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, but a mutation is only interesting if you can see what it does to the cell carrying it. Sequencing DNA and RNA from the same single cell has been the bottleneck. We built scG2P, which co-captures somatic DNA mutations and mRNA transcripts from the same cell at scale. Applied to esophageal tissue from older adults, more than half of over 10,000 cells carried clonal driver mutations, predominantly in NOTCH1 and TP53. NOTCH1-mutant clones disproportionately occupy immature differentiation states, staying in the tissue and continuing to divide instead of maturing and shedding from the surface.
Normal tissue is a competition between clones playing out over decades. Using large-scale single-cell phylogenetics, we reconstruct when clones arose, how fast they expanded, and which ones displaced their neighbors, 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.
Full list, newest first. Also on Google Scholar.
dyuan@nygenome.org
New York Genome Center, 101 Avenue of the Americas, New York, NY 10013
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