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. 2022 Apr 21;13:2169. doi: 10.1038/s41467-022-29857-6

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© The Author(s) 2022

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. 2 — Genomic landscape of 70 exocrine PDPCOs, including PDACs, IPMNs, and ACCs (left), and 4 neuroendocrine PDPCOs (right). The figure shows exonic mutations; noncoding mutations in UTR, upstream/downstream, intronic, ncRNA and intergenic regions; and CNVs. CAS-DAC-23 with WES of blood DNA; CAS-NEN-2 without sequencing of blood DNA. PDPCO patient-derived pancreatic cancer organoid, PDAC pancreatic ductal adenocarcinoma, NEN pancreatic neuroendocrine neoplasm, IPMN intraductal papillary mucinous neoplasm, ACC acinar cell carcinoma, CNV copy number variation.