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. 2023 Oct 21;31(4):31. doi: 10.1007/s10577-023-09741-9

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© The Author(s) 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 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/.

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Fig. 3 — Consequences of p53 loss. Cells that lose p53 function can become aneuploid by various means, including supernumerary centrosomes, DNA damage, and altered proliferation and cellular surveillance mechanisms. Supernumerary centrosomes can result in multipolar spindles and/or lagging chromosomes, causing CNAs and WGD. Unresolved DNA damage can contribute to replication stress and mitotic errors (e.g., chromosome anaphase bridges) likely resulting in structural CNAs (sCNAs) or WGD. The combination of p53 loss with alterations in driver genes affects proliferation and surveillance mechanisms, resulting in aneuploid progeny with sCNA and/or numerical CNAs (nCNA)