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This review systematically summarizes the core patterns of metabolic reprogramming in HCC, dissect the molecular mechanisms of metabolic crosstalk at the tumor–immune interface, and discusses the role of immunometabolic remodeling in therapeutic resistance.
This integrative multi-omics study identified HSPE1 as a candidate BD risk gene with immune-cell-related regulatory evidence, providing insight into BD pathogenesis and supporting functional validation.
A hierarchical logical relationship of heterogeneous EGFR-TKI resistance mechanisms is clarified to provide evidence-based references for individualized post-resistance clinical decision-making, and offer feasible directions for subsequent translational research and therapeutic optimization.
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