Primary Appointment

Our aim is to establish preventive therapy in high risk individuals that efficiently suppresses AP-1 activity due to estrogenic stimulation of mammary epithelial cells. A primary factor activated by estrogen is AP-1, a critical regulator of breast cell growth and invasion and a marker of poor prognosis in breast cancer. The goal of this proposal is to investigate how activation of the AP-1 transcription factor by estrogen regulates estrogen-regulated genes, mammary tumor development and breast cancer growth. Specifically, we will characterize the molecular environment and associated proteins required for the collaborative interaction of ER and AP-1, study the potential of a dominant negative AP-1 protein to suppress oncogene-induced mammary tumor formation and determine its tumor suppressive potential in vivo.

I have comprehensive background in molecular and cellular biology and completed postdoctoral training in cancer prevention research. In my postdoctoral position I have characterized the interaction of AP-1 with retinoid receptors to up-regulate the growth suppressive gene IGFPB6. At the Department of Clinical Cancer Prevention I am establishing a high content imaging facility which will greatly further our ability to perform quantitative cell based assays with multiparametric readouts. Such experiments are particularly suitable to characterize the interactions of distinct transcription factors, study their impact on gene expression and cell cycle on a cell-by-cell basis. Given the necessary expertise, and my interest in nuclear receptor biology and revealing novel mechanisms by which nuclear hormone receptors can be targeted to block cancer formation, I will contribute to the success of the proposed research.

Last updated: 2/7/2013