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. 2021 Jan 4;22:4. doi: 10.1186/s13059-020-02222-w

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© The Author(s) 2021

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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — HMs bear basic transcriptomic hallmarks of PDAC. a Principal component analysis based on whole transcriptome showed that HMs have similar transcriptome as PTs. As showed in first two principal components that HMs and PTs are closed clustered together. b Compared to Ns, there are many common DEGs shared by PTs and HMs, including 2500 upregulated and 1983 downregulated genes. c Similar as PTs, HMs showed basic molecular hallmarks including loss of pancreatic phenotype, anti-apoptosis, inflammation, metabolic remodeling, dysregulated signaling pathways, and ECM remodeling. Genes showed in heatmap were those common DEGs identified in b. d PTs and HMs shared similar tumor-infiltrating-lymphocytes profiles