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GEN’s editor in chief, John Sterling, interviews life science academic and biotech industry leaders on important research, technology, and trends. These podcasts will keep you informed with all the important details you need.
The growth of cancerous tumors is fueled, at least in part, by the buildup of free radicals. Thus it makes sense that cancer should respond to treatment with antioxidants, which inhibit the rogue radicals, or with pro-oxidants, which go the opposite direction, increasing oxidative stress on cancer cells to the point of vanquishing them.
Being able to monitor a marker of oxidative stress that is associated with the activation of tumor cell growth pathways, particularly at an early stage, and then tailor treatments accordingly should allow for more targeted studies and might improve the odds of success with antioxidants and pro-oxidants.
Now, researchers at the University of Michigan report in the September 22 issue of PNAS that they have developed such a monitoring system.
During this week's podcast Dr. Kate Carroll talks about why the treatment of cancer with antioxidants and pro-oxidants has so far met with limited success. She describes the development of a promising method of monitoring oxidative stress in cancer cells that depends on detecting sulfenic acid in proteins. Dr. Carroll goes on to discuss how a sulfenic-acid patient profile can be used in cancer therapy.
She also lists the kinds of cancer that might be susceptible to sulfenic acid detection and offers insights on her team's next stage of research designed to move this work forward.
Kate Carroll was born in Morgan Hill, California on March 16, 1974. From 1992-1996 she attended Mills College in Oakland, California were she majored in Biochemistry and carried our undergraduate research on prokaryotic transcription with Mike Chamberlin at the University of California, Berkeley. In 1997 Carroll moved to Palo Alto to attend graduate school at Stanford University. Here she joined Suzanne Pfeffer's laboratory as an American Heart Association Fellow and received her doctorate in 2003 for research on the mechanism of intracellular protein transport. Carroll's results were published in Science and provided the first molecular details for how protein transport machineries recognize their cargo-receptors. Carroll then joined Carolyn Bertozzi's laboratory as a Damon Runyon Postdoctoral Fellow at the University of California, Berkeley where she developed chemical methods to study bacterial sulfur metabolism and dissected the mechanism of catalysis by the enzyme APS reductase. In these studies, Carroll uncovered a new protein drug target against latent tuberculosis infection. In 2006 she joined the Chemistry Department and the Life Sciences Institute at the University of Michigan where she is currently an assistant professor. Prof. Carroll’s research interests span the disciplines of chemistry and biology with an emphasis on studies of sulfur metabolism pertinent to disease states. Her lab focuses on the development of novel tools to study of post-translational modification of cysteine residues, profiling changes in protein oxidation associated with cancer and neurodegeneration, and exploiting this information for development of diagnostic and therapeutic approaches. In addition, her group investigates sulfur pathways that are essential for infection and long-term survival of pathogens such as Mycobacterium tuberculosis. Kate Carroll has received a Scientist Development Award from the American Heart Association (2008), a Special Fellow Award from the Leukemia and Lymphoma Society (2006) and a Research Scholar Award from the University of Michigan (2006).