Presenter: Skylar Hartley
Authors: Skylar Hartley, Richard Warner, Saraswati Sukumar
Faculty Advisor: Doug Sainsbury
Institution: Dixie State University
Melanoma is a deadly skin cancer that begins in the melanocytes and has the ability to metastasize. Nearly 60% of melanomas contain a mutation in the BRAF gene—a proto-oncogene that controls cell growth. Dabrafenib, a BRAF inhibitor, is commonly used to treat BRAF mutated melanoma, but has a response rate of approximately 50%. It is often combined with other chemotherapies to increase the response rate through vertical inhibition. Rifapentine has shown promising results inhibiting the mTOR pathway in cells, an important pathway that regulates cell survival. A melanoma cell line derived from the lung of a fifty-year-old female, CACL, harbors a BRAFV600E mutation. Another melanoma cell line, SK-Mel-2, contains an activating NRAS mutation and was used as a control. We hypothesized that combining rifapentine and dabrafenib will produce a synergistic cytotoxic effect in CACL cells. This was tested using a PrestoBlue assay to determine the IC50 of dabrafenib and the IC50 of the drugs combined using CACL and SK-Mel-2 cells.