ArticleGenome biology2022
Refining colorectal cancer classification and clinical stratification through a single-cell atlas.
Article in Genome biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 157 papers.
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Who cites it
157 citing papers in PubMed, 194 citations in OpenAlex.
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- USP48 functions as a suppressor of colorectal cancer via SELENBP1 stabilization.Translational oncology · 2026Article
- Methylation-Associated Differentiation Features Define Biological and Prognostic Heterogeneity in CMS4 Colorectal Cancer.International journal of molecular sciences · 2026Article
- Article
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- Multi-layer molecular profiling defines an immune-active colorectal cancer subtype with therapeutic relevance.Molecular therapy. Nucleic acids · 2026Article
- RNA Metabolism Genes as Prognostic Biomarkers and Therapeutic Targets in Colorectal Cancer Based on the Analysis of Single-Cell and Bulk-RNA Sequencing Data.Journal of cellular and molecular medicine · 2026Article
- ScSpTITH: a rank-correlation framework for robust quantification of multi-dimensional tumor heterogeneity.Human genetics · 2026Article
- DKC1 promotes colorectal cancer progression and therapy resistance by dysregulating sphingolipid biosynthesis.Nature communications · 2026Article
- Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Multi Omics Integration in Colorectal Cancer: From Molecular Insights to Precision Oncology.Cancers · 2026Review
- Smoking promotes colorectal cancer via the CKAP2L/AREG axis.International journal of oncology · 2026Article
- Molecular subtyping and prognostic model construction based on endosome-related genes in colorectal cancer.Journal of gastrointestinal oncology · 2026Article
- ASCL2 drives colorectal cancer metastasis through transcriptional activation of TDGF1.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- AKAP12-LMOD1 signaling defines stromal CAF activation and epithelial junction loss in colorectal cancer.Scientific reports · 2026Article
- POSTNOncology reports · 2026Article
- Integrated single-cell transcriptomic atlas of human gastric and colorectal tissues across diverse phenotypes.Scientific data · 2026Article
- A differential single-cell transcriptome atlas of left-sided and right-sided colorectal cancer.Discover oncology · 2026Article
97 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
31 authors at 12 institutions in 3 countries.
Funding
Abstract
backgroundColorectal cancer (CRC) consensus molecular subtypes (CMS) have different immunological, stromal cell, and clinicopathological characteristics. Single-cell characterization of CMS subtype tumor microenvironments is required to elucidate mechanisms of tumor and stroma cell contributions to pathogenesis which may advance subtype-specific therapeutic development. We interrogate racially diverse human CRC samples and analyze multiple independent external cohorts for a total of 487,829 single cells enabling high-resolution depiction of the cellular diversity and heterogeneity within the tumor and microenvironmental cells.
resultsTumor cells recapitulate individual CMS subgroups yet exhibit significant intratumoral CMS heterogeneity. Both CMS1 microsatellite instability (MSI-H) CRCs and microsatellite stable (MSS) CRC demonstrate similar pathway activations at the tumor epithelial level. However, CD8+ cytotoxic T cell phenotype infiltration in MSI-H CRCs may explain why these tumors respond to immune checkpoint inhibitors. Cellular transcriptomic profiles in CRC exist in a tumor immune stromal continuum in contrast to discrete subtypes proposed by studies utilizing bulk transcriptomics. We note a dichotomy in tumor microenvironments across CMS subgroups exists by which patients with high cancer-associated fibroblasts (CAFs) and C1Q+TAM content exhibit poor outcomes, providing a higher level of personalization and precision than would distinct subtypes. Additionally, we discover CAF subtypes known to be associated with immunotherapy resistance.
conclusionsDistinct CAFs and C1Q+ TAMs are sufficient to explain CMS predictive ability and a simpler signature based on these cellular phenotypes could stratify CRC patient prognosis with greater precision. Therapeutically targeting specific CAF subtypes and C1Q + TAMs may promote immunotherapy responses in CRC patients.
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