Archive for category: Current Members

Our lab focuses on investigating the molecular mechanisms that drive normal breast development and how these processes become disrupted in cancerous tissue. More specifically, we are interested in the role of stem and progenitor cells in both normal and carcinogenic development, especially the molecular drivers of breast epithelial differentiation. Previous work recently established the transcription factor Slug (SNAI2) as a luminal differentiation suppressor. My project seeks to determine the effect of aging on mammary progenitor cells, specifically in regard to the role of Slug as a regulator of breast epithelial differentiation. I am also working to show that this transcription factor may also have a novel function as an RNA binding protein.

Raymond and Beverly Sackler Fellow

Breast tumors and other solid cancers do not exist in a vacuum and is a disease composed not only of cancer cells, but also the surrounding stromal cells making up the tumor microenvironment. My research interests are focused on the role of the surrounding fibroblasts in modulating the rigidity of the tumor microenvironment and its contribution to the promotion and progression of breast cancer.

American Cancer Society Postdoctoral Fellow
B.S. Biology, Yale University
Ph.D. Genetics, Yale University

Project Title: “Functional Investigation of the Long Tail Drivers of Human Breast Cancer”

Cancer exome sequencing has revealed that 20% of cancers lack mutations in even a single known or putative driver gene, indicating that we must look to the “long tail” distribution of mutated genes in order to complete our knowledge of cancer genetics. Since it is currently unknown how long tail drivers impact the proliferative pathways commonly deregulated in cancer, the investigation of these drivers is of central importance for basic and translational cancer research. Throughout my doctoral and postdoctoral work, I have pioneered genetic technologies to identify long tail drivers. These early works have served as the foundation for my current focus, which is to ask how such drivers mechanistically cause the dysfunction of major proliferative signaling pathways in order to promote transformation and tumorigenesis.

MD-PhD Trainee

B.S University of California, Davis

Basal-like breast cancer (BLBC) is an aggressive breast cancer subtype for which there is currently no effective targeted treatment. Our lab previously identified the transcriptional repressor Slug is frequently overexpressed in BLBC, and Slug is an important regulator of luminal differentiation. I carried out a chemical screen to identify potential homeostatic regulator(s) of Slug protein. In doing so, my goal is to pinpoint druggable regulators for developing rational therapeutic strategies to molecularly dampen Slug hyperactivity, and ultimately improve our abilities to treat and improve outcome of patients diagnosed with BLBC.