Research: FLEX Fund Research Scholars

This annual award supports a scientist at the post-doctoral level.

2011-2013: Gregory J. Block M.Sc., Ph.D. (see Miller Lab)

Study: "Mechanism of Wnt Signaling in Facioscapulohumeral Muscular Dystrophy," mentoring researcher — Daniel Miller. Total award $100,000 for 2-year fellowship began April 15, 2011 and will terminate April 14, 2013.

Gregory Block

I hail from the Great White North, a product of the University of Toronto biochemistry machine. There, I obtained my Honours (with a 'U') Bachelor of Science in Human Biology, and a Masters in Biochemistry.

My masters thesis focused on understanding the contribution of a proteinaceous substructure within the nucleus, called the PML body, to transcriptional regulation. The Bazett-Jones Lab planted the seed for what would become a long-term fascination with the little blue dot found at the center of a cell.

I did my Ph.D at Tulane University in New Orleans, under the supervision of Darwin Prockop. Two thirds of the way into my degree our lab nucleated the Texas A&M Institute for Regenerative Medicine. My work in the Prockop lab was devoted to understanding the mechanisms by which stromal cells isolated and expanded from the bone marrow (MSCs) contribute to tissue repair. I identified a molecule that was secreted by the MSCs, called Stanniocalcin-1 (STC1), that reduced cell death in injured cells. During my tenure in the lab, I described how STC1 acted as a anti-apoptotic protein, how the molecule regulated calcium signaling immediately after injury, and how STC1 facilitated its anti-apoptotic effects.

I joined the Miller lab in June 2009 with the goal of combining my interests in nuclear organization with cell therapy and stem cells. My goal is to develop creative assays to understand the pathogenesis of Facioscapulohumoral Muscular Dystrophy, a disease of a peculiar genetic lesion that has defied explanation for nearly 20 years.

2010-2012: Barbara D. Page, Ph.D. (see Tapscott Lab)

Study: "Using model organisms to identify new therapies and understand the pathogenesis of Facioscapulohumeral Muscular Dystrophy," mentoring researcher — Stephen Tapscott. Total award $100,000 for 2-year fellowship began Nov. 1, 2010 and terminates Oct. 31, 2012.

Barbara Page

I am honored to be an FSH Scholar. Previously, I obtained my Ph.D. in Dr. Michael Snyder’s laboratory at Yale University while studying how chromosomes segregate using yeast as a model organism. For my postdoctoral fellowship in the laboratory of Dr. James Priess at the Fred Hutchinson Cancer Research Center (FHCRC), I wanted to continue to use the elegant tools of genetics, but apply them to a new biological question. Using a tiny worm known as Caenorhabditis elegans, I studied how cell fate decisions are made during development.

My research as an FSH Scholar in Dr. Stephen Tapscott’s laboratory at the FHCRC focuses on using these two different model organisms to better understand facioscapulohumeral muscular dystrophy (FSHD) and develop new therapies to treat patients with this disease. Recent experiments suggest that FSHD may be caused in part by the inappropriate expression of a gene known as DUX4. Thus, a possible line of therapy for patients with FSHD would be the use of drugs that could reestablish silencing of the DUX4 gene. My first project uses the yeast Schizosaccharomyces pombe to screen for small molecules that can increase gene silencing. My second project involves trying to better understand how genes like DUX4 normally function. We have discovered a DUX4-like gene in the model organism C. elegans, which we have named dux-1. Using the powerful genetic tools of this organism, we hope to establish C. elegans as a model system for FSHD in order to better understand the regulation of DUX4 and its possible normal role in development. These two 'high risk/high reward' projects have the potential to rapidly identify new compounds and targets for therapy for patients with FSHD.

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