Cynthia J. Burrows

University of Utah

Election Year: 2014
Primary Section: 14, Chemistry
Membership Type: Member


Cynthia Burrows is Distinguished Professor of Chemistry and Thatcher Presidential Endowed Chair of Biological Chemistry at the University of Utah. She is a recognized expert in the chemistry of DNA damage, particularly chemical modifications related to oxidative stress occurring on guanine, one of the bases of DNA and RNA. She identified hyperoxidized structures in DNA and elucidated their effects on DNA structure and biochemistry. Burrows was born in St. Paul, Minnesota, in 1953, and she grew up there and later in Boulder, Colorado. She received a BA degree in 1975 from the University of Colorado, Boulder, and then studied physical organic chemistry at Cornell University, obtaining a PhD in Chemistry in 1982. From 1981-83, she was an NSF-CNRS postdoctoral fellow at Université Louis Pasteur in Strasbourg, France. She then held faculty appointments at the University of Stony Brook, NY (1983-1995) and at the University of Utah (1995-present). Burrows has served as Senior Editor of the Journal of Organic Chemistry (2001-2013) and since 2014 as Editor-in-Chief of Accounts of Chemical Research.

Research Interests

Cynthia Burrows leads a research team investigating the chemical structures and mechanisms by which DNA and RNA bases, notably guanine, undergo transformations under conditions of oxidative stress. These studies underlie the biology of age-related disorders such as cancer. Inflammation, metabolism and radiation generate reactive oxygen species that alter the structure of guanine in such a way as to affect the integrity of the genome, leading to mutations in DNA and to changes in both duplex and quadruplex folding patterns. The Burrows laboratory uses the tools of organic chemistry to synthesize and characterize site-specifically modified DNA and RNA strands, allowing the study of proteins that interact with modified bases such as those involved in replication, transcription and repair. Notably, Burrows and coworkers identified hyperoxidized hydantoin lesions in DNA that are highly mutagenic and appear to play significant roles in signaling for DNA repair. Nanopore technology employed by the group has moved this field forward by providing a single-molecule method of analyzing the effects of base damage on DNA folding and opens the door to single-molecule sequencing of DNA modifications.

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