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. 2021 Apr 27;11:9010. doi: 10.1038/s41598-021-88489-w

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© The Author(s) 2021

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 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/.

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Altered molecular pathways in inflamed UC tissue. (A) IPA canonical pathway and upstream regulator analysis revealed similarly enriched pathways across three independent cohorts (1: GSE4183, n = 8 healthy control, n = 9 UC-inflamed; 2: GSE14580, n = 6 healthy control, n = 24 UC-inflamed; 3: GSE38713, n = 13 healthy control, n = 15 UC-inflamed; IPA, FDR < 0.05). (B) Hierarchical clustering, as shown by representative heatmap, revealed two distinct clusters of UC samples separated by the UC₁₀₀ signature (generated from GSE4183, GSE14580, GSE38713) differentiating between inflamed UC and matched uninflamed transcriptomes from an independent cohort (GSE107593) (n = 24 UC-inflamed, n = 24 UC-matched uninflamed). (C) Presence of the UC₁₀₀ signature represented as a score in inflamed UC compared to uninflamed matched control transcriptomes from an independent cohort (GSE107593) (p = 4.65e^-08). (D) Disease and function enrichment analysis for UC₁₀₀ signature (IPA, p < 0.05).