ArticleMolecular therapy. Nucleic acids2026
Multi-layer molecular profiling defines an immune-active colorectal cancer subtype with therapeutic relevance.
Article in Molecular therapy. Nucleic acids, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Colorectal cancer (CRC) exhibits substantial heterogeneity in response to immunotherapy, highlighting the critical need for improved stratification strategies. Here, we established a robust multi-omics framework by integrating transcriptomic, epigenetic, and mutational profiles, identifying three cancer subtypes (CS1-CS3). Among these, the CS3 subtype emerged as a distinct immunogenic class characterized by genomic instability and robust immune activation, capturing a subset of immune-inflamed tumors classified as clinically microsatellite-stable (MSS) that may be overlooked by routine microsatellite instability (MSI) testing. Single-cell transcriptomics further supported this immune-active state by revealing enrichment of pro-inflammatory myeloid populations and specialized epithelial states. Longitudinal analysis of independent immunotherapy cohorts revealed that CS3 signature activity exhibits response-dependent dynamics. While elevated baseline CS3 activity was associated with favorable clinical outcomes, significant post-treatment score reductions were primarily enriched among patients achieving radiographic complete response (CR). To facilitate clinical translation, we derived an 11-gene prognostic model for risk stratification and leveraged pharmacogenomic screening to prioritize actionable combination candidates, including multi-kinase and epigenetic inhibitors. Collectively, these findings characterize a therapeutically relevant immune-active subtype and provide a comprehensive framework of biomarkers and actionable targets to advance precision immunotherapy in CRC.
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