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Neuroblastoma (NB) 1 is the most common extracranial tumor in childhood and accounts for nearly half of neoplasms diagnosed during infancy (Maris, 2010; Brodeur, 2003). A striking feature of these tumors has been their heterogeneous course, which ranges from spontaneous regression to inevitable progression and death (Brodeur, 2003). Current pharmacological approaches in the treatment of NBs include standard combination chemotherapy using dose-intensive cycles of carboplatin, etoposide, cyclophosphamide, and doxorubicin, with the addition of topoisomerase I inhibitors. For intermediate-risk NB, a high rate of survival among patients may still be achieved with significant reduction of doses and duration of chemotherapy (Baker et al., 2010). The retinoic acid analogue isotretinoin (13-cis-retinoic acid) is additionally used in high-risk NB patients with progressive or recurrent disease (Maris, 2010; Reynolds et al., 2003). Animal cancer models have offered valuable preclinical testing systems for studying the impact of specific genes in the appearance and the progress of the disease as well as the efficacy of novel therapeutic regimes. Animal models of NB have been developed by subcutaneous inoculation (xenografting) of established human NB cell lines in immunocompromised mice; for instance, the cell line SK-N-BE2c was successfully used to develop an animal model and test the effects of imatinib (Meco et al., 2005). Yet, the major

Interplay Between Protein Kinase C Isoforms Alpha and Epsilon, Neurofibromin, and the Ras/MAPK Pathway in Neuroblastoma Differentiation