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. 2018 Jun 27;9:2500. doi: 10.1038/s41467-018-04664-0

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — SREBP-1 protects vemurafenib-resistant cells from lipid peroxidation. BRAF^V600E-mutant PDX tumors (mel6 model) were transplanted into nude mice (NMRI-Fox1nu) which were blindly administered vehicle (n = 8), fatostatin (20 mg/kg) (n = 10), vemurafenib (20 mg/kg) (n = 10) or a combination of vemurafenib and fatostatin (n = 10) (daily by oral gavage). a Tumor size was measured blindly with digital calipers every 3 days. The tumor pictures in (b) show the tumors that represent the median of their respective cohort. c Expression of Ki67 protein in PDX tumors that represent the median of their respective cohort. Scale bars indicate 100 μm. d Lipidomics of PDX tumor homogenate. e MDA quantification of PDX tumor homogenate. The data represent the average over all mice for each cohort compared to the control. Data are represented as mean ± s.e.m. (**p < 0.01)