I earned a B.A. (with Distinction; Honors in Microbiology) from the U. of Kansas and the M.S. and Ph.D. in Medical Microbiology from the U. of Wisconsin, Madison. I completed an NIH Postdoctoral Fellowship in the laboratory of Dr. Julia Levy at the U. of British Columbia where I studied aspects of immune dysregulation associated with malignancy. I joined the Department of Immunology at the Michigan Cancer Foundation (now Karmanos Cancer Institute) as a Scientist and Assistant Professor in the Department of Pathology, Wayne State University School of Medicine. I was Chief of the Laboratory of Immunology and Associate Member at MCF until I joined the U. of Maryland as an Associate Professor of Pathology. I am currently Professor of Pathology with Tenure, a member of the Program in Oncology of the Marlene and Stewart Greenebaum Cancer Cancer, Leader of the Hormone Responsive Cancers Program, UMGCC and an Investigator of the Baltimore VA Medical Center. As a member of the Hormone Responsive Cancers Program of the Greenebaum Cancer Center, I collaborate with both clinical and basic research investigators to develop innovative approaches to diagnose, treat and prevent breast and prostate cancer. My research centers on dissecting the role of inflammatory pathways in the promotion of cancer progression.
Breast cancer; mechanisms of metastasis; inflammation; immune therapy
My laboratory is interested in identifying the mechanisms by which breast cancers grow and metastasize and in developing therapeutic strategies against breast cancer. Our goal is to understand the role of inflammation in promoting tumor progression. We have shown that overexpression of cyclooxygenase-2 is an indicator of aggressive disease and preclinical studies indicate that cyclooxygenase inhibitors limit tumor growth and spread. We have shown that specific targeting of the COX-2 pathway at the level of prostaglandin E receptor EP4 avoids the potential toxicities of COX-2 inhibition while preserving anti-metastatic activity. Recently we have shown that breast cancer stem-like cells with heightened tumorigenic potential and a treatment resistant phenotype have elevated levels of EP4 and are more sensitive to inhibition by EP4 antagonists than the non-stem cell population. These findings have led to the design of a clinical trial to examine efficacy of an EP4 antagonist in advanced malignancy. We have also discovered that the chemokine receptor CXCR3 promotes metastasis. CXCR3 ligands can promote or inhibit tumor growth and metastasis depending on levels of ligand expression. Current studies examine mechanisms by which cyclooxygenase inhibitors enhance anti-tumor immunity. We are also investigating how cytokines and chemokines and their specific receptors modify tumor behavior. We have identified therapeutic activities for several cytokines and are developing strategies to inhibit chemokine receptors that promote tumor metastasis. Working with Dr. Kundu, we have identified a novel and potent inhibitor of metastasis isolated from the Taro plant. Current studies are designed to identify the active moiety and to discern the mechanism of action.