I am a postdoctoral fellow in the Landau Lab at Weill Cornell Medicine and the New York Genome Center, where I develop single-cell technologies that link mutations and cell states.
I trained as a biomedical engineer. My doctoral work at Columbia used engineered materials to probe how mechanical cues shape T cell activation, which is where my interest in single-cell heterogeneity started.
Somatic mutations accumulate in every tissue as we age, and a key insight is how a genotype contributes to cell state and behavior. We built scG2P to co-capture somatic DNA mutations and mRNA transcripts from the same cell at scale. Applied to esophageal tissue from older adults, more than half of cells carried clonal driver mutations. In this mutation landscape, we revealed that NOTCH1- and TP53-mutant clones disproportionately occupy immature differentiation states, staying in the tissue and continuing to divide instead of maturing and shedding from the surface.
Clonal competition occurs in normal tissue over decades. Using large-scale single-cell phylogenetics, we reconstruct a timeline of when clones arose, which mutations initiated expansion and which genetic events follow, and how fast clones expanded, turning a static snapshot of mutations into a history of the tissue.
My doctoral work at Columbia asked how the physical properties of an antigen-presenting surface shape a T cell’s response. T cell activation turns out to be biphasic in substrate stiffness, and soft elastomer fiber scaffolds can expand T cells from patients whose cells expand poorly by conventional methods — a route to personalizing cell therapy manufacturing.
Cover image reproduced from Cancer Discovery 16(4), © American Association for Cancer Research. Artwork by Bianca Dunn.
Image: Weill Cornell Medicine Newsroom
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dyuan@nygenome.org
New York Genome Center, 101 Avenue of the Americas, New York, NY 10013
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