Abstract: The long-term goal of my research is to understand the mechanisms by which gene transcription is altered in disease states, focussing principally on breast cancer and during early development. To realise these goals, my colleagues and I use embryonic stem cells and breast cancer cell lines as model systems to study the mechanisms that govern regulated transcription from mammalian genes in response to endogenous and exogenous signals. Because of their widespread use in endocrine therapy, our work has placed an emphasis on the mode of action of steroid hormone receptors in response to natural ligands, as well as synthetic agonists and antagonists. We pay particular attention to the principles that permit the modulation of transcriptional responses via sequence specific binding of transcription factors. In this area, my research team has extensively studied the potential regulatory role of chromatin architecture in modulating the activity of these transcriptional effectors. In pursuing this line of investigation, I anticipate that discoveries with respect to the way gene transcription is altered in normal, and pathological states, will have implications for the deregulated control of gene expression that is characteristic of cancer. In today's lecture I will touch on both glucocorticoid regulation of transcription in breast cancer cells and functions of epigenetic enzymes in stem cell biology.
Sponsors: This lecture is sponsored by Office of the Vice President for Diversity, Equity, and Multicultural Affairs; Office of the Vice Provost for Faculty and Academic Affairs; Office of the Vice Provost for Research; College of Arts and Sciences; Department of Biology; and Medical Sciences Program.