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Mentor: Dawn Quelle, PhD
Year Entered Into Program: 2007 (MSTP) 2009 (PhD Program)
PhD Institution: University of Iowa, 2015 (MD, PhD)
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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