Jenifer Prosperi, Ph.D.
1234 Notre Dame Ave.
A134 Harper Hall
South Bend, IN 46617
Phone: (574) 631-4002
Research Program Membership
Indiana University School of Medicine-South Bend
Previous studies have indicated that the adenomatous polyposis coli (APC) tumor suppressor gene is mutated or silenced by hypermethylation in 18-70% of sporadic breast cancers depending on subtype; however, the molecular mechanisms downstream of APC loss remain unexplored. Using transgenic mouse models, we demonstrated that Apc mutation promotes Polyoma middle T antigen (PyMT)-mediated breast tumorigenesis independently of Wnt/??-catenin signaling. Interestingly, focal adhesion kinase (FAK)/Src/JNK signaling was required for the enhanced proliferation mediated by Apc mutation. Remarkably, Apc loss was sufficient to change the tumor histopathology from solid to squamous adenocarcinomas, which resembled metaplastic breast cancer, a highly aggressive breast cancer subtype. We are currently focused on two projects: 1. Delineation of the mechanism by which APC loss hyper-activates signaling through FAK/Src/JNK, and the subsequent downstream effect of this enhanced signaling. 2. How APC loss in mammary tumor cells impacts responsiveness to chemotherapeutic agents.
Post-doctoral Fellowship - University of Chicago, Chicago, IL 2007-2012
Ph.D. - The Ohio State University, Columbus, OH 2006