Bio


I am from State College, Pennsylvania and earned a BS with Honors in Microbiology from Penn State in 2020. I moved west to complete my PhD in Biomedical Sciences at UCSF between 2020 and 2026 in the lab of Ross Okimoto, where I modeled ultra-rare sarcomas driven by fusion oncogenes. I am currently a Schmidt Science Fellow in Jenn Brophy's lab where I am learning synthetic biology in the context of yeast and plants with the goal of rewiring gene expression to shape development.

Honors & Awards


  • Schmidt Science Fellow, Schmidt Sciences (2026-Present)
  • Ruth L. Kirschstein NRSA F31 Fellow, National Cancer Institute, NIH (2024-2026)

Professional Education


  • PhD, University of California, San Francisco, Biomedical Sciences (2026)
  • BS (Honors), The Pennsylvania State University, Microbiology (2020)

Current Research and Scholarly Interests


I am a primarily lab-based (but computationally competent) biologist with a broad interest in understanding both how cells evolve to cause disease and how we might leverage similar strategies to engineer new behaviors into organisms. I enjoy doing science in diverse research areas (previously including malaria, chromatin remodeling in yeast, and several types of cancer), and I am excited to continue this trend by building synthetic biology tools for deployment in plants as a postdoc.

All Publications


  • Osteosarcoma PDX-Derived Cell Line Models for Preclinical Drug Evaluation Demonstrate Metastasis Inhibition by Dinaciclib through a Genome-Targeted Approach. Clinical cancer research : an official journal of the American Association for Cancer Research Schott, C. R., Koehne, A. L., Sayles, L. C., Young, E. P., Luck, C., Yu, K., Lee, A. G., Breese, M. R., Leung, S. G., Xu, H., Shah, A. T., Liu, H. Y., Spillinger, A., Behroozfard, I. H., Marini, K. D., Dinh, P. T., Pons Ventura, M. V., Vanderboon, E. N., Hazard, F. K., Cho, S. J., Avedian, R. S., Mohler, D. G., Zimel, M., Wustrack, R., Curtis, C., Sirota, M., Sweet-Cordero, E. A. 2023: OF1-OF16

    Abstract

    Models to study metastatic disease in rare cancers are needed to advance preclinical therapeutics and to gain insight into disease biology. Osteosarcoma is a rare cancer with a complex genomic landscape in which outcomes for patients with metastatic disease are poor. As osteosarcoma genomes are highly heterogeneous, multiple models are needed to fully elucidate key aspects of disease biology and to recapitulate clinically relevant phenotypes.Matched patient samples, patient-derived xenografts (PDX), and PDX-derived cell lines were comprehensively evaluated using whole-genome sequencing and RNA sequencing. The in vivo metastatic phenotype of the PDX-derived cell lines was characterized in both an intravenous and an orthotopic murine model. As a proof-of-concept study, we tested the preclinical effectiveness of a cyclin-dependent kinase inhibitor on the growth of metastatic tumors in an orthotopic amputation model.PDXs and PDX-derived cell lines largely maintained the expression profiles of the patient from which they were derived despite the emergence of whole-genome duplication in a subset of cell lines. The cell lines were heterogeneous in their metastatic capacity, and heterogeneous tissue tropism was observed in both intravenous and orthotopic models. Single-agent dinaciclib was effective at dramatically reducing the metastatic burden.The variation in metastasis predilection sites between osteosarcoma PDX-derived cell lines demonstrates their ability to recapitulate the spectrum of the disease observed in patients. We describe here a panel of new osteosarcoma PDX-derived cell lines that we believe will be of wide use to the osteosarcoma research community.

    View details for DOI 10.1158/1078-0432.CCR-23-0873

    View details for PubMedID 37703185