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Role of PI3K Inhibitors in Sensitizing Neuroblastoma Cells to Apoptosis

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Pediatric Cancer, Volume 4

Part of the book series: Pediatric Cancer ((PECA,volume 4))

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Abstract

The phosphatidylinositol 3′-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway is aberrantly activated in most cancers and represents a key mediator of cell survival, for example by antagonizing apoptosis signaling. Recently, increased phosphorylation of Akt was identified as a novel marker of poor prognosis in primary neuroblastoma specimens, indicating that PI3K/Akt presents a clinically relevant molecular target. A variety of pharmacological approaches have been developed over the last years to block distinct elements of the PI3K/Akt/mTOR axis. The current review will focus on the potential of PI3K inhibition to sensitize neuroblastoma for apoptosis induction and to overcome treatment resistance. Such a strategy may pave the avenue to more effective treatment options for children with neuroblastoma.

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Acknowledgements

The expert secretarial assistance of C. Hugenberg is greatly appreciated. Work in the author’s laboratory is supported by grants from the Deutsche Forschungsgemeinschaft, the Deutsche Krebshilfe, the Bundesministerium für Forschung und Technologie (01GM1104C), Else-Kröner-Fresenius Stiftung, Wilhelm-Sander Stiftung, Novartis Stiftung für therapeutische Forschung, IAP6/18 and the European Community (ApopTrain, APO-SYS).

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Correspondence to Simone Fulda .

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Fulda, S. (2013). Role of PI3K Inhibitors in Sensitizing Neuroblastoma Cells to Apoptosis. In: Hayat, M. (eds) Pediatric Cancer, Volume 4. Pediatric Cancer, vol 4. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-6591-7_4

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