Linying Zhu, PhD

University of Chinese Academy of Sciences, PhD, Cell Biology

National Cancer Institute, NIH, Postdoctoral Fellow, Molecular Biology

Dr. Linying Zhu had robust training in molecular and cell biology in the PhD and postdoctoral studies. She had successfully improved the efficiency of hepatocyte lineage conversion from fibroblasts and applied these findings to cell therapy in patients. Inspired by the deep understanding of chromatin biology and genome biology, she developed a novel genome-wide method for detecting DNA supercoiling, providing new insights into how DNA topology influences transcriptional regulation. These experiences led her to focus on topoisomerases, the key players for maintaining DNA topology and great targets for cancer therapy. In collaboration with Dr. Yilun Sun, she had contributed to studies uncovering the repair mechanisms of topoisomerase-DNA protein crosslinks and their implications for genomic stability and cancer therapy. She also extended her research by exploring how HDAC inhibition can enhance immuotherapy responses in small-cell lung cancer by influencing tumor plasticity and immune microenvironment. Currently, she is leading a project to identify novel TOP3A inhibitors.

Cancer therapy, Topoisomerases, Supercoiling, DNA repair, Cell plasticity.

• Sun Y, Jenkins L, Touny L, Zhu L, et al. Flap endonuclease 1 repairs DNA-protein cross-links via ADP-ribosylation–dependent mechanisms. Sci. Adv. (2025).
• Ghafoor A*, Zhu L*, et al. HDAC inhibition unlocks tumor plasticity and enhances immunotherapy response in Myc- Driven Small Cell Lung Cancer. bioRxiv (2025)
• Yao Q,* Zhu L,* Shi Z, Banerjee S, Chen C. Topoisomerase-modulated genome-wide DNA supercoiling domains colocalize with nuclear compartments and regulate human gene expression. Nat Struct Mol Biol. (2025)
• Ma X*, Cao X*, Zhu L*, et al. Pre-existing chromatin accessibility of switchable repressive compartment delineates cell plasticity. National Science Review (2022)
• Ji S*, Zhu L*, Gao Y.  et al. Baf60b-mediated ATM-p53 activation blocks cell identity conversion by sensing chromatin opening. Cell Res (2017).