As part of the Content Development group in Research & Foundation, I perform a range of functions to support short- and long-term development of QIAGEN's products and assay technologies. Most of our work at the Frederick site is focused on targeted NGS applications for basic and translational research. I have contributed to assay panel design and data analysis specs for our QIAseq Targeted RNA (gene expression analysis by digital RNA-seq) and RNAscan fusion detection products, the QIAseq Immune Repertoire RNA kit, and other targeted sequencing applications currently in product development for future launch. I also perform market research and technology assessment to identify and prioritize long-term NGS development projects, and I support our more longstanding product lines such as PCR arrays, methylation, and ChIP-PCR assays by designing new disease- or pathway-focused panels, converting existing panels to cover new species, and working with customers to tailor semi/full custom assay panels for their research.

As a postdoc in Kent Hunter's lab, my project focused on using genetically engineered mouse models to investigate the role of the ARID4B gene in the metastatic progression of breast cancer. I identified several novel polymorphisms in the Arid4b C-terminal domain that modulate its binding to the mSIN3A chromatin remodeling complex, and found that high ARID4B expression in clinical specimens was predictive of a 2-fold increased risk of metastatic progression.

In 2004 I relocated with Dr. Greenberg's lab to FHCRC, where I continued my graduate thesis project investigating the role of FGF signaling in prostate cancer angiogenesis.

As a graduate student in the lab of Dr. Norman Greenberg, I investigated the role of FGF signaling in prostate cancer progression, with a specific focus on angiogenesis. I developed a novel method to quantitate vascular volume based on 3D confocal microscopy of tumors that were fluorescently labeled in vivo. By applying that technique to a genetically engineered mouse model expressing an inducible FGFR1 in the prostate, I was able to quantitatively image the earliest stages of angiogenesis. I used microarray analysis of induced tumors, as well as cell-based reporter assays, to identify a novel signaling pathway whereby FGFR1 activation results in differential regulation of Ang-1 and Ang-2.

In the lab of Dr. David Clemmons (Division of Endocrinology) I maintained cell lines expressing IGF binding proteins, collected conditioned media and purified IGFBPs using column chromatography, generated rabbit polyclonal antibodies, and performed radioimmunoassays to analyze levels of IGFBPs in patients with Type I diabetes. I also performed chromatography and protease assays to isolate IGFBP-specific protease activity, which enabled the identification of complement components C1r and C1s as endogenous IGFBP5 proteases.