David Schlaepfer

Professor, Moores Cancer Center, UC San Diego Professor, Reproductive Medicine, UC San Diego

The Schlaepfer laboratory seeks to understand how cancers spread from their tissue of origin to other sites in the body. Key steps in this process are the acquisition of a motile phenotype and the ability of cancer cells to survive upon detachment from the primary tumor. Enhanced cell migration enables the cancer to invade into surrounding tissue or vasculature, and augmented cell survival enables cancer cell growth in other parts of the body.

Their research interests are focused upon the molecular signaling events that control cell migration and survival. They hypothesize that there are important intracellular signaling proteins that act to integrate and regulate both motility and survival signals within cells. One such integrator is focal adhesion kinase (FAK), an intracellular protein-tyrosine kinase that is associated with, and activated at, sites of integrin receptor binding to extracellular matrix proteins.

Elevated FAK expression has been correlated with increased tumor growth and spread. However, the molecular signaling connections of FAK in the processes of tumor progression remain unclear. Schlaepfer and his colleagues are using live-cell imaging, recombinant viral vectors, RNA interference, cell culture-based signaling, and mouse tumor growth and experimental metastasis assays to elucidate the molecular connections of FAK and other integrin-associated signaling proteins in the processes of tumorigenesis.

They believe that obtaining a better understanding of why cancer cells become invasive and how they move will aid the design of strategies that block this process and restrict the spread of cancer through the body.

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