Cancer genome sequencing has revealed hundreds of distinct mutations that drive tumorigenesis. In many tumor types, mutations frequently co-occur or are mutually exclusive, suggesting that certain pairs cooperate to improve cancer cell fitness while others are redundant or even incompatible. Moreover, specific signaling pathways that are activated by cancer-causing mutations have context-dependent effects that can promote cell transformation in some contexts and aggressive cancer phenotypes in later stages of tumor progression. The projects in this space are aimed at understanding these gene-gene and gene-environment interactions.

Here we use high-throughput in vivo screening and traditional mouse modeling approaches to elucidate cancer cell autonomous and non cancer cell autonomous dependencies. Please contact David to learn more about joining this team.