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. 2016 Nov 25;35:97. doi: 10.1186/s40880-016-0162-7

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© The Author(s) 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 — Proposed mechanism of acquired resistance to the multikinase inhibitor sorafenib in hepatocellular carcinoma (HCC). Highly angiogenic HCCs are initially responsive to sorafenib treatment. Over time, tumor cells become more invasive which promotes co-option of liver vessels in the face of angiogenesis blockade. EMT epithelial-to-mesenchymal transition