I started my lab at Genentech in 2010. This was immediately following a postdoctoral fellowship at UCSF, where I was working with murine models harboring functionally switchable proteins to assess, in vivo, the dependence of tumor initiation and maintenance on key oncogenes and tumor suppressors.
What attracted me to Genentech was the unique environment of extraordinary basic scientific discovery and research, combined with world-class translational expertise, truly bench-to-beside. The responsibility and opportunity to actively participate in improving the lives of patients drives the progress and innovation at Genentech. Such an environment provides both excitement and meaning to my research.
Nature, 2013, ISSN: 0028-0836
An adaptive, continuous and complex dialogue exists between tumor cells and their surroundings during cancer initiation and progression. The recapitulation of this dynamic interplay between tumor cells and host during disease progression represents a difficult challenge. In autochthonous tumor models lesions initiate within a tissue and evolves together with extracellular matrix, vascular endothelial cells, and immune cells, providing a unique opportunity for modeling such complexity.
My group’s responsibility is the development and application of genetically engineered murine models to pre-clinically inform oncology target selection and drug development. We are currently utilizing and creating murine tumor models of lung, pancreas, breast, melanoma, colorectal and prostate cancer. By employing models that faithfully represent the human pathologies, we interrogate the impact of investigational and approved therapeutics with the primary goal of understanding mechanism of action.
In addition to evaluating primary responses within these models, a large effort in the lab is to understand how the selective pressure of drug treatment influences the emergence of resistance, with the ultimate aim of identifying mechanisms that lead to relapse in patients.
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