My laboratory is interested in the relationship of hyperplastic growth with malignant breast tumor formation. A fundamental GAP in our understanding of the natural history of breast cancer development is the lack of a molecular basis that explains how the loss of cellular differentiation underlies the desensitization of cells to the growth inhibitory influences of the microenvironment. My laboratory has found evidence that such events are strongly influenced by alterations in the signaling pathways that mediate the cross-talk between “polarity” proteins and core pathways involved in cell proliferation. In particular, we are focused on how the differential expression of the Amot family of adaptor proteins mediates the balance between growth arrested and differentiated ductal epithelia with highly proliferative and de-differentiated carcinomas. Our long term goal is to use such information to identify histologically significant markers that indicate whether normal appearing or hyperplastic tissues are likely to develop malignant carcinomas.


Biochemistry, Molecular Biology, Oncology, Cellular Biochemistry, Molecular Biochemistry
PhD, University of Texas Southwestern Medical Center at Dallas, Cell and Molecular Biology, 2001
BS, University of Kentucky, Biology, 1993