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. 2023 Sep 27;73(3):496–508. doi: 10.1136/gutjnl-2023-330748

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© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution 4.0 Unported (CC BY 4.0) license, which permits others to copy, redistribute, remix, transform and build upon this work for any purpose, provided the original work is properly cited, a link to the licence is given, and indication of whether changes were made. See: https://creativecommons.org/licenses/by/4.0/.

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Modelling the RPLS signature in iCCA single cell RNA-sequencing data. (A) Annotation of tumours as long survivor (LS)-iike or rapid progressor (RP)-like based on tumour cell expression of the tumour-origin RPLS signature (ESCAPE tool, p values derived by Wilcoxon test). (B) Differentially expressed pathways and processes (ESCAPE with KEGG and Hallmarks gene lists) between LS-like and RP-like tumour cells. (C) Cell type-specific transcription factor activities (DoRothEA), cytokine activities (CytoSig) and ligand:receptor interactions (CellChat) unique to RP-like tumours in GSE125449 and GSE151530, including the potential and current druggability of tumour surface receptors. (D) Differential expression of myeloid cell type and functional signatures in LS-like and RP-like myeloid cells (ESCAPE, Wilcoxon test). (E) T cell subtype annotation using ProjectTILs (p values from Fisher’s exact test). (F) RP-specific ligand-receptor interactions tumours in GSE125449 and GSE151530 involving immunomodulatory targets (highlighted in bold; defined by CRI iAtlas). iCCA, intrahepatic cholangiocarcinoma.