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. 2022 Dec 3;8:478. doi: 10.1038/s41420-022-01259-z

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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. 2 — A The full view of whole chromosomal copy number in 176P and 176R tissues by whole-genome sequencing (WGS). B The copy number of some cancer-related genes in 176P and 176R tissues. C The mutation profiles of cancer-related genes were consistent in 176P and 176R tissues. D Cells derived from 176P and 176R tissues were well divided into two groups after t-SNE algorithm analysis by single-cell RNA sequencing. E According to the k-means clustering algorithm, all the cells were divided into two separated subgroups when k = 2. Cells derived from 176P and 176R tissues were dominant in cluster 1 (pink) and cluster 2 (green), respectively. F Volcano plot displayed differentially expressed molecules of cluster 1 and cluster 2 when fold change ≥2. G Venn diagram showed differentially expressed molecules in 176P and 176R tissues detected by protein mass spectrometry. A total of 2983 molecules expressed both in 176P and 176R tissues, among which 1004 molecules were upregulated after acquired Trastuzumab resistance when fold change ≥ 1.5.