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. 2021 Jun 18;12:3742. doi: 10.1038/s41467-021-23957-5

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© The Author(s) 2021

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 — Microarray-based gene expression and cluster analysis to compare the molecular profiles of mammary tumors that originated in MMTV-tTA TetO-Kras^G12D (yellow arrows, N = 4 biological replicates) and WAP-Cre EF1-tTA TetO-Kras^G12D (red arrows, N = 4 biological replicates) transgenic females with reference sets from diverse genetically engineered, as well as chemical-induced and radiation-induced mammary cancer models. Note that the TetO-Kras^G12D transgene is under the control of the tetracycline-responsive transactivator (tTA) in both models. In contrast to the epithelial-specific expression of the tTA under the MMTV-LTR, the WAP-Cre-mediated activation of oncogenic KRAS in the luminal epithelium is under the control of the ubiquitously active EF1-tTA, which is untethered from a differentiation state and allows neoplastic cells to assume diverse developmental fates.