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. 2019 Dec 11;21:141. doi: 10.1186/s13058-019-1233-x

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© The Author(s). 2019

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. 5 — Genomic aberrations in primary tumors and corresponding organoids. Representations of copy number variations (a), indels (b), and clinically relevant SNPs (c) of driver oncogenes and tumor suppressor genes relevant to breast cancer. Genomic DNAs of primary tumors (T) and corresponding organoids (O) from three different patients (P1100, P1116, P1117) were analyzed by whole-genome sequencing (detailed information in the “Methods” section). Represented SNPs (black boxes) are PIK3CA (RCV000024623.6, RCV000154512.1, RCV000201232.1), PTEN (RCV000008256.2, RCV000008257.2, RCV000128455.2, RCV000162649.3, RCV000212882.1), RUNX2 (RCV000177104.2), and BMPR1A (RCV000034703.1, RCV000120253.2, RCV000131909.2). Note that organoids show different or much less genomic aberrations compared to primary tumors