Abstract
Chimeric antigen receptor T-cell (CAR-T) therapy has achieved remarkable success in hematologic malignancies, yet its extension to solid tumors and its broader accessibility remain constrained by several interlocking challenges. Identifying tumor-specific surface antigens that are absent from healthy tissue is far more difficult in solid cancers than in B-cell malignancies, where CD19 provided a nearly ideal target. In addition, the immunosuppressive solid tumor microenvironment, characterized by regulatory T cells, myeloid-derived suppressor cells, and inhibitory cytokine signaling, actively blunts the effector function and persistence of infused CAR-T cells.
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