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Since ROS-dependent DNA damage is markedly increased in myeloid cells after Bcr-Abl transformation 18 , we hypothesize that blocking dTTP and dCTP supply might exacerbate replication stress and DNA damage in Bcr-Abl-transformed cells, thereby jeopardizing cell survival

found that, the TME induces metabolic insufficiency in intratumoral CD8 + T cells by suppressing mitochondrial biogenesis

Integrating ferroptosis-inducing approaches with gemcitabine therapy may offer a novel strategy to bypass conventional resistance mechanisms

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