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. 2022 Jul 18;24:51. doi: 10.1186/s13058-022-01542-y

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 6 — Tumorigenic capacity of Dusp4NULL Trp53Δ MYCAMP cells is associated with chromosome 5 amplification. A Whole-genome sequencing of PMEC-derived cell lines with Dusp4 loss, Trp53 loss, and/or MYC amplification. Dusp4NULL Trp53Δex7 MYCAMP cells (tumor forming) or Dusp4FLOX Trp53Δex7 MYCAMP cells (not tumor forming). B FISH for chromosome 5 centromeric amplicon in DPM tumors compared to normal murine mammary gland tissue. C Representative images of FISH in metaphase spreads from DPM and Dusp4FLOX cells. In the right panel is a magnification of chromosome 5