Dr. Sears received her Bachelor’s degree in Biology from Reed College (1986), Portland Oregon. She received her Ph.D. in Cell Biology from Vanderbilt University (1993), Nashville Tennessee, and conducted her post-doctoral studies at Duke University in the Genetics Department. Dr. Sears is a full professor in the Department of Molecular and Medical Genetics at Oregon Health & Science University. She is Co-Director of the Brenden-Colson Center for Pancreatic Care and a senior member in the Knight Cancer Institute. Dr. Sears has received funding from the National Institutes of Health, the Department of Defense, the Susan G. Komen Foundation, the Leukemia and Lymphoma Foundation, as well as several other private foundations. She has received both research and business innovation awards in the areas of cancer biology, therapeutics, and technology advancement.

The Sears lab studies cellular signaling pathways that control tumor cell behavior, with a focus on their convergence on the c-Myc oncoprotein and how this impacts Myc’s expression, activity, and its regulation of cell fate. Myc is constitutively overexpressed in the majority of human tumors and studies have demonstrated that this affects both tumor cell state (proliferation, differentiation, metabolism) as well as cross-talk with the tumor microenvironment affecting immune surveillance and vasculature. Dr. Sears’ work has identified a complex signaling pathway that coordinately post-translationally regulates c-Myc’s DNA binding and transcriptional activity with its turnover via ubiquitin-mediated proteolysis and she has demonstrated that c-Myc is post-translationally stabilized with increased activity in the majority of human tumors. The Sears lab has modeled post-translational activation of c-Myc in genetically engineered mice, where they have developed accurate mouse models of human breast and pancreatic cancer. Dr. Sears’ lab is pursuing new therapeutic strategies to target Myc by reversing its post-translational activation. This work has lead to the development of a new small molecule activator of the tumor suppressor phosphatase PP2A. This drug is orally available and has demonstrated dramatic inhibition of tumor growth and significant extension of survival in mouse breast and pancreas cancer models.