An unanswered question in public health is whether anti-oxidation prevents or promotes cancer. Although anti-oxidation has historically been viewed as chemo-preventive, emerging evidence suggests that antioxidants can actually support neoplasia. We posit that this contention is rooted in the fact that reactive oxygen species (ROS) do not operate indiscriminately, but rather, function as selective, diverse secondary messengers with distinct functions. By functionally interrogating individual redox switches in PDA cells and the surrounding tumor microenvironment,  our laboratory aims to test the therapeutic principle that the specific redox dependencies of PDA cells can be exploited to target tumor cells while sparing normal tissues. 

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