Abstract
307 ISSN 2045-0907 10.2217/CNS.13.25 © 2013 Future Medicine Ltd CNS Oncol. (2013) 2(4), 307–310 CNS tumors are the most common solid tumors of childhood [1]. Although treatment advances have improved survival for some pediatric CNS diseases, there unfortunately remains a group of tumors associated with signif icantly poorer prognosis. Among these are high-grade gliomas (HGGs), which, despite aggressive manage ment, usually recur and are associated with 5-year survival outcomes between 15 and 35% [2]. Diffuse intrinsic pontine glioma (DIPG), a highly malignant brainstem tumor with median survival of less than 1 year [3], remains a constant therapeutic challenge. High-risk metastatic medulloblastoma with cerebrospinal fluid dissemination at presentation is associated with 5-year survival rates between 40 and 70% despite intensive treatment regimens [4]. In addition, rare malignancies, such as atypical teratoid rhabdoid tumors, although often demonstrating response to chemotherapy, are associated with early relapse and a median survival of only 17 months [5]. Oncolytic virotherapy, which uses viruses to selectively infect and destroy cancer cells [6], offers a novel treatment approach for poor prognosis pediatric CNS tumors. While there is extensive literature on oncolytic virotherapy for adult brain malignancies, such as HGG, work on pediatric CNS tumors is currently only just gathering steam. With no open clinical trials focused on oncolytic virotherapy in pediatric CNS tumors, we can currently only draw upon available preclinical models, alongside adult and limited pediatric clinical data, to progress the exciting future potential of this treatment modality. The majority of preclinical studies of oncolytic virotherapy for pediatric CNS tumors evaluate eff icacy in medulloblastoma. Over 15 years ago, Lasner et al. published that herpes simplex virus (HSV) variant 1716 could infect and destroy D283 medulloblastoma cells and demonstrated that intratumoral injection of the virus into D283 tumor-bearing mice conferred a statistically significant increase in survival compared with control murine models [7]. Pyles et al., 1 year later, also demonstrated therapeutic potential in a double-mutant modified HSV strain 3616UB that was
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