 My name is Joyce Schroeder. I'm a professor at the University of Arizona in the Arizona Cancer Center and Department of Molecular and Cellular Biology. We recently published a paper in OncoTarget called LGL1 Prevents Metaplastic Survival Driven by Epidermal Growth Factor Dependent Migration. This was a work performed by Erin Greenwood, who recently received her PhD in my laboratory. The work focuses on the role of a polarity protein called LGL1, also known as Hugga1. This is a polarity protein that's frequently lost in breast cancer. We previously showed that when this polarity protein is lost, breast epithelial cells gain a migratory capacity and lose their apical basal as well as planar polarity. This work was done to try to understand how LGL1 loss was accomplishing those phenotypes. The reason I'm interested in LGL1 and its role as a potential tumor suppressor in breast cancer comes from my interest in the role of polarity in general as a tumor suppressor. I've worked on the epidermal growth factor receptor most of my career and discovered that its localization and trafficking is altered dramatically during cancer progression. And so we wanted to try and understand the correlation between EGFR function and loss of polarity in epithelial cells. And what we discovered was upon loss of LGL1, EGFR does become mislocalized and it drives a number of cancerous phenotypes including increased migration, increased survival, and activation of the hippo pathway regulator TAS. So we know that TAS is a driver of breast cancer metastasis and a cancer stem cell phenotype. And we found that by loss of polarity through knockdown of LGL1 or by simply mislocalizing EGFR itself, we could drive activation of TAS and that we're driving it into the nucleus. So for me this is a very exciting discovery to tie together loss of polarity, EGFR, misregulation, and then activation of this cancer stem cell phenotype.