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. 2022 May;11(5):858–868. doi: 10.21037/tlcr-22-311

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2022 Translational Lung Cancer Research. All rights reserved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0.

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NLRP3 depletion inhibits PDAC progression. PDAC formation and progression were analyzed in a mouse model of PDAC with or without NLRP3 knockout. P48Cre; LSL-KrasG12D [KC or KC NLRP3 (+/+)] mice were bred with NLRP3-KO mice to obtain KC NLRP3 (−/−) mice. The KC NLRP3 (+/+) mice were used as controls. (A) Representative immunohistochemical images for NLRP3 staining at 6 months. (B,C) Quantification of percentage of healthy acinar area (B) and ducts at different stages (C) at 6 months. N=5. Scale bars were 50 µm. *, P<0.05. NLRP3, NLR family pyrin domain containing 3; KC, LSL-Kras^G12D; ADM, acinar-to-ductal metaplasia; PDAC, pancreatic ductal adenocarcinoma; KO, knockout; PanIN, pancreatic intraepithelial neoplasia.