I am a first-year PhD student in the Genetics Department at Stanford University. My main interest is to use statistical and machine learning approaches to better understand complex traits in a human disease context. Broadly, I hope to use these results to identify elements of biological pathways that may be amenable to therapeutic intervention.
Download my CV.
M.Phil. in Biological Sciences, 2022
University of Cambridge | Wellcome Sanger Institute
B.S. in Genetics, 2021
North Carolina State University
B.S. in Computer Science, 2021
North Carolina State University
Thesis Title: Multi-omics Integration to Characterize Mechanisms of Molecular QTL from a Sepsis Cohort.
Over the course of 10 months, I worked to better understand the cis and trans regulatory architecture of gene and protein expression from the Genomic Advances in Sepsis (GAinS) cohort. I performed multiple analyses, including weighted correlation network analysis, colocalization of molecular QTL, fine mapping of QTL loci, and integration of cell-type-specific ATAC-seq peaks.
Thesis Title: Meta-Analysis of Expression Quantitative Trait Loci between Two Pre-Collaborative Cross Mouse Cohorts.
The broad theme of my work as an undergraduate was to use publicly-available gene expression data to combine knowledge across studies in large mouse populations and ask higher-order biological questions. Specifically, we analyzed genotype and gene expression data from genetic reference panels (GRPs) such as the Collaborative Cross and Diversity Outbred mouse populations.
Project Title: Deciphering Quantitative Phenotypes in Complex Diseases using Gene Co-Expression Modules
I spent two summers at the Jackson Laboratory studying the genetics of Late-Onset Alzheimer’s Disease (LOAD) in three human cohorts. We used gene co-expression modules to identify pathological axes of variation in gene expression. The modules were used to stratify patients and identify genetic modifiers of LOAD cases.
We used weighted correlation network analysis on bulk RNA-Seq data from three Late-Onset Alzheimer’s Disease (LOAD) human cohorts. From this analysis, we derived submodules of genes that represented biological pathways implicated in LOAD. We leveraged this analysis to subtype our patients and identify genetic loci that are associated with the stratified patients and submodules.