Contingent upon concentration, reactive oxygen species (ROS) influence cancer evolution in apparently contradictory ways, either initiating/stimulating tumorigenesis and supporting transformation/proliferation of cancer cells or causing cell death. To accommodate high ROS levels, tumor cells modify sulfur-based metabolism, NADPH generation, and the activity of antioxidant transcription factors. During initiation, genetic changes enable cell survival under high ROS levels by activating antioxidant transcription factors or increasing NADPH via the pentose phosphate pathway (PPP). During progression and metastasis, tumor cells adapt to oxidative stress by increasing NADPH in various ways, including activation of AMPK, the PPP, and reductive glutamine and folate metabolism.

根据浓度，活性氧（ROS）以明显矛盾的方式影响癌症的进化，要么启动/刺激肿瘤发生并支持癌细胞的转化/增殖，要么导致细胞死亡。为了适应高 ROS 水平，肿瘤细胞会改变硫基代谢、NADPH 生成以及抗氧化转录因子的活性。在启动过程中，基因变化通过激活抗氧化转录因子或通过戊糖磷酸途径 (PPP) 增加 NADPH，使细胞能够在高 ROS 水平下生存。在进展和转移过程中，肿瘤细胞通过多种方式增加 NADPH 来适应氧化应激，包括激活 AMPK、PPP 以及还原性谷氨酰胺和叶酸代谢。