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. 2022 May 14;28(18):1934–1945. doi: 10.3748/wjg.v28.i18.1934

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©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/

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Association of common genetic alterations and pancreatic ductal adenocarcinoma pathogenesis. The progression from the early to invasive stage of pancreatic ductal adenocarcinoma (PDAC) is supported by different genes alteration at different stages. KRAS mutation transforms the normal pancreatic ductal cells to pancreatic intraepithelial neoplasia (PanIN). The PanIN1A, PanIN1B and PanIN2 are low grade PanIN. Additional mutation such as CDKN2A is required to develop PanIN2. As the disease deteriorates, additional genes mutation such as TP53, SMAD4 and BRCA2 are involved to develop high grade PanIN3 and eventually invasive PDAC. PDAC: Pancreatic ductal adenocarcinoma. The figure in this review paper is created by using BioRender.com by the authors.