ArticlePloS one2026
Integrated multi-omic analysis characterizes an IFNγ-responsive-to-myeloid-suppressive immune continuum in immune-active hepatocellular carcinoma.
Article in PloS one, 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
Immune-active hepatocellular carcinoma (HCC) is commonly treated as a single inflamed phenotype, although its internal immune heterogeneity remains incompletely defined. We integrated public bulk transcriptomic, single-cell, spatial transcriptomic, proteomic, phosphoproteomic, and treatment-cohort data to test whether this heterogeneity is better represented by discrete states or a continuous immune axis. In 112 checkpoint-high TCGA-LIHC tumors, an inflamed-minus-myeloid axis showed structured heterogeneity but no robust empirical bimodality: the observed kernel-density curve had one prominent mode and none of 1,000 bootstrap resamples contained two or more prominent modes. IFNγ-responsive-associated and myeloid-suppressive-associated labels were therefore retained only as operational summaries of opposing axis tendencies, and the biological polarity persisted across alternative definitions of immune-active entry. A fixed 10-gene within-sample rank template-contrast score transferred the axis to independent HCC cohorts. Transcriptomic analyses based on gene sets non-overlapping with the compact panel and original state-defining genes supported the IFNγ-oriented end, whereas spatial analyses showed local cross-end coexistence with reduced immediate-neighbor mixing relative to a count-preserving random-label null, and paired proteomic/phosphoproteomic analyses showed concordant myeloid-oriented associations involving macrophage, fibroblast/extracellular-matrix, hypoxia, SPP1-integrin-FAK, and myeloid-receptor programs. Direct application of the frozen transfer score to four public HCC immunotherapy cohorts yielded heterogeneous, imprecise response associations (pooled Hedges' g = 0.10, 95% CI -0.42 to 0.61) and did not establish clinical response prediction. These results support a structured IFNγ-responsive-to-myeloid-suppressive continuum within immune-active HCC. The framework is transferable across public datasets but requires prospective HCC-specific clinical validation, while functional perturbation studies are needed before causal or therapeutic claims.
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