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Consistently, emerging studies indicated that modulation of oxidative stress, ablation of CD36 (a scavenger receptor known for its function as a fatty acid transporter) (43, 44), or overexpression of GPX4 (44, 45) suppressed lipid peroxidation, restored tumor-infiltrating CD8 + effector functions, and enabled tumor control
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PEG-ASP), which demonstrates a significantly prolonged half-life and reduced immunogenicity in the treatment of acute lymphoblastic leukemia (ALL) [231,232]
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