Chuan He Named a Winner of 2017 Paul Marks Prize for Cancer Research

Chuan He, a CR-PSOC investigator, was one of three recipients of the 2017 Paul Marks Prize for Cancer Research. The award, given by Memorial Sloan Kettering (MSK), recognizes promising investigators aged 45 or younger at the time of nomination for their efforts in advancing cancer research.  He will receive an award of $50,000 and give a scientific presentation at a symposium held at MSK.


Dr. He is the John T. Wilson Distinguished Service Professor in Chemistry, Biochemistry, and Molecular Biology at the University of Chicago; director of U of C’s Institute for Biophysical Dynamics; and a Howard Hughes Medical Institute (HHMI) investigator. He is also director of the Synthetic and Functional Biomolecules Center at Peking University in China.

He is an expert in the field of cancer epigenetics and RNA modification biology. Epigenetics involves variations in the way that genes are expressed that don’t affect the actual DNA sequence. “The human genome contains 3 billion base pairs but only roughly 20,000 genes,” he says. “We have tens of trillions of cells, and about 200 different tissue or cell types. Epigenetics facilitates cell differentiation into different identities, despite having the same genetic sequence in an individual human being.”

His major contribution to the field is that he was the first to put forward the idea that modifications to RNA are reversible and can control gene expression. Control of RNA, the molecule that carries DNA’s “message” to the protein-making machinery of the cell, is one of the major ways that affects the outcomes of gene expression.

“When I started this work back in 2008 and 2009, we knew that proteins called writers could install modifications to RNA molecules that altered their function, but no one knew that there were also proteins called erasers that could undo these changes,” Dr. He explains. His team went on to identify for the first time the eraser proteins, and in later work characterized a series of reader proteins that explain how RNA methylation functioned.

“This research laid down the mechanistic pathways for our current understanding of how these modifications impact biological outcomes, including those related to cancer,” he says. “Cancer and other diseases can hijack aberrant RNA methylation to gain a survival advantage, allowing cells to proliferate and grow out of control.”

These types of RNA changes are known to play a role in many types of cancer, including endometrial cancer, acute myelogenous leukemia, and glioblastoma. Dr. He’s work forms some of the foundations for developing potential future therapies that target RNA methylation effectors against human cancer.

He earned his doctorate in chemistry from MIT.

Original article posted on the Memorial Sloan Kettering Cancer Center blog. Written by Julie Grisham.