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. 2016 May 16;16:314. doi: 10.1186/s12885-016-2346-6

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© Crivellaro et al. 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 1 — Tumor suppressors network associated with the BCR-ABL/PI3K/AKT pathway. Schematic representation of the BCR-ABL/PI3K/AKT pathway and the role of PTEN and FOXO tumor suppressors. This carton highlights how BCR-ABL inactivates PTEN through CKII-mediated phosphorylation and HAUSP-mediated changes of cellular compartmentalization. Furthermore, BCR-ABL promotes FOXO inactivation through the regulation of its cellular localization. We also speculate on the putative regulation of FOXO localization through HAUSP in CML, although BCR-ABL/HAUSP/FOXO connection has to be demonstrated