I am interested in understanding how genomic sequence dictates gene expression and how this process goes awry in cancer. My work focuses the ETS family of human transcription factors. 50-70% of all prostate cancers harbor a chromosomal rearrangement that results in the over-expression of one of four ETS genes (ERG, ETV1, ETV4, or ETV5). This aberrant ETS gene expression causes increased migration and extracellular matrix invasion of prostate cells and results in cellular transformation when paired with other mutations common to prostate cancer (PTEN deletion, AR over-expression). However, not all ETS genes promote prostate cancer. Fourteen ETS genes are expressed at moderate to high levels in the normal adult prostate, and at least two of these (EHF and SPDEF) can act as tumor suppressors in prostate cells. My lab utilizes a multi-disciplinary approach to study ETS protein function in an effort to identify mechanisms specific to the oncogenic ETS proteins. In particular, we use genomic localization techniques such as ChIP-seq to identify specific genomic targeting mechanisms. These mechanisms are then studied in detail using in vitro biochemical assays and tested for biological relevance using cell-based assays. In the future we hope that this work will provide targets for the development of drugs that specifically target oncogenic ETS function.
Post-doctoral Fellowship - University of Utah, Salt Lake City, UT 2009
Ph.D. - University of Wisconsin, Madison, WI 2002
