Member Biography

Steven Welc

Steven Welc, Ph.D.

635 Barnhill Drive
Indianapolis, IN 46202
Phone: (317) 274-7816

Research Program Membership

Associate member:

Dr. Welc's research interests include:

My research interests lie at the interface of muscle biology and immunology. I am primarily interested in the regulatory role of the immune system and its affects on muscle health, pathology and function. The relevance of my research to cancer biology is multi-faceted. 1) Most recently I have focused on the role of myeloid cells in the context of muscular dystrophy. Specifically, genetically modifying immune cells to express therapeutic transgenes and using infiltrating immune cells as vectors to target gene therapy to diseased muscle affecting stem cell proliferation and differentiation. In some cases I am modifying the expression of oncogenes like leukemia inhibitory factor (LIF) to treat muscular dystrophy, thus making tumor formation a possible unintentional negative outcome. I try to mitigate the likelihood of tumorigenesis with targeted promoters to limit these potential consequences. Furthermore, genetic mutations associated with muscular dystrophies (i.e. dystrophin deficiency) already present an increased risk of rhabdomyosarcoma. Thus, I am working to develop translational immunotherapeutics that affect stem cell differentiation making tumorigenesis a concern as an indirect negative consequence. 2) Sarcopenia or muscle wasting is highly prevalent in cancer. Cancer patients with sarcopenia have higher rates of many adverse outcomes including survival. Muscle-resident immune cells are gaining increasing recognition for their role in regulating muscle health beyond the contexts of trauma or disease. For example, I was a major contributor to a recent project demonstrating that aging of the immune system promotes sarcopenia. Our ability to study the role of immune cells in muscle is limited due to muscle being a heterogeneous tissue thus our interpretation of tissue level transcriptomics or epigenomics is limited by the integration of all cell types within the tissue sample. Alternatively, the dissociation of tissues to single cell suspensions for antibody labeling and cell sorting is an arduous process that removes cells from their native environment which can cause activation affecting the transcriptome. I am working with a mouse model to allow for the tagging of mRNA by Cre-expressing cells thus enabling in vivo transcriptomic analysis of Cre- expressing cells. Upon successful development of this mouse model I intend to use it as a tool allowing for us to assay changes to the transcriptome of myeloid lineage cells to begin to test the contributions of myeloid lineage cells to cancer cachexia. 3) Clinical observations suggest that chemotherapeutics result in increased prevalence of myocarditis an inflammatory cardiomyopathy. I have a growing interest in understanding the pathophysiology of chemotherapeutic induced cardiomyopathy and intend to pursue this as a new area of research.

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More Publications »

Ph.D. - University of Florida, Gaineville, FL 12/2012

Post-doctoral Fellowship - University of California LA, Los Angeles, CA 01/2019