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. 2020 Dec 9;588(7837):331–336. doi: 10.1038/s41586-020-2969-2

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© The Author(s), under exclusive licence to Springer Nature Limited 2020, corrected publication 2021

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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Extended Data Fig. 5 — a. A line-by-line view of brain metastatic potential and its associated features at genetic, expression, metabolite, and gene dependency levels. Mutation: mutant (MUT), wild-type (WT). Copy number: data are binarized, with deletion (DEL) cutoff < = -1 and amplification (AMP) cutoff > = 1. Expression signatures: 1. Hallmark: PI3K/AKT/MTOR signalling, 2. GO: ERBB signalling pathway, 3. GO: ERBB2 signalling pathway, 4. Burton: adipogenesis peak at 8hr, 5. GO: carnitine metabolic process, 6. Reactome: mitochondrial fatty acid beta oxidation, 7. GO: short chain fatty acid metabolic process. Data not available for the cell lines are marked with X. b, c, Scatter plots showing the correlation of SREBF1 in vitro dependency and brain metastatic potential in MetMap500 (a) and MetMap125 (b). Strong inverse correlation was observed for breast cancer in both datasets. Each dot represents a cell line.

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