Demonstrates superior tumor suppression in murine OSCC models, indicating effective immunotherapy.
to generate hydroxyl radicals via the Fenton reaction, triggering ferroptosis. In murine OSCC models, this combination induces immunogenic cell death and successfully reprograms tumor-associated macrophages from a pro-tumor M2 to an anti-tumor M1 phenotype. The treatment additionally induced robust immunogenic cell death, as evidenced by calreticulin exposure and HMGB1 release, leading to enhanced dendritic cell maturation. Consequently, the treatment achieved superior tumor suppression and significantly reduced recurrence compared to controls, establishing a robust and sustained antitumor immune response. This localized platform presents a promising strategy for managing OSCC by effectively overcoming the limitations of current therapies.
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Li et al. (2026) studied this question.
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