Some of Jun Xia’s earliest research was on the molecular makeup of the whitefly, a little-used model organism. But to Xia, it wasn’t just a research tool relegated to the lab. In China, where Xia was born and earned his undergraduate degree, these winged creatures are highly invasive and devastate crops.
“It was exciting because I knew what was going on in an organism that a lot of other people didn’t have insight into,” he said.
Xia, now a postdoctoral student at Baylor College of Medicine, feels that same excitement in his current research. He is studying endogenous DNA damage, which occurs seemingly organically in DNA. It’s distinct from the kind caused by external risks such as smoking or UV radiation. Even though it’s common, endogenous damage hasn’t received much attention from the scientific community, Xia said.
Cancer’s ability to appear as if from nowhere took on a personal meaning when a seemingly healthy cancer researcher on Xia’s thesis committee developed soft tissue sarcoma. He died in 2017 at the age of 43. “I don’t know why it happened,” Xia said. “But it inspired me to want to understand cancer systematically and quickly.”
Xia’s mission is to figure out why cancer develops this way. Last year, he and his colleagues found a network of genes and proteins that could cause DNA damage in E. coli, a model bacterium. They also found homologs of the same molecules in humans. Identifying these molecules also means that scientists might be able to use them to detect cancer risk before an individual develops disease. Xia is now using mouse models to test that idea.
— Shraddha Chakradhar