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. 2020 Jun 15;10:9654. doi: 10.1038/s41598-020-66561-1

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© The Author(s) 2020

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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Mir34a knockout accelerates the development of ADM and PanIN lesions from a young age. (A) Macroscopic view of the pancreas of Kras^G12D; Mir34a^Δ/Δ mice compared to Kras^G12D controls and haematoxylin eosin (HE) staining on whole slide and a 20 × zoomed in area, at 1 month of age. Scale bar 50 µm. (B) Quantification of the amount of pancreatic tissue remodelled (with ADM and PanIN lesions), expressed as percentage, in Kras^G12D; Mir34a^Δ/Δ mice compared to Kras^G12D controls at 1 month of age (N ≥ 3 per group). (C) Macroscopic picture and HE staining of the pancreas from Kras^G12D; Mir34a^Δ/Δ mice compared to Kras^G12D controls at 3 months of age. Scale bar 50 µm. (D) Quantification of the area of pancreatic tissue remodelled shown in percentage, in Kras^G12D; Mir34a^Δ/Δ mice compared to Kras^G12D controls at 3 months of age (N ≥ 7 per group). (E) Quantification of the amount of ADM and PanIN lesions per high power field (HPF) in Kras^G12D; Mir34a^Δ/Δ mice compared to Kras^G12D controls (N ≥ 7 per group).