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Amy Brock

Amy Brock

· Associate Professor Biomedical Engineering

University of Texas at Austin · Biomedical Engineering

Active 1984–2024

h-index27
Citations4.8k
Papers10753 last 5y
Funding$7.4M2 active
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About

Amy Brock is an Associate Professor in the Department of Biomedical Engineering at The University of Texas at Austin. She received her Ph.D. in Biomedical and Biological Sciences from Harvard University and holds a B.S. in Biology from the Massachusetts Institute of Technology. Brock carried out postdoctoral work at Boston Children’s Hospital and the Wyss Institute for Biologically Inspired Engineering at Harvard before joining UT Austin in 2013. Her research interests include cancer systems biology, heterogeneity and cell state plasticity, models of cancer progression, and response to therapy. She is the Raymond F. Dawson Centennial Teaching Fellowship in Engineering and is associated with the Brock Lab and the Center for Computational Oncology. Outside of her academic pursuits, she enjoys sailing on Lake Travis with her family, gardening, playing board games, and spending time with her five children.

Research topics

  • Biology
  • Genetics
  • Biochemistry
  • Evolutionary biology
  • Endocrinology
  • Cell biology
  • Neuroscience
  • Cancer research
  • Computational biology
  • Pathology
  • Chemistry

Selected publications

  • Multifunctional barcoding with ClonMapper enables high-resolution study of clonal dynamics during tumor evolution and treatment

    Nature Cancer · 2021 · 109 citations

    Senior authorCorresponding
    • Biology
    • Computational biology
    • Evolutionary biology
  • A hybrid model of tumor growth and angiogenesis: In silico experiments

    PLoS ONE · 2020 · 74 citations

    • Cell biology
    • Biology
    • Cancer research

    Tumor associated angiogenesis is the development of new blood vessels in response to proteins secreted by tumor cells. These new blood vessels allow tumors to continue to grow beyond what the pre-existing vasculature could support. Here, we construct a mathematical model to simulate tumor angiogenesis by considering each endothelial cell as an agent, and allowing the vascular endothelial growth factor (VEGF) and nutrient fields to impact the dynamics and phenotypic transitions of each tumor and endothelial cell. The phenotypes of the endothelial cells (i.e., tip, stalk, and phalanx cells) are selected by the local VEGF field, and govern the migration and growth of vessel sprouts at the cellular level. Over time, these vessels grow and migrate to the tumor, forming anastomotic loops to supply nutrients, while interacting with the tumor through mechanical forces and the consumption of VEGF. The model is able to capture collapsing and breaking of vessels caused by tumor-endothelial cell interactions. This is accomplished through modeling the physical interaction between the vasculature and the tumor, resulting in vessel occlusion and tumor heterogeneity over time due to the stages of response in angiogenesis. Key parameters are identified through a sensitivity analysis based on the Sobol method, establishing which parameters should be the focus of subsequent experimental efforts. During the avascular phase (i.e., before angiogenesis is triggered), the nutrient consumption rate, followed by the rate of nutrient diffusion, yield the greatest influence on the number and distribution of tumor cells. Similarly, the consumption and diffusion of VEGF yield the greatest influence on the endothelial and tumor cell numbers during angiogenesis. In summary, we present a hybrid mathematical approach that characterizes vascular changes via an agent-based model, while treating nutrient and VEGF changes through a continuum model. The model describes the physical interaction between a tumor and the surrounding blood vessels, explicitly allowing the forces of the growing tumor to influence the nutrient delivery of the vasculature.

  • Single cell transcriptome profiling of the human alcohol-dependent brain

    Human Molecular Genetics · 2020 · 127 citations

    • Biology
    • Genetics
    • Neuroscience

    Alcoholism remains a prevalent health concern throughout the world. Previous studies have identified transcriptomic patterns in the brain associated with alcohol dependence in both humans and animal models. But none of these studies have systematically investigated expression within the unique cell types present in the brain. We utilized single nucleus RNA sequencing (snRNA-seq) to examine the transcriptomes of over 16 000 nuclei isolated from the prefrontal cortex of alcoholic and control individuals. Each nucleus was assigned to one of seven major cell types by unsupervised clustering. Cell type enrichment patterns varied greatly among neuroinflammatory-related genes, which are known to play roles in alcohol dependence and neurodegeneration. Differential expression analysis identified cell type-specific genes with altered expression in alcoholics. The largest number of differentially expressed genes (DEGs), including both protein-coding and non-coding, were detected in astrocytes, oligodendrocytes and microglia. To our knowledge, this is the first single cell transcriptome analysis of alcohol-associated gene expression in any species and the first such analysis in humans for any addictive substance. These findings greatly advance the understanding of transcriptomic changes in the brain of alcohol-dependent individuals.

Recent grants

Frequent coauthors

  • Thomas E. Yankeelov

    The University of Texas at Austin

    74 shared
  • Donald E. Ingber

    Boston Children's Hospital

    35 shared
  • David A. Hormuth

    Livestrong Foundation

    24 shared
  • Silva Krause

    22 shared
  • Kaitlyn E. Johnson

    The University of Texas at Austin

    21 shared
  • Angela M. Jarrett

    The University of Texas at Austin

    20 shared
  • Grant Howard

    The University of Texas at Austin

    18 shared
  • Andrea Gardner

    The University of Texas at Austin

    17 shared

Awards & honors

  • Raymond F. Dawson Centennial Teaching Fellowship in Engineer…

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