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. 2023 Jan 17;19(4):827–838. doi: 10.1007/s12015-023-10508-2

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© The Author(s) 2023

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/.

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Fig. 2 — Progression model for pancreatic cancer based on the monophyletic model. Inflammatory responses in the pancreas induce cell apoptosis (①). PGE2 and wound-healing signals are activated to repair the injured tissues through NSC division and differentiation (②). NSCs dedifferentiate and adopt a novel status termed acinar-ductal metaplasia because of the gene mutation accumulation (③). NSCs become malignant CSCs (④). PGE2 and wound-healing signals maintain the division and proliferation of CSCs and lead to tumors