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. 2020 Aug 18;22:91. doi: 10.1186/s13058-020-01328-0

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 1 — Study cohort. a Recruitment and specimen retrieval flow chart. Sample information and numbers are shown on the left of the central chart and patient information and numbers are shown on the right. b Actionable alterations. Pie chart shows the percentage breakdown of patients and the level of actionable alterations their samples contain. Patients with at least one level 1 actionable alteration amounted to 49% (n = 114). Patients with a level 2 actionable alteration accounted for 25% (n = 57). Patients without an actionable alteration amounted to 26% of the cohort (n = 60). c Level 1 actionable alteration breakdown by number of samples. AKT1 mutations (3%, n = 4), BRCA1/2 germline variants (7%, n = 9), ESR1 mutations (12%, n = 16), ERBB2 mutations (10%, n = 14), PIK3CA mutations (52%, n = 71) and PTEN mutations (17%, n = 23). ERBB2 amplifications are not included. d Level 2 actionable alteration breakdown by number of samples. ARID1A mutations (12%, n = 21), ATM mutations (1%, n = 2), BRCA1/2 non-germline mutations (12%, n = 21), CDH1 mutations (27%, n = 48), ERBB3 mutations (5%, n = 9), HRAS mutations (1%, n = 1), IGF1R mutations (3%, n = 6), INPP4B mutations (5%, n = 9), MAP2K4 mutations (4%, n = 7), MAP3K1 mutations (9%, n = 16), MDM2 amplifications (7%, n = 12), PIK3R1 mutations (6%, n = 11) and RB1 mutations (8%, n = 14)