Findings reveal TP63's role in reducing survival through inhibiting ferroptosis in EGFR-mutant lung cancer, suggesting new treatment strategies.
Clinically, high TP63 expression correlates with reduced overall survival in EGFR-mutant NSCLC patients. These findings define a critical TP63-GPX4 ferroptosis axis that safeguards tumor cell survival during therapeutic stress, highlighting ferroptosis induction as a potential therapeutic strategy to overcome EGFR-TKI resistance.
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Li et al. (2023) studied this question.
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