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Abstract
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.