B.A., University of Chicago, 1986
Ph.D., University of Chicago, 1996
phone: (336) 716-7078
“I have learned from my mentors that training young scientists is a responsibility that should not be taken lightly. I try to maintain a lab environment that encourages critical thinking and an open exchange of ideas. I will guide the people who work with me to develop experimental and analytical skills that will help them to become independent scientists, while they work together with me to accomplish the research goals of the lab.” Mechanisms of anti-tumor immunity
Research in the laboratory focuses on two main areas: 1) the use of molecular imaging techniques to follow cellular anti-tumor immune responses in vivo, and 2) prostate cancer biology.
Recently developed molecular imaging techniques provide biologists with the ability to detect cellular and molecular interactions within the environment of the intact living subject. The use of radioisotoic and optical whole-body imaging modalities in combination can provide a sensitive readout of cell movement in real time. We have previously demonstrated in a mouse tumor model, that the localization of T cells to the site of the tumor can be detected using PET (positron emission tomography) imaging. Our goal is to follow lineage-specific and activation dependent anti-tumor T cell responses in vivo, using PET and bioluminescent optical imaging techniques. A murine bone marrow reconstitution model is under development to visualize the development of primary and secondary immune responses. We will utilize it to study the kinetics of T cell localization to experimental prostate cancers. We anticipate that this system can also be used for studies of autoimmunity as well as responses against viruses and other pathogens.
We are studying the role of Prostate Stem Cell Antigen (PSCA) in the development and progression of prostate cancer. PSCA is a GPI-anchored cell surface protein that is expressed in a restricted set of human and murine tissues, and is overexpressed in approximately 50% of human prostate cancers and bone metastases, and in a subset of bladder and pancreatic cancers. We and others have shown that murine PSCA is also overexpressed in experimental prostate cancers. Recent data from our lab suggests that the loss of PSCA expression leads to increased incidence of prostate cancer metastasis in a mouse model of prostate cancer. In order to determine the molecular basis for the putative growth control exerted by PSCA, we are currently examining the signaling pathways in which PSCA may be involved, as well as attempting to identify binding partners for PSCA.