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During tumor progression, ROS may interact with hypoxic responses, leading to stabilization of HIF-1 and increased expression of VEGF, which ultimately promotes angiogenesis and adaptive tumor survival ( In vitro evidence indicates that cisplatin, which is well known to induce DNA damage, can also trigger mitochondrial dysfunction, leading to increased mitochondrial-derived ROS and downstream oxidative signaling that may participate in determining cell fate, including apoptosis ( in vivo studies on ROS in HGSOC, this review selectively focuses on in vitro studies examining the mechanisms by which ROS reinforce stage-specific tumorigenic programs in HGSOC

These SULT families include at least 13 different members

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