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. 2020 Oct 5;11:4977. doi: 10.1038/s41467-020-18701-4

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© The Author(s) 2020

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. 3 — a DCCs from BM of 21 non-metastasized (M0-stage, n = 30 DCCs) and five metastasized (M1-stage; n = 11 DCCs) breast cancer patients were analyzed for CNAs. The cumulative frequency of genomic aberrations is given in yellow and blue indicating genomic gains and losses, respectively. M0-stage (b, c n = 30; d, e n = 29 and M1-stage (n = 11) DCCs and EpCAM+ BM cells of seven healthy donors, i.e. patients without malignant disease (HD; n = 15 cells) were analyzed by single cell RNA sequencing. b Principal component analysis of the top 500 most variable genes or top 100 most variable epithelial and B cell genes. c DCCs were tested for enrichment in pathways identified to be enriched in LRCs over QSCs/nLRCs (see Fig. 2d). d The heatmap displays log2 normalized read counts of mRNA expression of IL6 signaling pathway genes as listed in the NCI-Nature PID expanded by the LIFR gene. e Venn diagram for the gene-members of the four pathways (d) that are expressed in at least half of bone marrow DCCs (except for the BMX (5/40) and CEBPD (19/40) genes, Supplementary Fig. 1d). Pathway-private genes are annotated by their number, shared genes are named explicitly (see also Supplementary Table 5). See Supplementary Table 1 for patient/sample-ID allocation.