October 20, 2025
At The University of Kansas Cancer Center, the next generation of cancer researchers is gaining hands-on experience and mentorship as trainee members. This initiative provides graduate students and postdoctoral fellows with valuable opportunities for professional development.
In this trainee spotlight, we introduce Aninda Dey, PhD, a postdoctoral fellow whose curiosity about the molecular mechanisms driving cancer has led him to investigate the role of oxidative stress in its development. In the Q&A, Dr. Dey shares what inspired his career path, his current research focus and how being a cancer center trainee member has supported his growth as a scientist.
What inspired you to pursue a career in cancer research?
In high school, I was deeply intrigued by nucleic acid structures, genetic code, and various molecular mechanisms. I often wondered how such intricate processes could work so perfectly. Even now, observing the symmetry of DNA or the semiconservative mode of replication, I see a remarkably ordered and functional system within the microscopic world. For me, the central question always has been: how can such precise rules operate within the chaos? I felt there must be fundamental principles underlying it all, and this curiosity inspired me to study biochemistry and molecular biology.
For my graduate research work, I was motivated by a broader question: what are the most crucial challenges that will shape the future of human health, such as cancer? I wanted to contribute to research and generate new data that could make a real difference. I feel fortunate to have the opportunity to work in cancer research during my graduate and postdoctoral training.
Tell us about your research.
During my PhD, I studied a group of proteins called TET, which help DNA demethylation, which in turn regulate how genes are turned on and off. My dissertation focused on how these proteins remove certain chemical marks (methyl group) from DNA.
In my current postdoctoral research, I study oxidative DNA damage, which happens when cells produce too many reactive oxygen species (ROS), which damages DNA. ROS can come from normal metabolic processes, environmental toxins, or radiation. When ROS react with DNA, they can produce DNA lesions, or changes such as base alterations (8-oxo-guanine), strand breaks, and cross-linking. If these are not corrected, it can result in mutations and genomic instability which are linked to cancer.
My first project under the mentorship of Dr. Ryan Barnes is to develop a new tool that allows us to study one of these common oxidative DNA damage markers, called 8-oxo-guanine, across the entire genome. Eventually, I plan to use the tool to study how TET might also help repair DNA damage.
Which aspects of the trainee membership benefits are most valuable to you in advancing your career in cancer research?
Trainee membership has offered many valuable opportunities. My PhD work primarily centered on enzyme biochemistry, studying how enzymes function. During my postdoctoral training under Dr. Ryan Barnes, I have been learning cell biology techniques, such as immunofluorescence microscopy. Combining my background in biochemistry with these new skills in cell biology is helping me grow into an independent researcher.
Are there specific milestones or achievements you hope to reach in the coming years?
My long-term goal is to become an independent researcher after completion of my postdoctoral training.
In addition to publishing scientific research, securing funding represents a milestone for any cancer researcher. This year, I received the Biomedical Research Training Fellowship from the University of Kansas Medical Center, and my next goal is to obtain an external fellowship, such as one offered by the American Cancer Society.