Cancer &

Full list of author information is available at the end of the articleReactive oxygen species (ROS) have emerged as potent signaling molecules with the ability to modulate a num-ber of cellular signaling processes, owing to their ability to modify proteins, including via oxidation of specific cysteine residues [1,2]. ROS have also been found to directly regulate key enzymes of matter/energy metabol-ism. The mitochondrial tricarboxylic acid (TCA) cycle by ROS through its iron cluster [3]. Moreover, there is evidence for redox-dependent changes associated with malignancy-related metabolic alterations in breast can-cer development [4]. In addition, the glycolytic enzymes glyceraldehyde 3-phosphate dehydrogenase [5] and the tumor-specific M2 splice variant of pyruvate kinase [6-8] have both been shown to be inhibited by the oxidation of specific cysteine residues, apparently redirecting car-bon flux through the pentose phosphate pathway and away from the glycolytic pathway to generate ROS