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Cancer kills nearly 700 thousand people each year in the United States, making the discovery of novel therapeutic targets an urgent need. The c-MYC gene is a cancer-driving gene that is commonly found to be overabundant in tumors. Relevant to the research in our lab, the c-MYC gene promoter sequence is highly enriched with guanines (G’s). G-rich DNA or RNA sequences can form “knot-like” structures termed G-quadruplexes that act as regulatory checkpoints for transcription. For transcription to proceed, the G-quadruplex must be untied. The cell contains enzymes that unwind G-quadruplexes. The major enzyme responsible for untying G-quadruplexes is Dhx36. Dhx36 is overabundant in most cancers and increases c-MYC expression. For this study, I will determine if overexpression of Dhx36 initiates tumorigenesis and/or increases the progression of established tumors. I hypothesize that Dhx36 overexpression will initiate tumorigenesis and accelerate tumor growth. I will test this hypothesis using novel transgenic mouse tumor models. c-MYC expression levels will be assessed using qRT-PCR and RNA sequencing technologies. I expect completion of this work will contribute to the basic understanding of cancer pathogenesis and begin to establish Dhx36 as a novel therapeutic target.

Credits: Taylor Karns, Tyler Osborne, Michael Reisinger, Siara Sandwith, Philip Smaldino Ph.D.

Faculty Mentor: Dr. Phil Smaldino

Department of Biology

Graduate