ArticleCancer informatics2026
Development and Validation of a Six-Gene Signature of Myeloid Antigen Presentation Dysfunction Based on Single-Cell and Multi-Cohort Transcriptomics for Predicting Prognosis and Recurrence of Hepatocellular Carcinoma.
Article in Cancer informatics, 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
backgroundMyeloid antigen-presentation dysfunction is a central but incompletely translated immune state in hepatocellular carcinoma (HCC). This study aimed to develop a compact prognostic and recurrence model directly anchored in single-cell-defined myeloid antigen-presentation loss.
methodsIn this prognostic prediction-model development and validation study, GSE149614 was used as the single-cell discovery cohort. Tumor and normal myeloid cells were extracted, antigen-presentation (AP) module scores were calculated, and AP-loss candidate genes were identified using pseudobulk aggregation. Candidate genes were projected to TCGA-LIHC, GSE14520, and GSE76427 bulk transcriptomic cohorts. Survival-oriented model refinement was performed in GSE14520 using overall survival (OS) and recurrence-free survival (RFS), followed by validation with Kaplan-Meier analysis, Cox regression, fixed-time AUC, clinicopathological comparison, pathway scoring, targeted cell-cell communication analysis, and nomogram construction.
resultsA total of 13,784 myeloid cells were analyzed, including 8,209 tumor-infiltrating myeloid cells and 5,575 normal myeloid cells. Tumor-associated myeloid cells showed lower AP scores than normal myeloid cells (P = 0.04054). A compact six-gene signature consisting of SMOX, CSF1, AQP9, FLNB, COL7A1, and MXI1 was established. In GSE14520, the signature predicted poor OS (HR = 1.94, 95% CI: 1.41-2.65, P = 3.73e-05) and poor RFS (HR = 1.60, 95% CI: 1.23-2.08, P = 4.63e-04). In TCGA-LIHC, it also predicted inferior OS (HR = 1.49, 95% CI: 1.12-1.99, P = 5.83e-03). High-risk tumors showed enhanced glycolysis, hypoxia, epithelial-mesenchymal transition (EMT), angiogenesis, and IL6-JAK-STAT3 activity, with reduced antigen-presentation and IFNG response signals.
conclusionsWe report a compact single-cell-derived myeloid AP-loss signature for HCC prognosis and recurrence stratification. The model links clinical risk to a biologically interpretable myeloid dysfunction state and broader tumor microenvironment remodeling.
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