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. 2019 May 28;1(1):vdz004. doi: 10.1093/noajnl/vdz004

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© The Author(s) 2019. Published by Oxford University Press, the Society for Neuro-Oncology and the European Association of Neuro-Oncology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 1 — PI3K inhibition in diffuse intrinsic pontine glioma (DIPG). Schematic pathway representing the role of PI3K and mitogen-activated protein kinase (MEK) inhibition and relevant signaling molecules (A). Multiple points of compensation and feedback inhibition are a feature of the two pathways. ERK and the downstream kinase ribosomal S6 protein kinase (RSK) can compensate for AKT in the activation of mammalian target of rapamycin complex 1 (mTORC1) via inhibitory tuberous sclerosis complex 2 (TSC2) phosphorylation. Cross-inhibition occurs via MEK suppression of PI3K by promoting the membrane localization phosphatase and tensin homolog (PTEN), and AKT suppression of RAS activation via RAF inhibition. Cell viability following PI3K inhibitor treatment in SU-DIPG-IV (B) and SU-DIPG-XIII (C) cells. Errors bars SD.