Immunoediting Driven by Therapy and the Development of Cancer Immune Evasion

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Anticancer treatments can eradicate immune-visible tumor cells while selecting for populations capable of immune evasion.
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Therapy-induced immunoediting involves a continuum of pre-existing escape, immune activation, selective bottleneck, residual equilibrium, and subsequent escape.
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Genetic alterations and therapy-resistant stem-like states diminish tumor visibility and immune-cell access, contributing to immune evasion.
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Longitudinal biomarkers may identify residual equilibrium, allowing for mechanism-matched treatment adaptation before relapse occurs.
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Contemporary frameworks categorize resistance into primary, adaptive, and acquired forms, influenced by both tumor-intrinsic and tumor-extrinsic mechanisms.

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