Abstract
SummaryIn recent years, novel insight into molecular mechanisms has allowed the identification of drug targets for various pediatric brain tumors. The aim of this article is to give an overview of new treatment options in neurofibromatosis type 1 (NF1), novel tyrosine kinase inhibitors that target oncogenic gene fusions in pediatric brain tumors, and antiangiogenesis as promising therapy especially in recurrent medulloblastoma.
Highlights
The survival rates of pediatric brain tumor patients improved constantly during the end of the 20th century
Neurofibromatosis type 1 (NF1) is the most common genetic tumor predisposition syndrome associated with the development of central nervous system (CNS) tumors with an incidence of 1 in 3000
The MEK inhibitor selumetinib was evaluated in a pediatric trial for inoperable neurofibromatosis type 1 (NF1)-associated plexiform neurofibroma and demonstrated high volumetric response rates with tolerable side effects [6, 7]
Summary
Summary In recent years, novel insight into molecular mechanisms has allowed the identification of drug targets for various pediatric brain tumors. The aim of this article is to give an overview of new treatment options in neurofibromatosis type 1 (NF1), novel tyrosine kinase inhibitors that target oncogenic gene fusions in pediatric brain tumors, and antiangiogenesis as promising therapy especially in recurrent medulloblastoma
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