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INFORMATION FOR

    Kathryn Miller-Jensen, PhD

    Professor
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    Professor

    Biography

    Dr. Miller-Jensen is working on systems-scale approaches to study immune cell heterogeneity with a focus macrophage innate immune cells. Macrophages are critical for healthy tissue function and are also an important emerging target for cancer immunotherapy. Other areas of interest include the role of cell-to-cell heterogeneity in latent HIV infection in T cells.

    Departments & Organizations

    Education & Training

    PhD
    MIT, Chemical Engineering

    Research

    Overview

    Dr. Miller-Jensen's research program focuses on a quantitative, systems biology approach to studying changes in intracellular signaling, particularly after viral infection. Her laboratory has a significant focus on HIV infection and viral latency, which is a very important indirect human carcinogen. In addition, they have several ongoing efforts that are relevant to other aspects of cancer research. First, they use experimental models of latent HIV infection to study the dynamics and heterogeneity of transcriptional activation in different chromatin environments (see Miller- Jensen et al., Integrative Biology, 2012). The primary application of this work is to design therapeutic strategies to activate and treat latent HIV, which could have a dramatic impact on cancer incidence in this population. The findings are also useful for understanding chromatin-mediated heterogeneity in cancer (see Miller-Jensen et al, Trends in Biotechnology, 2011). Dr. Jensen also has an NCI U01 contract grant in collaboration with Prof. Rong Fan in the Dept. of Biomedical Engineering at Yale to develop a micro-chip device to detect cytokine and phosphorylation signatures in single cells. They will apply this technology to measure heterogeneity in cancer cell lines and primary tumor samples, as well as following viral infection. Finally, the Miller-Jensen Lab is collaborating with Prof. Paul Turner of Yale Ecology and Evolutionary Biology to study how strains of vesicular stomatitis virus (VSV) that were evolved on different host cell lines differentially activate the cellular innate immune response in different cell lines. They are particularly interested in the response of cancer cell lines with impaired innate immune signaling, and plan to build predictive models of signaling and apoptosis analogous to previous work Dr. Miller-Jensen published on adenoviral vector-mediated apoptosis in cancer cell lines (see Miller-Jensen et al, Nature, 2007). One potential application of this work is to design more effective VSV-based oncolytic vectors.

    Specialized terms: Systems biology, signal transduction, virus-host interactions

    Medical Research Interests

    Biomedical Engineering

    Research at a Glance

    Yale Co-Authors

    Frequent collaborators of Kathryn Miller-Jensen's published research.

    Publications

    2024

    2023

    2022

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