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. 2018 Apr 3;135(5):649–670. doi: 10.1007/s00401-018-1842-y

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© The Author(s) 2018

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.

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Fig. 4 — a Integration of a clonal evolution and cancer stem cell model for gliomagenesis. This model assumes that sequential mutations and selection pressure drive the evolution of cancer stem-like cells. At the same time, these stem-like cells may give rise to more differentiated (i.e., phase IV) offspring that may divide further but rapidly become growth arrested. b According to this model these cells may be senescent and contribute to the cancer phenotype by eliciting a microenvironment response via SASP. SASP senescence-associated secretory phenotype; ILs interleukins; CXCLs chemokines (C–X–C motif); CCLs chemokines (C–C motif)