ArticleFrontiers in immunology2026
A multi-dimensional omics framework identifies GPR35 as a driver of M2 macrophage activation and poor prognosis in colorectal cancer.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- An Epithelial-Mesenchymal Transition-Driven Transcriptional Index Stratifies Immunosuppression and Therapeutic Resistance in Bone Malignancies.International journal of genomics · 2026Article
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8 authors.
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Abstract
Introduction: Colorectal cancer (CRC) remains a leading cause of global cancer mortality, with therapeutic outcomes heavily reliant on the tumor microenvironment (TME). While immunotherapy has revolutionized treatment for distinct subsets, the mechanisms driving immune evasion in the majority of patients remain elusive. Methods: In this study, we constructed a comprehensive single-cell atlas of the CRC TME by integrating multi-cohort scRNA-seq data. Results: Through non-negative matrix factorization (NMF), we identified nine intratumoral heterogeneity meta-programs (MPs), among which MP8 was robustly linked to M2 macrophage activation. High-dimensional WGCNA further pinpointed GPR35 as a master regulator within the MP8-associated gene network. Clinical analysis across four independent cohorts validated GPR35 as a significant predictor of poor prognosis. Functionally, GPR35 knockdown Discussion: Collectively, our findings identify GPR35 as a novel cancer cell-intrinsic driver of immune evasion and immunotherapy resistance, positioning it as a promising therapeutic target to sensitize "cold" CRC tumors to immune checkpoint blockade.
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