it has been assumed that the genomic and expression aberrations of long-term established cell lines resemble, and are representative, of the primary tumor from which the cell line was derived. Indeed, the cell line-based research has been performed, not only for the definition of the molecular biology of several cancer models, but also for the investigation of new targeted therapeutic agents in a prior step to clinical practice. The use of tumor-derived cell lines has been highly relevant for the testing and development of new therapeutical agents, with several cancer cell-line panels having been developed for drug sensitivity screening and new agents’ discovery (Sharma et al, 2010). Controversial concerning the ability of tumor-derived cell lines to accurately reflect the phenotype and genotype of the parental histology has been documented. A previous report of Greshock and coworkers using array-based Comparative Genomic Hybridization (aCGH) data of seven diagnosis-specific matched tumors and cell lines showed that, on average, cell lines preserve in vitro the genetic aberrations that are unique to the parent histology from which they were derived, while acquiring additional locus-specific alterations in long-term cultures (Greshock et al, 2007). In contrast, a study on breast cancer cell lines and primary tumors highlight that cell lines do not always represent the genotypes of parental tumor tissues (Tsuji et al, 2010). Furthermore, a parallel genomic and expression study on glioma cell lines and primary tumors states that in this specific cancer type, cell lines are poor representative of the primary tumors (Li et al, 2008). Given the importance of the use of cell lines as models for the study of the biology and development of tumors, and for the testing of the mode of action of new therapeutical agents, the knowledge of which genomic alterations are tumor-specific or which are necessary for the maintenance of the cell line in culture, becomes essential.