A multiscale model reveals how ERK/p38-regulated dormancy shapes tumor-immune dynamics and immunoediting outcomes

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The study introduces a new ERK-p38-structured model to describe cancer-immune interactions and tumor dormancy as a continuous phenotype.
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The model links intracellular signaling to tumor behavior, highlighting the role of ERK and p38 in regulating immune susceptibility and stress responses.
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Increased p38 activation under immune pressure promotes immune evasion, while p38 inhibition enhances tumor sensitivity to immune-mediated killing.
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The research identifies critical thresholds in the mean ERK/p38 phenotype that influence tumor fate and dynamics in response to immune pressure.
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The findings suggest that phenotypic plasticity is crucial for understanding immunoediting and improving therapeutic responses in cancer.

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