Mapping single-cell transcriptomes in the intra-tumoral and associated territories of kidney cancer
Ruoyan Li(Wellcome Sanger Institute), John R. Ferdinand(University of Cambridge), Kevin W. Loudon(University of Cambridge), Georgina Bowyer(University of Cambridge), Sean Laidlaw(Wellcome Sanger Institute), Francesc Muyas(European Bioinformatics Institute), Lira Mamanova(Wellcome Sanger Institute), Joana B. Neves(The Royal Free Hospital), Liam Bolt(Wellcome Sanger Institute), Eirini S. Fasouli(Wellcome Sanger Institute), Andrew Lawson(Wellcome Sanger Institute), Matthew D. Young(Wellcome Sanger Institute), Yvette Hooks(Wellcome Sanger Institute), Thomas R. W. Oliver(Cambridge University Hospitals NHS Foundation Trust), Timothy Butler(Wellcome Sanger Institute), James N. Armitage(Cambridge University Hospitals NHS Foundation Trust), Tev Aho(Cambridge University Hospitals NHS Foundation Trust), Antony C. P. Riddick(Cambridge University Hospitals NHS Foundation Trust), Vincent J. Gnanapragasam(University of Cambridge), Sarah J. Welsh(Cambridge University Hospitals NHS Foundation Trust), Kerstin B. Meyer(Wellcome Sanger Institute), Anne Y. Warren(Cambridge University Hospitals NHS Foundation Trust), Maxine Tran(The Royal Free Hospital), Grant D. Stewart(University of Cambridge), Isidro Cortés‐Ciriano(European Bioinformatics Institute), Sam Behjati(Cambridge University Hospitals NHS Foundation Trust), Menna R. Clatworthy(University of Cambridge), Peter J. Campbell(Wellcome Sanger Institute), Sarah A. Teichmann(Wellcome Sanger Institute), Thomas J. Mitchell(University of Cambridge)
Cited by 246Open Access
Abstract
T cell clonotypes largely defines their exhaustion state with intra-tumoral spatial heterogeneity that is not well explained by somatic heterogeneity. De novo mutation calling from single-cell RNA-sequencing data allows us to broadly infer the clonality of stromal cells and lineage-trace myeloid cell development. We report six conserved meta-programs that distinguish tumor cell function, and find an epithelial-mesenchymal transition meta-program highly enriched at the tumor-normal interface that co-localizes with IL1B-expressing macrophages, offering a potential therapeutic target.
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