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. 2017 Jan 25;15:8. doi: 10.1186/s12964-017-0163-4

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© The Author(s). 2017

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 — Model of oncogenic HH/GLI signaling in AML. Activation of HH/GLI in leukemic (stem) cells of AML patients can be activated by HH ligand derived from adjacent BM stromal cells expressing low levels of the HH inhibitor HHIP. GLI expression in AML cells can enhance radio- and chemoresistance, and promote leukemogenesis by epigenetically repressing cell-cycle inhibitors (e.g. p15) or by synergistic cross-talk with oncogenic FLT3/STAT5 signaling. LIC: leukemia initiating cell; Me: DNA methylation