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Reviews of this body of work describe proposed pathways that include VEGFR2 signaling, nitric oxide synthesis through the Akt-eNOS axis, and ERK1/2 signaling (McGuire 2025)
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In vitro and preclinical studies demonstrate that inhibiting key regulators (e.g., GPX4) effectively induces ferroptosis, reducing GBM cell viability and tumor growth [11]
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