Chuan He, PhD

Bio

Dr. Chuan He is the John T. Wilson Distinguished Service Professor in the Department of Chemistry and Department of Biochemistry and Molecular Biology at the University of Chicago. He received his bachelor of science degree in 1994 from the University of Science and Technology of China and his Ph.D. in chemistry from the Massachusetts Institute of Technology in 2000. After training as a Damon-Runyon postdoctoral fellow at Harvard University, he joined the University of Chicago as an assistant professor, rising to associate professor in 2008 and full professor in 2010. He was selected as an investigator of the Howard Hughes Medical Institute in 2013.

 

Dr. He’s research spans a broad range of fields including chemical biology, RNA biology, epigenetics, biochemistry, and genomics. His recent research concerns reversible RNA and DNA methylation in biological regulation. In 2011, his group discovered reversible RNA methylation as a new mechanism of gene expression regulation. His laboratory characterized several key reader proteins that bind preferentially to m6A-modified RNA and regulate their stability and translation. In 2020, Dr. He’s laboratory reported prevalent m6A methylation on chromatin-associated regulatory RNAs (carRNAs), which regulates chromatin state and global transcription.

 

He is the winner of the 2017 Paul Marks Prize in Cancer Research, 2023 Wolf Prize in Chemistry, and 2023 Falling Walls Science Breakthrough of the Year, Life Sciences.

Refolding and Reactivation of Mutant p53 in Breast Cancer Therapy

The p53 protein acts as one of the body’s most important defenses against cancer, helping damaged cells repair themselves or die before they become tumors. In up to 80% of triple-negative breast cancers (TNBC), p53 is mutated, preventing it from doing its job and allowing cancer to grow more aggressively. These mutations are associated with poorer outcomes, and there are currently no approved therapies that directly target many of them.

 

This research is developing a new class of small molecules designed to restore mutant p53 to its healthy shape, effectively turning the protein back “on” so it can once again suppress tumor growth. Early laboratory studies have shown that this approach can reactivate one of the most common p53 mutations found in triple-negative breast cancer, causing cancer cells to die while largely sparing healthy cells.

 

This innovative strategy could lead to a first-of-its-kind targeted treatment for patients with aggressive breast cancers driven by p53 mutations, offering new hope where few treatment options currently exist.

Chuan He, PhD

University of Chicago

News & Articles

3 Chicago Hospitals Team Up to Fight Breast Cancer in New Clinical Trial

Top Chicago Hospitals Join Forces in the Chicago Breast Cancer Research Consortium

Three Chicago Hospitals Collaborate on Breast Cancer Clinical Trial

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