About
Hi! I'm a computational biologist. In broad terms, I'm interested in how cells turn genes on and off at the right time and place in development, and where this goes wrong in disease. More precisely, I use integrative computational analyses of multi-modal genomics data together with deep learning to understand how transcription factors shape cell identity during development and disease, with particular interest in how transcription factor binding sites are organized in regulatory elements in the genome. Since 2023, I've been a postdoctoral scientist jointly in Anshul Kundaje's and Will Greenleaf's labs in the Department of Genetics at Stanford. At Stanford, I've been puzzling over how to use sequence-to-function deep learning models to understand mechanisms of gene regulation in human cell types.
Between 2018 and 2023, I did my PhD with Claudia Kleinman in the Quantitative Life Sciences program at McGill University in Montreal, Canada, focusing on data-driven approaches to identify cell-of-origin in pediatric brain tumors. Before that, I studied Computer Science and Biology at McGill. I care about computational biology that emphasizes reproducibility, transparency, and re-use.
Publications
* co-first author ^ co-corresponding author
Sensitive, direct detection of non-coding off-target base editor unwinding and editing in primary cells
We present a new assay, beCasKAS, to sensitively detect off-target edits from CRISPR base editors, and show how non-coding off-target genome edits can be triaged for epigenetic dysregulation in silico using deep learning.
A unified lexicon of predictive DNA sequence motifs from ENCODE transcription factor binding and chromatin accessibility assays
FOXR2 targets LHX6+/DLX+ neural lineages to drive CNS neuroblastoma
We analyzed single-cell profiles of the developing brain together with molecular profiles from patient samplesto nominate cell-of-origin, which enabled rationally guided mouse modeling of FOXR2-activated CNS neuroblastoma, a rare pediatric brain tumor subtype
TULIPs decorate the three-dimensional genome of PFA ependymoma
K27M in canonical and noncanonical H3 variants occurs in distinct oligodendroglial cell lineages in brain midline gliomas
Using single-cell and bulk transcriptomics and epigenomics, we provide molecular evidence that deadly childhood gliomas with K27M mutations in different Histone 3 variants arise from distinct anatomical domains in the developing brain
Histone H3.3G34-Mutant Interneuron Progenitors Co-opt PDGFRA for Gliomagenesis
We show that despite being histologically considered gliomas, a subtype of Histone 3 mutant childhood brain tumors likely arise in the interneuron lineage in the developing telencephalon; and that these tumors co-opt the PDGFRA oncogene to drive tumorigenesis
Healthcare for All!: Access to healthcare for migrants with precarious status in the Parc-Extension neighbourhood of Montreal, Quebec
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