Aaron Hobbs, Ph.D.

RAS family small GTPases have been my top research interest since I began graduate school. Constitutively active RAS family GTPases are involved in numerous cancers, and RAS has been considered “undruggable” for decades. While the “undruggable” veneer has finally been shattered, developing effective RAS-targeted therapies remain a top priority in the cancer field. My studies on RAS can be grouped into two themes. First, I have extensive experience examining the role of thiol oxidation on modifying the biochemical properties and signaling of KRAS and RAS superfamily GTPases. Second, utilizing KRASG12R as a model, I demonstrated that all RAS mutations are not created equal. KRASG12R is present in approximately 15% of pancreas cancer patients yet is rare in other cancers. Pancreatic cancer has a low five-year overall survival rate of 11%, which highlights a clear need for effective therapeutic strategies. My research contributions describing mutation-specific signaling have shifted the paradigm in the RAS field, definitively showing a role for mutant-specific effector signaling and highlights my overall research objective, developing mutation-selective therapies for RAS-mutant cancers.