Nicole Rusk

The paper analyzes the evolutionary trajectories of high-level copy-number amplifications in cancer cell genomes to distinguish between extrachromosomal and intrachromosomal amplification mechanisms.

This study tracks clonal evolution of drug resistance in ovarian cancer using structural variants in cfDNA, finding polyclonal resistance with dominant high-fitness clones and genomic features linked to drug resistance.

The paper quantifies viral mimicry in genomes across species and shows how repetitive elements maintain pathogen-like features under selection.

This study shows that ongoing whole-genome doubling in ovarian cancer promotes cell diversity and immune dysregulation through chromosomal instability and quiescent states.

This study identifies MAPK activation and cellular plasticity as complementary resistance mechanisms to EGFR TKI in lung adenocarcinoma using single-nuclei RNA sequencing and clinical data.

The paper identifies impaired T cell priming and KLF2-dependent quiescence in gastric cancer draining lymph nodes as mechanisms limiting immune responses.

The paper introduces a scalable Bayesian method for phylogenetic tree inference from single-cell whole genome sequencing data, demonstrating its application on three datasets.

GeneVector uses mutual information-based dimensionality reduction to identify transcriptional programs and classify cell types across single-cell RNA-seq datasets.

This paper introduces TCRi, an information theoretic framework to analyze TCR and gene expression data from cancer patients, showing improved characterization of clonotypes and their phenotypic changes post-therapy.

This paper introduces a pooled sequencing strategy to address intratumoral genetic heterogeneity in cancer, showing it improves mutation detection and risk stratification while reducing costs.