生物
免疫系统
趋化因子
髓样
多细胞生物
癌症研究
结直肠癌
细胞
电池类型
基因表达谱
免疫学
癌症
基因表达
基因
遗传学
作者
Karin Pelka,Matan Hofree,Jonathan Chen,Siranush Sarkizova,Joshua D. Pirl,Vjola Jorgji,Alborz Bejnood,Danielle Dionne,William Ge,Katherine Xu,Sherry Chao,Daniel R. Zollinger,David Lieb,Jason Reeves,Christopher A. Fuhrman,Margaret L. Hoang,Toni Delorey,Lan Nguyễn,Julia Waldman,Max Klapholz
出处
期刊:Cell
[Cell Press]
日期:2021-08-26
卷期号:184 (18): 4734-4752.e20
被引量:477
标识
DOI:10.1016/j.cell.2021.08.003
摘要
Immune responses to cancer are highly variable, with mismatch repair-deficient (MMRd) tumors exhibiting more anti-tumor immunity than mismatch repair-proficient (MMRp) tumors. To understand the rules governing these varied responses, we transcriptionally profiled 371,223 cells from colorectal tumors and adjacent normal tissues of 28 MMRp and 34 MMRd individuals. Analysis of 88 cell subsets and their 204 associated gene expression programs revealed extensive transcriptional and spatial remodeling across tumors. To discover hubs of interacting malignant and immune cells, we identified expression programs in different cell types that co-varied across tumors from affected individuals and used spatial profiling to localize coordinated programs. We discovered a myeloid cell-attracting hub at the tumor-luminal interface associated with tissue damage and an MMRd-enriched immune hub within the tumor, with activated T cells together with malignant and myeloid cells expressing T cell-attracting chemokines. By identifying interacting cellular programs, we reveal the logic underlying spatially organized immune-malignant cell networks.
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