cancer-immunotherapy
How does cisplatin boost checkpoint therapy?
Open access · cc by · source: Europe PMC
Cisplatin-triggered tumor ferroptosis polarized N1 neutrophils and remodeled cold NSCLC tumors toward hotter T-cell/Th1 states, synergizing with ferroptosis activators in EGFR-mutant settings.
Key findings
Cisplatin induced tumor-cell ferroptosis then N1 neutrophil polarization that helped convert “cold” to “hot” tumors via T-cell infiltration and Th1 differentiation; ferroptosis activation synergized with chemoimmunotherapy in EGFR-mutant NSCLC models.
Methodology
Studied cisplatin effects on ferroptosis and neutrophil polarization in NSCLC models (including A549/LLC systems), assessed T-cell infiltration/Th1 differentiation, and tested ferroptosis-activator combinations aimed at EGFR-mutant immunotherapy resistance.
Limitations
Mouse/cell mechanisms may not fully predict human EGFR-mutant responses; clinical dosing/schedule optimization was not a randomized patient trial here.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
Triggering tumor ferroptosis can help checkpoint therapy in cold tumors (preclinical).
In EGFR-mutant NSCLC models, cisplatin-driven tumor ferroptosis polarized N1 neutrophils and supported T-cell/Th1 programs that synergized with immune checkpoint inhibitor therapy.
Evidence for the claim as stated.
Cisplatin-induced ferroptosis aided ICI efficacy in cold tumors vs IRE1/JNK blockade reduced ferroptosis-linked kidney I/R injury
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
Cisplatin-induced ferroptosis aided ICI efficacy in cold tumors vs IRE1/JNK blockade reduced ferroptosis-linked kidney I/R injury
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