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. 2022 Feb 24;3(2):232–250. doi: 10.1038/s43018-022-00337-6

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© The Author(s) 2022

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. 1 — a, Top, oncoprint plot showing single-nucleotide variants and insertion–deletions (indels) for commonly mutated genes in cancer. Annotations for each model include hormone receptor (HR) status for ER and PR, HER2 status, pathology (invasive ductal carcinoma (IDC), mixed, phyllodes, invasive lobular carcinoma (ILC), inflammatory or metaplastic) and whether the sample was from the primary breast tissue or a metastatic site. Bottom, specific gene-level CN alterations are displayed. b, Unsupervised clustering of the PDX models was performed using root mean squared scaling of transcript abundance in the PAM50 gene set.