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. 2020 Oct 30;40(2):322–333. doi: 10.1038/s41388-020-01530-6

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© The Author(s) 2020, corrected publication 2023

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 Aberrant growth of normal murine mammary gland cells transformed by overexpression of EGFR (NME cells) was normalized by the addition of the EGFR inhibitor AG1478 (1 µM). (Inset shows a typical small, acinar structure.) After 14 days of drug treatment, an AG1478-resistant (AGR) colony from these 3D cultures was isolated and characterized by differential gene expression analyses in comparison to the parental NME cells. b Human mammary epithelial cells transformed by overexpression of HER2 (HME2 cells) were cultured in the presence of lapatinib (1 µM) until lapatinib-resistant (LAPR) cells emerged. The LAPR cells were characterized by differential gene expression as compared to parental HME2 cells. c The differentially expressed genes in both ErbBi resistance models were compared. Genes similarly regulated by >2-fold upon acquisition of resistance to either AG1478 or lapatinib are listed.