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Address: 2-551 BSB
Phone: (319) 335-7663
Mentor: Dawn Quelle, PhD
Undergraduate Institution: University of Oklahoma, BS
Year Entered Into Program: 2007 (MSTP) 2009 (PhD Program)
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy that has a late diagnosis and is highly resistant to many treatments. For these reasons, PDAC is the fourth leading cause of cancer deaths in the United States. My research is focused on understanding the genetic alterations and protein modifications of the ARF-p53 tumor suppressor pathway and other growth suppressive pathways in the development of PDAC. I am specifically interested in characterizing a novel growth inhibitor, NIAM (Nuclear Interactor of ARF and MDM2), which has been shown in our lab to enhance ARF and p53 activity. Preliminary studies suggest NIAM also has anticancer activities apart from the ARF-p53 pathway that include sustaining genomic stability, suppressing proliferation, and sensitizing human pancreatic cancer cell lines to the DNA damaging agent, doxorubicin. My studies will 1) test the hypothesis that NIAM is inactivated in advanced human PDAC, 2) determine how altered NIAM expression affects the tumorigenic properties of PDAC cell lines, and 3) define the molecular mechanisms by which NIAM contributes to DNA damage checkpoints that normally protect our cells.
Muniz, V.P., Askeland, R.W., Zhang, X., Francis-Reed, S.M., Tompkins, V., McDowell, B.D., Button, A., Smith, B.J., Weydert, J., Mezhir, J.J., and Quelle, D.E.: Partner of ARF isoform 1A promotes oxaliplatin resistance in tumor cells and is a new marker of survival for resected pancreatic ductal adenocarcinoma patients. Manuscript submitted to Annals of Surgery.
Francis-Reed, S.M., Tompkins, V., Hagen, J., Cryderman, D.E., Wallrath, L.L. and Quelle, D.E. NIAM is a novel chromatin associated protein that activates p53 through Tip60 acetyltransferase. Manuscript in preparation for submission to Cell Cycle, December 2012.
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