Eric Snyder, MD, PhD
Pathobiology Prize, United States and Canadian Academy of Pathology (2009)
Burroughs Wellcome Career Award for Medical Scientists (2011)
NIH K08 Career Development Award (2011)
UCSF Program for Breakthrough Biomedical Research Award (2014)
Growing up in Painted Post, NY, I was blissfully ignorant of the world of biomedical research. Fortunately, my undergraduate advisor at Penn State suggested I give research a try, and I was immediately hooked. After graduation, I moved to St. Louis to pursue MD/PhD studies at Washington University. By this point, my research interests had solidified around the clinically compelling and intellectually fascinating problem of cancer. I pursued PhD studies on the p53 tumor suppressor protein with Dr. Steven Dowdy. This work included a brief detour to San Diego when Steve decided to move the lab halfway through my thesis. I then moved on to Boston for an Anatomic Pathology residency at Brigham and Women’s Hospital followed by a postdoctoral fellowship with Dr. Tyler Jacks at MIT.
During my clinical training, I learned to recognize the wide range of distinct identities, or differentiation states, that can be adopted by human tumors. As a postdoc in the Jacks lab, I used conditional murine genetics to dissect the molecular regulators of lung adenocarcinoma identity. I made the surprising observation that normal lung epithelial cells harbor a latent gastric differentiation program that can emerge during lung cancer progression. These clinical and research experiences inspired me to establish an independent research program to further investigate the molecular basis of cancer cell identity. The overall goal of my laboratory at the Huntsman Cancer Institute is determine how the loss of cellular identity and acquisition of alternative differentiation states contributes to cancer progression and alters therapeutic response. In the long term, we hope that studies in our lab will help lay the groundwork for the design of therapeutic strategies based on both targetable genetic mutations and intrinsic tumor differentiation state.