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. 2023 Jan 21;9:21. doi: 10.1038/s41420-023-01330-3

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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 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. 7 — Chronic or acute exposure of non-squamous epithelia to genotoxic agents would drive G2/M arrest via the DNA damage response. In turn, G2/M checkpoints would drive benign hyperplastic squamous differentiation (squamous metaplasia). Unrepaired cells would undergo terminal post-mitotic squamous differentiation. In the event of additional mutations (AM) hitting the G2/M checkpoints, cells overcoming the cell division block would proliferate bearing genomic instability, eventually resulting in cancer. Ep: epithelium. Created with BioRender.com.